Professional Documents
Culture Documents
Notice
Knowledge and best practice in this eld are constantly changing. As new research and experience broaden
our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate.
Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or formula, the method
and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on
their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of
the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or
property arising out of or related to any use of the material contained in this book.
The Publisher
Printed in Canada
Larry P. Tilley
Mark A. Oyama
To Dave, whose support enables my dreams; and my father, who inspired them.
Meg M. Sleeper
Contributors
vii
viii Contributors
Virginia Luis Fuentes, MA, VETMB, PhD, Marc S. Kraus, DVM, DACVIM
CertVR, DVC, DACVIM (Cardiology), (Cardiology and Internal Medicine)
DECVIM-CA (Cardiology), MRCVS Lecturer
Senior Lecturer in Small Animal Medicine Department of Clinical Sciences
Veterinary Clinical Sciences College of Veterinary Medicine
Royal Veterinary College Cornell University
Hatfield, United Kingdom Ithaca, New York
Echocardiography and Doppler Ultrasound Treatment of Cardiac Arrhythmias and Conduction
Disturbances
Anna R. M. Gelzer, Dr.med.vet., DACVIM
(Cardiology) Elizabeth A. McNiel, DVM, PhD,
Assistant Professor DACVIM (Oncology), ACVR
Department of Clinical Sciences (Radiation Oncology)
College of Veterinary Medicine Assistant Professor
Cornell University Department of Veterinary Clinical Sciences
Ithaca, New York College of Veterinary Medicine
Treatment of Cardiac Arrhythmias and Conduction University of Minnesota
Disturbances St. Paul, Minnesota
Pericardial Disorders and Cardiac Tumors
Rebecca E. Gompf, DVM, MS, DACVIM
(Cardiology) Sydney Moise, DVM, MS, DACVIM
Associate Professor of Cardiology (Cardiology and Internal Medicine)
Department of Small Animal Clinical Sciences Professor of Medicine, Section Chief Cardiology
University of Tennessee Department of Clinical Sciences
College of Veterinary Medicine College of Veterinary Medicine
Knoxville, Tennessee Cornell University
The History and Physical Examination Ithaca, New York
Treatment of Cardiac Arrhythmias and Conduction
Rosemary A. Henik, DVM, MS, DACVIM Disturbances
(Internal Medicine)
Clinical Associate Professor E. Christopher Orton, DVM, PhD, DACVS
Department of Medical Sciences Professor
University of Wisconsin Madison Department of Clinical Sciences
Madison, Wisconsin Veterinary Medical Center
Systemic Hypertension Colorado State University
Fort Collins, Colorado
Lynelle R. Johnson, DVM, PhD, DACVIM Cardiac Surgery
(Internal Medicine)
Assistant Professor Mark A. Oyama, DVM, DACVIM
Department of Veterinary Medicine and Epidemiology (Cardiology)
College of Veterinary Medicine Associate Professor
University of CaliforniaDavis Department of Clinical Studies
Davis, California School of Veterinary Medicine
Cor Pulmonale and Pulmonary Thromboembolism University of Pennsylvania
Philadelphia, Pennsylvania
Richard D. Kienle, DVM, DACVIM Canine Cardiomyopathy
(Cardiology) Appendix 2: Common Cardiovascular Drugs
Staff Cardiologist
Bay Area Veterinary Specialists Brian A. Poteet, MS, DVM, DACVR, ABSVM
San Leandro, California; Director,
Owner Gulf Coast Veterinary Diagnostic Imaging
Mission Valley Veterinary Cardiology Gulf Coast Veterinary Specialists
Gilroy, California Houston, Texas
Feline Cardiomyopathy Radiology of the Heart
Contributors ix
In the last 5 years there have been a number of field of canine and feline cardiology. The fourth edi-
excellent textbook chapters and journal articles tion has been carefully revised, edited, and updated
describing new findings in the field of canine and to reflect the latest technologies and approaches to
feline cardiology. However, for the practicing vet- cardiac care.
erinarian and veterinary student, the amount of The methods of diagnosis of heart diseases in the
information is overwhelming. Many veterinarians dog and the cat are described in Section I The first
and students have stated, in past surveys, the diffi- five chapters follow the sequence that the veterinar-
culty in keeping up with cardiovascular advances in ian uses in approaching the patient. Chapter 1 cov-
the most time-effective way. The Manual of Canine ers the history and physical examination; Chapter
and Feline Cardiology, now in its fourth edition, has 2, radiology of the heart; Chapter 3, electrocardi-
been updated to continue to meet the need for a cur- ography; Chapter 4, echocardiography and Doppler
rent textbook that can provide useful and practical ultrasound; and Chapter 5, special diagnostic tech-
information on cardiac disease in the dog and cat. niques for evaluation of cardiac disease.
We have worked hard to make this book a most reli- Section II presents in a step-by-step fashion a
able source for practicing cardiovascular medicine description of the various cardiac disorders that oc-
in the dog and cat. For the new edition, we have cur in the dog and cat, starting in each chapter with
expanded the number of contributors, with each general considerations (e.g., definitions, incidence,
chapter written by an expert. We have also worked pathophysiology, etiology), history, physical exam-
to conserve reading time by using an easy-to-use ination, electrocardiography, thoracic radiography,
format. The Manual of Canine and Feline Cardiol- special diagnostic techniques, differential diagno-
ogy, Fourth Edition, is unique as a quick reference sis, and finally, the therapeutic approach.
with consistency of presentation. The new edition Section III includes chapters describing the
now also has generous use of figures and charts, treatment of cardiac failure, treatment of arrhyth-
with many in color. mias and conduction disturbances, and two sepa-
This practical approach to the diagnosis and rate chapters on cardiopulmonary arrest and resus-
therapy of cardiac disease will be useful to a wide citation and on emergency management and critical
audience, from the veterinary student to the fully care in cardiology. Chapters on anesthesia of the
trained cardiologist. The approach is largely clini- cardiac patient, cardiac surgery, and pacemaker
cal and includes the practical as well as the most therapy complete this section.
sophisticated methods for diagnosis and therapy. Appendix 1, Canine Breed Predilections for
Cardiovascular disorders in the dog and cat Heart Disease, represents the most current listing
represent a substantial portion of diseases seen of breed-associated cardiac disorders.
in the average veterinary practice. It is important Appendix 2 is a cardiopulmonary drug formu-
for veterinary students and practitioners to under- lary that contains extensive cardiopulmonary drug
stand the principles of diagnosis and treatment of tables with indications, dosages, side effects, con-
the numerous cardiovascular disorders. New chap- traindications, and drug interactions. An extraordi-
ters that have been added include cardiac surgery, nary array of new cardiovascular drugs has become
cor pulmonale, pulmonary thromboembolism, and available, and both students and veterinarians have
pacemaker therapy. A table of canine breed pre- difficulty deciding which drugs from various drug
dilections for heart disease has been added to the classes should be prescribed.
appendixes. Appendix 3, Echocardiographic Normals, is
Since the third edition of this textbook was pub- an easy-to-refer-to list of normal values by body
lished, there has been tremendous growth in the weight and breed.
xi
xii Preface
The Manual of Canine and Feline Cardiology, as a reference for the advanced student and the vet-
Fourth Edition, will help to eliminate the aura of erinarian with expertise in cardiology.
mystery that surrounds the diagnostic and thera-
peutic principles of veterinary cardiology. The Larry P. Tilley
teaching principles that are presented will allow Francis W. K. Smith, JR.
even the novice to make an intelligent assessment Mark A. Oyama
of a cardiac case. This manual will be useful to a Meg M. Sleeper
wide audience, but comprehensive enough to serve
Acknowledgments
The completion of this manual provides a welcome much you know until they know how much you
opportunity to recognize in writing the many indi- care. That saying was Johns philosophy and one
viduals who have helped along the way. All authors that all of us should follow.
have board certification and are uniquely qualified Finally, a special thank you goes to Tony Winkel,
to give an update or review of their respective dis- Editor, Elsevier, whose vision and support were
ciplines. critical for this fourth edition. The unique format
In addition to thanking veterinarians who have and use of numerous images demonstrates the edu-
referred cases to us, we would like to express our cational vision he had. For this edition, we would
gratitude to each of the veterinary students, interns, also like to thank Shelly Stringer, Developmental
and residents whom we have had the pleasure of Editor and the rest of the Elsevier staff, including
teaching. Their curiosity and intellectual stimula- everyone in the Production Department. They are
tion have enabled us to grow and prompted us to all meticulous workers and kind people who made
undertake the task of writing this manual. the final stages of preparing this book both inspir-
The last edition was co-edited by John Karl ing and fun.
Goodwin, and since then he has unfortunately
passed away. Johns teaching principles in vet- Larry P. Tilley
erinary medicine were clearly drawn from clinical Francis W. K. Smith, JR.
experience, and this edition continues to maintain Mark A. Oyama
that focus. I will always remember what John had Meg M. Sleeper
posted on a wall at his office: No one cares how
xiii
SECTION I
Introduction
Medical History
Despite the technical nature of many cardiovascu-
Signalment
lar diagnostics, such as electrocardiography and
echocardiography, the history and physical exami- Age
nation remain the most crucial steps in establish- Young animals usually present with congenital
ing the correct diagnosis. Findings from a careful diseases (e.g., patent ductus arteriosus [PDA]),
history and physical examination prompt the clini- whereas older animals usually present with ac-
cian to the probability or presence of heart disease. quired diseases, such as degenerative diseases
Results of the cardiovascular physical examination (e.g., mitral and tricuspid regurgitations) or neo-
will usually allow the clinician to make a tentative plastic diseases (e.g., heart base tumor). Excep-
diagnosis or formulate a specific differential diag- tions can occur because cardiomyopathies can
nosis. The history and physical examination also occur in young dogs and cats (aged 6 months
provide important information regarding the stage oryounger), and older dogs can have congeni-
of heart disease present, which may significantly tal heart defects that were not diagnosed when
impact therapy. theywere young (e.g., PDA, atrial septal de-
A good history and physical exam are invalu- fect). Also, cardiac disease in older animals can
able in making a diagnosis of heart disease and be modified or affected by other concurrent dis-
helping to differentiate heart disease from pul- ease processes (e.g., collapsing trachea, renal or
monary disease. liverdisease).
Besides helping to make the diagnosis, a good
history and physical exam help to tell the extent Breed
of the problem, how well the animal is respond- Certain cardiac defects are more common in some
ing to previous therapy, if the owner is able to breeds of animals; however there can be a regional
medicate the animal consistently, and if other difference in the rate of occurrence of cardiac prob-
medical problems are present. lems. See Appendix for a summary of some of the
cardiac defects found in certain breeds of dogs and
cats.
Key Point
Clinicians should do a thorough history and Sex
physical exam in order to properly diagnose Males are more susceptible to certain cardiac dis-
and treat an animal with heart disease. eases (e.g., male cocker spaniels to endocardiosis
of the mitral valve, and large-breed males to dilated
Chapter 1 The History and Physical Examination
cardiomyopathy). However, sick sinus syndrome It will also define the animals attitude and be-
occurs in the female miniature schnauzer and PDA havior by asking if the animal is listless and
is more common in females than in males. depressed or alert and playful. Does the animal
tire easily with exercise?
Weight It covers the family history of the siblings and
The animals weight influences several aspects of parents, especially if congenital disease is present
treatment including the dose of cardiac medication in the patient.
to use, evaluation of the response to diuretic medi- It will ask about the health of other pets in the
cation, and the monitoring of cardiac cachexia. A household.
Pickwickian syndrome (characterized by severe It includes the results of previous tests done on
obesity, somnolence, and hypoventilation) can oc- the patient.
cur in an animal that is so obese that its ability to It covers other relevant information that may help
breathe is restricted. to identify the patients problem(s), such as what
and how much is being fed and the patients ap-
Utilization of the Animal petite and water consumption. How frequently is
It is important to know how an animal is going to the animal urinating, and does it have any diar-
be used when giving a long term prognosis for a rhea? Does the patient have any vomiting or re-
cardiac disease. For example, hunting dogs with gurgitation? Has the patient had any seizures or
severe heartworm disease may not be able to hunt syncopal episodes? What is the patients repro-
again after treatment. Also, some animals with con- ductive status? Does the patient have any lame-
genital heart defects may have normal life spans ness or paresis? Is the patient coughing, sneezing,
and may make good pets; however, they should not or having difficulty breathing? Has the patient
be used for breeding purposes, because the defect had any previous trauma? Where is the animal
could be perpetuated. housed (e.g., indoors, outdoors, fenced-in yard)?
It includes information about other diseases such
as hyperthyroidism, chronic renal disease, respi-
ratory diseases, or other diseases that can also af-
Key Point fect the heart or can affect how the animals heart
The age, breed, and sex of the animal may disease is treated.
help the clinician to make an accurate diag- Once a problem is identified, more specific ques-
nosis; however, there are always exceptions tions can be asked such as the character of a
to every rule, so a clinician should not ignore cough, when the cough occurs, and stimuli evok-
the fact that an animal could have an atypical ing the cough.
problem for its age, breed, or sex. Common presenting complaints for cardiac dis-
ease include dyspnea or tachypnea, coughing,
exercise intolerance, syncope, abdominal swell-
ing, cyanosis, anorexia or decreased appetite, and
History
poor growth or performance.
A good history will establish the presence of a Other symptoms can be associated with cardio-
cardiac problem, help to differentiate between vascular disease. Polydipsia and polyuria are
cardiac and respiratory problems, and help to common in animals on diuretics or that have a
monitor the course of the disease and the re- concurrent disease (e.g., renal disease), whereas
sponse to therapy. It must be done carefully oliguria occurs with severe left-heart failure. He-
to prevent an owner from giving a misleading moglobinuria is found with the postcaval syn-
history. drome of heartworm disease.
It includes several key questions such as the rea- Cardiac drugs such as digitalis, quinidine, and
son the animal is being presented, the problems procainamide can cause vomiting and diarrhea.
noted by the owner, the onset and duration of the Regurgitation occurs with congenital vascular
problem(s), the progression of the disease, any ring anomalies. Right-heart failure can cause in-
known exposure to infectious diseases, vaccina- testinal edema and a protein-losing enteropathy
tion history, any current medications the animal resulting in diarrhea. Cats with cardiomyopathy
is receiving, the animals response to any medica- can develop hemorrhagic enteritis secondary to
tions that have been given, and the owners ability thromboembolism of the gastric or mesenteric
to give the medication(s). arteries.
Section I Diagnosis of Heart Disease
Table 1-1 Characteristics of Coughs and Their Associated Causes in Dogs and Cats
Type of Cough Causes
Acute cough Tonsillitis, pharyngitis, tracheobronchitis, acutebronchitis,
pleuritis, acute left heart failure (dogs)
Chronic cough Right or left heart disease, heartworms, enlarged left
atrium compressing the left mainstem bronchus (dog
only), pulmonary neoplasia, asthma (cat only), chronic
respiratory problem, chronic bronchitis (dog only)
Acute onset, soft that rapidly becomes Pulmonary edema
worse in dogs with dyspnea
Mild, intermittent cough, harsh, low Chronic heart disease
pitched in dogs
Loud, harsh, dry, sudden onset followed Tracheobronchitis
by gag in dogs
Honking, high-pitched in dogs Collapsing trachea or bronchi
Chronic, paroxysmal, loud, honking Large airway disease
with excitement in dogs
Cough after drinking in dogs Cardiac disease, collapsing trachea, chronic tracheitis,
tracheobronchitis, laryngeal paralysis, dysphagia
Cough after eating in dogs Pharyngeal dysfunction, megaesophagus, vascular ring
anomalies, esophageal diverticula, esophageal foreign
bodies, esophageal tumors
Cough without an inciting factor Cardiac, pulmonary, or extrapulmonary disease
Chapter 1 The History and Physical Examination
Key Point
back up quickly, and are normal before and after
Hemoptysis is a sign of a very serious underly-
ing abnormality in the lungs, which may be the syncopal episode.
caused by either a severe cardiac or respira- Box 1-3 lists the causes of syncope in dogs and
tory problem. cats.
In a dog with no other cardiac problems, syncope
may be associated with severe bradycardias (e.g.,
third degree heart block or sick sinus syndrome),
Syncope
or with marked sustained tachycardias (e.g., atrial
Syncope is a loss of consciousness due to inad- or ventricular tachycardias), which are usually
equate cerebral blood flow. It can reoccur and is paroxysmal (i.e., they come and go).
usually brief. Small dogs with chronic, severe mitral regurgita-
Syncope can be hard to differentiate from sei- tion that cough when they get excited can have
zures. Animals usually fall over suddenly, get syncopal episodes.
Chapter 1 The History and Physical Examination
Box 1-3 Causes of Syncope in Dogs and Box 1-4 Causes of Weakness and
Cats Exercise Intolerance
Disease with very poor cardiac output (e.g., dilated Cardiac disease with myocardial dysfunction (e.g.,
cardiomyopathy) dilated cardiomyopathy)
Severe bradycardia (e.g., complete heart block, sick Cardiac disease with obstruction to left ventricular
sinus syndrome) outflow (e.g., subaortic stenosis, hypertrophic
Severe sustained tachycardias (e.g., atrial or ventri obstructive cardiomyopathy)
cular tachycardia) Decreased arterial oxygen (e.g., pulmonary edema,
Severe hypertrophic cardiomyopathy in cats pleural effusion or other pulmonary diseases)
Systemic hypotension including arteriolar dilator Inadequate ventricular filling (e.g., arrhythmias, peri-
therapy cardial diseases)
Severe pulmonary hypertension Drug toxicities
Severe subaortic stenosis Severe anemia
Severe pulmonic stenosis Severe metabolic disease
Small dogs with severe mitral regurgitation that Severe respiratory diseases
cough when excited Severe systemic diseases
Tetralogy of Fallot
Ascites
Weakness and Exercise Intolerance
Ascites is an accumulation of fluid in the
Weakness and exercise intolerance are nonspe- abdomen.
cific signs of heart disease. Many diseases such Ascites caused by cardiac problems is either
as severe anemia, systemic diseases, metabolic due to the right heart being unable to pump the
diseases (e.g., hyperadrenocorticism), drug tox- blood presented to it or because of pericardial
icities, and severe respiratory diseases can cause disease, in which the blood cannot get into the
these signs. See Box 1-4 for causes of weakness right heart. In either case the blood accumulates
and exercise intolerance. in the liver and spleen and causes congestion
Because most animals do not exercise very hard, and increased venous pressure. Eventually fluid
weakness and exercise intolerance are uncom- leaks out of the capsule of the liver causing the
mon presenting complaints. Some owners think ascites.
Section I Diagnosis of Heart Disease
Ascites is seen more frequently with right-heart Box 1-5 Causes of Ascites in the Dog
failure in dogs due to acquired diseases (e.g.,
tricuspid regurgitation due to endocardiosis, ad- Advanced heartworm disease
vanced heartworm disease, dilated cardiomyopa- Dilated cardiomyopathy
thy, pericardial effusions, restrictive pericarditis) Large atrial septal defect
Large ventricular septal defect
and congenital heart defects (e.g., tricuspid dys- Pericardial effusion
plasia, large ventricular septal defect, large atrial Restrictive pericarditis
septal defect). See Figure 1-1 for an example of Tricuspid dysplasia
ascites and Box 1-5 for a list of causes of ascites Tricuspid regurgitation due to endocardiosis
in the dog.
Ascites is less common in cats and is usually
due to tricuspid dysplasia but occasionally can
be seen with other problems such as dilated Cyanosis is a very insensitive way of detecting
cardiomyopathy. hypoxemia in dogs and cats because the oxy-
Large amounts of ascites will put pressure on the gen saturation has to be very low to cause it and
diaphragm, resulting in tachypnea or dyspnea. animals have darker mucous membranes, which
Ascites associated with right-heart failure is makes cyanosis harder to detect until it is severe.
usually a modified transudate and accumulates Right-to-left shunting cardiac defects such as
slowly. tetralogy of Fallot result in low oxygen satura-
tion plus high deoxygenated hemoglobin levels,
Key Point which make affected animals cyanotic. These pa-
Decompensated heart diseases that result in tients also have polycythemia, and the increased
ascites may not have an associated murmur number of red blood cells has increased amounts
(e.g., pericardial effusion, some dilated cardio- of reduced hemoglobin, which contributes to the
myopathies, heartworm disease). Thus, any cyanosis.
time ascites occurs, right-heart failure must be Cyanosis gets worse with exercise because the
included in the differential diagnosis. peripheral vascular resistance will decrease while
the pulmonary vascular pressure is unchanged
so more deoxygenated venous blood will go
Cyanosis
systemically.
Cyanosis is blue-tinged mucous membranes
of the gums, tongue, eyes, ears, and so on and Key Point
is associated most commonly with right-to-left
shunting congenital heart defects. Occasionally it Cyanosis is a very late finding in severe car-
diac disease, except in right to left shunting
is seen with severe left-heart failure or severe re-
congenital heart defects, and so it is an in-
spiratory disease. It is rarely seen with abnormal sensitive indicator of membrane oxygenation
hemoglobin production. and cardiac function.
Weight Loss
Weight loss occurs in dogs with chronic, severe
right-heart failure (e.g., severe tricuspid regurgi-
tation, dilated cardiomyopathy, advanced heart-
worm disease).
Weight loss in cats is usually associated with
hyperthyroidism or infiltrative bowel disease, al-
though cats with chronic right-heart failure can
also lose weight.
Cardiac cachexia is the loss of total body fat and
lean body mass, especially skeletal muscle, de-
spite a normal appetite and adequate therapy for
Figure 1-1. Notice the severe ascites in this dog with right-
heart failure due to severe pulmonic stenosis and severe tri- the underlying heart disease. It can be a rapid
cuspid dysplasia. loss of body condition in some dogs with dilated
Chapter 1 The History and Physical Examination
cardiomyopathy (Figure 1-2). See Box 1-6 for a Box 1-6 Problems Contributing to Cardiac
list of the problems that contribute to cardiac ca- Cachexia in the Dog
chexia in dogs.
Weight loss is associated with: Ascites
Ascites. Dogs with ascites may have mild discom- Cardiac medications causing anorexia and vomiting
fort from the fluid which makes them reluctant Electrolyte imbalance causing anorexia
to eat. Also, the ascites and congested liver will Increased energy use by the body
compress the stomach so that the animal feels Increased tumor necrosis factor
Malabsorption
full after eating only a small amount of food. The
Maldigestion
fluid also restricts gastric emptying. Finally, if an Protein losing enteropathy
unpalatable diet is fed, the animal is even more
reluctant to eat and does not consume enough
calories to keep from losing weight.
Malabsorption caused by the congestion of the
intestines secondary to the ascites.
Congestion of the pancreas, which may decrease
its function of secreting enzymes for digestion,
resulting in maldigestion.
Systemic venous and lymphatic hypertension
from right-heart failure causing a secondary in-
testinal lymphangiectasia that results in a pro-
tein-losing enteropathy.
Increased effort to breath and increased myocar-
dial oxygen consumption that result from the de-
creased cardiac output. These two problems result
in an increased use of energy and therefore calories
by the heart and lungs. The activation of the sym-
pathetic nervous system, which also results from
the decreased cardiac output, causes increased en-
ergy use by the rest of the body.
Use of cardiac medications such as digoxin, mex-
iletine, quinidine, procainamide, diltiazem, and
occasionally other drugs that can cause anorexia
and/or vomiting. Digoxin also has a direct effect
on the small bowel, where it inhibits sugar and
amino acid transport.
Electrolytes, especially sodium and potassium,
are adversely affected by diuretics, angiotensin
converting enzyme inhibitors, and digoxin. When
Key Point
Weight loss and cardiac cachexia are due to
multiple factors. It is very important to make
sure that an animal with ascites is being treat-
ed appropriately for heart failure and that the
animals digoxin levels, electrolytes, and renal
function are being monitored. It is also impor-
tant to calculate the animals caloric require-
ment and make sure it is eating enough to
meet its requirements. Special high caloric di-
ets and multiple small meals may be needed to
insure adequate caloric intake. Appetite stimu-
Figure 1-2. Great Dane with cardiac cachexia secondary to lants have been tried with varying success.
dilated cardiomyopathy.
10 Section I Diagnosis of Heart Disease
potassium levels are abnormal, they contribute to dilated left atrium or left ventricle, and pieces
anorexia. break off and lodge in the distal aorta or other
Dogs with chronic congestive heart failure have artery. When the thrombus lodges in the aortic
increased tumor necrosis factor that inhibits the bifurcation, the cat will exhibit severe pain in
activity of lipoprotein lipase (hydrolyzes chylo- the first few hours after the embolism and the
microns) and therefore interferes with the con- distal limbs will be cold and may be slightly
version of triglycerides to free fatty acids. swollen. The pads on the rear feet will be cya-
notic (Figure 1-5). The cats pulses cannot be
detected, and the nails on the affected legs do
Paresis
not bleed when cut short.
Cats with acute, posterior paresis (Figure 1-3) Acute, posterior paresis is rare in dogs but it has
or paresis of one front leg (Figure 1-4) often been associated with emboli from severe, vegeta-
have thromboembolism secondary to cardio- tive endocarditis of the aortic or mitral valve.
myopathy. The thrombi tend to form in the Shifting leg lameness in dogs has also been as-
sociated with bacterial endocarditis.
Key Point
Paresis in the rear limbs of the cat is usually
due to emboli that form in the left atrium sec-
ondary to left atrial enlargement secondary
to cardiomyopathies. Shifting leg lameness
or posterior paresis in the dog can be due to
emboli from vegetations on either the mitral
or aortic valve.
Figure 1-3. Cat with a saddle thrombus secondary to a left Physical Examination
atrial thrombus due to hypertrophic cardiomyopathy.
Observation
The animals attitude and behavior can give clues
as to the severity and kind of problems that the
animal is having. It is important to note whether
the animal is depressed or alert, and listless or
active.
An animal that refuses to lie down may have Hypertension in cats will cause decreased pu-
severe pulmonary edema, pleural effusion, peri- pillary responses due to retinal detachment or
cardial effusion, pneumothorax, diaphragmatic hemorrhage. Also, a fundic exam may reveal pap-
hernia, or respiratory disease (Box 1-7). illedema (swelling of the optic disc) along with
An animal that stands with elbows abducted and hemorrhage or retinal detachment.
head extended as well as open-mouth breathing Retinal hemorrhages also can occur with polycy-
with flared nostrils has severe respiratory distress themia and bacterial endocarditis.
and needs immediate therapy. Central retinal degeneration occurs in about one
The rate and rhythm of respirations can help de- third of cats with dilated cardiomyopathy caused
termine the underlying problem. Tachypnea and by taurine deficiency. The areas of degeneration
panting are usually due to excitement; however, are horizontal, linear, and hyperreflective.
expiratory dyspnea usually indicates lower air- The ears have no significant changes associated
way disease, and inspiratory dyspnea usually in- with the cardiovascular system.
dicates upper airway disease. Cyanosis can sometimes be recognized by evalu-
The nature and type of coughing is helpful if it ating the color of the pinna.
occurs during the course of the physical exam. Examine the nose for signs of disease and for
The presence of dependent ventral edema can patency.
give the clinician an idea as to the source of In the mouth, mucous membrane color and perfu-
theanimals problem. If edema is present in sion should be noted. A perfusion time of greater
the neck, head, and forelimbs only, then it usu- than 2 seconds suggests decreased cardiac out-
ally indicates an obstruction of the cranial vena put; however, most animals with congestive heart
cava or a mediastinal mass. If edema is present failure have normal mucous membrane color un-
in the entire body, then pleural effusion with or til their heart failure is severe. So, mucous mem-
without ascites is usually present. Other causes brane color and perfusion are very insensitive
of edema (e.g., hypoproteinemia) should also be ways to evaluate adequate circulation.
considered. Cyanosis is due to hypoventilation or poor dif-
Elevated temperature may be seen with an infec- fusion across the alveoli produced by multiple
tious disease or subacute bacterial endocarditis. different factors (see history section discussed
previously).
Hyperemic mucous membranes (dark red to
Key Point muddy) may indicate an increased packed cell
By observing an animal, the presence and se-
volume (polycythemia), which can be second-
verity of a respiratory problem can be deter- aryto a chronic right-to-left vascular shunt
mined quickly. Animals with severe dyspnea (Figure 1-6).
should be handled gently to avoid stress and Pale mucous membranes indicate anemia or poor
should be treated immediately. perfusion.
The mucous membranes of the mouth should
becompared with the posterior membranes
Head
Check for any asymmetry and swellings.
The eyes should be examined for changes that
could indicate systemic diseases.
Diaphragmatic hernia
Pneumothorax
Severe pericardial effusion
Severe pleural effusion
Severe pulmonary edema
Severe respiratory disease Figure 1-6. Hyperemic mucous membranes in a dog with
polycythemia due to Tetralogy of Fallot.
12 Section I Diagnosis of Heart Disease
(e.g., vagina, prepuce), because differential cya- The entire jugular vein can be distended indicat-
nosis can occur in a right-to-left shunting PDA. ing increased systemic venous pressure caused
Check the oral cavity for severe dental tartar, gin- by right-heart failure, pericardial disease, or ob-
givitis, or pyorrhea, which can serve as sources struction of the cranial vena cava (e.g., heart base
of sepsis leading to bacteremia and possibly tumor). Only about 70% of dogs with right-heart
endocarditis. failure have distended jugular veins, and cats
rarely have distended jugular veins with right-
Key Point heart failure. See Box 1-9 for causes of jugular
Mucous membrane color and perfusion are distension.
insensitive signs of cardiac function, so when Mediastinal masses such as lymphosarcoma can
they are abnormal, the animals cardiac or re- compress the cranial vena cava causing a dis-
spiratory problem is severe. tended jugular vein; however, they also usually
cause pleural effusion and head and neck edema.
Arterial pulses can mimic a jugular pulse; how-
Neck
ever, when light pressure is applied to the area of
The jugular pulse should be evaluated while the the jugular pulse, the arterial pulse will continue,
animal is standing with its head in a normal posi- whereas the jugular pulse will stop.
tion. Any pulse going over one third of the way The hepatojugular reflex is a distension of the jug-
up the neck is abnormal and can be due to any of ular veins that occurs when the abdomen is com-
several factors. See Box 1-8 for causes of abnor- pressed for 10 to 30 seconds. It is caused by an
mal jugular pulses. increased return of blood to the right heart from the
Abnormal jugular pulses occur in right-heart fail- abdomen. However, the right heart is not normal
ure due to tricuspid regurgitation or dilated car- and cannot handle the increased venous return, so
diomyopathy, when the right ventricle contracts the blood from the cranial vena cava cannot enter
and the blood flows back into the right atrium and the heart and the jugular veins become distended.
up the jugular veins due to the insufficient tricus- This reflex is present with both right- and left-heart
pid valve. failure and indicates increased blood volume in the
Abnormal jugular pulses occur with pulmonic peripheral venous system due to an inability of the
stenosis and pulmonary hypertension, when the heart to circulate the blood properly.
right atrium contracts against a hypertrophied, Cats with left-heart failure may have distended
noncompliant right ventricle so that only some of jugular veins only when lying down and the jugu-
the blood enters the right ventricle and the rest lar veins return to normal when they sit or stand.
goes back up the jugular veins.
With heartworm disease, abnormal jugular pulses
occur because there is both a stiff, hypertrophied
Box 1-9 Causes of Distended Jugular Veins
right ventricle and tricuspid regurgitation which
both contribute to the jugular pulses. Right-heart failure (e.g., tricuspid regurgitation,
Arrhythmias such as second or third degree heart dilated cardiomyopathy)
block or premature beats cause abnormal jugular Pericardial diseases
Heart base tumor
pulses because the sequence of atrial and ven-
Mediastinal mass
tricular activation is disrupted so that the atrium
contracts against a closed tricuspid valve sending
blood back up the jugular veins.
Key Point
Box 1-8 Causes of Abnormal Jugular Jugular vein distention can be present with
Pulses both right- and left-heart failure, but may be
present in only 70% of these cases. Abdominal
Arrhythmias ultrasound is a sensitive, noninvasive method
Heartworm disease of determining increased venous pressure by
Pulmonary hypertension detecting distended hepatic veins; however,
Pulmonic stenosis the ultrasound only confirms the presence of
Right-heart failure (e.g., tricuspid regurgitation, di- increased venous pressure and not the cause
lated cardiomyopathy) of it.
Chapter 1 The History and Physical Examination 13
A central venous pressure can be obtained on Box 1-10 Causes of Shifting of the
animals with distended jugular veins. It is most Palpable Apex Beat or Point
useful in the diagnosis of restrictive pericardial of Maximum Intensity
disease where less invasive tests have not con-
firmed the diagnosis. Cardiac enlargement
A young dog with regurgitation due to a mega- Collapsed lung lobes on the right
esophagus may have a congenital vascular ring Diaphragmatic hernias
anomaly. Pectus excavatum
Lying down
Masses displacing the heart
Tracheal Palpation Pleural effusions
The presence of ascites can be difficult to ascer- The femoral pulse rate should be taken. Nor-
tain in obese animals. The clinician should put mal rates in dogs are 70 to 180 beats per minute
one hand on one side of the abdomen and the (bpm). Puppies can have a normal rate of 220
other hand on the other side, and then tap the bpm. Normal rates in cats are 160 to 240 bpm.
abdomen. If a fluid wave is felt by the hand on The rhythm of the pulses should be noted. There
the opposite side of the abdomen, then ascites is should be a pulse for every heartbeat. Pulse defi-
present. cits usually indicate incomplete ventricular fill-
Check for signs of hepatomegaly and splenomeg- ing, as seen in arrhythmias.
aly. The presence of ascites, splenomegaly and Arterial pulse pressure (femoral pulse quality) is
hepatomegaly, usually indicates right-heart failure the difference between the arterial systolic pres-
due to dilated cardiomyopathy, tricuspid regurgi- sure and the diastolic pressure. Pulse quality can
tation, heartworm disease, pericardial disease, or normally vary depending on the animals confor-
congenital heart disease. Another possibility is an mation, age, hydration, heart rate, cardiac func-
obstruction of the posterior vena cava. tion, and level of excitement or activity.
Palpate for any masses. The intensity of the pulse should be palpated.
Palpate the kidneys as chronic renal failure can Normal pulses are strong and have a rapid rate of
lead to systemic hypertension that can affect the rise and fall.
heart. Table 1-3 lists the pulse quality and the cause for
Most ascites due to right-heart failure is a modi- each type of pulse.
fied transudate on cytology and accumulates Hypokinetic (weak) pulses are due to decreased
slowly. cardiac output (e.g., congestive heart failure, hy-
povolemia), decreased peripheral vascular resis-
Key Point tance, increased arterial compliance, or slower
Ascites can be due to right-heart failure or rate of rise due to delayed emptying of the left
other heart problems such as pericardial effu ventricle (e.g., subaortic stenosis). Dogs will
sion; however, it can also be due to other have normal pulses until the stroke volume is
noncardiac problems. Further tests are indicted markedly decreased with severe congestive heart
to determine the cause of ascites.
failure so pulses are an insensitive indicator of If an area, especially dorsally, in the thorax sounds
cardiac output. hyperresonant, then pneumothorax may be present.
Hyperkinetic (strong) pulses rise and fall quickly If an area, especially ventrally, sounds hyporeso-
and are due to large left ventricular stroke vol- nant, then pleural effusion may be present.
umes with rapid diastolic runoffs (e.g., PDA,
aortic regurgitation). They are called B-B shot Key Point
or water-hammer pulses. Fear, fever, severe Percussion can be a rapid way of determining
bradycardia, thyrotoxicosis, and anemia can also the presence or absence of pleural effusion.
produce this type of pulse.
The pulses can be abrupt or jerky with mitral regur-
Stethoscope
gitation and ventricular septal defects as a greater
volume of blood is ejected in early systole. The main components of the stethoscope are the
Pulsus alternans occurs when the pulse is alternately bell, diaphragm, tubing, and ear pieces. The bell
weak and then strong in patients with normal si- transmits both low-frequency (20 to 300 cycles
nus rhythm. It is frequently associated with severe per second [cps]) sounds when light pressure is
myocardial failure (e.g., dilated cardiomyopathy). used and high-frequency (300 to 1000 cps) sounds
Pulsus bigeminus occurs when weak pulses alter- when firm pressure is used to apply it to the thorax.
nate with strong pulses. This is associated with It is best for hearing third and fourth heart sounds.
arrhythmias such as ventricular bigeminy where The diaphragm attenuates low frequencies and se-
a normal heart beat alternates with a ventricular lectively transmits the high frequencies. It is best
premature beat. The weak pulses occur because for hearing the first and second heart sounds.
the premature beat causes the ventricles to con- Most stethoscopes combine the bell and dia-
tract before they are adequately filled so a smaller phragm into a dual-sided, combination-style
than normal volume of blood is ejected by the left chest piece. Some stethoscopes have the bell and
ventricle, causing weak pulses. The difference diaphragm as one piece. With these stethoscopes,
between the normal and abnormal pulses may simple fingertip pressure allows one to switch
be accentuated due to the fact the ventricles have from low- to high-frequency sounds. There is no
more time to fill on the normal beats so that the interruption in sound as there is in a traditional
normal pulses feel even stronger. two-sided stethoscope, resulting in added conve-
Pulsus paradoxus is an alteration of the pulse nience and efficiency in auscultation.
strength during respiration due to changes in A practical tubing length on a stethoscope is ap-
ventricular filling. There is an increase in pulse proximately 14 to 18 inches. If the tubing is too
strength on expiration and a decrease in strength long, then it will attenuate all the heart and lung
on inspiration in normal animals; however, this sounds.
change is exaggerated and easier to feel when Ear tubes should angle forward to conform to the
cardiac tamponade is present. anatomy of the ear canals. A stethoscope with
Pulses feel erratic when an animal has atrial variable sizes of ear pieces is ideal because each
fibrillation. person can find the correct size earpiece that fits
comfortably in the ear canal and shuts out extra-
Key Point neous sounds.
The quality of an animals pulse is not a good For dogs and cats less than 15 pounds, a pediatric
indication of the severity of its cardiac prob- stethoscope that has a smaller headpiece should
lem because only very advanced heart disease be used.
will cause weak pulses; however, pulse defi- Electronic stethoscopes have improved dramati-
cits are very good indicators of the presence cally in the past 10 years. In addition to electronic
of an arrhythmia. amplification of heart sounds and murmurs, most
electronic stethoscopes currently allow the user to
record and play back sounds at either normal or
Percussion
half speed. This feature is useful for judging and
Percussion can be used to determine the presence timing the shape or quality of murmurs in tachy-
of masses or fluid lines, especially in the thorax. cardic patients and for judging the timing of tran-
It will elicit a hollow sound (hyperresonance) sient heart sounds such as clicks or gallops. Some
over the lungs and a dull sound over solid struc- models also provide the ability to record graphic
tures (hyporesonant). representations of sounds in a digital file format
16 Section I Diagnosis of Heart Disease
(i.e., a phonocardiogram) that can be stored on crackling due to the rubbing of hair. Extraneous
a computer, possibly even becoming part of the sounds will occur if auscultation is not performed
patients medical record. A new electronic stetho- in a quiet area.
scope (Figure 1-7), the 3M Littman Model 3000, Auscult the heart and lungs separately.
features useful ambient noise reduction circuitry Auscult the entire thorax on both sides.
that appears to overcome most if not all of the The areas of auscultation of the heart are
problems of background noise amplification that shown in Figure 1-8. Table 1-4 lists the areas of
plagued previous models. auscultation.
The pulmonic valve area is on the left side. In
Key Point the dog, it is between the second and the fourth
Not every stethoscope is ideal for everyone. intercostal spaces just above the sternum. In the
Ideally, a clinician should try various stetho-
scopes to find the one that works best for him
or her.
Auscultation
This is the most helpful part of the cardiac exami-
nation; it should be done carefully and systemati-
cally. The animal should be standing so that the
heart is in its normal position. This avoids the
problem of positional murmurs caused by the
heart rubbing against the chest wall when an ani-
mal is lying down.
Common artifacts heard include respiratory
clicks and murmurs, rumbles due to shivering Figure 1-7. 3M Littman electronic stethoscope.
and twitching, and movement sounds such as (Courtesy 3M Health Care, St. Paul, Minn.)
Figure 1-8. Areas of auscultation in the dog. M is the mitral valve area, A is the aortic valve area, P is the pulmonic valve area,
and T is the tricuspid valve area. (From Gompf RE: The clinical approach to heart disease: history and physical examination. In Fox
PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Chapter 1 The History and Physical Examination 17
Figure 1-9. Heart sounds and their relationship to the ECG. The first heart sound is S1. The second heart sound is S2. The third
heart sound is S3 and the fourth heart sound is S4. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Box 1-12 Causes of Changes in the First Box 1-13 Causes of Changes in the Second
(S1) Heart Sound (S2) Heart Sound
Loud S1 Loud S2
Anemia Atrial septal defect
Excitement Mild valvular pulmonic stenosis
Exercise Patent ductus arteriosus
Fear Pulmonary embolism
Fever Pulmonary hypertension
Hyperthyroidism Systemic hypertension
Mitral regurgitation Valvular aortic stenosis
Positive inotropic agents Ventricular septal defect
Pregnancy Soft S2
Systemic hypertension Dilated cardiomyopathy
Tachycardia Hypothyroidism
Thin animals Marked aortic regurgitation
Soft S1 Shock
Bradycardias Significant pulmonic stenosis
Decreased cardiac output Valvular aortic stenosis
Diaphragmatic hernias Split S2
Emphysema Atrial septal defect
Hypothyroidism Heartworms
Left bundle branch block Mitral stenosis
Negative inotropic agents Pulmonary hypertensionmoderate to severe
Obesity Pulmonic stenosis
Pericardial effusion Right bundle branch block
Pleural effusion Right to left patent ductus arteriosus
Severe aortic or mitral regurgitation Ventricular premature beat from left ventricle
Severe heart failure Paradoxical split S2
Shock Left bundle branch block
Thoracic masses Left ventricular failure
Variable S1 Severe systemic hypertension
Arrhythmias Significant aortic regurgitation
Split S1 Subaortic stenosis
Atrial or ventricular premature beats Ventricular premature beats from the right ven-
Cardiac pacing tricle
Right bundle branch block Absent S2
Stenosis of mitral or tricuspid valve Arrhythmias
such as hypertrophic cardiomyopathy or third The precise cause of the click is unknown, but it
degree heart block. It may also be heard in dogs may be due to the mitral valve buckling into the
with ruptured chordae tendineae. left atrium (mitral valve prolapse) in dogs with
A gallop rhythm is an S3, S4, or combination early mitral regurgitation because many of these
(summation) of the two. Gallops are of a low fre- animals develop a mitral regurgitation murmur
quency and can be difficult to hear. A gallop can later in life. This is a benign finding and is not
be a very early sign of heart failure, preceding usually associated with heart failure.
clinical signs. Ejection sounds are high frequency sounds gen-
Systolic clicks are short, mid- to high-frequency erated in early systole due to hypertension, dila-
clicking noises that occur in systole between S1 tion of the great vessels, or opening of abnormal
and S2 (see Figure 1-9). They are usually loud- semilunar valves such as in valvular pulmonic
est over the mitral and tricuspid areas. A sys- stenosis.
tolic click may come and go and may change its
position in systole (gets closer to or further away Key Point
from S2) and may change its intensity. The presence of a gallop is an indication of
A systolic click can be hard to differentiate from a cardiac disease in small animals.
gallop, especially if the animals heart rate is fast.
20 Section I Diagnosis of Heart Disease
Functional murmurs are divided into physiologic The loudness of a murmur does not indicate the
and innocent murmurs. severity of the underlying problem.
Physiologic murmurs have a known cause such as A murmur should be described by using the
increased cardiac output or decreased blood vis- following classification. First, the murmur
cosity and occur with anemia, hypoproteinemia, should be identified as to its timing in the car-
fever, increased blood pressure, pregnancy, hyper- diac cycle (e.g., systolic, diastolic, continuous).
thyroidism, and an athletic heart. These are high Also, the duration of the murmur (e.g., early
frequency murmurs occurring in the early to mid- systolic, holosystolic, pansystolic) should be
systolic phase, are loudest over the aortic and pul- noted (Figures 1-10 and 1-11).
monic areas and rarely radiate to other areas. Table Next the site at which the murmur is loudest
1-6 lists the types of murmurs and their causes. (PMI) (e.g., valve area) and where it radiates due
Innocent murmurs have no known cause and are to blood flow through the defect (e.g., other valve
not associated with any cardiac problem. These areas where it can be heard) should be noted.
murmurs are soft systolic murmurs (no louder than The intensity or loudness of the murmur can be
grade 3) and usually just occur in young animals. evaluated based on the following scale: grade I/
They can be located over any valve area but are VI can only be heard after listening for several
most frequent over the mitral and aortic areas. Also, minutes and sounds like a prolonged first heart
these murmurs should disappear by the time of the sound; grade II/VI is very soft, but can be heard
animals last vaccinations (5 months of age). immediately; grade III/VI is low to moderate in
Pathologic murmurs are caused by underlying intensity; grade IV/VI is very loud, but a thrill
heart or vessel disease such as stenosis of valves cannot be palpated on the thorax; grade V/VI is
or outflow tract or great vessels, valvular regur- very loud, and a thrill can be palpated on the tho-
gitation, or abnormal intracardiac or extracardiac rax; grade VI/VI can be heard without the use of
shunts. Refer to individual defects in the follow- a stethoscope or with the stethoscope slightly off
ing chapters for a description of the murmurs as- the thoracic wall.
sociated with each defect. The quality or shape of the murmur is subjective,
but can be evaluated according to graphic appear-
ance on phonocardiogram (see Figures 1-10 and
Table 1-6 Types of Heart Murmurs and Their 1-11). Regurgitant murmurs are plateau shaped
Causes
(e.g., equal loudness throughout). Ejection murmurs
Murmur Cause are usually decrescendo, crescendo, or diamond
shaped. Machinery or continuous murmurs are
Physiologic Anemia
Athletic heart
diamond-shaped and peak at S2, continuing
Fever through all of systole and most of diastole. Blow-
Hypoproteinemia ing murmurs are decrescendo murmurs (e.g., de-
Hypertension crease in intensity).
Hyperthyroidism The pitch or frequency of the murmur can also
Pregnancy be described. Some murmurs are high, medium
Innocent No known cause or low pitched, or a mix. Also, they can be harsh,
Pathologic Aortic regurgitation blowing, or musical.
Aorticopulmonary septal defect
Arteriovenous fistula
Atrial septal defect Other Sounds Auscultated in the Thorax
Mitral dysplasia Normal respiratory sounds include referred
Mitral regurgitation
sounds from the trachea that are commonly heard
Mitral stenosis
Patent ductus arteriosus over the lungs. Vesicular sounds are due to air
Pulmonic regurgitation moving through the small bronchi and are louder
Pulmonic stenosis on inspiration. Bronchial sounds are due to air
Subaortic stenosis moving through the large bronchi and trachea
Tetralogy of Fallot and are heard best on expiration. Bronchovesicu-
Tricuspid Dysplasia lar sounds are the combination of the above two
Tricuspid regurgitation and are heard best over the hilar area.
Tricuspid stenosis
Abnormal respiratory sounds include attenuated
Ventricular septal defect
sounds as well as increased, abnormal sounds.
22 Section I Diagnosis of Heart Disease
Figure 1-10. Timing and duration of murmurs. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Figure 1-11. Timing and quality of murmurs. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Chapter 1 The History and Physical Examination 23
Attenuated bronchovesicular lung sounds are due pericarditis. Wheezes are relatively high pitched,
to thoracic masses, pleural effusion, pneumothorax, musical sounds and are often a sign of pulmonary
obesity, pneumonia, shallow breathing, or early pathology.
consolidation of the pulmonary parenchyma.
Rhonchi are due to air passing through partially
Suggested ReadingS
obstructed airways in the bronchial tubes or
smallest airways. Rhonchi from the large bronchi Buchanan J: Prevalence of cardiovascular disorders. In
are low pitched, sonorous, and almost continu- Fox PR, Sisson DD, Moise NS, eds: Textbook of ca-
ous. They are heard best on inspiration. Rhonchi nine and feline cardiology, ed 2, Philadelphia, 1992,
from the small bronchi are high pitched, sibilant, WB Saunders.
or squeaky, and are heard best on expiration. Gompf RE: The clinical approach to heart disease: his-
tory and physical examination. In Fox PR, ed: Canine
Crackles are interrupted, crepitant, inspiratory
and feline cardiology. New York, 1988, Churchill
sounds heard in many disease conditions and are Livingstone.
not pathognomonic for pulmonary edema. They Kittleson MD: Signalment, history, and physical ex
are due to opening of alveoli or airways that are amination. In Kittleson MD, Kienle RD, eds: Small
collapsed or partially filled with fluid or bubbles animal cardiovascular medicine. St Louis, 1998,
bursting in the airways. They are further defined Mosby.
as fine or coarse in quality. Sisson DD, Ettinger SJ: The physical examination. In
Other sounds which can be ausculted include Fox PR, Sisson DD, Moise NS, eds: Textbook of ca-
pleural friction rubs. Pleural friction rubs are nine and feline cardiology, ed 2, Philadelphia, 1999,
grating, rubbing sounds heard during inspira- WB Saunders.
tionandexpiration owing to the moving of two Smith FWK, Keene B, Tilley LP: Heart sounds. In
Smith FWK, Keene B, Tilley LP, eds: Interpretation
relatively dry, roughened pleural surfaces against
of heart sounds, murmurs, arrhythmias, and lung
each other.Pericardial friction rubs are short, sounds: a guide to cardiac auscultation in dogs and
scratchy noises produced by pericarditis and catsCD ROM and manual. Philadelphia, 2006,
heart movement. Pericardial knocks are diastolic WB Saunders.
sounds that occur in animals with constrictive
Chapter 2
u0010 Exposure technique will vary depending on equip- A normal heart can appear diseased and vice
ment and film-screen combinations. The current versa when positioning is not adequate.
standard for veterinary radiographic equipment is
a 300 mA/125 to 75 kVp machine. Guidelines for proper exposure and positioning of p0020
The current standard for economic film-screen a lateral thoracic radiograph (Figure 2-1) include:
combination imaging systems is the rare earth Radiographic exposure should be adequate to u0030
systems. Because of the motion created by res- define the dorsal spinous process of the cranial
piration, relatively high-speed (400) film-screen thoracic vertebrae superimposed on the scapula.
combinations that allow shorter exposure times To ensure a lateral projection, the dorsal heads of
are best suited for thoracic radiography. the ribs should be superimposed.
24
Chapter 2 Radiology of the Heart 25
t0010
TABLE 2-1 Small Animal Thoracic Radiographic Technique Chart Using a 400-Speed Film-Screen
System and Standard Radiographic Equipment*
Thickness (cm)
mA Time mAs kVp
Table Top
300 1/60 5 17 18 19 20 21 22 23 24 25 26 27 28 cm
76 78 80 82 84 86 88 90 92 95 90 101
Technique rules of thumb: Change exposure(1) 10% KVp; (2) two thirds of mAs.
*Single-phase fully rectified 300mA 125 KVp generator focal-film distance = 38.
1 3
Heart
A 2
2
Abdomen
B
2 3
f0010
Figure 2-1. A, Guidelines for proper exposure and positioning of a lateral thoracic radiographic projection. (1) Exposure should
allow delineation of the thoracic vertebral dorsal spinous process superimposed over the scapula. (2) The forelimbs should be pulled
forward to provide an unsuperimposed view of the cranial thorax. (3) The dorsal rib heads should be superimposed (compare with
B). (4) The exposure should be performed during inspiration, which provides maximum separation between caudal cardiac margin
and diaphragmatic cupula. B, Improperly positioned lateral thoracic radiographic projection (compare with A). (1) Nonsuperimposed
left and right rib heads. (2) The oblique projection markedly distorts cardiac silhouette conformation and intrathoracic position. (3)
Expiratory phase radiographic exposure with poor lung volume between caudal cardiac margin and cupula of the diaphragm.
26 Section I Diagnosis of Heart Disease
L L
DV DV
3
2
2
2
1
A 1 B
3
4
f0020
Figure 2-2. A, Guidelines for proper exposure and positioning of a dorsoventral/ventrodorsal thoracic radiographic projection.
L, Lateral; DV, dorsoventral. (1) The radiographic exposure should provide outline definition of thoracic vertebra superimposed
over the cardiac silhouette. (2) Exposure should be increased (usually a 10% kVp increase with obesity as suggested by an increase
in thoracic body wall thickness). (3) The thoracic vertebral dorsal spinous processes should be superimposed over the body por-
tions for the entire length of the thoracic spine. (4) Adequate lung volume between caudal cardiac margin and cupula indicates
an inspiratory phase radiographic exposure. B, Improperly positioned dorsoventral radiographic projection. Thoracic vertebral
dorsal spinous processes projected over the left hemithorax (1) and the sternal vertebra projected over the right hemithorax (2),
indicating an oblique thoracic dorsoventral radiographic projection. A lack of lung volume between caudal cardiac margin (3) and
cupula (4) indicates an expiratory phase radiographic exposure.
The forelimbs should be pulled forward so that The dorsal lung fields are hyperinflated, and the
they are not superimposed over the cranial thorax vessels to the caudal lung fields are magnified
or cranial margin of the heart. owing to increased object-film distance. This
The radiographic exposure is taken during full produces an improved radiographic definition
inspiration, identified as an adequate lung field of the large pulmonary arteries and veins of
spacing between the caudal margin of the heart the caudal lung fields. The DV projection also
and the cupula of the diagram. Two primary allows increased detection of early pulmonary
disease considerations for consistent expiratory infiltrates (most commonly with cardiac dis-
phase radiographs are: ease in the hilar and caudodorsal lung fields).
Obesity and Pickwickian syndrome, where the However, an improperly positioned DV/VD
overabundance of abdominal fat prevents ade- projection is worthless for cardiac radiographic
quate inspiratory distraction of the diaphragm interpretation.
Upper airway disease, which most commonly
causes obstruction during the inspiratory phase
of respiration Key Point b0020
Although the DV projection is preferred, a
Dorsoventral/Ventrodorsal Projection straight (symmetric) projection is the ultimate s0060
The dorsoventral (DV) radiographic projection is goal, with patient compliance determining p0030
preferred over the ventrodorsal (VD) for cardiac which projection (DV vs. VD) is attainable.
evaluation for two reasons:
The anatomic positioning of the heart in the DV u0040
p0040 projection is less dependent on thoracic cavity con- Guidelines for proper exposure and positioning for
formation (deep-chested vs. barrel-chested breeds). the DV/VD projections (Figure 2-2) include:
Chapter 2 Radiology of the Heart 27
u0050 Radiographic exposure should be sufficient to formation of early cardiogenic pulmonary edema.
define the outline of the thoracic vertebrae super- Adequate exposure is critical to ensure definition
imposed over the cardiac silhouette. of caudal pulmonary vasculature superimposed
The kVp should be increased 10% from tech- over the cupula of the diaphragm.
nique-chart values for obese patients. Examina- The radiographic detection of caudodorsal pul-
tion of the thoracic body wall thickness on the monary vasculature is the best objective parame-
VD view should assist in evaluation of obesity. ter for the detection of pulmonary edema. Vessels
The dorsal spinous processes of the thoracic in the normal lung are detected by their soft tissue
vertebrae should be centered over the vertebral opacity contrasting with the normal radiolucent
bodies along the full length of the thoracic spine. gas-filled lung parenchyma surrounding them.
The thoracic sternal vertebrae also should be su- As pulmonary parenchyma (interstitial spaces as
perimposed over the thoracic spine and be essen- well as alveoli) become filled with edema fluid,
tially indistinguishable radiographically. the normal radiographic soft tissuegas contrast
The radiograph is taken during full inspiration, is lost, and delineation of the vessels diminishes.
identified as an adequate lung field spacing be- In other words, the vessels start to disappear
tween caudal cardiac margin and cupula of the from radiographic detection with the increased
diaphragm. opacity of the surrounding edematous lung pa-
renchyma (Figure 2-3).
The phase of inspiration is critical when using this
s0070 Projection Selection in method for interpretation both in the DV/VD and
Cardiac-Related Pathology in the lateral projections. Pulmonary pathology
can be mimicked when underinflation decreases
s0080 Pulmonary Edema
the parenchymal gas content per unit volume,
u0060 The DV is preferred over the VD projection for thus decreasing the radiographic contrast be-
radiographic detection of pulmonary edema. The tween lung parenchyma and associated vascu-
DV view accentuates pathology in the dorsal lung lature. This is especially true in older patients,
field, which is the most common location for the which already have slightly increased pulmonary
L L
DV DV
Heart Heart
A B
LAa LAa
LA LA PV
PV
Alv
f0030
Figure 2-3. A, Normal radiographic definition and contrast of pulmonary venous vasculature (PV) with surrounding normal
radiolucent lung parenchyma. L, Lateral; DV, dorsoventral; LA, left atrium; LAa, left atrial auricular appendage. B, Radiographic
obliteration of pulmonary venous vasculature (PV) by alveolar consolidation (Alv) of hilar and caudal lung lobes, a characteristic
distribution for cardiogenic pulmonary edema.
28 Section I Diagnosis of Heart Disease
parenchymal radiographic opacity owing to age- degree of respiratory compromise should always
related pulmonary degenerative changes (intersti- be assessed prior to thoracic imaging.
tial fibrosis, bronchial mineralization, heterotopic If significant amounts of pleural effusion are sus-
pulmonary bone formation). pected, increasing radiographic exposure to ab-
dominal technique-chart levels results in better
intrathoracic radiographic contrast. When pos-
s0090 Pleural Effusion
sible, thoracocentesis and fluid drainage prior to
u0070 Pleural effusion is radiographically evident as fo- radiography is always preferred.
cal areas of increased soft tissue opacity located
within the thoracic cavity. It causes separation of
lung lobes from both the thoracic wall and the ad- Radiographic Anatomy s0100
jacent lobes. This is seen on the lateral projection
Lateral Thoracic Radiographic Projection s0110
as an increase in the soft tissue thickness of the
caudodorsal thoracophrenic angle and diaphragm Cardiac Parameters s0120
as well as linear soft tissue opacities (pleural fis- Even though the lateral radiographic projection de- p0050
sures) at anatomic locations comparable with fines the cranial-caudal and dorsal-ventral dimen-
interlobar fissures (Figure 2-4). Pleural effusion sions of the thorax, the anatomy of the heart of the
also contributes to loss of definition of the cra- dog and the cat as it resides in the thorax also al-
nial and caudal margins of the heart, producing a lows this projection to detail the left and right as-
radiographic positive-silhouette sign. pects of the heart. This is because in the dog and the
In cases of pleural effusion, the VD projection is cat the heart is slightly rotated along its base-apex
much preferred over the DV view for detection axis, such that the right cardiac chambers are posi-
and delineation of cardiac size and shape. If intra- tioned more cranially and the left chambers posi-
thoracic fluid volumes are severe enough, the heart tioned more caudally. Thus, the cardiac silhouette
can effectively disappear on the DV view because as it appears on the lateral projection defines the
of the relative distribution of the fluid and heart right side of the heart along the cranial margin and
in the thoracic cavity. The positive-silhouette the left side is defined by its caudal margin (Figures
phenomenon is accentuated in the DV compared 2-6 to 2-8).
with the VD view (Figure 2-5). However, patient The canine and feline heart shape or radiographic p0060
positioning for the DV projection puts less silhouette is ovoid, with the apex more pointed in
physiologic demand on the patient compromised conformation than the broader base. This base-
by pleural effusion and thus is favored over theVD apex difference in conformation is accentuated
projection. The patients physiologic stability and in the cat. The heart axis is defined by drawing a
1 1
1
L L
VD DV
A B
f0050
Figure 2-5. A, Ventrodorsal (VD) thoracic radiographic projection of pleural effusion consisting of pleural fissure lines (closed
arrows) with blunting of the thoracophrenic angles (open arrows). Note that the cardiac silhouette is still well outlined. B, Dorso-
ventral (DV) thoracic radiographic projection of pleural effusion. The intrathoracic fluid distribution creates a positive silhouette
sign where a complete loss of the cardiac silhouette has occurred. Thus, the VD projection (A) is preferred for cardiac silhouette
definition in the presence of pleural effusion. L, Lateral.
CrVC PAS LP RP
CaV C
RA
TV
f0060 ra PV RV
Figure 2-6. Schematic lateral thoracic radiographic projection of the relative position and size of the right-side structures of the
heart. Note the more cranial position of the right chambers of the heart. CrVC, Cranial vena cava; PAS, main pulmonary artery;
PV, pulmonic valve; ra, right atrial auricular appendage; RV, right ventricle; RA, right atrium; LP, left pulmonary artery; RP, right
pulmonary artery; TV, tricuspid valve; CaVC, caudal vena cava.
30 Section I Diagnosis of Heart Disease
Aa LA
CVC
MV
LVI
Trachea TB CVC
LA
RA
LV
RV Abdomen
f0080
Figure 2-8. Schematic lateral thoracic radiographic projection outlining the approximate location of the four heart chambers.
TB, Tracheal bifurcation; CVC, caudal vena cava; RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle.
line from the tracheal bifurcation (carina) to the Apso, Bulldog) tend to have more globular-shaped
apex at an angle approximately 45 degrees to the hearts, with increased sternal contact of the cra-
sternal vertebrae. This angle can decrease in the cat nial margin of the heart. The heart chambers can
with age and is often called a lazy heart. It has be roughly defined by a line connecting the apex
been postulated that this may be related to a loss to the tracheal bifurcation and a second line per-
of aortic connective tissue elasticity. This is most pendicular to the base-apex axis and positioned at
often seen in cats older than 7 years. Shallow, the level of the ventral aspect of the caudal vena
barrel-chested dog breeds (Dachshund, Lhasa cava (see Figure 2-8).
Chapter 2 Radiology of the Heart 31
VHS = S + L
f0090 Measured in vertebral units beginning at T4.
Figure 2-9. Schematic representation parameters for the vertebral scale system of cardiac size. The vertebral heart sum (VHS) is
the sum of the long axis cardiac dimension (L) and the maximal perpendicular short axis dimension (S). S and L are measured in
vertebral units beginning at T4. CVC, Caudal vena cava.
p0070
p0100 The dorsal cardiac margin includes both atria, A more objective determination of cardiac size
pulmonary arteries and veins, the cranial and caudal has been formulated for the dog and uses a verte-
vena cavae, and the aortic arch (see Figures 2-6 to bral scale system in which cardiac dimensions are
2-8). The cranial border is formed by both the right scaled against the length of specific thoracic ver-
ventricle and the right atrial appendage, resulting in tebrae (Figure 2-9). In lateral radiographs the long
the radiographically defined cranial waist (see Fig- axis of the heart (L) is measured with a caliper
ures 2-6 and 2-8). The caudal margin is formed by the extending from the ventral aspect of the left main
left atrium and left ventricle, with the atrioventricular stem bronchus (tracheal bifurcation hilus, carina) to
junction defined as the radiographic caudal waist. the left ventricular apex. The caliper is repositioned
p0080 The base-to-apex cardiac dimension or length along the vertebral column beginning at the cranial
occupies approximately 70% of the DV distance of edge of the fourth thoracic vertebra. The length of
the thoracic cavity at its position within the thorax. the heart is recorded as the number of vertebrae cau-
For objective measurements it is important to mea- dal to that point and estimated to the nearest tenth
sure thoracic cavity distance between the thoracic of a vertebra. The maximum perpendicular short
spine and the sternum at an axis perpendicular to axis (S) is measured in the same manner beginning
the thoracic spine. at the fourth thoracic vertebra. If obvious left atrial
The cranial-caudal dimension or width as it ap- enlargement is present, the short axis measurement p0090
pears on the lateral projection is measured at its is made at the ventral juncture of left atrial and cau-
maximum width (which is usually at the level of dal vena caval silhouettes.
the ventral aspect of the insertion of the caudal vena The lengths in vertebrae (v) of the long and p0110
cava) and perpendicular to the base-apex axis. This short axes are then added to obtain a vertebral
classically has been defined as between 2.5 (deep- heart sum (VHS), which provides a single number
chested conformation breeds [Setters, Afghans, representing heart size proportionate to the size
Collies]) and 3.5 (barrel-chested conformation of the dog. The average VHS in the dog is 9.7 v
breeds [Dachshunds, Bulldogs]) intercostal spaces (range 8.5 to 10.5 v). Caution must be exercised in
(ICS) in the dog and 2.5 to 3.0 ICS in the cat. The somebreedsthathave excessively disproportionate
ICS measurement is made at an axis perpendicular skeletalbody weight conformations. An example is
to the long axis of the ribs. Thus, the cardiac width the English Bulldog, which has relatively small tho-
distance determination may have to be shifted in racic vertebrae and commonly has hemivertebrae
axis angle before comparison to ICS length. as well; thus, a normal heart may be interpreted
32 Section I Diagnosis of Heart Disease
Heart
f0100 PA PV
Figure 2-10. Pulmonary vascular anatomy in the lateral thoracic projection. Cranial lung lobe branch of the pulmonary artery
(PA), cranial lung lobe branch of the pulmonary vein (PV), end-on view of the right main pulmonary artery (RPA) as it traverses
the thorax from left to right, and left main pulmonary artery (LPA). TB, tracheal bifurcation (carina); BCrL, Bronchus to a cranial
lung lobe.
as large with the VHS method. Although the VHS The pulmonary arteries and veins should be equal
concept is more precise, clinical judgment is still in size. The width of the vessels where they cross
necessary to avoid over diagnosing or under diag- the fourth rib should not exceed the width of the
nosing heart disease. narrowest portion of that rib at its juncture with the
rib head (the dorsal aspect of the rib near the tho-
s0130 Vessel Parameters racic spine). The dorsal section of the rib is used as
p0120 The main pulmonary artery (pulmonary trunk) can- a reference to adjust for radiographic magnification
not be seen on the lateral projection owing to a pos- owing to thoracic conformation.
itive-silhouette sign with the craniodorsal base of
Dorsoventral and Ventrodorsal Projections s0140
the heart. The left pulmonary artery can sometimes
be seen extending dorsal and caudal to the tracheal Cardiac Parameters s0150
bifurcation (carina). The right pulmonary artery is The heart is rotated on its long axis such that the p0150
frequently seen end-on as it leaves the main pul- right chambers are oriented both right and cranially,
monary artery immediately ventral to the carina and the left chambers reside both left and caudal.
(Figure 2-10). This end-on appearance may be con- The degree of rotation is less in the cat. The cranial-
fused with a mass lesion on normal radiographs and caudal rotation is most significant when defining
is accentuated in cases of pulmonary hypertension the location of the left and right atria, respectively.
such as heartworm disease. The pulmonary veins The canine heart appears radiographically as an p0160
are best identified as they enter the left atrium cau- elliptical opacity with its base-apex axis orientation
dal to the heart base. approximately 30 degrees to the left of the midline.
p0130 Using the larger, more proximal segments of the The width of the heart across its widest point is usu-
mainstem bronchi as a reference, the pulmonary ar- ally 60% to 65% of the thoracic width at its loca-
teries are dorsal to the bronchus, and the pulmonary tion within the thorax. In the cat the cardiac axis
veins are ventral to the bronchus (see Figure 2-10). is most commonly on or close to midline, and its
p0140 The vessels to the cranial lung lobes are usu- width does not usually exceed 50% of the width
ally seen as two pairs of vessels, each with their of the thoracic cavity during full inspiration. The
respective bronchi. The more cranial pair of vessels cardiac silhouette may be artificially increased in
generally corresponds to the side on which the lat- the obese patient owing to an excessive amount of
eral projection was made. Thus, in the right lateral pericardial fat. In these cases, the cardiac silhouette
projection, the right cranial lobar vessels are more margin appears to be less well defined or blurred
cranial than vessels of the left cranial lung lobe. because the margin of contrast between soft tissue
Chapter 2 Radiology of the Heart 33
AA
PAS
AV
LV
Aot
Da
f0110
Figure 2-11. Schematic anatomy of the chambers and vasculature of the left ventricular outflow tract of the heart in the dorso-
ventral radiographic projection. LV, Left ventricle; Aot, aortic outflow tract; AV, aortic valve; AA, aortic arch; PAS, pulmonary artery
segment; Da, descending aorta.
PAS
rpa lpa
LA
Pv
f0120
Figure 2-12. Schematic anatomy of the pulmonary vasculature in the dorsoventral projection. PAS, Main pulmonary artery
(radiographic descriptionpulmonary artery segment); lpa, left pulmonary artery; rpa, right pulmonary artery; LA, left atrium; Pv,
pulmonary veins.
(heart), fat (pericardial), and air is not as distinct as vertical in the thorax and thus produces a smaller
that between soft tissue and air. and more circular cardiac silhouette conformation.
Evaluating the obesity of the patient by evalu- The broad, barrel-chested breeds produce a radio- p0170
ating the thickness of the abaxial thoracic wall graphic silhouette that appears wider than that of
and width of the mediastinum (as well as exam- standard breeds.
ining the patient) will assist in the determination The margins of the heart that create the car- p0180
of pericardial fat contribution to cardiac size. In diac silhouette contain a number of structures that
deep, narrow-chested breeds, the heart stands more often overlap. A clock face analogy can be used to
34 Section I Diagnosis of Heart Disease
LAu
2
LA
2
f0130
Figure 2-13. Dorsoventral thoracic radiographic projection of a dog with severe left atrial (LA) enlargement. The left atrial
auricular appendage (LAu) contributes to the cardiac silhouette at the 2 to 3 oclock position (1). The body of the left atrium su-
perimposed over the caudal cardiac silhouette produces a radiolucent mach line, a radiographic edge effect caused by an acute
change in soft tissue thickness (2).
RAa
PAS
RA
PV
RV
CVC
f0140
Figure 2-14. Schematic anatomy of the chambers and outflow tract of the right side of the heart in the dorsoventral radio-
graphic projection. RV, Right ventricle; RA, right atrium; RAa, right atrial auricular appendage; PV, pulmonic valve; PAS, mainstem
pulmonary artery segment; CVC, caudal vena cava.
s implify the location of these structures. The aortic segment (PAS) (Figures 2-12 and 2-13). In the
arch extends from the 11 oclock to 1 oclock posi- cat, the body of the left atrium proper forms the 2
tion (Figure 2-11). The main pulmonary artery is to 3 oclock position of the cardiac silhouette. In
located from the 1 to 2 oclock position, with its the dog, the left atrium is superimposed over the
radiographic designation as the pulmonary artery caudal portion of the cardiac silhouette in the DV
Chapter 2 Radiology of the Heart 35
p rojection (see Figure 2-12). With severe cases of substantiated on multiple radiographic views where
left atrial enlargement in the dog, the left auricular applicable.
u0080 appendage contributes to the definition and enlarge- Evaluate the radiographs for technical quality,
ment of the cardiac silhouette at the 2 to 3 oclock positioning, and proper exposure. If the study is
position (Figure 2-13). The left ventricle forms the substandard, then stop right here and repeat the
left heart margin from the 2 to 6 oclock position radiographic study.
(see Figure 2-11). The right ventricle is located Determine the phase of respiration.
from the 7 to 11 oclock position (the right ven- Review the entire thoracic cavity: spine, sternum,
tricle does not extend to the apex of the heart) (Fig- diaphragm, thoracic wall, ribs, cranial and caudal
ure 2-14). The right atrium is located at the 9 to 11 mediastinum, conformation and position of the
oclock position (see Figure 2-14). Pericardial fat diaphragm.
in the dog can asymmetrically contribute to cardiac Review the portion of the cranial abdomen in-
silhouette enlargement at the 4 to 5 oclock and 8 to cluded in the projection. Thoracic radiographic
11 oclock positions. exposure is usually half of that required for ab-
dominal imaging but a cursory evaluation of ab-
s0160 Vessel Parameters dominal contrast, detail, and hepatic size (using
p0190 The pulmonary arteries originate from the main gastric axis) can be performed.
pulmonary artery or the PAS with the right branch Evaluate the position, course, and diameter of the
coursing transversely, superimposed over the trachea and mainstem bifurcations.
cranial portion of the heart silhouette, extending Evaluate the position of the cardiac apex and cau-
beyond the right heart margin at approximately the dal mediastinum.
8 oclock position (see Figure 2-12). The left pul- Evaluate the size, shape, and course of the main
monary artery branch courses caudally, superim- pulmonary artery and peripheral pulmonary ar-
posed over the caudal left ventricular portion of the teries and veins.
heart, and extends beyond the left heart margin at Evaluate the lung fields for hyperinflation or un-
approximately the 4 oclock position. The pulmo- derinflation and for distribution and pattern of
nary veins are best seen as they enter the left atrium increased or decreased opacity.
along the caudal margin of the cardiac silhouette Evaluate the cardiac margin (cranial, caudal, right,
(see Figure 2-12). Compared with the pulmonary left, clock position segmentation) for enlarge-
arteries, they are clustered in a more axial position. ment, abnormal position, or conformation.
Thus, the pulmonary arteries extend to both the cra-
nial and caudal lung fields in a more abaxial posi-
tion relative to the pulmonary veins. NoncardiacRelated s0180
p0200 The aortic arch is within the cranial mediasti- Variables that can Mimic
num at the cranial heart margin and is normally Radiographic Signs of
not visible. The descending aorta is superimposed Cardiac Disease
over the heart and extends caudally, dorsally, and
Cardiac Position s0190
medially. The left lateral margin of the aorta can
be seen to the left of the vertebral column on both Pulmonary pathology (such as lung consolida- u0090
DV and VD views (see Figure 2-11). The caudal tion, atelectasis, or pleural disease) can cause a
vena cava courses cranially from the diaphragm mediastinal shift and alter the position and axis
to the right of midline and into the right caudal of the heart in the thoracic cavity.
margin of the heart (see Figure 2-14). This is one Mediastinal mass lesions can affect the cardiac
of the most useful landmarks for determination position and axis, as well as obscure the cranial and
of proper orientation of the DV radiograph on a cardiac margins when in contact with the heart, by
viewbox. producing a radiographic positive-silhouette sign.
Pneumothorax can produce disproportionate
hemithoracic volume changes, altering cardiac
s0170 Radiographic position and axis. Pneumothorax commonly
Interpretation produces elevation of the cardiac apex from the
p0210 A systematic evaluation of the entire thoracic sternum. This is supported by other radiographic
cavity involves adherence to and inclusion of the signs of pneumothorax:
following steps with each radiographic interpreta- Premature termination of lung vasculature into
tion. Abnormalities supportive of disease should be the periphery of the thoracic cavity
36 Section I Diagnosis of Heart Disease
Lung lobe margin detection as it contrasts with Uneven lung inflation secondary to disease or
nonparenchymal free intrathoracic gas previous lobectomy can produce a mediastinal
Sternal conformational abnormalities due to con- shift and resultant apex shift.
genital defects or previous trauma can alter car- If radiographs are taken on diseased, recumbent pa-
diac position and axis. tients or patients during or immediately following
general anesthesia, then hypostatic congestion and
atelectasis of the dependent lung fields can produce
Cardiac Size and Lateral Projection s0200
a mediastinal shift, altering cardiac position.
Younger animals appear to have larger hearts Pectus excavatum or funnel chest sternal con- u0100
relative to their thoracic size than do mature formation due to congenital deformities
patients.
The heart appears smaller on inspiration than
s0230 on expiration. During expiration increased ster- Evaluation of Heart
nal contact of the right heart margin and dorsal Chamber Enlargement
elevation of the trachea occurs, falsely suggesting
s0240 Right atrial enlargement
right-heart enlargement.
s0250 Anemic or emaciated patients often have small Radiographic Signs
u0120 hearts owing to hypovolemia and are hyperin- Lateral projection (Figure 2-15):
flated to compensate for hypoxemia. In deep- Elevation of the trachea as it courses dorsally
chested conformation breeds, the cardiac apex over the right atrium
can be elevated far enough from the sternum to Accentuation of the cranial waist. Preferential
mimic pneumothorax. enlargement of the more dorsal margin of the
cranial margin of the cardiac silhouette defines
s0210 Cardiac Position, Dorsoventral/
selective enlargement of the right atrial auricu-
Ventrodorsal Projection
lar appendage.
s0220 Malposition of the Cardiac Apex to the Right Increased soft tissue opacity of the cranial
or Left aspect of the cardiac silhouette owing to in-
u0110 Malposition of the heart to the right is normal creased soft tissue thickness of the right atrium
variant in the cat. superimposed over the right ventricle
Ao Pa RA LA CVC
Abdomen
Aa
PaS
LAa
RA
Normal heart
LV
RV
f0160
Figure 2-16. Cardiac silhouette changes associated with vessel and chamber enlargement in the dorsoventral radiographic
projection. Aa, Aortic arch; PaS, main pulmonary artery; LAa, left atrial auricular appendage; LV, left ventricle; RV, right ventricle;
RA, right atrium.
LA
4 RA
3 LV
RV
2 Abdomen
1
Trachea
3 5
4
LA
RA
2
RV LV
180
Figure 2-18. Schematic representation of radiographic signs associated with left- heart enlargement in the lateral projection.
(1) Rounding and widening of the cardiac apex conformation. (2) Straightening and increased vertical axis of the caudal cardiac
margin. (3) Left atrial enlargement with characteristic right-angular caudodorsal margin conformation. (4) Dorsal elevation of the
intrathoracic portion of the trachea, carina, and mainstem bronchi. The angle between the thoracic spine axis and the trachea is
diminished to the point of becoming parallel. (5) Separation of normally superimposed caudal mainstem bronchi. Left more dorsal
in position than the right. RA, Right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Chapter 2 Radiology of the Heart 39
s0550
Evaluation of the Radiographic Diagnosis s0460
Pulmonary Circulation of Heart Failure
p0220 The radiographic diagnosis of heart failure is de-
Undercirculation s0470
pendent upon recognition of imbalances in the
Radiographic Signs blood and fluid distribution within the body. This s0480
Lung field more radiolucent than normal owing circulatory imbalance is the result of diminished u0280
to lack of pulmonary vascular volume cardiac output into the pulmonary or systemic
Hyperinflation due to hypoxemia or ventilation/ vascular systems or reduced acceptance of blood
perfusion mismatch by the failing ventricle (hypertrophy), or both. De-
Pulmonary arteries smaller than normal; may be pending on which side of the heart is most severely
smaller in size when compared with correspond- affected, blood is shifted from the systemic to the
ing pulmonary veins pulmonary circulation (left-heart failure) or from
the pulmonary to the systemic circulation (right-
s0490 Causes of Pulmonary Undercirculation heart failure).
u0290 Congenital disease: pulmonic stenosis, te-
Right-heart failure s0560
tralogy of Fallot, reverse PDA (right-to-left
shunting) Physiologic Phenomenon s0570
In right-heart failure, an inadequate right ven- u0340
s0500 Differential Diagnosis tricular output into the pulmonary arteries ex-
u0300 Emphysema, chronic obstructive pulmonary ists concurrently with a reduced acceptance of
disease blood from the systemic veins. The blood vol-
Hyperinflation ume and pressure in the splanchnic and systemic
Pneumothorax veins are elevated. The venous congestion causes
Overexposure hepatomegaly.
Pulmonary thromboembolism With further progression of right-heart failure,
Hypovolemia, shock (the heart will also be a progression of systemic hypertension leads to
smaller than normal) increased amounts of fluid, solutes, and protein
Hypoadrenocorticism (Addisons disease); the escaping from the capillary beds of the major
heart may also be smaller than normal organs. The lymphatic circulation is overtaxed,
and fluid exudes into the serosal cavities, pro-
s0510 Overcirculation
ducing ascites, pleural, and even pericardial
s0520 Radiographic Signs effusions.
u0310 Both the pulmonary arteries and the veins are The extracardiac radiographic signs of progres-
enlarged sively worsening right-heart failure are hepato-
Arteries are frequently larger than the veins megaly, ascites, and then pleural effusion.
Pulmonary thoracic opacity is increased because
of larger vascular volume Radiographic Signs s0580
Right-sided cardiomegaly (see Figures 2-15 u0350
s0530 Causes of Pulmonary Overcirculation through 2-17). Patients with concentric cardiac
u0320 Dirofilariasis (arteries are larger than correspond- hypertrophy (e.g., pulmonic stenosis), thin-
ing veins) walled cardiomyopathy, or acute arrhythmias
PDA: both arteries and veins enlarged often may not have dramatic radiographic cardio-
Left-to-right shunts (ventricular and atrial septal megaly. Thus, subtle cardiac silhouette changes
defects): both arteries and veins enlarged in both the DV and the lateral projections must
Congestive heart failure: veins may be larger than be considered significant with supportive clinical
arteries if mainly left sided; both arteries and evidence of cardiac disease.
veins enlarged with concurrent left- and right- Hepatomegaly: rounded liver margin, which ex-
sided failure tends caudal to last rib; displacement of stomach
Fluid overload caudally and to the left
Ascites: abdominal distention; diffuse loss of
s0540 Differential Diagnosis intra-abdominal detail
u0330 Underexposure Pleural effusion
Expiratory phase of respiration Generalized increase in thoracic opacity
Chapter 2 Radiology of the Heart 41
Visualization of interlobar pleural fissures (see Engorgement and distention of the pulmonary
Figures 2-4 and 2-5, A) veins, especially in the hilar area as they enter
Obliteration of cardiac silhouette definition the left atrium. On the DV view these are iden-
(best demonstrated on the DV projection) (see tified as the more axial of the caudal vascula-
Figure 2-5, B) ture (see Figure 2-12).
Separation of pulmonary visceral pleural mar- The diameter of the pulmonary veins is greater
gin away from thoracic wall (see Figures 2-4 than that of their corresponding pulmonary ar-
and 2-5) teries (best seen on the lateral projection with
cranial lobar vessels) (see Figure 2-10).
s0590 Causes of Pleural Effusion Secondary to Right- The radiopacity of the lung parenchyma distal
Heart Failure and peripheral to the hilus is unchanged.
u0360 Decompensated mitral and tricuspid insufficiency Interstitial edema
Decompensated pulmonic stenosis, tetralogy of Diffuse increased radiopacity of the lung fields
Fallot owing to a hazy interstitial opacity is apparent.
Dirofilariasis (caval syndrome) The margins of the pulmonary veins and arter-
Pericardial effusion with tamponade ies are indistinct owing to perivascular edema.
Restrictive pericarditis As the lung parenchyma surrounding the pul-
monary vasculature fills with fluid, the normal
s0600 Differential Diagnosis pulmonary radiographic contrast between gas
u0370 Pleuritis (air-filled lung) and soft tissue (blood-filled
Chylothorax vessels) is lost. Thus, the pulmonary vascu-
Hemothorax laturebecomes indistinct and begins to dis
Pyothorax appearin the surrounding, fluid-filled lung
Hypoproteinemia parenchyma.
Neoplasia (pleural, mediastinal, cardiac, pulmo- In some patients, fluid accumulates around ma-
nary, primary, or metastatic) jor bronchi, producing prominent peribronchial
markings.
s0610 Left-heart failure
Alveolar edema
s0620 Physiologic Phenomenon Radiographic signs
u0380 In left-heart failure, inadequate left ven Fluid enters the alveolar air spaces and
tricular output into the aorta occurs, and a peripheral bronchioles, causing a coales-
diminished acceptance of blood from the pul- cent fluffy alveolar infiltrate. Air broncho
monary veins entering the left atrium results. grams(black tubes in a white radiopaque
This causes pulmonary venous congestion background) and air alveolograms (lung
and leakage of fluid into the pulmonary in- parenchyma with the radiopacity of liver
terstitium, with progression to flooding of the containing no vascular markings) are pres-
alveoli. ent. In the cat, cardiogenic alveolar consoli-
Clinically, this evolves as a progression of physi- dations can appear as a very well margined,
ologic events: pulmonary venous congestion, in- cloudlike conformation area of increased
terstitial pulmonary edema, alveolar edema, and pulmonary radiopacity.
lung consolidation. The margins of the pulmonary vessels are
usually completely obscured (see Figure 2-3,
s0630 Radiographic Signs B). The alveolar infiltrate is of greatest opac-
u0390 Left-sided cardiomegaly (see Figure 2-18). Pa- ity in the perihilar area, fading peripherally.
tients with concentric cardiac hypertrophy (e.g., In the dog, alveolar edema can be asymmet-
aortic stenosis), thin-walled cardiomyopathy rical, with the right lung fields more severely
(large- and giant-breed dogs), or acute arrhyth- affected than the left (best seen on the DV
mias often may not have dramatic radiographic projection).
cardiomegaly. Thus, subtle cardiac silhouette Differential diagnosis for pulmonary edema
changes in both the DV and lateral projections Neurogenic: electrocution, head trauma, post
as well as noncardiac changes (pulmonary vas- seizure, encephalitis, brain neoplasm
cular changes, pulmonary edema, etc.) must be Hyperdynamic (excessive negative intratho-
evaluated. racic pressures): choking, strangulation, up-
Pulmonary venous congestion per airway obstructions
42 Section I Diagnosis of Heart Disease
Trachea CVC
1
2
3 Abdomen
Congenital defects
Patent ductus arteriosus N In In In In In In In N/In Left Volume
Pulmonic stenosis In In N/De N/De N In N/De N/De In Right Pressure
Aortic stenosis N N/In N/In In In N N N/In N Left Pressure
Ventricular septal defect N In In In N N/In In In N/In Left Volume
Tetralogy of Fallot N/In In N/De N/De N De/N/In De De N Right Pressure
Atrial septal defect In In N/In N N N/In N/In N/In N/In Left Volume
Acquired heart disease
Mital insufficiency N N/In In In N N N In N Left Fluid
Tricuspid insufficiency In In N N N N N N In Right Fluid
Aortic insufficiency N N In In N/In N N In N Left Fluid
Hypertrophic cardiomyopathy In In In In N N N/In N/In N/In Left>Right Myocardial
Dilated cardiomyopathy In In In In N N N/In N/In N/In Right>Left Myocardial
Pericardial effusion In In In In N N N/De N/De In Right Tamponade
RA, Right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; MPAs, main pulmonary artery segement; PAb, pulmonary artery branches; PV, Pulmonary vein; VC, caudal vena cava;
In, enlarged or increased; De, smaller or decreased; N, normal.
Chapter 2 Radiology of the Heart
43
44 Section I Diagnosis of Heart Disease
f0200
Figure 2-20. Right lateral view of the thorax taken with a flat panel detector system (DR). Note that all structures (bone, lung,
pulmonary vessels, spine, etc) are visible in the same image. There are no areas of overexposure or underexposure.
f0220
Figure 2-22. Technique independence. These three exposures were made with different mAs settings and identical kVp (90). A,
1.8 mAs. B, 2.5 mAs. C, 5.0 mAs. Note that all three exposures appear similar and are diagnostic. The computer software corrects
for under or overexposure automatically. This decreased the number of retakes and increases productivity. On the other hand, if
image A is magnified, it will appear much grainier than the other images.
46 Section I Diagnosis of Heart Disease
Electrocardiography
Larry P. Tilley and Francis W. K. Smith, Jr.
Electrocardiographic abnormalities are often pres A positive electrode is placed on the left side of the
ent with hypothyroidism and hyperthyroidism. chest, over the heart, and the negative electrode is
A pronounced sinus arrhythmia may be present placed in the area of the right shoulder or neck.
in animals with elevated vagal tone (often seen Esophageal ECG electrode lead for surgical mon
with diseases affecting the respiratory tract, cen itoring (Figure 3-3.) This technique is very use
tral nervous system, and gastrointestinal tract). ful as complexes recorded are increased in size,
providing an increased accuracy for diagnosing
an arrhythmia during surgery.
Principles of Hand-held, wireless ECG and ECG real time
Electrocardiography computer display represents new technology for
recording electrocardiograms (Figures 3-4 and
Surface Electrodes are Placed in a
3-5.)
Designated Fashion to Obtain Standard
Electrocardiographic Leads
Recording The
A lead consists of the electrical activity mea
Electrocardiogram
sured between a positive electrode and a negative
electrode. The electrocardiogram should be recorded in an
Electrical impulses with a net direction toward area as quiet and as free of distraction as possible.
the positive electrode will generate a positive Noises from clinical activity and other animals
waveform or deflection. Electrical impulses with may significantly affect rate and rhythm. Any
a net direction away from the positive electrode use of electrically operated equipment, such as
will generate a negative waveform or deflection. clippers, may cause interference and should be
Electrical impulses with a net direction perpen minimized during the electrocardiogram. In some
dicular to the positive electrode will not generate cases, fluorescent lighting may result in electrical
a waveform or deflection (isoelectric). interference.
Standard electrocardiographic lead systems are The patient should ideally be placed in right lat
used to create several angles of assessment. A sin eral recumbency.
gle lead would provide information on only one Electrocardiographic reference values were
dimension of the current (e.g., left vs. right). Two obtained from animals in right lateral recumbency.
leads would allow two-dimensional information Limbs should be held perpendicular to the
(e.g., left vs. right and cranial vs. caudal). As many body. Each pair of limbs should be held paral
as 12 leads may be acquired simultaneously. lel, and limbs should not be allowed to contact
one another.
The animal should be held as still as possible
Standard Lead Systems
during the electrocardiogram. When possible,
The standard leads are I, II, III, aVR, aVL, and aVF panting should be prevented.
(Figure 3-1, Box 3-1). Placement of electrodes to When dyspnea or other factors prevent stan
generate each lead is illustrated in Figure 3-2. dard positioning, the electrocardiogram may be
Leads I, II, and III are bipolar limb leads. These recorded while the animal is standing, or, less
are termed bipolar because the electrocardiogram ideally, sitting.
is recorded from two specific electrodes. Electrode placement
Leads aVR, aVL, and aVF are augmented unipolar Alligator clips or adhesive electrodes may be
leads. To generate these, two electrodes are elec used. To reduce discomfort, teeth of alligator
trically connected (as a negative electrode) and clips should be blunted and the spring should
compared with the single electrode (positive). be relaxed.
Precordial chest leads are obtained using an explor Limb electrodes are placed either distal or prox
ing unipolar positive electrode at specific locations imal to the elbow (caudal surface) and over the
on the chest. These leads may provide additional stifle. Electrodes placed proximal to the elbow
information or supportive evidence of cardiac cham may increase respiratory artifact.
ber enlargement. They are also useful in evaluating Each electrode should be wetted with 70 % iso
for the P wave when limb leads are equivocal. propyl alcohol to ensure electrical contact.
The base-apex lead is often used in equine Recording the electrocardiogram
electrocardiography and may also be used in Approximately three to four complete complexes
small-animal practice for rhythm assessment. should be recorded from each lead at 50mm/s.
Chapter 3 Electrocardiography 51
Figure 3-1. The limb leads (I, II, III, aVR, aVL, aVF) surround the heart in the frontal plane as shown in the top part of the
figure (feline). The circled limb lead names indicate the direction of electrical activity if the QRS is positive in that lead. The
mean electrical axis in this canine ECG (bottom part of the figure) is +90. Lead I is isoelectric. The lead perpendicular to lead I
is aVF (see axis chart on top). Lead aVF is positive, making the axis +90. If lead aVF had been negative, the axis would have
been90. (From Tilley LP: Essentials of canine and feline electrocardiography. ed 3, Malvern, Penn: 1992, Lea & Febiger.)
Figure 3-2. A, Three bipolar standard leads. By means of a switch incorporated in the instrument, the galvanometer can be
connected across any pair of several electrodes. Each pair of electrodes is called a lead. The leads illustrated here are identified as
I, II, and III. B, Augmented unipolar limb leads aVR, aVL, and aVF. (From Tilley LP: Essentials of canine and feline electrocardio
graphy: interpretation and treatment, ed 3, Malvern, Penn, 1992, Lea & Febiger.)
will shift to the right. Because the left ven The MEA may be determined using the six stan
tricle is normally the dominant ventricle, the dard leads and the Bailey axis system (see Figure
normal MEA is to the left. A degree system is 3-1). If there is a lead with isoelectric QRS com
usedif the MEA is directly to the left, then it plexes, then the MEA equates to the lead on the
is said to be 0 degrees; if the MEA is directly Bailey axis perpendicular to the isoelectric lead.
downward, then it is 90 degrees, and if it is The MEA may also be determined by plotting
directly to the right, then it is 180 degrees. The the net amplitude of a lead I QRS complex (hori
MEA of the normal dog is 40 to 100 degrees. zontal axis) and the net amplitude of a lead aVF
For the cat, the MEA is more variable, ranging QRS (vertical axis). The intersection will provide
from 0 to 160 degrees. the vector equal to the MEA (see Figure 3-1).
54 Section I Diagnosis of Heart Disease
Figure 3-3. Esophageal ECG electrode and temperature probe positioned for surgical monitoring. This technique is very useful as
complexes recorded are increased in size, providing an increased accuracy for diagnosing an arrhythmia during surgery.
Evaluation of Waveforms
P Wave
Atrial enlargement patterns (Figure 3-9)
The P wave is generated by atrial depolarization.
Atrial enlargement may result in an increase in
width or height of the P waves recorded in leadII.
Enlargement of the right atrium may result in an
increased P wave height. This is referred to as P-
pulmonale. The height of the P wave should not
exceed 0.4 mV (dog) or 0.2 mV (cat). Chronic pul
monary disease may result in P-pulmonale in the
absence of heart disease.
Figure 3-4. Hand-held, wireless ECG and ECG real time Enlargement of the left atrium may result in
computer display. (Courtesy Vmed Technology, Redmond, an increased P wave width or duration. This
Wash. www.vmedtech.com.) is referred to as P-mitrale. The duration of the
P wave should not exceed 0.04 second (dog or
cat). Left atrial enlargement may also result in
The MEA may be approximated by inspecting notching of the P wave.
leads I and aVF. Presence or absence of P waves
If the net direction of the lead I QRS is posi There is no minimum height or duration forthe P
tive, then the MEA is to the left. If the net wave. In some cases, P waves maybeindistinct.
deflection of the lead I QRS is negative, then In this situation, carefully evaluate all leads for P
the MEA is to the right. wave activity. If P waves cannot be discerned in
If the net direction of the lead aVF QRS is pos any of the limb leads, evaluation of chest leads is
itive, then the MEA is downward or caudal. If recommended.
the net deflection of the lead aVF QRS is nega P waves may be absent in several arrhythmias,
tive, then the MEA is upward or cranial. including atrial fibrillation and atrial standstill.
The approximate angle can be estimated by P waves may be superimposed on other wave
examining the relative amplitudes of leads I forms in ventricular tachycardia and supraven
and aVF. tricular tachycardia (SVT).
Determine the rhythm. Variation of P wave height is a normal finding
Compare patient values with reference values in the dog and a manifestation of alterations in
(Table 3-1). vagal tone.
Chapter 3 Electrocardiography 55
Figure 3-5. Wireless ECG printout report from laptop computer software system in Figure 3-4. (Courtesy Vmed Technology,
Redmond, Wash. www.vmedtech.com.)
SA
node
LA
A-V
node
RA
A-V
node
P LBB
Positive RBB
electrode P
P
RV LV R
Q
P
Q S
Figure 3-7. Sequence of electrical impulse conduction and cardiac chamber activation as it relates to the electrocardiogram.
(Modified from Tilley LP: Essentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Philadelphia, 1992,
Lea & Febiger.)
Figure 3-8. Close-up of a normal feline lead II P-QRS-T complex with labels and intervals. Measurements for amplitude (mil
livolts) are indicated by positive (+) and negative () movement; time intervals (hundredths of a second) are indicated from left
to right. Paper speed, 50 mm/s; sensitivity 1 cm=1 mV. (From Tilley LP: Essentials of canine and feline electrocardiography:
interpretation and treatment, ed 2, Philadelphia, 1985, Lea & Febiger.)
Chapter 3 Electrocardiography 57
Canine Feline
Heart rate (HR) Puppy: 70-220 bpm 120-240 bpm
Toy breeds: 70-180 bpm
Standard: 70-160 bpm
Giant breeds: 60-140 bpm
Rhythm Sinus rhythm Sinus rhythm
Sinus arrhythmia
Wandering pacemaker
P wave
Height Maximum: 0.4 mV Maximum: 0.2 mV
Width Maximum: 0.04 s (Giant breeds 0.05 s) Maximum: 0.04 s
PR interval 0.06-0.13 s 0.05-0.09 s
QRS
Height Large breeds: 3.0 mV maximum Maximum: 0.9 mV
Small breeds: 2.5 mV maximum
Width Large breeds: 0.06 s maximum Maximum: 0.04 s
Small breeds: 0.05 s maximum
ST segment
Depression No more than 0.2 mV None
Elevation No more than 0.15 mV None
QT interval 0.15-0.25 s at normal HR 0.12-0.18 s at normal HR
T waves May be positive, negative, or biphasic usually positive and<0.3 mV
Amplitude range0.05-1.0 mV in
any lead
Not more than of R wave
amplitude
Electrical axis +40 to + 100 0160
Chest leads
CV5RL (rV2) T positive; R<3.0 mV
CV6LL (v2) S<0.8 mV; R<3.0 mV R<1.0 mV
CV6LU (V4) S<0.7 mV; R<3.0 mV R<1.0 mV
V10 QRS negative; T negative except in T negative. R wave/Q wave<1
Chihuahua
S,Second.
*Measurements are made in lead II unless otherwise stated.
Not valid for thin, deep-chested dogs under 2 years old.
Figure 3-10. Severe right ventricular enlargement in a dog with pulmonic stenosis. There is a right axis deviation of approxi
mately 110 degrees. Note the deep S waves in leads I, II, III, aVF, and CvsLU. The T wave is positive in V10. (From Tilley LP: Es
sentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Philadelphia, 1992, Lea & Febiger.)
A
C
Chapter 3 Electrocardiography
Figure 3-11. A, Electrocardiogramelectrical alternans. B, ElectrocardiogramST segment elevation. C, ElectrocardiogramST segment depression.
59
60
Section I
D
Diagnosis of Heart Disease
Figure 3-11, contd. D, Electrocardiogramnormal sinus arrhythmia. E, Electrocardiogramsinus arrest. F, Electrocardiogramatrial premature complexes.
G
Torsades de pointes (turning about a point) is a not exceed one-fourth the height of the R wave,
rare arrhythmia in the dog. It is a form of poly one-fourth the height of the Q wave (if Q wave is
morphic ventricular tachycardia or flutter in greater than R wave), or 0.5 mV to 1.0 mV in any
which the amplitude of the complexes increases lead.
and decreases in size so that they appear to twist The T wave should be positive in CV5RL in dogs
around the baseline. Human patients with tors 2 months of age and should be negative in V10,
ades de pointes are at risk for sudden death. except in the Chihuahua.
Prominent T waves may occur with myocardial
Possible Formulas for Corrected QT intervals. hypoxia, interventricular conduction distur
Many formulas and methods for correcting the QT bances, ventricular enlargement, and in some ani
interval for the effects of heart rate, including log mals with heart disease and bradycardia.
arithmic, hyperbolic, and exponential functions, Prominent and peaked T waves are associated
but they also have limitations. These limitations with hyperkalemia.
result from both physiological and computational Small, biphasic T waves may occur with
problems. The Bazetts formula, for example, hypokalemia.
predicts an ever-increasing increment in the Nonspecific T wave changes may occur with
QT interval as the heart rate slows and an ever- metabolic disturbances (hypoglycemia, anemia,
decreasing increment as the rate rises, both of which shock, fever), drug toxicity (digoxin, quinidine,
are physiologically improbable. In addition, all procainamide), and neurologic disease.
these formulas do not account for the effects of T wave alternans has been reported second
autonomic tone on the QT interval independent ary to hypocalcemia, increased circulating cat
of the effects on rate. They also do not account for echolamines, and sudden increases in sympathetic
the relatively slow adaptation of repolarization to tone.
changes in rate. Fridericias formula (QT divided
by the cube root of the R-R interval) is a modi
fication of Bazetts formula. This modification is Arrhythmias and
important, because Bazetts formula will over Conduction Disturbances
correct for rates higher than 60 bpm. Van de Wa An arrhythmia (or dysrhythmia) refers to an
ter formula (study was done in dogs) involves irregularity in the cardiac rhythm. In general, an
regression analysis yielding the following equa arrhythmia denotes an abnormality of the car
tion: QTc=Van de Water formula=QT87(60/ diac rhythm, although in the dog the term normal
HR1). Recent publications have recommended sinus arrhythmia is used to describe the normal
the use of the log-log formula for correcting the variation in heart rate associated with respiration
QT interval for heart rate (Linear regression with (see Box 3-2).
logcHR as the covariate: QT=a + b (logcHR); Arrhythmias may be classified according to
a & b are constants). their origin.
Prolongation of the QT interval may occur with Supraventricular arrhythmias arise from the
interventricular conduction disturbances that atria or AV node.
are associated with prolongation of the QRS Ventricular arrhythmias arise from the
complexes, bradycardia, ethylene glycol toxic ventricles.
ity, strenuous activity, or CNS disturbances. QT Arrhythmias may be classified according to
prolongation has been reported with many drugs their rates.
and electrolyte imbalances. These include hypo Arrhythmias with slow rates are referred to as
kalemia, hypocalcemia, quinidine, procainamide, bradyarrhythmias.
bretylium, tricyclic antidepressants and many Arrhythmias with rapid rates are referred to
anesthetics. as tachyarrhythmias.
Shortening of the QT interval may occur with Arrhythmias may be classified according to
hypercalcemia, hyperkalemia, or digoxin therapy. their regularity.
Fibrillation is an irregular, chaotic rhythm.
Tachycardia is a regular (non irregular) rhythm.
T Wave
Examples: Atrial fibrillation is an irregular,
The T wave is quite variable in the dog and cat. chaotic arrhythmia originating from the atria;
In most leads, the T wave may be positive, nega ventricular tachycardia is a regular arrhythmia
tive or biphasic. The height of the T wave should originating from the ventricles.
64 Section I Diagnosis of Heart Disease
There are several pathophysiologic causes of Check for pauses in the rhythmperiods of
arrhythmias. inactivity greater than two R-R intervals.
Abnormal automaticity of normal pacemaker Check for P waves occurring prematurely
cells (occurring earlier than expected)distinguish
Shift of the pacemaker from the SA node to from normal sinus arrhythmia, where P wave
other areas of the heart rate increases during inspiration. Premature
Conduction blocks that terminate or slow nor P waves will noticeably break the rhythm. Pre
mal conduction through the heart mature P waves indicate the presence of atrial
Abnormal pathways of impulse conduction premature complexes (APCs).
through the heart Check for QRS complexes occurring prema
Spontaneous impulse formation in any area of turely. These may occur without preceding
the heart P wave, may be superimposed on P wave,
Systemic approach to arrhythmia recognition and or may follow P wave with shortened PR
evaluation interval. Premature QRS complexes indicate
Any lead may be used for arrhythmia evalua presence of VPCs.
tionlead II is generally used as waveforms
are usually best defined in this lead. A signifi
cant duration of artifact-free lead II should be
Key Point
carefully evaluated.
Determine if P waves are present. Examine all Remember, a ventricular premature complex
leadsP waves may be small or isoelectric in is premature. A ventricular complex occurring
several leads. You must distinguish baseline after a pause is not prematureit is a ven
tricular escape complex.
motion (artifact) from P waves. P waves are
generally consistent in size and distance from
associated QRS complex. The presence of
P waves indicates a sinus (originating from SA
node) rhythm. Evaluation of PR interval
D etermine if an atrial (P wave) and ven PR interval may vary slightly with changes in
tricular (QRS complex) association exists. vagal tonethis would also result in a sinus
There should be a P wave for every QRS arrhythmia.
complex. If there are a greater number of P Progressive prolongation of the PR interval
waves or QRS complexes, then an arrhyth signals first degree AV block.
mia exists. P waves without associated QRS complexes
P waves should slightly precede QRS are usually indicative of second degree AV
complexes. block
If P waves follow the QRS complex, then AV Shortened PR interval may be seen with
dissociation exists, and the rhythm is ventric increased sympathetic tone and pre-excitation
ular or junctional rather than sinus. syndromes (presence of accessory pathway
There should be a QRS complex following bypassing AV node).
each P wave. If not, then a conduction distur Evaluation of QRS complexes
bance is present. Height of R wave and duration of QRS complex
Determine the regularity of the rhythm. Presence of prominent S waves
Normal sinus rhythminsignificant (less Morphology of QRS complexes should not
than 10%) variation in the P-P or R-R vary significantly. Variation may be caused by:
intervals VPCs or ventricular escape complexes
Normal sinus arrhythmiasignificant (more Fusion beatssimultaneous occurrence of
than 10%) variation in the P-P or R-R VPC and normal QRS
intervals Electrical alternans
A pattern of irregularity is usually noted Intermittent bundle branch block
the heart rate increases during inspiration Artifact
and decreases during expiration in a cycli Premature QRS complexes suggest VPCs;
cal pattern. QRS complexes without P waves and oc
This may be referred to as a respiratory curring after a pause suggest ventricular
sinus arrhythmia. escape complexes.
Chapter 3 Electrocardiography 65
Key Point
Disturbances of Sinus
QRS complexes should not vary in their mor
phology in a normal animal.
Impulse Formation
Sinus Arrest
When the SA node fails to discharge as expected,
Normal Rhythms a pause in the rhythm will occur. The duration
of the pause is at least twice the preceding R-R
Normal Sinus Rhythm interval. When severe, pause duration may be 5
Normal rhythm in the dog and cat to 12 seconds (Figure 3-11, E).
P wave for every QRS complex, regular rhythm For survival, the pause is ended by a ventricular
Rate between 60 bpm and 180 bpm for the dog, escape complex, junctional escape complex, or
depending on size of dog and degree of anxiousness normal complex.
Rate between 140 bpm and 240 bpm for the cat, Causes include fibrosis of the SA nodal tis
depending on degree of anxiousness sue, greatly increased vagal stimulation, drug
Rate and rhythm dependent on SA nodal dis influences (digoxin, beta blockers), and rarely
charge. This is highly influenced by changes in neoplasia.
autonomic tone. An elevated sympathetic tone If severe and frequent, intermittent weakness or
will increase rate of SA nodal discharge; an ele syncope may occur.
vated parasympathetic (vagal) tone will decrease
rate of SA nodal discharge. Sinus Bradycardia
A sinus rhythm with an abnormally slow rate
Normal Sinus Arrhythmia May be physiologicduring sleep, the heart rate
Normal in the dog, generally abnormal in the cat of many dogs drops to 30 to 40 bpm. Calm ani
A pattern of irregularity is presentthe heart mals or athletic animals at rest may have a physi
rateincreases during inspiration and decreases ologic sinus bradycardia.
during expiration in a cyclical pattern (Figure Elevated vagal tone may result in a sinus bradycardia.
3-11, D). Drug-inducedanesthetics and sedatives, di
Irregularity is secondary to fluctuations in vagal goxin, calcium channel blockers, beta blockers
tone associated with the respiratory cycle. Pathologichypothermia, hypothyroidism, sick
When respiratory effort is increased (brachyce sinus syndrome (SSS)
phalic breeds, animals with respiratory disease), Specific therapy for sinus bradycardia is not
fluctuations in vagal tone may be dramatic, pro warranted unless clinical signs (weakness,
ducing a pronounced sinus arrhythmia. reduced cardiac output) have developed as a
Normal sinus arrhythmia is a rhythm of high result of the arrhythmia.
vagal tone and low sympathetic tonethis situ
ation is rare in dogs with congestive heart failure. Sinus Tachycardia
The presence of a sinus arrhythmia in a dog with A sinus rhythm with an abnormally rapid rate
severe cough is more supportive of primary respira May be physiologicassociated with exercise,
tory disease rather than congestive heart failure. stress, anxiousness, pain
Drug-inducedatropine or glycopyrrolate,
Wandering Sinus Pacemaker methylxanthines (theophylline), excessive thyroid
The origin of SA nodal discharge may change as supplementation, catecholamines (epinephrine,
a consequence of alterations in vagal tone. This dobutamine)
is noted on the electrocardiogram as a cyclical Pathologicfever, shock, hyperthyroidism, ane
change in the height of the P wave. At times, the P mia, hypoxia, and congestive heart failure
wave may become isoelectric and not detectable. Specific therapy for sinus tachycardia is usually
Often associated with normal sinus arrhythmia or indicated for rate control in congestive heart fail
pronounced sinus arrhythmia. ure patients.
66 Section I Diagnosis of Heart Disease
A
Section I
B
Diagnosis of Heart Disease
F
Chapter 3 Electrocardiography
Figure 3-12, contd. D, Electrocardiogramthird-degree AV block. E, Electrocardiogramright bundle branch block. F, Electrocardiogramunifocal ventricular premature
complexes.
69
70
Section I
G
Diagnosis of Heart Disease
Figure 3-12, contd. G, Electrocardiogrammultiform ventricular premature complexes. H, Electrocardiogramrun of ventricular premature complexes.
Chapter 3 Electrocardiography 71
Third-Degree Atrioventricular Block The presence of an LBBB does not impair car
(Complete Heart Block) diac performance directly, but is a marker of sig
All conduction through the AV node is blocked. nificant heart disease.
Atrial and ventricular depolarizations are no lon
ger coordinated and occur independently of one Key Point
another. Ventricular depolarization is initiated by Complete heart block will occur if right bun
discharge of a ventricular escape focus. dle branch block (RBBB) develops in an ani
Electrocardiographic features (see Figure 3-12, D) mal with LBBB.
There is no association between P waves and
QRS-T complexes.
P waves are of normal morphology and usually Left Anterior Fascicular Block
occur at a normal rate. There is a block in the left anterior fascicle of the
QRS complexes are of ventricular origin left bundle branch slowing depolarization of the
morphology. left ventricle.
Ventricular rate is typically 30 to 50 bpm. Electrocardiographic features
Causes include fibrosis of the AV node, drug-in QRS duration is within normal limits
duced (digoxin), infiltrative disease, Rickettsial Left axis deviation (dog less than 40 degrees,
myocarditis, hyperkalemia. cat less than 0 degrees)
Usually associated with clinical signs of weak Small Q wave and tall R wave in leads I and
ness or collapse. Complete AV block warrants aVL (small Q wave not consistent)
implantation of a permanent pacemaker in most Deep S waves in leads II, III, and aVF
cases. (exceeding R wave)
Associated with feline hypertrophic cardiomy
Left Bundle Branch Block opathy, other diseases associated with left ven
A conduction delay or block in both the left pos tricular hypertrophy, hyperkalemia, ischemia,
terior and the left anterior fascicles of the left bun and post-cardiac surgery
dle. A supraventricular impulse activates the right
ventricle first through the right bundle branch. Key Point
Left ventricular depolarization is delayed.
Electrocardiographic features (Figure 3-14) Left anterior fascicular block does not directly
impair cardiac function, but if present, then
Prolongation of QRS duration (>0.08 second
one should look for underlying etiologies.
for the dog;>0.06 second for the cat)
QRS wide and positive in leads I, II, III, and aVF
Unlike VPCs, the QRS complex is associated
with a preceding P wave. Right Bundle Branch Block
May be difficult to distinguish from left ven There is block of the right bundle branch, delay
tricular enlargement pattern ing depolarization of the right ventricle.
Causes include structural heart disease (car Electrocardiographic features (Figure 3-12, E)
diomyopathy, congenital anomalies, neoplasia, QRS duration increased
trauma, fibrosis) Prominent S waves in leads I, II, III, and aVF
Figure 3-14. Intermittent left bundle branch block in a dog. The QRS complexes are wider and taller than normal in the fourth,
fifth, and sixth complexes. (From Fox PR, Sisson D, Moise NS, eds: Textbook of canine and feline cardiology, St Louis, 1999,
Elsevier.)
Chapter 3 Electrocardiography 73
output may be significantly impaired, and Atrial Premature Complexes with Aberrant
the arrhythmia predisposes to ventricular Conduction
fibrillation. When the impulse of an APC encounters an area of
refractoriness (AV node, bundle of His, or ventricu
Ventricular Fibrillation lar myocardium), it may terminate or continue with
Completely irregular, chaotic variable fibril aberrant conduction. The latter may result in a wide
lation potentials, indicating lack of organized and bizarre QRS configuration resembling a beat of
ventricular depolarization and impending ventricular origin.
death Most often occurs at slow heart rates
Electrocardiographic features (Figure 3-15, B) QRS may take the form of RBBB.
There is no evidence of organized cardiac
depolarization (absence of P-QRS-T waves)
Wavy, undulating baseline Escape Rhythms
Coarse ventricular fibrillation is character Junctional Escape Beat
ized by large wavelets. When not activated by atrial depolarization, the
Fine ventricular fibrillation is characterized junctional AV nodal area may spontaneously dis
by small wavelets. charge. This impulse results in ventricular depo
larization in a normal fashion. Junctional escape
Key Point beats may occur when there is a significant pause
in the sinus rhythm.
Ventricular fibrillation indicates cardiopul Electrocardiographic features
monary arrest, and immediate restoration of Inverted P wave, occurring before, during, or
rhythm is required to preserve life.
just after QRS complex
Normal or relatively normal QRS complex
Ventricular Asystole Occurs after significant pause in sinus rhythm
Lack of any significant ventricular electrical activity Clinical significancethis complex is adaptive
Electrocardiogram demonstrates flat baseline and helps to maintain cardiac output in the face
occasional ventricular escape complexes may of a slow rate or sinus arrest.
occur
A terminal rhythm requiring immediate restora
Key Point
tion of rhythm to preserve life
Junctional escape beats should not be sup
pressed.
Disturbances of Both
Impulse Formation and Junctional Rhythm
Impulse Conduction Succession of junctional escape beats in absence
Sick Sinus Syndrome of adequate sinus node function
SSS is a progressive heart disease charac Rate of junctional escape rhythm is typically
terized by a variety of arrhythmias, including 40 to 60 bpm.
sinusbradycardia, sinus arrest, paroxysmal This rhythm is adaptive and should not be sup
atrial tachycardia (bradycardia-tachycardia pressed. Correction of the cause of sinus node
syndrome), intermittent AV nodal block, and dysfunction is warranted.
lack of ventricular escape complexes (Figure
3-15, C). Ventricular Escape Beat
Breeds predisposed include Miniature Schnau When not activated by atrial depolarization, a
zers, Cocker Spaniels, Dachshunds, Pugs, West ventricular focus may spontaneously discharge.
Highland White Terriers. SSS is most common in This impulse results in an abnormal ventricular
older female dogs. depolarization, but contraction is not affected.
The cause is unknown but likely involves idio Ventricular escape beats may occur when there is
pathic degeneration of the conduction system. a significant pause in the sinus rhythm and lack of
Most cases are presented with a history of inter junctional escape complexes.
mittent weakness and collapse. Electrocardiographic features
Medical therapy may be successful in some cases; Ventricular escape beat occurs following a
many require pacemaker implantation. pause in the rhythm
A
C
Chapter 3 Electrocardiography
QRS wide and bizarre, consistent with ventric Ventricular parasystole focus is located within
ular origin ventricular myocardium and produces regularly
Clinical significancethis complex is adaptive spaced QRS complexes. When the focus dis
and helps to maintain cardiac output in the face charges during the ventricles refractory period,
of a slow rate or sinus arrest. a QRS will not be created.
Suggested Readings Miller MS, Tilley LP, Detweiler DK: Cardiac electro
physiology. In Dukes physiology of domestic ani
Davis AS, Middleton, BJ: Relationship between QT mals, ed 11, Ithaca, NY, 1993, Cornell.
interval and heart rate in Alderley Park beagles, Redfern WS, Carlsson L, Davis AS, Lynch WG, Mac
Record, 145:248-250, 1999. Kenzie I, et al: Relationships between preclinical
Detweiler DK: The dog electrocardiogram: a critical cardiac electrophysiology, clinical QT interval prolon
review. In MacFarlane, PW, Lawrie, TDV, eds: Com gation and torsade de pointes for a broad range of
prehensive electrocardiography: theory and practice drugs: evidence for a provisional safety margin in
in health and disease, New York, 1998, Pergamon drug development. Cardiovasc Res, 58, 32-45, 2003.
Press. Smith, FWK, Tilley, LP, Miller, MS: Disorders of cardiac
Ettinger SJ Le Bobinnec G, Cote E: Electrocardiography. rhythm. In Brichard, SJ, Sherding, RG, eds: Manual
In Ettinger SJ, Feldman EC, eds: Textbook of Vet of small animal practice, ed 3, St Louis, 2007, WB
erinary internal medicine, ed 5, St Louis, 2000, WB Saunders.
Saunders. Smith FWK, Tilley, LP, Miller, MS. Electrocardiography.
Finley MR, Lillich JD, Gilmour RF, Freeman LC: In Brichard, SJ, Sherding, RG, eds: Manual
Structural and functional basis for the long QT syndrome: of small animal practice, ed 3, St Louis, 2007,
relevance to veterinary patients. J Vet Med 17:473-488, WB Saunders.
2003. Tilley LP: Essentials of canine and feline electrocardio
Kittleson MD: Electrocardiography. In Kittleson MD, graphy, ed 3, Ames, Iowa, 1992, Blackwell.
Kienle RD, eds: Small animal cardiovascular medi Tilley LP, Miller MS, Smith FW, Jr: canine and feline
cine, St Louis, 1998, Mosby. cardiac arrhythmias: self-assessment. Ames, Iowa,
Miller MS, Tilley LP, Smith FWK Jr, Fox PR, Electro 1993, Blackwell.
cardiography. In Fox PR, Sisson D, Moise NS, eds:
Textbook of canine and feline cardiology, St Louis,
1999, Elsevier.
Chapter 4
Figure 4-1. Right parasternal echocardiographic views. A, Long-axis four-chamber view optimized for left ventricular inlet.
B, Long-axis view optimized for left ventricular outflow tract. C, Short-axis view at the papillary muscle level.
Continued
80 Section I Diagnosis of Heart Disease
Figure 4-1. contd. D, Short-axis view at chordal level. E, Short-axis view at mitral valve level. F, Short-axis view at the heart base,
optimized for left atrium and aortic valve.
Continued
Chapter 4 Echocardiography and Doppler Ultrasound 81
Figure 4-1. contd. G, Short-axis view at the heart base, optimized for pulmonary artery. LA, Left atrium; LV, left ventricle; RA,
right atrium; RV, right ventricle; Ao, aorta; R, right coronary sinus of Valsalva; L, left coronary sinus of Valsalva; NC, noncoronary
sinus of Valsalva; PA, pulmonary artery; rPA, right pulmonary artery.
Tissue Doppler imaging (TDI), where the velocity times as a receiver or transmitter of ultrasound
of myocardial motion is displayed (Figure 4-5, E) waves, allowing the interrogation of blood flow
velocities within a specific region of interest.
This region of interest is represented as a sample
Spectral Doppler Echocardiography
volume on the cursor.
A graph of blood flow velocity against time Pulsed wave Doppler has limitations in the maxi-
is shown, usually with a simultaneous ECG mum velocities that it can display without ambigu-
display. ity: high velocities result in aliasing, where blood
Blood flow velocities toward the transducer are flow will be displayed as both positive and negative
displayed as positive (above the baseline), and velocities (i.e., signal wraps around the baseline).
blood flow velocities away from the transducer The velocity at which aliasing will occur depends
are displayed as negative (below the baseline). on the Nyquist limit (half the pulse repetition
The Doppler shift can also be represented by an frequency), with higher velocities without alias-
audible sound, because the shift in frequency is ing achieved at lower transducer frequencies, and
usually quite small and within the audible range reduced depth from the transducer.
(around 10 kHz), so that most machines will
show a visual spectral display with a simultane- Continuous Wave Doppler
ous audible signal. In contrast, with continuous wave (CW) Doppler,
Spectral Doppler is usually recorded with guid- ultrasound waves can be transmitted and received
ance from two-dimensional echocardiographic simultaneously. This allows much higher veloci-
images (2D-Doppler, or Duplex Doppler). This ties to be displayed, but it is not possible to draw
allows a cursor to be superimposed over a 2D any conclusions about the depth along the cursor
image, showing the angle of interrogation of the from where these velocities are originating (i.e.,
Doppler beam in two dimensions. there is range ambiguity).
Spectral Doppler can be further subdivided into
pulsed wave, continuous wave, and high-pulse High-Pulse Repetition Frequency Doppler
repetition frequency. High-Pulse repetition frequency Doppler is a form
of pulsed Doppler that shares some similarities
Pulsed Wave Doppler with CW Doppler. Frequent pulses of ultrasound
The ultrasound waves are transmitted as pulses waves are produced so that a number of sample
of waves, with the transducer acting at different volumes will be superimposed on the 2D image.
82 Section I Diagnosis of Heart Disease
Figure 4-2. M-mode echocardiograms of the left heart at the mitral valve chordal level (note that the 2D image is moved to the
left of the screen to allow correct placement of the cursor) (A); mitral valve leaflet level (B); aortic valve level.
Continued
Chapter 4 Echocardiography and Doppler Ultrasound 83
Figure 4-2. contd. (C). IVS, Interventricular septum; LV, left ventricle; LVFW, left ventricular free wall; RV, right ventricle;
Ao, aorta; LA, left atrium; LAur, left auricle.
This not only allows the display of higher veloci- indices, because they may be less influenced by
ties without aliasing, but also increases the num- loading conditions.
ber of possible sites from which the velocities are
being recorded. Applications
Doppler echocardiography is most often used to
Color Flow Doppler characterize abnormal direction or velocity of
Color flow Doppler represents the velocity and blood flow, or to indicate the origin of turbulent
direction of blood flow in color, superimposed blood flow. This is invaluable in valve disease or
on a black-and-white 2D image. In effect, the congenital heart disease, but Doppler echocardiog-
color is displayed within a very large sample vol- raphy may also be used to estimate flow volumes,
ume superimposed on the 2D image. Blood flow to assess systolic and diastolic function, and to ob-
away from the transducer is shown in blue, and tain information about intracardiac pressures.
blood flow toward the transducer is displayed in Abnormal blood flow direction may be noted
red (BART: blue away, red toward). Disturbed with conditions such as valvular insufficiency.
or turbulent flow may be displayed in green or Abnormal blood flow velocity may be a clinically
yellow. Aliasing may also occur in color flow useful finding, as the velocity of blood flow across
Doppler. an orifice is chiefly determined by the difference
in pressure. If there is a large difference in the
Tissue Doppler Imaging pressures in the chambers on each side of a valve,
More sophisticated machines may include fa- then the velocity of flow across the valve will be
cilities for recording the velocity of myocardial high. For example, during systole the pressure in
motion. The signals reflected by the moving the left ventricleisvery high, and the pressure
myocardium are high amplitude, but low veloc- in the left atrium is very low. If the mitral valve
ity. These myocardial velocities can be displayed is incompetent and regurgitation occurs, then
in spectral format, as a color display, or as color the velocity of the regurgitant jet traveling from
M-mode. It is believed that TDI indices may have the left ventricle to the left atrium will be very
advantages over conventional echocardiographic high, reflecting the large difference in pressures.
84 Section I Diagnosis of Heart Disease
C
Chapter 4 Echocardiography and Doppler Ultrasound 85
Figure 4-3. Doppler echocardiographic studies. A, Mitral inflow obtained from the
left caudal parasternal (apical) four-chamber view, with the cursor placed parallel with
mitral inflow, and a small sample volume placed at the tips of the mitral valve leaflets
when the mitral valve is open. The typical spectral Doppler waveform of mitral inflow
displays an early diastolic (E) wave and an atrial contraction (A) wave of filling. B, Aortic
flow obtained from the left caudal parasternal (apical) five-chamber view, showing
left ventricular outflow tract and placement of pulsed wave sample volume in ascend-
ing aorta. The typical spectral Doppler waveform of aortic flow is displayed. C, Aortic
flow obtained from the subcostal view, showing continuous wave cursor positioned
in ascending aorta. The typical spectral Doppler waveform of aortic flow is displayed.
D, Tricuspid valve flow obtained the left cranial parasternal view optimized for right
ventricular inflow. The pulsed wave sample volume is placed at the tricuspid leaflet tips,
with the probe in a cranial position. The spectral waveform is similar to that of mitral
inflow, although sometimes an additional systolic forward flow wave is recorded. E,
Pulmonary artery flow from the right parasternal short-axis view optimized for right
ventricular outflow (left panel) with the pulsed wave sample volume positioned in the
main pulmonary artery, and from the left cranial parasternal view optimized for the
pulmonary artery (middle panel). The typical spectral Doppler waveform of pulmonary
artery flow is displayed. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right
ventricle; CdCV, caudal vena cava; Ao, aorta; RVOT, right ventricular outflow tract; PA,
pulmonary artery.
86 Section I Diagnosis of Heart Disease
A B C
D E
Figure 4-4. Color flow echocardiographic studies of mitral regurgitation. A, Mild mitral regurgitation. The color jet occu-
pies<20% of the left atrial area. B, Moderate mitral regurgitation. The color mitral regurgitation jet occupies 20% to 40% of
the left atrial area. C, Severe mitral regurgitation. The color jet occupies>40% of the left atrial area (the jet is rebounding from
the dorsal LA wall in red), the vena contracta is wide, and a proximal flow convergence region can be seen. D, Right parasternal
long-axis view of a dog with severe mitral regurgitation, showing a large vena contracta width (black arrow). E, Left apical view of
a dog with severe mitral regurgitation, showing a large proximal flow convergence region. The white arrows indicate the borders
of the hemisphere where aliasing is occurring. The larger the hemispheres diameter for a particular aliasing velocity (in this case
69 cm/s), the more severe the mitral insufficiency.
B C D
Figure 4-5. Echocardiographic evaluation of ventricular diastolic function. A, Normal transmitral flow pattern demonstrating an
early filling wave (E) with higher velocity than the atrial contraction wave (A). B, Delayed relaxation transmitral flow pattern dem-
onstrating reduced amplitude and prolonged duration of the E wave. C, Pseudonormal transmitral flow pattern demonstrating a
normal E:A velocity ratio, but this is the result of the combined effects of delayed relaxation, increased LA pressures and increased
LV stiffness. D, Restrictive transmitral flow pattern. High LA pressures result in increased E wave amplitude despite delayed relax-
ation. Decreased LV compliance (sometimes with atrial systolic dysfunction) results in a diminished A wave. E, Pulsed wave tissue
Doppler (TDI) image of mitral annulus velocity, displaying a systolic wave (S), early diastolic wave (E) and atrial wave (A).
Figure 4-6. M-mode measurements of the left heart and aorta. A, M-mode at chordal level, showing measurements at end-diastole
(onset of QRS) and end-systole (peak septal motion). Septal thickness in diastole (IVSd), left ventricular diameter in diastole (LVDd), left
ventricular free wall in diastole (LVFWd), septal thickness in systole (IVSs), left ventricular diameter in systole (LVDs), left ventricular free
wall in systole (LVFWs). B, M-mode measurements at mitral valve level, showing an increased E-point to septal separation (EPSS) of
15.6 mm. C, M-mode measurements at the atrial and aorta level showing measurement of left atrial (LA) and aortic (Ao) diameter.
Chapter 4 Echocardiography and Doppler Ultrasound 93
Figure 4-7. Measurement of the left atrial (LA) and aortic (Ao) diameters from the right parasternal short-axis view (A) and LA
diameter from the right long-axis view optimized for the left ventricular inlet (B).
Figure 4-8. Echocardiographic evaluation of ventricular systolic function. A, M-mode of ventricular hypokinesis from a dog
with dilated cardiomyopathy (DCM) (left panel), normal ventricular motion from a healthy dog (middle panel), and ventricular
hyperkinesis from a dog with mitral regurgitation (MR) (right panel).
Continued
Dilated Cardiomyopathy
basis of a low fractional shortening value alone
Overt DCM is a relatively easy diagnosis to make, (especially in dogs of nonpredisposed breeds).
with global hypokinesis of a dilated heart in the Dilation of LA and LV
absence of any other lesions (Figure 4-11). Occult Dilation of RA and RV
DCM may be more difficult, and caution is required LV hypokinesis ( FS%, EF%)
in diagnosing DCM in asymptomatic dogs on the EPSS
Chapter 4 Echocardiography and Doppler Ultrasound 95
Figure 4-8. Contd. B, Measurement of left ventricular volume from a right parasternal long-axis view. The endocardial borders are
traced, with the left ventricular length measured from a line drawn across the mitral annulus to the apex. LA, Left atrium; RA, right atri-
um; RV, right ventricle. C, Spectral Doppler aortic blood flow velocity, showing preejection period (PEP) and LV ejection time (LVET).
Hypertrophic Cardiomyopathy
Thrombus or spontaneous echocontrast (smoke)
Feline hypertrophic cardiomyopathy (HCM) is may be present in left auricle
very common, and a spectrum of disease exists.
Severe HCM is easy to diagnose (Figure 4-12),
Pericardial disease
but mild HCM may be very difficult (focal hy-
pertrophy may be the only recognizable feature Pericardial effusions can be identified as an
that distinguishes mild HCM from a normal heart echo-free space around the heart, although
with a functional murmur). they may be confused with pleural effusions.
Septal or free wall thickness in diastole>6.0 Tamponade may be suggested by collapse of
mm on 2D and/or M-mode the right atrial wall. The heart may be affected
LA may or may not be dilated (depending on by a number of different neoplasms which can
degree of hemodynamic compromise) result in pericardial effusions, and these may
Systolic anterior motion of the mitral valve often be best imaged while some pericardial fluid is
present (hypertrophic obstructive cardiomyopathy) present.
96 Section I Diagnosis of Heart Disease
Figure 4-9. CW spectral Doppler recording of high-velocity flow in pulmonary artery in a dog with severe pulmonic stenosis. The
measured peak velocity of 5.47 m/s corresponds with a pressure gradient of 119.8 mm Hg across the pulmonic valve.
LV
4
LA
Figure 4-10. Right parasternal long-axis view of dog with myxomatous mitral valve disease, showing thickened, distorted
mitral leaflets with prolapse of the anterior leaflet.
Chapter 4 Echocardiography and Doppler Ultrasound 97
LV
LA
Figure 4-11. Right parasternal long-axis view of a dog with dilated cardiomyopathy, showing a rounded LV with normal mitral
valve morphology (and no mitral valve prolapse).
LV
LA
Figure 4-12. Right parasternal long-axis view of a cat with hypertrophic cardiomyopathy, showing marked LV hypertrophy.
Chemodectomas generally involve the heart base to image at this site. They may also infiltrate
and may be imaged as homogeneous soft tissue other areas of the heart (such as the septum
densities encircling the aortic and pulmonary ar- and ventricular walls) where they may have
tery roots. They may be associated with pericar- an irregular echotexture compared with sur-
dial effusion. rounding myocardium. Right atrial hemangio-
Hemangiosarcomas frequently affect the right sarcomas are often associated with pericardial
atrium, although they can be very difficult effusions.
98 Section I Diagnosis of Heart Disease
Introduction Technique
Many special diagnostic techniques are available Continuous electrocardiographic monitoring re-
for evaluation of animals with cardiovascular dis- quires an ECG unit with an oscilloscope or light-
ease. Ambulatory electrocardiographic equipment emitting diode (LED) display.
is available through various services, continu- Use of a chest lead configuration with adhesive
ous in-hospital electrocardiographic monitoring electrode patches will minimize artifacts on the
equipment is widely available, and several large tracing while allowing the patient the most free-
diagnostic laboratories provide specialized clinical dom for mobility.
pathology services. Additionally, veterinary car- Clip two 2- to 3-cm square areas at the left apex
diology referral centers are increasingly available and the heart base (where the apex beat is pal-
for special diagnostic techniques such as cardiac pable on the left chest and at the heart base caudal
catheterization. to the right or left scapula).
Clean and de-fat the area with 70% isopropyl al-
cohol. Allow to dry.
Continuous In-Hospital Place the positive electrode patch at the left api-
Electrocardiographic cal site and the negative electrode at the heart
Monitoring base site. A ground electrode may be placed at
Continuous electrocardiographic monitoring is either site (Figure 5-1).
recommended for hospitalized patients at risk of Apply a light chest wrap to secure the electrodes
heart rate or rhythm disturbances. These patients and wires.
include: If a multiple-lead electrocardiographic (ECG) unit is
Patients with congestive heart failure being used, then use the left arm electrode for the pos-
Patients hospitalized with clinical signs (e.g., itive electrode, the right arm electrode for the nega-
syncope) secondary to arrhythmia tive electrode lead, and lead I for display/recording.
Patients with systemic disease that puts them at If the patient is recumbent and unlikely to move, leads
risk for arrhythmias (e.g., shock, sepsis, gastric attached directly to the patient limbs can be used.
dilation-volvulus, etc.) Depending on the unit available, the signal
is transmitted to the machine by cables or by
*John Karl Goodwin contributed to previous versions of this chapter. radiotelemetry.
99
100 Section I Diagnosis of Heart Disease
Vagal Maneuver
The techniques listed below can be used for ele-
vating vagal tone. The patient should be restrained
and calm so that a good quality lead II ECG is
obtained prior to and during the technique.
Figure 5-1. Chest lead preparation in a Boxer. The
Ocular Pressure
negative lead should be placed in the upper patch behind
the scapula and the positive lead should be placed at the Moderately firm digital pressure is applied over
left apex (behind the elbow). This configuration can be used the closed eyelid to one or both eyes for a period
for in hospital continuous ECG monitoring or ambulatory of 5 to 10 seconds or until significant slowing of
monitoring.
the heart rate occurs.
Many ECG units will print out an ECG strip, which Carotid Body Massage
can be added to the permanent patient record. The carotid bodies are located in the area behind
the larynx. Apply moderate digital pressure around
the larynx while monitoring the ECG. Initiation of
Limitations
a gag response or a cough yields similar results
Excessive patient motion may result in displace- and suggests adequate pressure has been applied.
ment of electrodes or motion artifact in the ECG.
Adhesive patches may occasionally result in con-
Inhibition of Vagal Tone
tact dermatitis.
Two techniques are possible for abolishing vagal
tone and are useful if the patient is suspected to have
Provocative
a vagally mediated bradycardia. With either tech-
Electrocardiographic
nique, it is important to first obtain a baseline ECG.
Techniques
In some patients, the history or baseline ECG is sug- Postexercise Electrocardiography
gestive of pathologic arrhythmias, but a definitive Typically, strenuous leash running is used; how-
diagnosis is elusive. In these cases, vagal stimula- ever, the duration of exercise is not standardized.
tion or abolition may be informative. A provocative Evidence of exertion, such as panting, is sufficient
vagal maneuver will transiently elevate parasympa- to stop exercise and an immediate post-exercise
thetic tone. In normal animals, the technique typi- ECG is obtained. A delay of as little as 30 seconds
cally slows the heart rate or has no effect. However, may alter results, and heavy panting can result in
when there is sinoatrial or atrioventricular (AV) artifacts making the ECG difficult to interpret.
nodal dysfunction, or an abnormal sensitivity to
parasympathetic tone, transient sinus arrest or sig- Atropine Response Test
nificant AV block may occur. Similarly, a vagal ma- Atropine (0.04 mg/kg IV or IM) will result in
neuver may be diagnostic and/or therapeutic for an abolition of vagal influence. An ECG should be
ectopic supraventricular tachycardia. A sinus tachy- obtained 10 to 15 minutes after administration of
cardia typically slows over several seconds while an the drug for comparison with the baseline ECG.
ectopic supraventricular tachycardia may terminate
Clinical Utility
abruptly (see Frequently Asked Questions).
An ECG recorded immediately post exercise may Vagal Maneuver
demonstrate cardiac arrhythmias associated with in- Clinically useful in two scenarios:
creased sympathetic tone. Likewise, an atropine re- In the evaluation of dogs with a history of syn-
sponse test can be used to determine if a slow heart cope, a vagal maneuver may demonstrate sinus
rate is associated with elevated vagal tone, as can oc- arrest or AV block, suggestive of parasympathetic
cur with respiratory disease, gastrointestinal disease hypersensitivity or primary nodal disease.
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 101
In dogs with tachycardia, abrupt termination of the recording of the ECG increases the sensitivity of
arrhythmia with a vagal maneuver suggests an ec- arrhythmia detection. Major indications include:
topic supraventricular origin because ventricular Detection of transient arrhythmias associated
tachycardias are not usually sensitive to vagal tone; with syncope or periodic weakness.
however, lack of response is not helpful in differen- Screening of high-risk breeds for cardiomyopathy
tiating the origin of the tachycardia. The maneuver (e.g., Boxers, Doberman Pinschers).
can also be useful to differentiate sinus tachycardia Evaluation of frequency, severity, and significance
(no response or gradual slowing of heart rate) from of arrhythmias detected on in-hospital ECG.
pathologic ectopic supraventricular tachycardia (no Monitoring efficacy of antiarrhythmic therapy
responce or abrupt termination of tachycardia). (e.g., control of heart rate in patients with chronic
atrial fibrillation).
Postexercise Electrocardiography Determining the true incidence and type of ar-
This test can be performed in the evaluation of rhythmia in heart disease patients.
dogs with subaortic stenosis or occult cardio-
myopathy. In affected dogs, the combination of
Technique
exercise, myocardial disease and left ventricular
hypertrophy may result in electrocardiographic Modern Holter monitors use a high-fidelity digital
indicators of myocardial ischemia (i.e., ST seg- recorder to capture and store the cardiac electrical
ment depression or ventricular ectopy). Lack of re- activity for 24 hours. Some digital recorders are
sponse does not necessarily rule out heart disease. now capable of monitoring the patient for up to 7
In dogs with bradycardia, abolition of the arrhyth- days. Two to three simultaneous ECG chest leads
mia after exercise suggests a vagally mediated are typically recorded.
etiology. The increased availability of ambulatory Electrode sites are prepared by clipping, shaving,
ECG recordings has markedly reduced the use of cleaning and drying the chest.
post exercise ECGs in clinical practice. Adhesive patches are firmly adhered to the skin
(see Figure 5-1).
Atropine response test A chest wrap is essential for securing electrodes,
Sinus tachycardia with a heart rate greater than 135 wires and the recorder. A vest or harness can also
beats per minute suggests normal sinus node func- be used (Figure 5-2).
tion in the dog. Additionally, this response suggests Once the monitor has been applied, the animal re-
that medical management with vagolytic therapy turns home to resume normal activity. Very small
may be effective if the bradycardia is associated dogs and cats that find it cumbersome to ambu-
with clinical signs such as syncope or collapse and late with the monitor in place may respond better
implantation of a pacemaker is not possible. to hospitalization with cage restraint during the
24-hour recording session.
Key point
Provocative ECG techniques are easily per-
formed, relatively inexpensive, and can be
very helpful for diagnostic and therapeutic
purposes in animals with bradycardias and/or
tachycardias.
Ambulatory
Electrocardiography
(Holter Monitoring and
Cardiac Event Recording)
Indications
Routine in-hospital electrocardiography only pro-
vides a glimpse of the daily electrocardiographic
activity. Moreover, arrhythmia detection may be con- Figure 5-2. A vest can be placed over the light wrap, which
founded by iatrogenic changes in the autonomic ner- secures Holter or CER monitor electrodes in place. The vest has
vous system activity. A 24-hour ambulatory (Holter) pockets to hold the monitor and helps keep the device in place.
102 Section I Diagnosis of Heart Disease
defects, sternal recumbency to visualize pulmo- The standard cardiac catheterization procedure
nary arteries). for evaluation of congenital or acquired cardiac
A large bolus of contrast is rapidly injected intra- diseases typically includes measurement of intra-
venously. Typically, 1 ml of radiopaque contrast cardiac pressures, blood oximetry, and selective
per kg of body weight is used for the injection. angiocardiography. The most common indica-
Alternatively, the dose of iodine to be injected tion for cardiac catheterization is to ameliorate
can be calculated using 400 mg iodine/kg body congenital heart disease (e.g., pulmonic stenosis
weight as the desirable dose. or patent ductus arteriosus). For the purposes of
A fluoroscopy unit allows continuous assessment. diagnosis, advances in echocardiography have
If fluoroscopy is not available, radiographic expo- markedly reduced the need for routine cardiac
sures are obtained 2 to 8 seconds after the injection catheterization.
is initiated (depending on the structures of interest
and cardiovascular performance). Shorter times
Technique
should be used for evaluation of the right heart and
pulmonary arteries, longer times for evaluation of Anesthesia is usually required.
structures on the left side of the heart or animals Surgical preparation of the neck (carotid artery
with heart failure and slow circulation. or jugular vein) or inguinal area (femoral vein or
artery) is required.
Vascular access can be obtained by dissecting
Clinical Utility
down to the vessel or with a percutaneous cath-
Nonselective angiography is an alternative tech- eter introducer system using a modified Seldinger
nique primarily used to evaluate lesions that in- technique.
volve the right side of the heart, particularly when Catheter advancement to the chamber of interest
echocardiography or cardiac catheterization is ei- is performed under fluoroscopic or pressure wave
ther not an option or is inconclusive. form guidance (Figure 5-3).
Intravascular pressures are recorded from cham-
bers of interest. Pressures are typically recorded
Limitations, Risks, and Costs
before and after therapeutic interventions (e.g.,
Dilution of contrast material occurs as it moves balloon valvuloplasty) to assess procedure
through the circulation. Thus, nonselective angi- efficacy.
ography results in poor opacification of structures
that are very distal to the site of injection (e.g., Oximetry
left heart and systemic arteries). Blood samples are obtained from various cardiac
Timing of radiographs is difficult to predict and or great vessel locations to measure oxygen satu-
several attempts are often required unless fluoros- ration and to calculate shunt fraction in animals
copy is available. with congenital shunting defects.
Intravenous contrast agents may result in tran-
sient hypotension, cardiac arrhythmias, nephro- Angiocardiography
toxicity (especially in patients with pre-existing Radiopaque contrast material is injected
renal dysfunction), and allergic reactions. through the catheter(s) located at the appropri-
ate areas of interest, and the image is recorded
Key point on videotape, radiographic film, by cineangi-
Nonselective angiography is significantly ography or is digitally stored (Figure 5-4). Post
limited, particularly in the assessment of left processing can be performed on digital im-
heart structures. Echocardiography and/or ul- ages using digital subtraction techniques. The
trasound are preferred diagnostics. primary advantage over nonselective angio
graphy involves superior opacification of struc-
tures of interest.
Cardiac Catheterization Cardiac output may be determined using thermo-
dilution or indicator dye techniques.
Indications
Additional procedures such as balloon valvulo-
Generally, cardiac catheterization is defined as a plasty, patent ductus arteriosus coil occlusion,
combined angiographic and hemodynamic study endomyocardial biopsy, heartworm retrieval, and
undertaken for therapeutic or diagnostic purposes. cardiac pacing can be performed.
104 Section I Diagnosis of Heart Disease
Figure 5-3. Fluoroscopically obtained images of a balloon-tipped cardiac catheter being placed into the right heart. The cath-
eter is advanced to the heart via the jugular vein. The balloon on the tip of the catheter facilitates traversing the tricuspid valve
because it will tend to follow blood flow.
Contrast solutions can result in hemodynamic ab-
Clinical Utility
normalities. Patients with severe heart disease or
Angiocardiography is valuable to diagnose cases of renal disease are at a relatively higher risk.
complex heart disease and to guide therapeutic in- Infection, cardiac arrhythmias, air embolism,
terventions such as balloon valvuloplasty or patent vascular thromboembolism or perforation are
ductus arteriosus occlusion. The approach provides possible complications. With appropriate experi-
useful morphologic and physiologic information re- ence and case selection, mortality rate is low.
garding interventional responses to therapy.
Serologic Testing
Limitations, Risks, and Costs
Indications
Cardiac catheterization requires specialized
equipment and training and is typically limited to Animals with clinical signs suggestive of myo-
tertiary care facilities. cardial dysfunction resulting from infectious or
The technique can be time consuming. immune-mediated etiologies and animals at risk of
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 105
Cardiac Neurohormones
and Biomarkers
Cardiac Troponins
Indications
Cardiac troponin I and T are specific markers of
myocyte injury, ischemia, and necrosis. Cardiac
troponin I is more sensitive than cardiac troponin
T. Specific indications include cases of suspected
myocardial infarction, toxic myocardial disease
(e.g., secondary to doxorubicin), myocarditis, or
blunt myocardial trauma (e.g., vehicular injury).
Technique
A variety of human cardiac troponin I assays that
Figure 5-4. Selective aortogram demonstrating a patent cross-react with canine and feline cardiac tropo-
ductus arteriosus with radiographic contrast material crossing nin I are available, but standardization is lacking,
the ductus and entering the pulmonary artery (left to right making it difficult to compare results from dif-
flow).
ferent machines. Most cardiac troponin assays
accept either serum or heparinized or ethylenedi-
aminetetra acetic acid (EDTA) plasma. Some use
yocardial toxicity from chemotherapeutic agents
m whole blood. If testing is not performed within 12
are candidates. hours after collection, then the samples should be
Trypanosoma titer. Animals from Mexico, south- frozen until testing is done.
ern Texas, or other regions where Chagas disease
is endemic, with right-heart failure. Clinical Utility
Antinuclear antibody titer. Animals with heart Elevated cardiac troponin I has been demon-
failure or arrhythmias in addition to other clinical strated in a wide range of cardiac and extracar-
signs suggestive of immune-mediated disease. diac diseases. Concrete diagnostic, prognostic
Toxoplasmosis titer. Cats with myocardial dys- and therapeutic recommendations based on assay
function, fever, pneumonia, neurologic disease, results are not yet available; however, cardiac tro-
chorioretinitis or other signs compatible with ponin I results may give useful supportive infor-
toxoplasmosis. mation to the electrocardiographic, radiographic,
and echocardiographic findings in some patients.
Serial testing of individual patients is more likely
Technique
to be useful than one measurement at a single
Serum or plasma should be submitted to a labora- point in time.
tory that has the appropriate facilities to perform
the indicated serologic testing. Limitations
Since cardiac troponin I can be elevated with both
cardiac and extracardiac disease, the test does not
Clinical Utility
appear to be a useful screening tool for cardiac
In selected cases, these tests can be very useful in disease.
establishing an etiologic agent and in monitoring
patients at risk for myocardial toxicity. Results
must be interpreted in concert with the patients Natriuretic Peptides (Atrial
clinical signs. And B-Type)
Indications
Limitations, Risks, and Costs
Atrial natriuretic peptide (ANP) and B-type natriuretic
These tests are only limited by correct interpre- peptide (BNP) are produced by myocardial tissue in
tation. Otherwise, there are no particular risks. response to increased pressure and wall stress and are
Costs are dependent on the laboratory. markers for cardiac dysfunction and heart failure.
106 Section I Diagnosis of Heart Disease
Figure 5-5. Simultaneous lead I, II, and III ECG showing the effect of a vagal maneuver on a supraventricular tachycardia (atrial
fibrillation in this example). Note the dramatic slowing of the heart rate which results in clearer demonstration of the hallmarks of
atrial fibrillation (irregularly irregular rhythm, lack of P waves and fibrillation waves). 50 mm/sec; 10 mm/mV.
Cardiovascular Disease
Acquired primary valvular disease in dogs and cats Degenerative MVD is the most common car-
p0010 u0010
generally is degenerative or less commonly, infec- diac disease in the dog; it is an acquired disease,
tive. Other pathologic processes, such as neoplasia, and the prevalence is greatest in the geriatric
rarely affect the cardiac valves. Myxomatous de- population.
generation of the mitral valve is the most common Clinical evidence of degenerative valvular dis-
cardiac disease in the dog. Mitral valve incompe- ease is detected in approximately 30% of dogs
tence due to valvular degeneration can result in pro- aged 13 years and older.
gressive cardiac enlargement and, in some cases, MVD is a progressive disease, and subtle changes
congestive heart failure (CHF). Clinical signs, par- in valve structure precede the development of
ticularly cough due to compression of the mainstem clinically evident valvular dysfunction. Conse-
bronchi by an enlarged left atrium, may precede the quently, the prevalence of MVD detected by post-
development of CHF. The clinical consequences of mortem examination is higher than that reported
degenerative valvular disease are observed primar- in clinical studies.
ily in elderly, small-breed dogs. Postmortem evidence of advanced degenerative
Infective endocarditis (IE) is an uncommon form valvular disease was found in 58% of dogs older
p0020
of acquired valvular disease that is observed oc- than 9 years; when mild degenerative changes
casionally in dogs and rarely in cats. Middle-aged are included, the postmortem prevalence exceeds
medium- and large-breed dogs are affected most of- 90% in dogs older than 13 years.
ten. The clinical signs of IE relate to sepsis, throm- MVD may affect any breed of dog, but clinical
boembolism, and CHF. consequences of MVD are observed most often
in small-breed dogs. Miniature Poodles, Pomera-
nians, Yorkshire Terriers, Chihuahuas, and other
Degenerative Mitral Valve
s0020
merous designations for degenerative mitral value is sometimes clinically evident at a young age.
disease (MVD) have been proposed. The terms Male dogs are affected somewhat more often than
myxomatous valvular degeneration, myxomatous females.
transformation, mucoid degeneration, endocardio- Degenerative valvular disease is uncommon in
sis, chronic valvular disease, and degenerative val- cats, and when it occurs it seldom results in clin-
vular disease all refer to the same disorder. ical consequences.
110
Chapter 6 Acquired Valvular Disease 111
Key Point
b0010
Etiopathogenesis
s0050
tion of the valve leaflets as well as by thicken- vasoactive peptide endothelin in the pathogenesis
ing and, sometimes, lengthening of the chordae of MVD. Relative to mitral valve tissue obtained
tendineae. The appearance of a small number from healthy young dogs, degenerative mitral
of nodules at the free edge of the valve leaflet is leaflets had a greater density of endothelin recep-
the initial pathology. As the disease progresses, tors. Furthermore, the density of endothelin re-
these nodules increase in number and size and co- ceptors was related to the severity of MVD.
alesce. In severe cases, the leaflets are contracted, Because distinct breed predispositions are recog-
and the free edge of the leaflet rolls inward to- nized, it is likely that there is a genetic predis-
ward the ventricular endocardium (Figure 6-1). position for the development of MVD. Available
When severe, these abnormalities prevent coapta- evidence suggests that the tendency to develop
tion of the valve leaflets, resulting in mitral valve MVD is not subject to simple Mendelian inheri-
incompetence. tance but rather is a polygenic trait.
MVD is histologically characterized by the In Cavalier King Charles Spaniels, parental sta-
deposition of mucopolysaccharides primarily tus with respect to age and murmur intensity is
within the spongiosa layer of the valve leaflet. an important determinant of the prevalence of
Fibrosis of the valve is also present, but is not murmurs in 5-year-old offspring. Based on this,
the dominant histologic feature. Inflammatory it appears that the age at which MVD develops is
infiltrates are absent; MVD is a sterile, degen- inherited.
erative disease that bears no known relationship
Key Point
b0030
to endocarditis.
The cause of MVD is not known but genetic
b0020
diac dysfunction. Left-sided CHF is defined by MVD exhibits a broad spectrum of severity. In
u0050
the presence of cardiogenic pulmonary edema. most affected dogs, MVD does not cause clinical
Right-sided CHF refers to clinical signs that signs, and the disease is detected when a cardiac
result from systemic congestion; in dogs, asci- murmur is incidentally identified in patients pre-
tes is the most common manifestation of right- sented for routine health care or for management
sided CHF. of noncardiac disease.
Chapter 6 Acquired Valvular Disease 113
mias. Additionally, exertional syncope may result Figure 6-2. A phonocardiogram recorded from a 13-year-
old female spayed mixed-breed dog with a grade 4/6 systolic
when MR limits stroke volume so that cardiac murmur. The systolic murmur (sm) begins at the first heart
output does not adequately increase to meet the sound (S1), is evident throughout systole and obscures the
physiologic demands of exercise. Alternatively, second heart sound.
syncope on exercise or excitement or associated
with paroxysmal cough can result from sudden present when the murmur intensity is grade V/VI
onset of reflex-mediated bradycardia. or greater.
Other clinical signs related to reduced cardiac A high-frequency, mid-systolic click (Figure 6-3) is
performance, including tachypnea, exercise in- sometimes heard in older, small-breed dogs. These
tolerance, and abdominal distention caused by clicks may be associated with prolapse of the mitral
ascites, occasionally prompt owners of affected valve. In many dogs, clicks are a precursor of MR.
dogs to seek veterinary attention. Often, a soft systolic murmur of MR can also be
heard in patients that have systolic clicks.
Physical Findings When MR is severe, the third heart sound some-
s0090
The most notable feature of the physical ex- times is audible and results in an S3 gallop. Care
u0060
amination is a systolic murmur that is usu- must be taken to distinguish a mid-systolic click
ally heard best over the left cardiac apex. The from a gallop. In general, a systolic click is louder
murmur of MVD is indistinguishable from the than is the third heart sound, and in patients with
murmur caused by other disorders, such as IE MVD, a click typically is heard in association with
or dilated cardiomyopathy (DCM), which also findings that suggest mild MR. In contrast, an S3
can result in MR. Importantly, however, an ac- gallop usually reflects severe MR and generally
quired, left apical, systolic murmur in an older, is heard in patients with loud murmurs. Note that
small-breed dog is almost always due to MVD. S3 is sometimes audible in patients with DCM.
The intensity of the murmur depends on a num- However, DCM is typically a disorder of large
ber of factors, but severe MR usually causes and giant breed dogs.
a loud murmur. Severe MR associated with a The femoral arterial pulse is usually of normal
nonrestrictive regurgitant orifice can result in a strength when MR is present, but the pulse may
soft murmur but this is extremely uncommon in have a rapid rise. Very severe MR can be associ-
MVD. Phonocardiographically, the murmur of ated with diminished pulse strength.
MR typically has a plateau-shaped configura- Crackles may be heard in patients with pulmo-
tion meaning that the murmur has a similar in- nary edema. It should be recognized that the
tensity throughout systole; when the murmur is prevalence of primary respiratory diseases such
loud, the second heart sound may be obscured as chronic bronchitis in the patients most often
(Figure 6-2). affected by MVD is relatively high. Primary re-
An exaggerated apical impulse is often evident spiratory tract diseases can explain adventitious
on precordial palpation of patients with moderate pulmonary sounds, such as crackles, in the ab-
or severe MR. By definition, a precordial thrill is sence of pulmonary edema.
114 Section II Cardiovascular Disease
f0030
Figure 6-3. A phonocardiogram recorded from an 11-year-old male castrated Shih-Tzu. A mid-systolic click (click) is shown.
Abdominal palpation is usually normal in patients The presence of respiratory sinus arrhythmia (RSA)
with MVD, but hepatic enlargement or even asci- can also be of diagnostic value. Much of the mo-
tes may be present when there is severe tricuspid ment-to-moment heart rate variability observed in
valve disease, or when pulmonary hypertension healthy dogs is due to the effect of vagal discharge.
complicates the presentation of MVD. In patients with severe cardiac disease, there is little
vagal influence on heart rate and rhythm and as a
Key Point
b0050
as collapsing trachea and chronic bronchitis, are In contrast, the clinical signs of thin patients with
common in the patient group that is affected by loud murmurs and tachycardia are more likely to
MVD. In an individual patient, it can be difficult result from cardiac disease or CHF.
to determine whether cardiac disease or respira- Coughing in elderly, small-breed dogs that do not
tory disease bears the greatest responsibility for have cardiac murmurs is almost always due to
the development of clinical signs. Key Point
b0060
t0010
complementary data. The left atrium is left of, and caudal to, the right
atrium. Radiographically, it occupies the cau-
dodorsal area of the cardiac silhouette in the lat-
Large-Breed Dogs with Mitral Valve Disease eral projection.
A syndrome of severe MR and concurrent myo- In the absence of left atrial enlargement, the cau-
u0080
cardial dysfunction is recognized in medium- and dal portion of the trachea curves ventrally over
large-breed dogs. The fact that this observation the caudal aspect of the cardiac silhouette.
was made relatively recently is probably explained When the left atrium is enlarged, the caudal border
by the increasing availability of echocardiog- of the cardiac silhouette straightens, and the trachea
raphy and not by a change in the epidemiology is forced dorsally to varying degrees. With marked
of MVD. Before widespread availability of this left atrial enlargement, the left mainstem bronchus
technology, large-breed dogs with heart failure is narrowed, and the trachea adopts a path that is
s0110
generally were assumed to have primary myocar- parallel to the thoracic vertebrae. Occasionally, se-
dial disease. vere left atrial enlargement has the appearance of a
For reasons that are not known but may relate to mass that splits the mainstem bronchi.
the geometry or pattern of contraction of inher- In the ventrodorsal projection, the left atrium is
ently larger ventricles, large-breed dogs with MR located near the center of the cardiac silhouette.
are more apt to develop echocardiographically When enlarged, the left atrium splits the mainstem
evident myocardial dysfunction than are small- bronchi to varying degrees. This is apparent in well-
breed dogs. penetrated radiographs and results in an appearance
The gross appearance of the valvular lesions in that is sometimes known as the crab sign or the
large dogs tends to be less impressive than it is in bowlegged cowboy (Figures 6-4 and 6-5).
small breed dogs. Additionally, in the ventrodorsal view, enlargement
Perhaps because myocardial dysfunction compli- of the left atrium may cause a bulge which repre-
cates MVD in large dogs more often than it does sents the atrial appendage at the 3 oclock position.
in small dogs, the prognosis may be worse than in
smaller dogs. Radiographic Findings of Pulmonary
s0150
Figure 6-4. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from a 10-year-old mixed-breed dog with degen-
f0040
erative mitral valve disease. There is relatively mild but distinct left atrial enlargement, as evidenced by elevation of the trachea
and loss of the caudal waist in the lateral film.
f0050
Figure 6-5. A lateral thoracic radiograph obtained from a 14-year-old female spayed mixed-breed dog with severe mitral valve
incompetence due to degenerative disease. The left atrium is markedly enlarged, and the left mainstem bronchus is compressed.
Chapter 6 Acquired Valvular Disease 117
f0060
Figure 6-6. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from an 11-year-old female spayed Miniature
Poodle with degenerative mitral valve disease. The cardiac silhouette is markedly enlarged, and there is evidence of left atrial
enlargement. Pulmonary opacities compatible with edema are distributed throughout the lung; the edema is most noticeable in
the caudodorsal lung field.
pulmonary congestion and may precede the de- When tissue fluid weeps into the pulmonary
velopment of pulmonary edema. alveoli, it provides contrast with air-filled
A central, or perihilar, distribution often charac- structures such as the bronchi, resulting in air
terizes cardiogenic pulmonary edema in dogs. bronchograms. Alveolar pulmonary opacities
The development of interstitial pulmonary edema together with radiographic evidence of left atrial
precedes the appearance of alveolar edema. enlargement are diagnostic of left-sided CHF
Blurring of vascular detail in the presence of left atrial (Figure 6-6). The presence of alveolar pulmo-
enlargement and, sometimes, concurrent pulmonary nary edema indicates severe CHF that is almost
venous distention characterizes the radiographic ap- invariably associated with noticeable respiratory
pearance of interstitial pulmonary edema. distress.
118 Section II Cardiovascular Disease
f0070
Figure 6-7. A right parasternal short-axis echocardiographic image obtained from an 11-year-old male castrated Cocker Spaniel
with severe mitral valve regurgitation. The left atrium (LA) is markedly enlarged; the dimension of the body of the atrium is more
than twice the diameter of the aorta (Ao).
f0080
Figure 6-8. A right parasternal long-axis echocardiographic image obtained from a 15-year-old male castrated Cavalier King
Charles Spaniel with mitral regurgitation due to degenerative disease. The image was obtained during systole. The left atrium is
enlarged and there is distinct prolapse of the mitral valve leaflets. LV, Left ventricle; LA, left atrium.
MVD demonstrates variable degrees of left atrial Often, the tricuspid leaflets are affected, although
(Figure 6-7) and left ventricular dilation. Hypertro- seldom as markedly as the mitral valve.
phy is usually adequate to preserve a near-normal Evaluation of myocardial function in patients
relationship between the diastolic luminal dimen- with MR is difficult. When MR is moder-
sion and wall thickness. ate or severe, loading conditions imposed on
The mitral leaflets may be noticeably thicker the left ventricle are altered and left ventricu-
than normal, and prolapse of the leaflets into lar performance is hyperdynamic (Figure 6-9)
Chapter 6 Acquired Valvular Disease 119
f0130
f0090
Figure 6-9. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from an 11-year-old female
spayed Cavalier King Charles Spaniel. Left ventricular dilation and hypertrophy are evident. Left ventricular systolic performance
is hyperdynamic; the fractional shortening is 46%.
Figure 6-10. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from 12-year-old male cas-
trated Keeshond weighing 18 kg. There was Doppler evidence of severe mitral regurgitation due to degenerative valve disease. Left
ventricular systolic performance evaluated by fractional shortening is normal (38%) but the end-systolic left ventricular dimension is
markedly enlarged which provides evidence of systolic myocardial dysfunction. The cardiac rhythm is atrial fibrillation.
f0110
Figure 6-11. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from 12-year-old male
castrated Dalmatian. There was Doppler evidence of severe mitral regurgitation due to degenerative valve disease. Left ventricu-
lar systolic performance evaluated by fractional shortening is subnormal (22%) and the end-systolic left ventricular dimension
is markedly enlarged. These findings provide evidence of systolic myocardial dysfunction. An examination recorded three years
before this one had demonstrated mitral valve regurgitation and mildly hyperdynamic systolic performance. In the interim, the
end-diastolic and end-systolic left ventricular dimensions had enlarged. Large dogs are more apt to develop systolic myocardial
dysfunction as a consequence of mitral valve disease than are small dogs.
Chapter 6 Acquired Valvular Disease 121
f0120
Figure 6-12. A right parasternal long-axis echocardiographic image obtained from a 5-year-old female spayed Cavalier King
Charles spaniel with mitral regurgitation due to early onset degenerative disease. Color-flow Doppler mapping demonstrates mild
mitral valve regurgitation (MR). The color mosaic occupies less than 50% of the area of the left atrium and the jet is relatively
narrow at its origin (arrow). LV, left ventricle.
Figure 6-13. A right parasternal long-axis echocardiographic image obtained from a 12-year-old female spayed Whippet with
mitral regurgitation due to degenerative disease. Color-flow Doppler mapping demonstrates marked mitral valve regurgitation.
The color mosaic nearly fills the enlarged left atrium and more importantly with respect to evaluation of the severity of regurgita-
tion, the jet is very broad at its origin. LV, left ventricle.
methods are time consuming and have not found means of evaluating the severity of regurgita-
widespread clinical application. tion; a greater width indicates a larger orifice
The area of the color Doppler regurgitant jet and, more severe regurgitation (Figures 6-12 and
relative to that of the receiving chamber is one 6-13). The appearance of proximal flow conver-
means of semi-quantitatively evaluating the se- gencethe color Doppler appearance of accel-
verity of valvular regurgitation; however, many eration through the regurgitant orificesuggests
physiologic and technical factors influence the that MR is at least of moderate severity (Figure
size of the jet and this intuitively simple method 6-14).
has limitations. The width of the regurgitant jet The density of the regurgitant continuous wave
at its origin is another, perhaps more accurate, spectral Doppler signal is roughly proportional
122 Section II Cardiovascular Disease
f0140
Figure 6-14. A left parasternal apical echocardiographic image from a 13-year-old male castrated mixed-breed dog with mitral
regurgitation due to degenerative disease. Color-flow Doppler mapping demonstrates marked mitral valve regurgitation. The
region of proximal flow acceleration (arrow) is evident within the left ventricle (LV).
to the number of cells that move into the receiv- e chocardiography cannot provide a diagnosis of
ing chamber and is an alternative means of semi- CHF; it can only demonstrate that cardiac disease is
quantitatively evaluating regurgitant severity sufficiently severe that a diagnosis of CHF is plau-
(Figure 6-15). sible. Although the clinical signs associated with
Ultimately, it is important that the echocardio- MVD may have a sudden onset, the disease pro-
graphic assessment is clinically relevant: in vet- cess itself is chronic. Therefore, left atrial dilation
erinary patients in whom valvular repair is seldom and, usually, concurrent left ventricular dilation are
performed, the effect of valvular regurgitation might expected prior to the onset of clinical signs. Echo-
be of greater importance than its magnitude cardiographic evidence of MR in the absence of left
information regarding chamber size and myocardial atrial and left ventricular dilation is seldom of clini-
function is essential in placing Doppler findings in cal importance. In most cases, then, echocardiogra-
the appropriate clinical context. phy is not essential for the clinical management of
patients with MR. In patients with suspected MR,
Relative merits of radiography and echocardiography is likely to provide clinically
s0170
spectrum of severity. Often, the presence of MR (for example, patients in which the signalment is
is incidental to the presentation, and clinical signs atypical or there is the possibility that the murmur
such as cough are not the result of CHF or even is congenital)
heart disease, but, rather, result from primary re- When it is difficult to discern from thoracic radio-
spiratory disease. Therefore, in most cases, the graphs whether or not the left atrium is enlarged
thoracic radiograph provides the most useful diag- When sudden deterioration has occurred, and
nostic and prognostic information in patients with rupture of the chordae tendineae or left atrium is
MVD. Thoracic radiography not only provides an suspected
assessment of cardiac size but also allows visual- When it is important to evaluate systolic myocar-
ization of the pulmonary vessels and parenchyma. dial function
Thus, thoracic radiography provides an indirect When pulmonary hypertension is suspected
assessment of cardiac performance, and currently
it is the only widely available noninvasive route to
a diagnosis of CHF. Key Point
Echocardiography provides a noninvasive
b0080
p0070
f0150
Figure 6-15. A, Pulsed wave Doppler echocardiogram obtained from a dog with mitral valve incompetence due to degenera-
tive mitral valve disease. The pulsed wave sample volume was placed within the left atrium; during systole there is a dense, aliasing
multifrequency signal. B, Continuous wave Doppler study of the left atrium of a dog with severe mitral valve incompetence due
to degenerative mitral valve disease. The signal is quite dense, suggesting severe regurgitation.
124 Section II Cardiovascular Disease
diagnosis of arrhythmias but also can provide in- affect prognosis in people with asymptomatic
direct evidence of chamber enlargement. ventricular dysfunction, only limited efficacy
The electrocardiogram is an insensitive gauge of of ACE inhibitors in subclinical MVD has been
cardiac chamber size. Nevertheless, it is likely demonstrated.
that findings such as P mitrale are relatively spe- The possibility that enalapril might delay the onset of
cific; that is, when P waves in the caudal fron- heart failure in subclinical MVD has been addressed
s0180
tal leads (i.e., II, III, and aVF) are wide, the left by two separate clinical trials. In both the Scandina-
atrium is usually enlarged (Figure 6-16). vian Veterinary Enalapril Prevention (SVEP) Trial
Arrhythmias can complicate the presentation of and the Veterinary Enalapril Trial to Prove Reduc-
MVD. Most often, arrhythmias in MVD take the tion in Onset of Heart Failure (VETPROOF), dogs
form of supraventricular tachyarrhythmias that with subclinical MR were randomized to receive
reflect atrial stretch. Atrial premature complexes placebo or enalapril. Neither trial demonstrated a
and paroxysms of atrial tachycardia are relatively statistically significant effect of enalapril on time
common in patients with MVD. Atrial fibrillation to development of CHF. Although the result of the
develops occasionally and generally indicates VetProof trial was not statistically significant
advanced disease with marked atrial dilation. with respect to the primary end point, the data did
Ventricular arrhythmias (ventricular premature show a tendency toward a favorable treatment ef-
complexes) may develop in association with left fect. Atrial enlargement was an inclusion criterion
ventricular dilation and myocardial fibrosis. for VETPROOF but not for SVEP; however, it is
worthy of consideration that both trials included
Therapy
s0190
apy slows the progression of subclinical (asymp- tively long periods of follow-up. The inclusion of
tomatic) MVD is lacking. mildly affected patients in a clinical trial might
A theoretical, ideal treatment for MVD could be mask a treatment effect that is evident only for
used to prevent or reverse myxomatous degenera- patients with severe disease. It is therefore possible
tion. Unfortunately, drug therapy that affects this that a subpopulation of preclinical patients with
pathologic process has not been identified. severe MR and cardiomegaly would benefit from
In the absence of evidence that medical ACE inhibition. Although this hypothesis has not
therapy can alter the progression of valvular been specifically tested, it is partly refuted by the
degeneration, interest has been directed toward results of SVEP; in that trial, a treatment effect
the possibility that drug therapy might improve was not observed in the subset of dogs that had
prognosis in subclinical MVD by decreasing radiographic cardiomegaly at study entry.
MR or by modifying the process of ventricular The reason that ACE inhibitors do not appear
remodeling. to improve prognosis in subclinical MVD is not
f0160
Figure 6-16. An electrocardiogram recorded from a 13-year-old Beagle with physical findings of mitral valve regurgitation.
There is P-mitrale, and the R amplitude exceeds 3 mV, suggesting left atrial enlargement and left ventricular hypertrophy, respec-
tively. (Lead II, 50 mm/s, 1 mV=1 cm.)
Chapter 6 Acquired Valvular Disease 125
known; however, it should be recognized that the Cough caused by Airway Compression
widely cited clinical trials of ACE inhibition in Some dogs with MVD develop a cough that ap-
u0150
people with heart disease generally have enrolled pears to result from compression of the mainstem
people with past myocardial infarction or idio- bronchi by an enlarged left atrium. This type of
s0210
pathic DCM. MVD in people is generally treated cough can develop prior to the development of
surgically, and, indeed, medical therapy is not pulmonary edema.
recommended for asymptomatic people with MR. Radiographically, there is an enlarged cardiac
Pathophysiologic differences between people with silhouette with distinct evidence of left atrial
ventricular myocardial dysfunction and dogs with enlargement. The mainstem bronchi may be
MVD might also be relevant. In contrast to the noticeably narrowed. The pulmonary veins are
effect of renin-angiotensin-aldosterone system sometimes distended, but the pulmonary intersti-
(RAS) suppression in dogs with experimentally tium and parenchyma have a normal appearance.
induced, primary myocardial disease, neither ACE It is important to recognize that primary respiratory
inhibitors nor angiotensin II antagonists favorably tract diseases such as tracheal collapse and chronic
affect ventricular remodeling in dogs with experi- bronchitis are common in the same patient group
mentally induced MR. However, the syndrome that develops MVD. With very few exceptions,
that results from acute disruption of the mitral clinical signs related to MVD do not occur in the
valve in the laboratory may differ markedly from absence of radiographic left atrial enlargement.
spontaneous valvular degeneration associated with When radiographic findings suggest that the
chronic, progressive MR. Therefore, the clinical cause of cough is airway compression but not
relevance of these research findings is uncertain. pulmonary edema, the use of an antitussive such
Theoretical considerations aside, definitive evi- as hydrocodone or butorphanol is rational.
dence that ACE inhibitors improve prognosis in Vasodilation causes a decrease in systemic vas-
subclinical MVD is lacking. Although it might be cular resistance and, in the setting of MR, can
u0190
argued that trials to date have had inadequate sta- increase stroke volume through a decrease in
tistical power, it is likely that a favorable effect of the regurgitant fraction. Potentially these effects
ACE inhibition, if one exists, is modest; the results can decrease left atrial and pulmonary venous
of VETPROOF suggest that 2 years of therapy with pressures and perhaps, reduce left atrial size.
enalapril may delay the onset of pulmonary edema Cough due to compression of the airways gener-
by approximately 4 months. Based on available ally is associated with considerable chamber en-
data, the author generally does not treat dogs with largement and this latter finding is a risk factor
subclinical MVD. On a pragmatic level, the prac- for the ultimate development of heart failure. Be-
titioner is sometimes presented with subclinical cause of the proven favorable effect of ACE inhi-
patients for which radiographic findings suggest bition in patients with heart failure due to MVD,
that the development of frank heart failure is im- it is reasonable to administer an ACE inhibitor
minent. In cases where there is marked left atrial in addition to an antitussive, when cough results
enlargement and pulmonary venous distension, the from bronchial compression.
author prescribes an ACE inhibitor. It is notewor- Some of the benefits of ACE inhibition likely
thy that long-term ACE inhibition has not been as- relate to their neuroendocrine effects. Because
sociated with detrimental effects. Furthermore, it is of this and because the ACE inhibitors are not
possible that these drugs have benefits that relate potent vasodilators, a case might be made for
to effects on other geriatric disorders such as hy- the use of hydralazine or perhaps amlodipine
pertension or renal disease. Based on this and the for dogs with MVD and cough due to bronchial
suggestion of a favorable effect in the VetProof compression. Caution must be exercised if these
trial, ACE inhibition may be a therapeutic consid- drugs are used and patients should be monitored
eration for some patients with cardiac enlargement for the development of systemic hypotension.
and subclinical MR; however, the evidence to Diuretic administration effectively reduces car-
support this approach is neither direct nor strong. diac volumes and may also be efficacious. The
argument can be advanced that this may result in
harmful activation of the renin-angiotensin axis.
Key Point Therefore, in this clinical situation, add furose-
Medical therapy that slows the progression of mide to the drug regimen only when ACE inhibi-
MVD has not been identified. tion in combination with an antitussive, fails to
result in clinical improvement.
126 Section II Cardiovascular Disease
t0020
Table 6-2 Suggested Strategies for Diagnostic and Therapeutic Management of Canine
Degenerative Valvular Disease
Cough caused by
Subclinical MR Airway Compression CHF Advanced CHF
Diagnostic X-rays as indicated X-rays X-rays X-rays
approach by clinical Echocardiography Echocardiography Echocardiography
circumstances (i.e., recommended not usually EKG when auscultation
prior to elective when radiographic necessary but provides suggests pathologic
anesthesia, loud evidence of left potentially useful arrhythmia
murmurs particularly atrial enlargement is ancillary information
if associated with equivocal in most cases
tachycardia) EKG when EKG when
EKG when auscultation auscultation suggests
auscultation suggests pathologic pathologic arrhythmia
suggests pathologic arrhythmia
arrhythmia
Therapeutic Generally none Antitussive agent and Standard therapy for The following can be
approach indicated although in an ACE inhibitor CHF due to MR considered in addition
some circumstances, Short-term anti- consists of furosemide, to standard
the use of an ACE inflammatory dose an ACE inhibitor, and therapytreatment
inhibitor might be corticosteroids or moderate dietary salt should be tailored to
considered for patients therapeutic diuretic restriction the individual
with distinct cardiac trial considered for Triple diuretic therapy
enlargement (see text) refractory cases Amlodipine (or
Hydralazine)
Carvedilol
Spironolactone
Pimobendan
Nitroglycerin
When cough fails to respond to ACE inhibition marily of interventions that manipulate the deter-
and modest diuresis, it is important to consider minants of cardiac output and others intended to
the possibility that the cough results not from blunt the maladaptive neuroendocrine response
heart disease but rather from primary respiratory to cardiac dysfunction.
tract disease. In CHF due to MR, left ventricular filling pres-
sure (preload) is excessive, and the consequent
Treatment of Congestive Heart Failure caused increase in venous pressures causes tissue fluid to
s0220
by Mitral Valve Disease weep into the pulmonary interstitium and alveoli.
When MR causes clinical signs in people, the The administration of agents that reduce intravas-
u0160
disorder is treated surgically. Mitral valve re- cular volume, such as diuretics, or of agents that
pair with preservation of chordal attachments increase venous capacitance, such as nitroglyc-
is generally preferred to replacement of the erin, are therefore a mainstay of therapy.
valve with a prosthesis. Surgical treatment of Nitroglycerin is usually administered transder-
dogs with MVD has been reported. However, mally and is used most often as short-term therapy
expense and the need for expertise in open- in patients with fulminant edema, or occasionally
heart surgery performed during cardiopulmo- as adjunctive therapy in patients with advanced
nary bypass have limited the availability of this disease. The efficacy of transdermal nitroglycerin
approach. is uncertain, and in dogs with experimentally in-
Heart failure due to MVD generally is treated duced MR, the effect of nitroglycerin on filling
medically (Table 6-2). Unless the cause can be pressure did not differ from that of placebo.
definitively treated, heart failure is a terminal Furosemide, a potent agent that acts on the loop
syndrome. Therefore, medical management is in- of Henle, is the diuretic that is used most often
tended to alleviate clinical signs and to prolong in veterinary practice. It can be administered
life. Drug therapy of heart failure consists pri- orally or parenterally; the route of administration
Chapter 6 Acquired Valvular Disease 127
is chosen based upon the clinical status of the pimobendan increases the sensitivity of the con-
patient. The resultant decrease in intravascular tractile apparatus to available calcium, an effect
volume reduces left ventricular filling pressures, which also contributes to the inotropic effect.
allows lymphatic drainage of tissue fluid and, This latter property may be favorable because
resolution of edema. the increase in inotropic state is associated with a
It should be recognized that diuretics reduce pre- relatively low cost in terms of myocardial oxygen
load; this decrease in ventricular filling pressures consumption.
is generally well tolerated by patients with ven- Two recent clinical trials compared the ef-
tricular dilation and has obvious benefits when fects of pimobendan with an ACE inhibitor
edema is present. However, excessive diuresis in dogs with heart failure due to MVD. These
can result in hypotension related to low cardiac trials demonstrated that the clinical effects of
output, prerenal azotemia, and electrolyte distur- pimobendan and furosemide were not inferior
bances. It is generally believed that the optimal to established therapy consisting of furosemide
dose of furosemide is the lowest one that controls and an ACE inhibitor. For some clinical vari-
signs of congestion. ables, pimobendan was superior to the ACE
Importantly, many dogs with clinically evi- inhibitor. The effect of pimobendan when used
dent MVD cough in the absence of pulmonary together with an ACE inhibitor in dogs with
edema, and many of these patients have concur- valvular disease has not been addressed in
rent primary respiratory tract disease. Therefore, published trials to date. Therefore, the stage of
aggressive diuresis following radiographically disease at which pimobendan is most appro-
demonstrated resolution of pulmonary edema priately added to conventional therapy can be
is to be avoided. In most cases of CHF due to debated. It is reasonable to add pimobendan to
MVD, the administration of furosemide rap- the therapeutic regimen when there is clinical
idly and effectively resolves signs. Failure of deterioration despite administration of furose-
patients with MR and respiratory distress to mide and an ACE inhibitor. The concurrent use
respond promptly to diuretic administration of pimobendan, an ACE inhibitor, and furose-
should cause the practitioner to question the di- mide as initial therapy can probably be justi-
agnosis of CHF. fied when MVD results in severe heart failure.
Most patients that develop radiographic pulmo- When pet owners are constrained financially,
nary edema due to MR require lifelong diuretic and it is possible to prescribe only pimobendan
therapy. Early in the course of the syndrome, a or an ACE inhibitor, the available data suggest
dose of 1 mg/kg PO every 12 hours may be ade- that the use of either drug likely is appropriate.
quate, although the inevitable progression of MR In Beagles with mild MVD, chronic, oral adminis-
and CHF and renal tubular adaptations ultimately tration of pimobendan was associated with histo-
necessitate higher doses. logic valvular lesions that were more severe than
Moderate dietary salt restriction is suggested for those in a similar group of Beagles that received
patients with CHF due to MVD. benazepril. These data and a clinical case report
The benefits of ACE inhibition in CHF due to suggest that in some circumstances, pimobendan
MR have been demonstrated. Thus, the use might accelerate the development of degenerative
of an ACE inhibitor together with furosemide valvular lesions. Pimobendan is not indicated for
has become standard therapy for CHF due to the management of subclinical MVD.
MVD. When atrial tachyarrhythmias, particularly atrial
Pimobendan has recently been approved by the fibrillation, complicate MVD, the use of digoxin
United States Food and Drug Administration for (0.22 mg/m2 PO every 12 hours) is generally ac-
use in dogs; it is indicated for the management of the cepted. However, the role of digoxin in the man-
signs of mild, moderate, and severe CHF resulting agement of patients with CHF who are in normal
from DCM or atrioventricular valve insufficiency. sinus rhythm remains a point of controversy.
Previously, pimobendan had been licensed for Digoxin has two principal effects; it acts as a posi-
use in dogs with heart failure in Canada, Europe, tive inotrope and as a negative chronotrope. The
and Australasia. latter property is related to the autonomic effects
Pimobendan is an inodilator that has com- of the drug, which include a central vagomimetic
plex pharmacologic properties. It inhibits phos- effect and effects that may serve to normalize the
phodiesterase and therefore causes vasodilation baroreceptor dysfunction associated with CHF.
and an increase in inotropic state. Additionally, There is evidence to suggest that chronic activation
128 Section II Cardiovascular Disease
of the adrenergic nervous system is detrimental, adrenergic nervous system and RAS is ultimately
and that this abnormality may be partly reversed maladaptive and contributes to the progressive
by the administration of digoxin. nature of heart failure. The use of beta blockers
The need for digoxin in the patient with CHF due in this setting is consistent with this paradigm.
to MVD is difficult to assess. Because the com- Acutely, beta blockers have a negative effect on
monly used echocardiographic indices of contrac- cardiac performance and should be used in canines
tility depend on preload and afterload as well as with heart failure only with caution. Beta blocks-
myocardial function, they are difficult to interpret ers must be initiated at very low doses and titrated
when MR is severe. Furthermore, the results of to effect or target dose over the course of weeks.
clinical trials that enrolled people with heart fail- The use of beta blockers in patients with systolic
ure cast doubt on the intuitive notion that chronic failure is predicated on the belief that these agents
inotropic therapy is beneficial. preserve myocardial function. Although invasive
The effect of digoxin on dogs with heart failure measures may disclose myocardial function in dogs
and sinus rhythm has not been evaluated. How- with MR, the primary cause of clinical signs in pa-
ever, based on the results of a clinical trial that tients with MVD is likely the mechanical effect of
addressed the role of digoxin in people with heart the volume load. Nevertheless, studies of dogs with
failure, it seems likely that the magnitude of ef- experimentally induced MR suggest that beta block-
fect in dogswhether it is positive or negative ade may have a role in the management of MVD.
is probably small. Carvedilol is a third-generation beta blocker that
In patients with MVD and sinus rhythm, it is also an alpha adrenergic antagonist. Because of
seems most reasonable to reserve the use of this latter property, carvedilol is a weak vasodila-
digoxin for patients with advanced CHF and tor, which might make this beta blocker particu-
preserved renal function as digoxin is excreted larly well suited to the management of MVD.
almost entirely through the kidneys. When ad- The author considers the use of carvedilol, or a
ministering digoxin to dogs in sinus rhythm, less expensive alternative such as metoprolol or
aim for a blood concentration of 0.5 to 1 ng/mg atenolol, when echocardiographic findings sug-
on a sample obtained 8 to 10 hours postdose. gest incipient or patent myocardial dysfunction.
Higher concentrations likely are necessary and
appropriate when atrial fibrillation is present. Therapy of severe Congestive Heart Failure
s0240
ACE inhibitors are part of the standard therapeu- furosemide with a thiazide and a potassium-
u0170
tic approach to heart failure caused by MR. It is sparing diuretic such as spironolactonecan be
likely that the favorable effect of ACE inhibition considered for patients that require high doses of
is not simply the result of vasodilation. In ad- furosemide to remain free of congestive signs.
dition to this mechanical effect, ACE inhibition The use of three different diuretic agents inter-
serves to protect the heart from the apparently feres with nephron function at anatomically and
detrimental effects of RAS activation. functionally distinct sites; together, the drugs may
Pharmacologic ACE inhibition generally is not have synergistic effects, allowing the use of lower
complete, and because aldosterone may con- doses of the individual agents. Additionally, the
tribute to the development of myocardial fibro- use of a potassium-sparing agent such as spirono-
sis, more complete suppression of the RAS may lactone serves to limit some of the adverse effects
yield positive results. Accordingly, the use of that are associated with the use of high doses of
spironolactonea weak diuretic that antagonizes loop diuretics such as furosemide.
the effect of aldosteroneis considered as adjunc- Despite proven efficacy in the management of
tive therapy for patients with severe CHF due to heart failure due to MVD, the ACE inhibitors
MVD. In humans with CHF, the use of subdiuretic are not potent vasodilators. In some patients with
doses of spironolactone prolongs survival. CHF due to severe MVD, the use of hydrala-
Beta blockers decrease mortality in people with zine or perhaps the vasoselective calcium chan-
heart failure. Because these drugs have a po- nel blocker, amlodipine, in addition to an ACE
tent negative inotropic effect, the mechanism by inhibitor may be helpful. When vasodilators are
which beta blockers improve survival is not in- used in addition to ACE inhibitors, the initial dose
tuitively obvious. However, it is now recognized should be low; ideally, the dose is titrated to effect
that seemingly compensatory activation of the based on serial blood pressure determinations.
Chapter 6 Acquired Valvular Disease 129
f0170
Figure 6-17. An early systolic, right parasternal long-axis echocardiographic image obtained from an 8-year-old, fe-
male spayed Papillion. The anterior mitral valve leaflet (arrow) was flailthe leaflet is perpendicular to plane of the mitral
annulusbecause of rupture of a chorda tendineae. LV, Left ventricle.
u0270
Key Point
administered.
The authors standard medical therapy for It should be recalled that there are essentially
heart failure due to MVD consists of furose-
no circumstances under which diuresis will in-
mide, an ACE inhibitor, and in some cases, di-
goxin. Pimobendan has been approved for the crease stroke volume and renal blood flow. In
treatment of mild, moderate, and severe CHF contrast, judicious vasodilation in the setting of
due to MVD. Spironolactone and beta block- MR can do exactly that. Thus, the development
ers may have roles as adjunctive therapy. of azotemia is usually managed first by a cau-
tious reduction in the diuretic dose. Should cre-
atinine values fail to decrease, the diuretic can be
discontinued; the patients respiratory rate and
Complications of Mitral Valve Disease and character should be carefully monitored. If azo-
its treatment temia persists after discontinuation of diuretic
therapy, the ACE inhibitor can be discontinued,
s0250
diuretic and Angiotensin-Converting Enzyme and cautious intravenous infusion of fluid can be
inhibitor administration initiated.
Monitoring of renal function is suggested for
Rupture of chordae tendineae
s0270
f0180
Figure 6-18. Continuous wave Doppler study performed with the Doppler cursor through the right atrium of a dog with severe
endocardiosis. There is tricuspid valve regurgitation (TR); the peak velocity of the TR jet was nearly 5 m/s. This corresponds to a
systolic right atrialright ventricular pressure difference that is close to 100 mm Hg and provides evidence of severe pulmonary
hypertension. In this case, elevated left atrial pressure was partly responsible for pulmonary hypertension but the predicted
pulmonary artery pressure was out of proportion to any credible estimate of left atrial pressure. Reactive vasoconstriction of the
pulmonary arterioles may have contributed to the development of pulmonary hypertension.
in patients with normal cardiac dimensions is P is the pressure difference and v is the veloc-
uncommon. ity of the regurgitant jet). The right atrial pressure
Acute CHF due to chordal rupture is treated is approximated based on clinical findings; in
similarly to acute or decompensated heart failure the absence of right-sided CHF, the right atrial
caused by other disorders although there may be pressure is likely less than 10 mm Hg. Provided
a particular role for the intravenous administra- pulmonary stenosis (PS) is excluded by Doppler
tion of nitroprusside in addition to parenteral di- evaluation of the right ventricular outflow tract,
uretic administration. right ventricular and pulmonary artery pressures
The prognosis depends on numerous factors are equal during systole. Thus, measurement of
of which response to therapy is probably most the velocity of the TR jet can provide noninvasive
important. estimates of systolic pulmonary artery pressure
(Figure 6-18).
Pulmonary hypertension The cause of pulmonary hypertension associated
s0280
Pulmonary hypertension occasionally compli- with MVD is probably multifactorial. The pri-
u0210
cates the clinical presentation of MVD in the mary function of the right ventricle is to propel
dog. Doppler studies can provide noninvasive the stroke volume through the pulmonary vascu-
estimates of pulmonary artery pressure. Dop- lar tree to the left atrium. Elevations in left atrial
pler echocardiographic evidence of tricuspid pressure cause commensurate increases in right
valve regurgitation (TR) is commonly observed ventricular systolic pressure; if mean pulmonary
in patients with MVD. The velocity of the TR jet artery pressure does not exceed mean left atrial
is related to the systolic pressure difference be- pressure, there is no impetus for forward flow.
tween the right atrium and the right ventricle by The tendency for left atrial hypertension to cause
the modified Bernoulli equation (P = 4v2, where pulmonary hypertension is probably the primary
Chapter 6 Acquired Valvular Disease 131
explanation for high pulmonary artery pressures ten go on to develop CHF. When CHF develops, the
in most cases; however, in some patients, the disease is generally terminal. Even with palliative
increase in estimated pulmonary artery pressure medical therapy, survival is usually measured in
is disproportionate to any credible estimate of left months, with 8 to 14 months being typical.
atrial pressure. In these cases, pulmonary arte-
rial constrictionsometimes known as reactive
Infective Endocarditis
s0300
lated to the presence of concurrent pulmonary or The prognosis is generally grave, and most cases
airway disease. are terminal even with aggressive medical therapy.
There is no established therapy for patients with This latter point emphasizes the importance of de-
pulmonary hypertension associated with MVD. tecting IE, a disease that sometimes poses a consid-
Most vasodilators have a relatively predictable erable diagnostic challenge.
effect on the systemic vasculature; however, the
pulmonary arterioles respond inconsistently to
Prevalence and incidence
s0310
use of vasodilators in patients with pulmonary served occasionally in dogs but rarely in cats.
hypertension due to severe pulmonary vascular Mural endocarditis and infection of the tricuspid
disease is not without risk. If a vasodilator with valve are observed occasionally, as is infection
potent peripheral effects fails to decrease pulmo- of endocardial pacing leads; however, bacterial
nary vascular resistance, systemic hypotension or infection of the aortic or mitral valve leaflets is
detrimental increases in right ventricular pressure most common.
and myocardial oxygen demand may result. Middle-aged, large-breed male dogs, including
As initial therapy, interventions that reduce left German Shepherds and Boxers, are affected most
atrial pressure are reasonable. Diuretic therapy often.
should be tailored to rid the patient of radiographic In people, the presence of a congenital cardiac
evidence of pulmonary congestion or edema. Al- malformation is a risk factor for the development
veolar hypoxia is a stimulus for constriction of of IE. An association between congenital subval-
the pulmonary arterioles. If bronchoconstriction vular aortic stenosis and IE of the aortic valve has
associated with primary respiratory disease has been demonstrated, and it is likely that subvalvu-
contributed to the development of pulmonary lar aortic stenosis and, perhaps, other congenital
hypertension, the administration of bronchodila- malformations, are important factors in the epi-
tors may be helpful. demiology of IE in dogs.
When effective control of pulmonary conges-
tion or therapy of primary respiratory tract dis-
Etiopathogenesis
s0320
bly be related to pulmonary hypertension, the following factors are important in the pathogen-
use of sildenafil in addition to an ACE inhibitor esis of infective valvular endocarditis:
can be considered. Sildenafil is an inhibitor of Endocardial damage (which may result from
phosphodiesterase-V that appears to have a rela- valvular insufficiency, stenosis, or a shunting
tively selective effect on pulmonary arterioles. lesion)
When possible, systemic blood pressure should Activation of clotting factors
be monitored when therapy with this drug is initi- Bacteremia and colonization of a noninfective
ated (see chapter 9). thrombus
The development of a noninfective thrombus
Prognosis precedes valvular infection. Episodes of bac-
s0290
The prognosis associated with the development of teremia can result in infection of the thrombus
p0080
MVD depends on numerous factors. The major- and the initiation of a variably aggressive in-
ity of patients with MR due to MVD succumb to flammatory process that results in distortion and
noncardiac disease. In the absence of noncardiac destruction of the valve leaflets and their associ-
disease, patients with cough or syncope and distinct ated structures.
radiographic evidence of left atrial enlargement of-
132 Section II Cardiovascular Disease
In clinical cases of canine IE, a congenital car- valve leaflets contributes to valvular incompe-
diac malformation may represent a predisposition tence. The hemodynamic consequences of MR
for the development of the disease. Prostatitis, have been discussed previously.
pyelonephritis, or even dental disease can pro- IE of the aortic valve typically results in aortic valve
vide a source for the development of bacteremia; incompetence, which is a potentially catastrophic
often, however, the site of bacterial entry into the hemodynamic lesion. When the aortic valve be-
bloodstream remains undiscovered. comes incompetent, the left ventricle is filled dur-
Degenerative valvular disease has no known as- ing diastole by the pulmonary venous return and
sociation with IE. Interestingly, despite the preva- by the blood that enters through the regurgitant
lence of dental disease in patients with MR due to orifice. When severe, the increase in ventricular
MVD, IE is extremely uncommon in this patient filling pressures (diastolic ventricular pressures) is
group. reflected back upon the pulmonary venous circula-
Gram-positive bacteria such as the streptococci tion, resulting in pulmonary congestion and edema.
and staphylococci are most often implicated in In contrast to MR, aortic valve insufficiency (AI)
the development of IE. Valvular infection with causes a substantial increase in left ventricular after-
gram-negative organisms such as Escherichia load and therefore, myocardial oxygen demand. As
coli is less common. a result, myocardial dysfunction (cardiomyopathy
With regards to the etiology of IE, there has been of overload) is observed commonly and early in the
recent interest in the fastidious, intracellular or- course of aortic valve IE.
ganisms of the genus Bartonella. Four species Embolization of fragments from the endocardi-
of Bartonella have been documented to cause tis lesion occurs commonly. Sites where infected
canine IE. Although geographical distribution of thrombi lodge include the spleen, the kidney, and
Bartonella IE may not be uniform, Bartonella is occasionally the brain. Most often, embolization
an important cause of IE in northern California of the spleen is clinically silent; infarction of the
and probably elsewhere. Patients with Bartonella kidneys or central nervous system can be cata-
infection are often concomitantly seropositive strophic, resulting in renal failure and nervous sys-
for tick-borne diseases and Bartonella itself tem signs such as head tilt. Embolization of joints,
may be arthropod borne. Bartonella spp. are resulting in bacterial arthritis, can also occur.
difficult to culture using standard microbiological
Clinical presentation
s0340
more specifically, demonstration of Bartonella IE in dogs is observed most commonly in a sub-
u0250
antigens through polymerase chain reaction acute form. In these cases, historical evidence of
testing performed on bacterial isolates or valve prior illness or of infectious disease may be lack-
tissue. ing. A congenital cardiac murmur may or may
not have been detected. IE is also observed in an
acute form.
Pathophysiology
s0330
embolism, and cardiac dysfunction. IE results in ercise intolerance are observed most commonly.
intermittent shedding of bacterial organisms into The lameness is often mild and may be difficult to
the bloodstream, resulting in episodes of bacte- localize. The embolization of infected thrombi to
remia. Signs of sepsis, including pyrexia and, joints contributes to lameness, although immune
rarely, circulatory collapse, may be observed. complex arthropathy may be of equal etiologic
Sequelae of sepsis related to chronic antigenic importance.
stimulation and the consequent development of Clinical signs of sepsis may be more prominent in
immune complex disease are observed fairly patients that develop acute IE. The sudden onset of
commonly in IE. Polyarthritis is observed often, fever and the development of a new cardiac mur-
and glomerulonephritis can also develop. mur in the critically ill suggest the presence of IE.
In canine IE, it is often the destruction of the
valve leaflets and associated structures that is of Physical findings
s0360
greatest clinical importance. The development Fever is a common but not necessarily a consis-
u0260
of infected thrombi results in failure of the valve tent finding in patients with IE. Published cases
leaflets to coapt. Occasionally, perforation of the series of canine IE reflect the experience of re-
Chapter 6 Acquired Valvular Disease 133
ferral centers and are therefore biased. At some tachyarrhythmias, including atrial fibrillation,
point in the natural history of the disease it is are also observed.
likely that most patients are pyrexic; however, The association of third-degree atrioven-
fever associated with IE can be intermittent and tricular block with IE deserves mention. Occa-
may resolve before clinical presentation. sionally an aggressive aortic lesion will invade
The pulse rate is often elevated, as some degree the interventricular septum or, alternatively,
of cardiac dysfunction is commonly present at embolize the nodal coronary artery, resulting
the time of presentation. in destruction of the atrioventricular node or AV
The respiratory rate is elevated, and respiratory bundle. This catastrophic complication is relatively
distress is usually apparent, in patients that have uncommon, but lesser degrees of atrioventricular
developed CHF. block or intraventricular conduction delays, such as
A cardiac murmur is present in the majority of left bundle branch block, are observed fairly often.
patients with established valvular infection. MR Electrocardiographic evidence of cardiac cham-
results in a systolic murmur that is most easily ber enlargement is observed in patients that
heard over the left cardiac apex. Aortic valve survive long enough for the volume overload as-
IE usually results in a diastolic decrescendo sociated with IE to result in chamber dilation and
murmur that is typically heard most easily over the hypertrophy.
left cardiac base. A concurrent systolic murmur
related to the increase in left ventricular stroke Echocardiographic Findings
s0400
volume associated with AI results in a murmur The term vegetative endocarditis is generally used
u0290
There are no electrocardiographic findings that not eliminate IE from the differential diagnosis.
u0280
are diagnostic of IE. However, all manner of When vegetative IE of the aortic or mitral valve is
cardiac arrhythmias can be observed in asso- present, there is often echocardiographic evidence
ciation with this disease. Ventricular tachyar- of left atrial and left ventricular enlargement. Pre-
rhythmias, including ventricular tachycardia, mature diastolic closure of the mitral valve and
are relatively common, and supraventricular diastolic flutter of the anterior mitral valve leaflet
indicate severe AI (Figure 6-22). Some degree of
134 Section II Cardiovascular Disease
f0190
Figure 6-19. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from a 1-year-old German Shepherd with aor-
tic valve endocarditis. The cardiac silhouette is enlarged and there is evidence of left atrial enlargement. Pulmonary opacities
indicate the presence of pulmonary edema.
systolic myocardial dysfunction is typically pres- is relatively mild, and evidence of acute inflam-
ent when cardiac enlargement results from AI. mation may or may not be present.
Doppler echocardiography is used to confirm the Abnormalities in the serum chemistries are not
presence of valvular incompetence. specific and, when present, are secondary to the
disease process. Azotemia is relatively common
Laboratory data and can be pre-renal, as a result of poor renal per-
s0410
In many cases of IE, the hemogram reveals leu- fusion, or it can result from renal infarction. Hypo-
u0300
kocytosis, but this finding is not consistently albuminemia, hyperglobulinemia, and elevations in
present. In subacute cases of IE, the leukocytosis serum alkaline phosphatase may also be observed.
Chapter 6 Acquired Valvular Disease 135
f0200
Figure 6-20. Two-dimensional echocardiographic image obtained from a Boxer with aortic valve endocarditis. This left apical
five-chamber view demonstrates the presence of a large, highly echogenic nodule attached to one of the aortic valve leaflets.
f0210
Figure 6-21. Two-dimensional echocardiographic short axis image obtained from a 5-year-old female spayed Doberman Pin-
scher with mitral valve endocarditis. There is a discrete nodule attached to anterior mitral valve leaflet (arrow).
Figure 6-22. M-mode echocardiograms obtained from dogs with severe aortic valve incompetence due to bacterial endocardi-
f0220
tis. A, An M-mode echocardiogram obtained at the mitral valve level. There is diastolic flutter of the anterior mitral valve leaflet and
premature closure of the mitral valveindirect echocardiographic evidence of severe aortic valve incompetence. B, An M-mode
echocardiogram obtained at the aortic level. The motion of the visible aortic valve leaflet is chaotic because it is flail, having been
all but destroyed by an aggressive endocarditis lesion.
Most often, IE in dogs results from gram-positive nous route because high serum levels of drugs are
organisms, and agents such as the clavulanate achieved quickly and with certainty.
potentiated penicillins or the cephalosporins are When clinical signs of sepsis are prominent and
appropriate. Azithromycin may have a role in blood culture results are negative, initial therapy
the management of IE due to Bartonella spp. using a combination of intravenous gentamicin
In general, bactericidal agents are preferred. A (or amikacin) and ampicillin (or a cephalosporin)
long course of therapy, 6 to 8 weeks, is generally is justified. When patients are free of gastroin-
recommended. There may be some advantage testinal signs such as vomiting or diarrhea, oral
to initiating antibiotic therapy using the intrave- antibiotic therapy is probably appropriate.
Chapter 6 Acquired Valvular Disease 137
f0230
Figure 6-23. Lateral radiographic projection of a clinically normal Cocker Spaniel. The dimensions used to calculate the vertebral
heart sum (VHS) are shown. The vertebral bodies, beginning at the fourth thoracic vertebra are used as a scale.
Canine Cardiomyopathy
Mark A. Oyama
Dilated Cardiomyopathy
Introduction
Prevalence and Signalment
Cardiomyopathy is defined as a primary disease of
the heart muscle of unknown etiology. Disease of Surveys indicate that between two and six dogs are
the heart muscle secondary to toxins, nutritional de diagnosed with DCM per 600 case referrals. In cer
ficiencies, endocrinopathies, and infectious agents tain breeds, the prevalence of DCM is remarkably
is often regarded as a secondary cardiomyopathy. high. Approximately 25% of Irish Wolfhounds,
The most common form of canine cardiomyopathy 50% of male Doberman Pinschers, and 33% of
is dilated cardiomyopathy (DCM), which is charac female Doberman Pinschers develop DCM. The
terized by progressive ventricular dilation and loss of typical age at diagnosis is between 6 and 8 years;
myocardial contractility. Other forms of cardiomyo however, it is not uncommon to diagnose DCM in
pathy, such as hypertrophic cardiomyopathy (HCM), dogs as young as 3 years and as old as 12 years.
are rare in dogs. DCM is most common in adult Male dogs appear to be more frequently affected,
large breed dogs, and in particular the Doberman especially in the Doberman Pinscher breed.
Pinscher, Irish Wolfhound, Scottish Deerhound, and
Great Dane. The important features of canine DCM
Natural History
include (1) the presence of an asymptomatic or occult
phase during which diagnosis of disease is difficult, The clinical progression of DCM is best described
(2) the high prevalence of congestive heart failure, as occurring in two distinct phases.
and sudden death in severely affected dogs, and (3)
the need for aggressive and comprehensive medical Asymptomatic Occult Phase
therapy to help alleviate clinical signs. Boxers with No clinical signs are evident; however, myocar
cardiomyopathy possess a unique pathophysiology, dial or electrical abnormalities are present and
clinical presentation, and natural history, such that may include:
disease is best described as arrhythmogenic right Increased left ventricular and atrial dimensions
ventricular cardiomyopathy (ARVC). Sudden death Decreased myocardial contractility
from ventricular arrhythmias is very common in Ventricular premature beats
Boxers with ARVC, much more so than chronic con The duration of the occult phase is highly vari
gestive heart failure. Secondary cardiomyopathies able and thought to last for months to years.
due to nutritional deficiencies appear in breeds of During this phase, progressive heart enlargement
small and medium size, most notably in the Ameri and worsening arrhythmias occur.
can Cocker Spaniel. A highly fatal juvenile form of Occult phase ends with the appearance of the first
DCM is seen in the Portuguese Water Dog. clinical signs of disease.
139
140 Section ii Cardiovascular Disease
Figure 7-1. Lead II ECG tracing from a 7-year-old male, castrated Boxer with arrhythmogenic right ventricular cardiomyopa-
thy. Ventricular premature beats with left bundle branch block morphology are a common finding in dogs with this condition.
25 mm/sec; 0.5 cm/mV.
Chapter 7 Canine Cardiomyopathy 141
In Irish Wolfhounds, atrial fibrillation is of The chest radiographs in Doberman Pinschers
ten an early sign of disease as opposed to are often misleading in that heart enlargement
other breeds where atrial fibrillation is as is less striking than in other breeds with simi
sociated with advanced stages of disease. lar clinical signs. In these instances, cardiac
Holter monitoring detects arrhythmias with ultrasound helps to determine the magnitude
greater sensitivity and is recommended in of left-sided heart enlargement and systolic
dogs at high risk (i.e., dogs with a familial dysfunction.
history of disease). The chest radiographs in Boxers with ARVC
Greater than 100 ventricular premature are usually normal.
beats in a 24-hour period is highly sugges
tive of occult DCM or ARVC. Echocardiography
A total of 50 to 100 ventricular premature Echocardiography is widely used to quantify
beats in a 24 hour period is suspicious for heart enlargement and systolic function. Routine
disease and should be followed by another echocardiography is not particularly sensitive in
Holter examination in 2 to 6 months. detecting early changes in occult disease, nor is it
Day-to-day variability in the frequency of particularly helpful after a diagnosis of end-stage
arrhythmia can produce false-negative re disease is made. As such, the utility of echocar
sults, and if the initial Holter examination diography increases as disease moves out of the
is inconclusive, multiple Holter examina occult phase to the overt clinical phase then de
tions may be indicated, especially in dogs clines again as the patient advances into end-stage
with a family history of disease or in those disease. Early in the course of disease, many dogs
that have experienced syncope. possess normal echocardiographic examinations,
During the overt clinical phase, the following despite having a significant numbers of ventricu
may be detected: lar arrhythmias.
Occasional to frequent ventricular or supra Echocardiographic criteria are used to help di
ventricular premature beats agnose occult DCM.
Ventricular tachycardia In Doberman Pinschers, a left ventricular
Criteria for left ventricular or atrial enlarge end-diastolic diameter (LVIDd) > 46 mm
ment (see previous section) or a left ventricular end-systolic diameter
Left bundle branch block (LVIDs) > 38 mm is highly suggestive of
Atrial fibrillation (Figure 7-2) early disease. These values may not be ap
plicable to Dobermans with very large body
weights, and LVIDd > 49 mm or LVIDs
Key Points
> 42 mm may be better guides in this
The author regards Holter monitoring as population.
the current gold standard for detection of In Doberman Pinschers, fractional shortening
occult DCM in Doberman Pinschers. Holter is an unreliable index for occult DCM, as this
monitoring is relatively easy to perform and
breed typically has fractional shortening val
equipment is readily available to the general
practitioner through human and veterinary ues in the mid or low 20% range. Similarly,
medical suppliers. Many veterinary telemedi- large-breed dogs with athletic lifestyles com
cine or remote consulting practices lease monly display fractional shortening values in
Holter units and assist in result analysis. the mid 20% range, and longitudinal echo
cardiographic studies or Holter monitoring is
required to determine whether disease is truly
Chest Radiography present.
Chest radiographs are relatively insensitive to mild In Irish Wolfhounds, occult disease is defined
increases in the heart size. A single set performed as LVIDd > 61.2 mm, LVIDs > 41 mm, frac
in the asymptomatic occult phase contributes tional shortening < 25%, end-systolic volume
relatively little to the immediate diagnosis; how index > 41 ml/m2, or E-point to septal separa
ever, serial radiographs are well suited to monitor tion > 10 mm.
progressive heart enlargement and progression of Newer ultrasound modalities such as Dop
disease. In the overt clinical phase, radiographs pler tissue imaging may be more sensitive in
are invaluable in helping to diagnose congestive detecting early abnormalities of myocardial
failure and to monitor response to treatment. contractility.
142 Section ii Cardiovascular Disease
Figure 7-2. Lead II ECG tracing from a dog indicating atrial fibrillation and left ventricular enlargement. Note the irregular
rhythm, lack of P waves, and widened QRS complex. 50 mm/sec; 10 mm/mV.
Figure 7-3. 2-dimensional echocardiogram of the left ventricle (LV) and atrium (LA) of a Great Dane with dilated cardiomyo
pathy. Note the dilated ventricular and atrial chambers. RV, Right ventricle; RA, right atrium.
As disease progresses from occult to overt, Decreased systolic thickening of the left ven
echocardiography helps monitor heart enlarge tricular wall and interventricular septum.
ment, assess contractility, and evaluate second The echocardiogram in Boxers with ARVC is
ary mitral regurgitation. Echocardiography is usually normal. Subtle right ventricular dilation
used in conjunction with chest radiographs to or wall motion abnormalities may be noted.
help decide when to initiate therapy.
Common echocardiographic findings in dogs
Concomitant Abnormalities in Moderate or
with advanced occult or overt clinical disease
Severe Dilated Cardiomyopathy
include the following:
Moderate to severe left ventricular and atrial Azotemia is commonly detected in dogs that
enlargement (Figure 7-3). are receiving diuretic therapy and is typically
Reduced systolic motion of the left ventricular prerenal in nature.
wall and interventricular septum (Figure 7-4). Mild azotemia (blood urea nitrogen < 60 mg/
Mild to moderate mitral regurgitation sec dl and creatinine < 2.5 mg/dl) usually does
ondary to mitral annulus dilation. not require specific treatment or cessation or
Incomplete systolic opening of the aortic reduction of diuretic therapy.
valves. More severe azotemia (blood urea nitrogen
Decreased aortic blood flow velocity. > 80 mg/dl and creatine > 3.0 mg/dl) can con
Increased mitral valve E-point to septal sepa tribute to patient morbidity and may require
ration (normal < 6 mm) (Figure 7-5). reduction of angiotensin-converting enzyme
Chapter 7 Canine Cardiomyopathy 143
Figure 7-4. M-mode echocardiogram of the left ventricle of a Cocker Spaniel with dilated cardiomyopathy. Note the decreased
systolic motion of the interventricular septum (arrow) and left ventricular free wall (arrowhead).
Figure 7-5. M-mode echocardiogram of the left ventricle and mitral valve of a Brittany Spaniel with dilated cardiomyopathy.
Electronic calipers are being used to measure the E-point to septal separation (EPSS), which is markedly increased over normal.
(ACE) inhibitor and diuretic dose or parenteral require specific treatment. Severe hypoka
fluid supplementation. lemia (K+ < 2.5 mEq/l) can cause cardiac
If fluids are administered, then administer arrhythmias and contribute to muscle weak
ing half-strength saline or Ringers solution ness. Reduction of potassium-wasting di
will reduce the sodium load to the patient. uretics (e.g., furosemide) or institution of
ACE inhibitor therapy can be temporarily potassium-sparing agents (e.g., ACE inhibi
discontinued or the dosage reduced. Initia tors, spironolactone) is performed. Clini
tion of the ACE inhibitor therapy should be cally important hyperkalemia is uncommon
delayed or done with caution. and usually associated with reduced car
Aggressive parenteral fluid therapy can ag diac output, poor renal perfusion, and renal
gravate congestive heart failure and should failure.
be used with caution. Mild hyponatremia is common and is di
Many instances can be treated by reduc lutional in nature. Serum concentration of
tion of diuretics and allowing the patient to sodium is decreased secondary to water re
drink enough water to reestablish hydration tention and expansion of the plasma volume
on their own. despite elevated total body sodium content.
Azotemia reduces renal clearance of digoxin Mild hyponatremia does not require spe
and predisposes to toxicity. Serum digoxin cific treatment. In the authors experience,
levels should be determined especially if the profound hyponatremia (Na+ < 130 mEq/l)
patient displays anorexia, vomiting, diarrhea, signals a poor prognosis. Treatment requires
or frequent arrhythmias. reduction of diuretic dose, water restriction,
Electrolyte abnormalities are common in dogs and dietary sodium supplementation.
with congestive heart failure due to DCM. Most Hypothyroidism is a common concurrent dis
changes are mild and do not require specific ease in middle-aged to older dogs, especially
treatment. in Doberman Pinschers. A causal relationship
Potassium levels may be either increased between hypothyroidism and DCM is doubtful.
or decreased. Mild hypokalemia (K+ = 2.5 Supplementation does not improve survival.
to 3.0 mEq/l) is commonly associated with Natriuretic peptides are produced by the atrial
high doses of diuretics and usually does not and ventricular tissues in response to increased
144 Section ii Cardiovascular Disease
vasodilation. ACE inhibitors improve survival no known treatments that definitively slow pro
and quality of life in dogs with DCM. Dogs gression of disease in the occult state. Insofar as
with severe heart failure and poor renal per gradual derangement of neurohormonal activity is
fusion may become uremic while taking ACE associated with worsening cardiac function, use of
inhibitors, especially when high doses of di ACE inhibitors, beta blockers, and spironolactone
uretics are being concurrently used. has been suggested. Current recommendations are
Sodium nitroprusside elicits potent arterial based on small veterinary trials and extrapolation
and venous vasodilation and is very effective from human medicine. Three drug classes are typi
in cases of life-threatening heart failure. Due to cally considered during the occult phase.
the risk for hypotension, arterial blood pressure Use of beta blockade is scientifically supported in
monitoring is required during its use. Sodium virtually all human patients with left ventricular
nitroprusside is administered as a constant-rate systolic dysfunction with current or prior symp
infusion (CRI). toms, and consensus opinion extends this recom
Topical nitroglycerin produces minimal ve mendation to use in asymptomatic patients. In
nous vasodilation in dogs due to poor absorp dogs, sympathetic tone is increased during the oc
tion and low plasma concentrations. cult phase, thus providing rationale for administra
Antiarrhythmic agents suppress life-threatening tion of beta blockers in dogs with early disease.
ventricular arrhythmias and control the ventricu Use of ACE inhibition is scientifically supported
lar rate during atrial fibrillation. For ventricular in virtually all human patients with left ventricular
arrhythmias, drugs in classes I (e.g., lidocaine systolic dysfunction regardless of symptoms. In
and mexiletine), II (beta blockers), and III (e.g., dogs, the time course of ACE activation is uncer
sotalol) can be used alone or in certain combi tain. Although several studies indicate that height
nations. Drugs in class II and IV (calcium chan ened activity of the renin-angiotensin-aldosterone
nel blockers) and digoxin are used for atrial is not present in early disease, there is a need to
fibrillation. distinguish between circulating and local tissue
Beta-adrenergic blocking agents are extensively ACE activity. Though circulating ACE activity
used in humans with DCM. In dogs, little clini is not upregulated until later in disease, evidence
cal data exists. Beta-blocking agents blunt the suggests that a locally contained myocardial ACE
effects of chronic sympathetic nervous system system contributes much earlier in disease. Thus,
activity (i.e., tachycardia, arrhythmias, myocyte tissue-penetrating ACE inhibitors, such as benaz
death, ventricular remodeling, elevated activity epril or ramipril, may be beneficial.
of the renin-angiotensin-aldosterone system). Spironolactone is primarily used in humans with
Overly aggressive use may exacerbate conges symptomatic DCM; however, the benefit in pre
tive heart failure, and patients should be clini venting aldosterone-mediated remodeling may
cally stable before being titrated onto this class begin in earlier stages of disease.
of drug. Due to the high incidence of sudden death in
Inodilators are drugs that improve cardiac con Boxers and Doberman Pinschers, antiarrhythmic
tractility and elicit vasodilation. Pimobendan therapy is often initiated in asymptomatic dogs
is a calcium-sensitizing inodilator that increases based on Holter monitor findings. Dogs with runs
the myocardial response to calcium. Pimobendan
should be used in dogs with symptomatic disease
that are already receiving conventional therapy. Key Points
Pimobendan improves quality of life and is likely The natural history of cardiomyopathy is
to improve survival. substantially influenced by breed. Large- or
giant-breed dogs commonly develop atrial
fibrillation and congestive heart failure, while
Treatment of Asymptomatic Occult Disease Doberman Pinschers and Boxers with ARVC
Treatment in the occult phase represents both an commonly exhibit syncope, ventricular ar-
opportunity and a challenge. Clearly, treatments rhythmias, and sudden death. Thus, in Great
Danes, Irish Wolfhounds, and similar affected
that slow progression in this phase would help
breeds, treatment efforts should focus on the
delay or prevent symptomatic disease, yet the dis resolution of heart failure, whereas in Dober-
covery of effective drugs is hindered by the diffi man Pinschers and Boxers, antiarrhythmic
culty in performing large-scale prospective clinical therapy is commonly prescribed.
trials with sufficient statistical power. There are
146 Section ii Cardiovascular Disease
of ventricular tachycardia or R-on-T phenome Oral pimobendan (0.25 mg/kg every 12 hours)
non are started on sotalol (1.5 to 2.0 mg/kg every may be useful if intravenous positive inotrope
12 hours) or the combination of mexiletine (5 to therapy is not available.
8 mg/kg every 8 hours) and atenolol (0.3 to 0.4 When given orally, digoxin requires several days
mg/kg every 12 hours). The efficacy of this treat to reach effective concentration, and as such, has
ment in preventing sudden death is unproven. little role as an emergency positive inotrope. In
travenous digoxin commonly produces toxicity
Treatment of Overt Clinical Disease
and is not recommended.
Treatment of Severe Life-Threatening Supplemental oxygen therapy is administered either
Congestive Heart Failure in an oxygen cage (fraction of inspired oxygen =
Congestive heart failure is relieved through aggres 40%) or given nasally (50 to 100 ml/kg/min).
sive diuretic, vasodilator, and positive inotropic One of the most difficult clinical decisions is
therapy. whether or not to specifically treat ventricular
Manual removal of heart failure fluid should be arrhythmias. Overly aggressive treatment may
performed in all patients with clinically significant cause hypotension or predispose to even more
pleural or abdominal effusion, as this will rapidly malignant arrhythmias.
improve respiratory effort and alleviate distress. Ventricular premature beats and short runs of
Intravenous or intramuscular furosemide (3 to 8 mg/ ventricular tachycardia that occur at relatively
kg) is administered. When given parenterally, dura slow heart rates (< 160 bpm) typically do not
tion of effect is approximately 2 hours; therefore, require treatment. Often, resolution occurs
additional doses should be administered if the pa spontaneously once congestive heart failure
tients respiratory rate and effort have not improved and hypoxia are successfully treated.
within this time period. Patient recovery can be sig Rapid ventricular arrhythmias that are life-
nificantly hindered due to insufficient dosing of fu threatening are accompanied by clinical signs
rosemide during the first 12 hours of treatment. (i.e., weakness, syncope, hypotension, blanch
Efficacy of diuretic therapy is assessed by mon ing of mucous membranes). Intravenous lido-
itoring patient respiratory rate and effort, urine caine (2 mg/kg IV bolus followed by CRI of
output, and body weight. To confirm the reso 40 to 80 mcg/kg/min) or procainamide (6 to
lution of pulmonary edema or to reassess pa 8 mg/kg IV bolus followed by CRI of 20 to 40
tients that are not responding to therapy, chest mcg/kg/min) is often effective.
radiographs are performed 12 to 24 hours after Due to the high incidence of sudden death in
initiation of therapy. Boxers and Doberman Pinschers, aggressive anti
The presence of severe underlying renal dys arrhythmic therapy in these species is more com
function may necessitate lower doses and less monly warranted, and especially in dogs that have
frequent dosing. previously experienced syncope. Once stabilized,
Sodium nitroprusside (2 to 5 mcg/kg/min CRI) either oral sotalol or combination of mexiletine
is a very effective vasodilator. Nitroprusside can and atenolol are prescribed (see next section).
produce profound hypotension, and arterial blood
pressure monitoring is required when using it. Transitioning the Improved Emergency Patient
The infusion rate is adjusted to elicit a 15 mm Hg to Chronic Oral Treatment
decrease in mean blood pressure as long as the Aggressive emergency therapy successfully resolves
mean value does not fall below 70 mm Hg. acute heart failure in approximately 75% of dogs. In
Intravenous positive inotropes such as dopamine most dogs, significant improvement in clinical signs
(2 to 10 mcg/kg/min CRI) or dobutamine (5 to will be apparent within 48 hours. Patients refractory to
15 mcg/kg/min CRI) help improve cardiac out therapy beyond this point have a grave prognosis. As
put. High doses may aggravate ventricular ar the patient becomes increasingly stable, intravenous
rhythmias or cause sinus tachycardia. medications are gradually reduced and replaced with
Milrinone is a potent positive inotrope that acts oral medications. During this time, patient hydration
downstream of the myocardial beta adrenergic status, body weight, appetite, respiratory effort, elec
receptor. It increases contractility in patients re trolytes, and renal function continue to be monitored.
ceiving beta blockers or in patients that are not Once the patients respiratory rate and effort has im
responding to dopamine or dobutamine therapy. proved, parenteral furosemide is discontinued in fa
Milrinone is administered as a 30 to 50 mcg/kg vor of oral furosemide (typical oral dose: 1 to 2 mg/kg
loading bolus given intravenously over 10 min every 8 to 12 hours). Nitroprusside and dopamine
utes then CRI of 1 to 8 mcg/kg/min. or dobutamine are gradually reduced over 12 to 24
Chapter 7 Canine Cardiomyopathy 147
is done in patients with clinically stable heart c alcium overload, myocardial oxygen demand,
disease, and as such, beta blocking agents should and arrhythmia formation. Agents with combined
not be used in patient with active signs of con vasodilatory properties may offer additional adv
gestion (the exception would be emergency beta vantages in patients with severe DCM.
blocker use to control rapid atrial fibrillation). Ini Pimobendan (0.25 mg/kg PO every 12 hours)
tiation of beta blockade can acutely worsen con results in substantial improvement in quality of
tractility; thus patients are gradually titrated onto life. Pimobendan is typically used in patients
the medications over 4 to 8 weeks. Adverse side with severe disease, and as such, is used in con
effects include bradycardia, hypotension, and ex junction with diuretics, ACE inhibitors, and oc
acerbation of congestive heart failure. Clinicians casionally, digoxin. Benefit from pimobendan
who prescribe beta blockers must be prepared to during occult disease is possible, but requires
manage acute heart failure secondary to drug ini additional study.
tiation. In humans, beta blockers slow progression Aldosterone antagonists, such as spironolactone,
of disease and improve survival but do not dramat act as mild diuretics but even more importantly,
ically improve quality of life. Beneficial effects re reduce the proliferative effects of aldosterone
quire several months of continuous treatment, and within the myocardium and vasculature. Other
in dogs with end-stage disease, treatment may not beneficial properties include blunting of sym
be practical. Accordingly, both the maximum ben pathetic nervous activity and normalization of
efit and the minimum risk of beta blocker use are baroreceptor function. In the presence of severe
probably early in the course of disease. heart disease, ACE inhibition alone may not be
Metoprolol (initial dose of 0.1 to 0.2 mg/kg PO sufficient in suppressing aldosterone production,
every 12 hours followed by gradual titration to and in humans with heart failure, spironolactone
0.4 to 0.8 mg/kg PO every 12 hours over 4 to 8 improves survival.
weeks). Spironolactone (1 to 2 mg/kg PO every 12 hours)
Carvedilol(initial dose of 0.1 mg/kg PO every is commonly prescribed with hydrochlorothia
12 hours followed by gradual titration to 0.5 zide in dogs with severe heart disease. Due to
mg/kg PO every 12 hours over 4 to 8 weeks). its anti-proliferative effects, spironolactone
Calcium-sensitizing agents purportedly increase may also be beneficial in the occult and early
cardiac contractility while reducing cellular symptomatic stages of disease.
Amino acid deficiency is present in some breeds
with DCM (e.g., American Cocker Spaniels).
Key Points
Taurine supplementation (500 mg PO every
Beta blockade represents one of the cornerstones 12 hours for Cocker Spaniels) is recommended
of treatment in human patients with DCM. In in dogs with low plasma taurine concentration.
these patients, beta blockers slow progression of Concurrent l-carnitine supplementation (1
disease, improve systolic function, and prolong
g every 12 hours for Cocker Spaniels) is rec
survival. These benefits are dose dependent and
aggressive therapy yields the greatest results. In ommended in dogs with taurine deficiency.
canine patients, little is known about the ideal Alternatively, due to the relative expense of
timing, dose, and drug that should be used. In l-carnitine compared to taurine, l-carnitine is
healthy dogs, oral carvedilol doses ranging from withheld during the initial three months of tau
0.5 to 1.5 mg/kg PO every 12 hours blunt re- rine treatment and administered only to those
sponse to sympathetic stimulation with isopro- dogs that have not responded to taurine alone.
terenol. The appropriate dose for dogs with heart l-Carnitine deficiency was detected in a fam
disease is unknown, but it is likely to be lower ily of Boxers with left ventricular dilation and
than that used in healthy dogs. In dogs with systolic dysfunction. Supplementation (50
experimental mitral valve disease, oral carve- mg/kg PO every 8 to 12 hours) should be
dilol at 0.4 mg/kg PO every 24 hours reduced
considered in dogs with this presentation. The
heart rate, whereas in a small study of dogs with
advanced naturally occurring DCM, oral carve- value of supplementation in Boxers with ar
dilol at 0.3mg/kg PO every 12 hours did not re- rhythmias and no left ventricular dilation (which
sult in any measurable improvement in echocar- is the most common presentation) is doubtful.
diographic heart size or systolic function. Thus, Dogs that respond to amino acid supplementa
the effective dose of carvedilol in affected dogs tion can often reduce or discontinue conventional
is likely to be > 0.3mg/kg PO every 12 hours. heart failure medications (i.e., furosemide, ACE
inhibitors, digoxin); however, taurine and/or
Chapter 7 Canine Cardiomyopathy 149
c arnitine supplementation should continue in majority of dogs reported to have HCM are male
definitely. and of young age (typically < 3 yrs), suggesting a
Heart disease is accompanied by elevations of heritable etiology. The left ventricular hypertrophy
circulating cytokines and alterations of energy associated with HCM can be symmetrical (i.e., af
production, both of which may contribute to the fecting both the interventricular septum and left
heart failure syndrome of weight loss, muscle ventricular posterior wall equally) or asymmetric
wasting, and poor appetite. (in humans, the septum is typically more affected
Fish oil supplements can reduce interleu than the posterior wall). In the authors experience,
kin concentrations and help improve cardiac most cases of canine HCM involve symmetric
cachexia. LV hypertrophy. Significant left ventricular hy
Coenzyme Q10 is part of the mitochondrial re pertrophy causes diastolic dysfunction, left atrial
spiratory transport chain and supplementation enlargement, heart failure, and arrhythmias. Most
may improve quality of life. dogs with HCM are asymptomatic and the diag
The benefit of supplementary antioxidant vita nosis is made during evaluation of a heart murmur
mins E, A, or C is unknown. or arrhythmia. Echocardiography is the diagnostic
method of choice. Treatment is aimed at abolish
ing the obstructive component of disease with beta-
Prognosis
blocking agents (atenolol 0.5 to 1.0 mg/kg every
The time course from occult to symptomatic DCM 12 to 24 hours), alleviating heart failure with di
is highly variable and can be years. During this uretics, and suppressing arrhythmias. Sudden death
phase, serial echocardiographic and electrocardio appears to be more common than congestive heart
graphic exams are recommended. Sudden death can failure. Many dogs with HCM remain asymptom
occur during the occult phase, especially in Boxers atic for years.
and Doberman Pinschers. Once clinical signs such
as congestive heart failure develop, the long-term
prognosis is poor. Survival times derived from clin Frequently Asked Questions
ical studies are difficult to assess due to nonstan What Causes DCM?
dardized treatment, lack of ACE inhibitor use, and The etiology of primary DCM is unknown. DCM is a
statistical issues surrounding euthanasia. Median description of the hearts response to injury (i.e., dila
survival time is likely 3 to 4 months in Doberman tion and systolic dysfunction), and as such, may be the
Pinschers and 5 to 6 months in other breeds. Dogs end result of multiple causes. In fact, given the forms of
that survive greater than 7 months may do well DCM that are unique to different breeds, it is likely that
more than one etiology exists. Possible causes include
for an extended period of time. One-year survival genetic/familial, immune-mediated, infectious, toxic,
is approximately 10% to 15%. The presence of or nutritional. DCM in Doberman Pinschers may in
atrial fibrillation, biventricular congestive failure, volve specific components of the cytoskeleton or extra
and young age at time of presentation (< 5 years) cellular matrix. Cellular energy production is markedly
are associated with worse prognosis. Although the reduced in affected Doberman Pinschers, but whether
overall survival rate is disheartening, it is difficult these changes are primary abnormalities or secondary
to assess how any individual dog may fare. The au changes has yet to be determined. Boxers with ARVC
are thought to possess abnormal calcium cycling, which
thor suggests aggressive intravenous management is detected in certain forms of ARVC in humans.
of dogs with fulminant heart failure and reevalua
tion after 24 to 72 hours of therapy. Combination Therapy with Beta Blockers and
Pimobendan
There is a wealth of data supporting use of beta block
Hypertrophic ers in humans with DCM. Although these agents are
Cardiomyopathy effective at slowing pathologic ventricular remodel
ing and improving survival, they do relatively little
Hypertrophic cardiomyopathy (HCM) is an un to improve quality of life or exercise tolerance. In
common myocardial disease of dogs. HCM is char contrast, pimobendan, though not proven to improve
acterized by idiopathic concentric left ventricular survival in humans, has a marked benefit on quality
of life in dogs. A practice adopted by some cardiolo
hypertrophy, and can lead to heart failure or sud gists is to combine pimobendan and beta blocker use
den death. HCM, if accompanied by systolic ante in dogs with symptomatic DCM. The positive ino
rior motion of the mitral valve and left ventricular tropic effect of pimobendan may increase the like
outflow tract obstruction, is specifically referred to lihood of successful titration and tolerance of beta
as hypertrophic obstructive cardiomyopathy. The
150 Section ii Cardiovascular Disease
Kittleson MD, Keene B, Pion PD, Loyer CG: Results
blockers, and thereby achieve both increased quality
of the multicenter spaniel trial (MUST): taurine- and
and quantity of life.
carnitine-responsive dilated cardiomyopathy in Ameri
can cocker spaniels with decreased plasma taurine con
centration, J Vet Int Med 11(4):204-211, 1997.
Monnet E, Orton EC, Salman M, Boon J: Idiopathic di
Suggested Readings lated cardiomyopathy in dogs: survival and prognos
tic indicators, J Vet Int Med 9(1):12-17, 1995.
Borgarelli M, Tarducci A, Tidholm A, Haggstrom J: Ca
OGrady MR, OSullivan ML: Dilated cardiomyopa
nine idiopathic dilated cardiomyopathy. Part II: Patho
thy: an update, Vet Clin North Am Small Anim Pract
physiology and therapy, Vet J 162(3):182-195, 2001.
34(5):1187-1207, 2004.
Calvert CA, Pickus CW, Jacobs GJ, Brown J: Signal
Tidholm A, Svensson H, Sylven C: Survival and prog
ment, survival, and prognostic factors in Doberman
nostic factors in 189 dogs with dilated cardiomyopa
pinschers with end-stage cardiomyopathy, J Vet Int
thy, J Am Anim Hosp Assoc 33(4):364-368, 1997.
Med 11(6):323-326, 1997.
Tidholm A, Haggstrom J, Borgarelli M, Tarducci A:
Fuentes VL, Corcoran B, French A, et al: A double-blind,
Canine idiopathic dilated cardiomyopathy. I.
randomized, placebo-controlled study of pimobendan
Aetiology,clinical characteristics, epidemiology and
in dogs with dilated cardiomyopathy, J Vet Int Med
pathology, Vet J 162(2):92-107, 2001.
16(3):255-261, 2002.
Chapter 8
Feline Cardiomyopathy
Richard D. Kienle
Key PointS
Heart Disease
A normal thoracic radiograph does not pre-
clude the diagnosis of a cardiomyopathy.
Myocardial
Failure
Many asymptomatic cats with mild chang-
es and normal LA size will have a normal
thoracic radiograph.
Echocardiography, including Doppler
echocardiography, is essential for nonin-
vasive determination of a functional and
anatomic diagnosis. Before assigning a
diagnosis of cardiomyopathy based solely
Low Congestive upon morphologic/functional appearance,
Output
Failure
Heart a concerted effort should be made to rule
Failure out cardiac and extracardiac diseases that
might mimic the echocardiography of pri-
mary myocardial diseases.
Other diagnostic tests do not usually con-
tribute to the diagnosis of myocardial dis-
Figure 8-1. Venn diagram illustrates the various potential ease but are important for determining the
combinations of congestive heart (backward) failure, low-out- overall status of the patient, identifying con-
put (forward) heart failure, and myocardial failure (each repre-
comitant disorders, and assessing the effi-
sented by a circle) that may be detected in patients with heart
disease (the box). As all the circles reside in the box, each rep-
cacy or untoward effects of therapy. When
resents a form of heart disease, and the overlapping portions possible, routine biochemistries, urinalysis,
of the circles illustrate how the conditions may coexist. and hemogram should be performed prior
to pharmacologic intervention to establish
Physical Examination baseline values for the patient and to rule
out concurrent or secondary metabolic or
Early detection of disease should be a primary
hematologic disturbances.
goal. A thorough physical examination, with Chemical and cytologic evaluation of pleural
careful attention to auscultation, should be per- fluid with respect to protein concentration
formed. Many patients present with acute onset and cellularity can help determine whether
of dyspnea, paresis, lethargy, or anorexia; how- CHF underlies the production of pleural fluid.
ever, the majority of patients is asymptomatic and Cats with CHF can develop true chylous
will be identified after a murmur, gallop sound, effusion.
or other abnormality is identified during a routine Plasma and whole blood taurine concen
physical examination. The most common physi- trations should be measured in all cats
cal clues suggesting myocardial disease include: with echocardiographically documented
Systolic murmur (commonly heard along the ster- myocardial failure (see Taurine Deficiency
Induced Myocardial Failure).
nal border). This murmur may relate to either mitral
regurgitation or outflow tract obstruction or both.
Gallop sound, At normally rapid heart rates these
gallop sounds often represent a summation of the der and alert the clinician to secondary ramifications
third and fourth sounds. that may require attention; however, neither elec-
Dysrhythmia trocardiography nor thoracic radiography provides
Tachypnea/dyspnea adequate evidence for ruling out, confirming, or clas-
Muffled or harsh lung sounds sifying feline cardiac disease. Contrast radiography
Hypothermia or, preferably, echocardiography, is required to con-
Jugular pulses/distention firm or rule out and categorize myocardial disease.
Acute paresis associated with pain in regions Electrocardiography often shows:
with evidence of reduced peripheral perfusion Intraventricular conduction abnormalities (left
bundle branch block, left anterior fascicular
block pattern, pre-excitation syndrome)
Ancillary Tests
Increased amplitude of R waves
Thoracic radiography and electrocardiography may Ventricular arrhythmias are common but are
direct or reinforce suspicion that a cardiac disorder is generally mild with relatively infrequent single
present. They may also further characterize the disor- premature ventricular contractions.
154 Section II Cardiovascular Disease
Figure 8-2. A, Lateral thoracic radiograph from a cat with dilated cardiomyopathy demonstrates severe generalized cardio-
megaly. B, Dorsoventral thoracic radiograph from the same cat as in A.
Occasionally cats will have more complex ar- radiography. The author often delays radiography
rhythmias. Some cats with severe LA enlarge- until after stabilizing the patient (Figure 8-4).
ment will develop atrial fibrillation. Diagnostic and potentially therapeutic thoraco-
Thoracic radiography is most useful for detect- centesis should precede radiography in dyspneic
ing gross cardiac enlargement and clinical se- cats.
quelae to cardiac dysfunction (e.g., pulmonary
venous congestion, pulmonary edema, enlarged
Therapy
great veins, pleural effusion) (Figures 8-2 and
8-3). Restraint for radiographic procedures can Therapy should be based upon the clinical
be life threatening to dyspneic cats. Extreme andfunctional classification of the disease
caution should be taken before proceeding with process in the individual patient and not by
Chapter 8 Feline Cardiomyopathy 155
Figure 8-3. Lateral thoracic radiograph from a cat with hypertrophic cardiomyopathy demonstrates marked left atrial enlarge-
ment, pulmonary venous engorgement, and pulmonary edema.
to 0.50 mg/kg PO every 24 hours) are also quite Medical therapiesmost are untested and
effective in cats with CHF. Antiarrhythmic drugs unproven
may be indicated to control significant arrhythmias. Anticoagulation with heparin (220 units/kg IV fol-
Inotropic agents may be indicated in patients with lowed 3 hours later by maintenance dose of 66 to
myocardial failure or low-output heart failure. 200 U/kg SQ four times a day) is used to prevent
The judicious use of intravenous fluids may in- further thrombosis. Adjust dose to maintain the acti-
frequently be indicated in patients with signs of vated partial thromboplastin time at or slightly above
low-output heart failure, primarily in situations the upper limit of the normal reference range.
where the patient has stopped taking in oral Vasodilation with acepromazine (0.2 to 0.4 mg/
fluids, has received excessive treatment with kg SQ three times a day) or hydralazine (0.5 to
diuretics, or has concurrent renal dysfunction 0.8 mg/kg PO three times a day) is used to pro-
and there is concern about maintaining adequate mote collateral blood flow.
renal perfusion. Streptokinase and urokinase are significantly
Specific therapies designed to alter the natural less expensive than newer fibrinolytic agents
history of disease should be instituted concur- (e.g., tissue plasminogen activator), but little
rently and may, in some cases, in time, eliminate clinical experience has been reported. Tis-
the need for drugs to control heart failure (see sue plasminogen activator: Though clinically
specific conditions discussed later). effective thrombolysis has been documented in
All cats with myocardial failure should be sup- the cat, expense, morbidity associated with rapid
plemented with taurine (see section on Taurine reperfusion, and inability to prevent recurrence
DeficiencyInduced Myocardial Failure) until make this option impractical in most cases.
proven to be not taurine deficient and not taurine
responsive.
Prognosis
Several strategies to prevent an initial thromboem-
bolic event or to avoid recurrence of aortic throm- Inadequate information is available to make broad
boembolism in cats with cardiomyopathy have generalizations regarding prognosis for cats with
been devised and recommended. None of these myocardial diseases. Although echocardiography
strategies has been evaluated by controlled studies. provides the basis for diagnosis, clinical and ra-
Low-dose aspirin (25 mg/kg PO every 2 to 3 diographic data should be strongly considered for
days) is the most widely employed prophylactic prognostication.
measure. Although aspirin is known to exert anti- Cats with severe myocardial disease and
thrombotic effects, there is no objective evidence noevidence of heart failure may survive for
of its efficacy for the prophylaxis of systemic long periods of time. Conversely, cats with
aortic thromboembolism in cats. Recurrence of much less severe echocardiographic evidence
thromboembolic events in aspirin-treated cats of disease presenting with significant and
were as high as 75% in one study. difficult to control signs of heart failure may
Lovenox (enoxaparin),a low molecular weight survive for very short periods under the best of
heparin, has shown promise in anecdotal clini- situations.
cal settings. No large clinical trials have been The long-term prognosis for cats with thrombo
completed. The most commonly used dose is embolic disease is grave because mortality asso
1 mg/kg SQ every 12 to 24 hours. ciated with individual episodes is high, and recur-
Left untreated, the outcome of arterial occlusion rence is common despite prophylaxis.
will depend upon the extent of occlusion and time
to spontaneous reperfusion, either via the primary
Pathology
vessel or the collateral circulation. Cats may lose
the affected leg(s) because of ischemic necrosis, Gross examination of the heart provides use-
die of toxemia, remain paralyzed from peripheral ful anatomic information and should be per-
nerve damage, or regain full or partial function of formed when possible to confirm antemortem
the leg. Overall, response to presently available findings.
conservative or aggressive clinical intervention In most cases histopathologic evaluation adds
has been poor. little useful information and, unless readily avail-
Therapeutic options include: able at low cost, is not recommended unless
Surgical removal of emboli specific indications are present (see the section
Catheter embolectomy Specific Diseases).
Chapter 8 Feline Cardiomyopathy 157
Pleural effusion is common in cats with heart failure. Cats with severe HCM and moderate to severe
It can be a modified transudate, pseudochylous, or heart failure are usually presented to a veterinar-
true chylous in nature.Theexactpathophysiology ian because of respiratory abnormalities (tachy-
of pleural effusion secondary to heart failure is un- pnea and/or dyspnea) due to pulmonary edema,
known. The most likely possibility is that feline vis- pleural effusion, or both.
ceral pleural veins drain into the pulmonary veins Cats with HCM may develop systemic
such that elevated pulmonary vein pressure causes thromboembolism.
the formation of pleural effusion. Cats with HCM may die suddenly, often with no
Thrombi in cats with HCM may form in the prior clinical signs referable to heart disease or
left atrium or left auricle. LA thrombi commonly failure. The cause of the sudden death in these
break loose (become emboli) and are carried by blood cats is unknown.
flow most commonly to the terminal aorta where they In humans, sudden death appears to be either due
lodge. These thromboemboli occlude aortic blood to an arrhythmia, acute worsening of the outflow
flow and elaborate vasoactive substances that con- tract obstruction associated with stress or exer-
strict collateral vessels. The net result is cessation of cise, or a large thrombus occluding flow in the
blood flow to the caudal legs resulting in acute paresis/ left.
paralysis and pain. The incidence of sudden death in feline HCM
is probably under represented in the veterinary
literature because cats that die suddenly are not
Signalment and Presenting Complaints
presented or reported to veterinarians.
In cats the disease has been observed as young
as 6 months of age and as old as 16 years of age.
Echocardiography
In Maine coon cats that are going to develop
severe disease, HCM most commonly develops Cats with severe HCM have papillary muscle hy-
to its most severe stage in males by around 2 pertrophy, markedly thickened LV walls (7 to 10
years of age. Females are more variable but most mm), and usually an enlarged left atrium (Figure
frequently develop to an end-stage of wall thick- 8-5). The hypertrophy can be global, affecting all
ening by three years of age. The average age of areas of the LV wall or can be more regional or
onset and rate of progression in mixed breed cats segmental. Segmental forms can have the entire or
is unknown. a region of the interventricular septum or free wall
Males are affected more commonly than females. primarily affected, the apex primarily affected,
Cats with HCM may be completely asymptom- or the papillary muscles (and often the adjacent
atic, may be presented to a veterinarian with sub- free wall) primarily affected. Papillary muscle
tle signs of heart failure, may have moderate to hypertrophy may be the only manifestation of the
severe heart failure, or may be presented because disease.
of thromboembolic disease. Sudden death is also Because of these forms, HCM is a diagnosis that
a common presentation. should be made by examining several different
Asymptomatic cats can have mild to severe LV two-dimensional echocardiographic views and
thickening; however, those with severe thicken- measuring wall thicknesses in diastole from the
ing usually go on to develop heart failure. Cats thickest region or regions on the two-dimen-
with severe disease that appear to have no clini- sional images. M-mode echocardiography may
cal signs may show subtle signs of heart fail- miss regional thickening unless it is guided by
ure (e.g., tachypnea) that may be detected by the two-dimensional view. The LV end-diastolic
an observant owner. The respiratory rate is of- or end-systolic dimension may be normal or
ten increased in these cats at rest and they may decreased and end-systolic cavity obliteration
become more tachypneic or even dyspneic if may occur. An enlarged left atrium indicates
stressed. Stressed cats with severe HCM may increased LV end-diastolic pressure. Occa-
recover quickly following stress or may go on to sionally, a thrombus is imaged in the LA or its
develop fulminant heart failure. Cats with mild appendage.
to moderate thickening may never develop clini- SAM of the mitral valve may be identified by
cal signs referable to their disease and may live two-dimensional or, more commonly, by M-mode
normal lives. In others, the LV wall may pro- examination (Figure 8-6). Color flow Doppler
gressively thicken and complications may de- echocardiography can be used to demonstrate
velop when they are older. the hemodynamic abnormalities associated with
Chapter 8 Feline Cardiomyopathy 159
Figure 8-5. Echocardiograms from a cat with hypertrophic cardiomyopathy. A, Right parasternal long-axis view shows concen-
tric hypertrophy of the left ventricle (LV) and left atrial (LA) dilation. B, Right parasternal short-axis view shows the thick interven-
tricular septum and left ventricular wall and a comparatively small left ventricular chamber. C, M-mode echocardiogram at the
level of the left ventricle, showing the thickened myocardium and small LV cavity.
160 Section II Cardiovascular Disease
Figure 8-6. M-mode echocardiogram of the mitral valve from a cat with hypertrophic cardiomyopathy demonstrates systolic
anterior motion of the mitral valve. The mitral valve moves toward the interventricular septum in early systole (unlabeled arrows) and
returns to normal position shortly before the beginning of diastole. LV, Left ventricle; RV, right ventricle; MV, mitral valve. (Courtesy
Mark D. Kittleson, D.V.M., Ph.D.)
SAM. Two turbulent jets originating from the LV are likely many cats with mild to moderate HCM
outflow tract are seenone regurgitating back in the cat population that never progress to a more
into the left atrium and the other projecting into severe form of the disease, condemning owners to
the aorta. Spectral Doppler can be used to deter- pill their cat twice or even once a day for the rest
mine the pressure gradient across the region of of the cats life is questionable, given the lack of
dynamic subaortic stenosis produced by the SAM. data. Many veterinarians feel compelled to treat a
The pressure gradient roughly correlates with the patient with a disease, and some owners demand
severity of the SAM although it can be quite la- treatment for their pet, even if there is only a theo-
bile, changing with the cats level of excitement. retical case for using a drug. Consequently, when-
SAM is not present in all cats with HCM. The ever HCM is diagnosed in a cat the veterinarian
majority of cats with severe HCM have SAM. must explain the situation to each owner and try to
However, on the other end of the spectrum, some let the owner make an informed decision based on
cats develop SAM before they have any evidence their wishes and life style. Because no intervention
of wall thickening, when their papillary muscles is known to change the course of the disease, there
are thickened or long. Although the basilar region is no mandate to treat at this stage.
of the interventricular septum is often thickened Two classes of agents, oral beta blockers and oral
in diastole in cats with HCM, the basilar LV out- calcium channel blockers, have been advocated
flow tract does not need to be narrowed for SAM to improve LV filling and cardiac performance
to occur. in cats with HCM. Although there is no clear
Diastolic dysfunction in cats with severe HCM evidence as to which therapy is more beneficial
has been documented using Doppler tissue imag- in symptomatic individuals, many cardiologists
ing and measures of transmitral flow and relax- believe patients with documented HCM should
ation time. Cats with severe HCM routinely have receive one or the other as part of their chronic
a decrease in early diastolic wall motion of the LV management. Whatever the initial choice, re-
free wall and mitral valve annulus using Doppler sponse to therapy should dictate whether dose
tissue imaging. In addition, peak E wave veloc- adjustment, changing drug class, or discontinua-
ity is reduced, peak A wave velocity is increased, tion of therapy is warranted.
isovolumic relaxation time is prolonged, and rate
of deceleration of early inflow is reduced. Adrenergic Beta Blockers
Atenolol: 6.25 to 12.5 mg/cat every 12 hours.
Atenolol is supplied as 25 mg tablets.
Therapy
There currently is no evidence that any drug alters Calcium Channel Blockers
the natural history of HCM in domestic cats until Diltiazem is currently the preferred calcium
they are in heart failure. Diltiazem, atenolol, bena- channel blocker. Beneficial effects include less-
zepril, and enalapril are commonly administered ened edema formation and decreased wall thick-
to cats with mild to severe HCM that are not in ness in some cats. Exactly how these beneficial
heart failure on an empirical basis. Because there effects occur is open to debate. Only a few cats
Chapter 8 Feline Cardiomyopathy 161
experience a clinically significant decrease in In general, cats that present with heart failure
wall thickness in my experience. have a poor prognosis. A median survival time
Cardizem7.5 mg PO every 8 hours. This product after diagnosis of about 3 months is reported. Cats
is supplied as 30 mg tablets. One-quarter tablet is that present in heart failure and respond favorably to
given every 8 hours. therapy may do well for prolonged periods of time.
Dilacor XR: 30 mg PO every 12 hours. This In general, cats presenting with aortic throm-
product is supplied as 120, 180, and 240 mg cap- boembolism have a poor prognosis. A median
sules. Each large capsule can be opened to yield survival, after diagnosis, of about 2 months is re-
two, three, or four 60 mg tablets, which are then ported. Cats that survive the thromboembolic epi-
halved to achieve a 30 mg dose. sode may do well for extended periods; however,
CardizemCD: 45 mg PO every 24 hours. Cardi- these cats are generally at high risk for recurrence
zem CD is supplied as 180 mg capsules that con- of thromboembolism.
tain many smaller capsules. The larger capsule Owners should always be warned of the potential
can be opened and the smaller capsules divided for sudden death. The exact incidence of sudden
into a number that produces an appropriate dose. death in cats with HCM is unknown. It is in some
The smaller capsules can be divided into groups cats, it is the first and only clinical sign.
of four (45 mg each) and placed in smaller gelatin
capsules for administration. One capsule is then
Pathology
administered once per day.
In severe cases the entire LV wall may be im-
pressively thick. Papillary muscle hypertrophy is
Key Point usually prominent, and the LV cavity is usually
decreased in size owing to encroachment. Both
The authors generally use diltiazem first in cats symmetric and asymmetric (asymmetric septal
without outflow tract obstruction, tachycardia
hypertrophy) forms of hypertrophy are recog-
or arrhythmias. The authors generally use aten-
olol first in cats with outflow tract obstruction,
nized in cats. The left atrium is often enlarged,
tachycardia or arrhythmias. The authors may and, occasionally, a thrombus is present within
switch to the alternate therapy if the response the left atrium.
is suboptimal or becomes suboptimal. Cats with milder forms have less dramatic wall
thickening and normal or near-normal LV cham-
ber size. The LA may be normal or only mildly
enlarged. Occasionally, the disease is manifested
Prognosis
only by papillary muscle hypertrophy with nor-
Prognosis is generally based upon clinical pre- mal LV free wall and septal thickness. There is
sentation, echocardiographic evidence of elevated considerable variability in the degree and loca-
intracardiac pressures, and response to therapy. tion of the hypertrophy.
Inadequate data has been published to reach de- Myocyte hypertrophy is the hallmark of histo-
finitive conclusions; therefore, statements on prog- pathologic examination with approximately 30%
nosis are largely based upon clinical experience of the cases also having myocardial fiber disarray
and conjecture. involving at least 5% of the septal myocardium.
Asymptomatic cats with mild to moderate
hypertrophy and no LA enlargement are believed
Feline (Idiopathic) Dilated
to have a good long-term prognosis. Reported
Cardiomyopathy
average survival times are generally in the
range of 4 to 6 years. Asymptomatic cats with DCM is a disease of the ventricular myocardium
obvious wall thickening and LA enlargement (predominantly left) characterized by primary
are likely at higher risk for developing heart fail- myocardial failure.
ure. These cats are also believed to be at risk for
developing thromboembolic disease. Asymptom-
General Comments
atic cats with severe wall thickening and normal
LA size are occasionally observed. Although Prior to 1987, DCM was one of the most com-
it is tempting to predict that these cats are at monly diagnosed heart diseases in cats. Most
greater risk for progressive disease, inadequate cases at that time were likely a secondary car-
data are available. diomyopathy associated with nutritional taurine
162 Section II Cardiovascular Disease
deficiency. Primary idiopathic DCM is currently The degree to which alterations in diastolic func-
not a common cardiac condition in cats. Because tion contribute to decompensation of patients with
there are no published reports defining differences DCM is likely larger than previously appreciated.
between cats with myocardial failure associated
with taurine deficiency and with idiopathic DCM,
Signalment and Presenting Complaints
there is very little, if anything, known about idio-
pathic DCM in cats. The reported age at diagnosis ranges from 5
There is no reason to expect that clinical findings months to 14 years (mean age 7 to 8 years).
and results of ancillary tests (other than blood No sex predilection is evident.
taurine concentration and funduscopic examina- Cats with DCM may have a variable period of
tion) should be dramatically different between lethargy, anorexia, and malaise prior to overt
these disorders. signs of CHF.
Myocardial failure secondary to other causes Cats may present with no prior signs and an acute
(e.g., long-standing congenital or acquired LV onset of CHF or systemic thromboembolism.
volume overload or toxic, ischemic, nutritional,
or metabolic problems that may underlie myo-
Physical Examination
cardial failure) must be ruled out to definitively
assign a diagnosis of idiopathic DCM. Physical examination is similar to that of other
The underlying etiology remains unknown and may forms of myocardial disease.
represent a common endpoint to many processes.
Ancillary Tests
Key Point
Ancillary tests are similar to taurine deficiency
Although myocardial failure secondary to myocardial failure (see next section); however,
taurine deficiency is now quite rare in cats, one must rule out taurine deficiency using whole
all cats with myocardial failure should be as-
blood and plasma taurine assays.
sumed to be taurine deficient until shown not
to be taurine responsive.
Therapy
For acute CHF, see the earlier section on treatment of
Pathophysiology
CHF in the Therapy section of General Information.
The underlying abnormality leading to clini- Cats with DCM and signs of low-output heart
cal manifestations in cats with idiopathic DCM failure (cardiogenic shock) represent a therapeu-
is primary systolic myocardial failure. End- tic challenge. Suggestions based upon clinical
systolic LV volume increases owing to a reduc- experience with cats with myocardial failure as-
tion in myocardial pump function. As a result, sociated with taurine deficiency are presented in
stroke volume and cardiac output decrease. Neu- the section on this disorder.
rohumoral compensatory mechanisms promote
an increase in intravascular volume and end-dia-
Prognosis
stolic pressures, stimulating eccentric hypertrophy
(dilation). At these larger LV end-diastolic vol- There are no reports documenting the clinical char-
umes, the geometry of the ventricle is such that acteristics of cats with idiopathic DCM thatdo not
small changes in chamber dimension during sys- respond to taurine supplementation. There is no
tole provide adequate stroke volume and cardiac evidence that clinical intervention alters the pro-
output; however, working at these larger volumes gression of myocardial failure in patients that do
is energetically inefficient for the ventricle. At any not respond to taurine supplementation. The ex-
point in this degenerative process that end-diastolic pected survival time for patients is more a function
pressures rise too high or cardiac output drops too of their clinical condition at the time of diagnosis
low, the patient may present with signs of CHF or than of the treatment they receive.
low-output heart failure, respectively (Figure 8-7). Asymptomatic cats diagnosed because a murmur
The factors that contribute to patients going from or gallop is identified during a routine physical
asymptomatic, well-compensated myocardial examination may survive for years with myocar-
failure, to a symptomatic, uncompensated state dial failure before developing signs of CHF or
are poorly understood. low-output heart failure.
Chapter 8 Feline Cardiomyopathy 163
A B
C D
E F
Figure 8-7. Dilated cardiomyopathy in a cat. A, Right parasternal long-axis view showing dilation of the left atrium (LA)
and left ventricle (LV). B, Systolic color Doppler image of the same view as in A showing modest secondary mitral and tricus-
pid valve regurgitation. C, Left apical four-chamber view showing the dilated left atrium and ventricle. D, Right parasternal
short-axis view showing left ventricular dilation. E, Right parasternal short-axis view at the heart base showing moderately
severe left atrial dilation. F, M-mode recordings at the level of the ventricles [1], mitral valve [2], and aortic valve [3]. There
is marked dilation of the left atrium and left ventricle and decreased left ventricular systolic motion. In addition, the opening
motion of the mitral valve is decreased, and the distance between the open mitral valve and ventricular septum (EPSS) is
markedly increased (10 mm). RA, Right atrium; RV, right ventricle. (From Nyland TG, Mattoon JS: Small animal diagnostic
ultrasound, ed 2, Philadelphia, 2002, WB Saunders.)
A B
C D
Figure 8-8. Atypical (restrictive?) cardiomyopathy in the cat. A, Right parasternal long-axis view showing marked dilation of
the left atrium (LA), right atrium (RA), and right ventricle (RV). Note that the left ventricle (LV) is neither dilated nor thickened.
B, Right parasternal short-axis view from the same cat as in A showing marked right and left atrial dilation. In addition, a ball-like
thrombus is visible within the dilated left auricle (arrow). C, Right parasternal long-axis view of another cat with biatrial dilation,
a nonhypertrophied and nondilated left ventricle, and mild secondary tricuspid valve regurgitation. D, M-mode recording at the
mitral valve level from the same cat as in A and B. The right ventricular wall, septal, and left ventricular wall thicknesses are normal,
but all show mildly hyperdynamic systolic motion. The mitral-septal distance (EPSS) is normal. (From Nyland TG, Mattoon JS:
Small animal diagnostic ultrasound, ed 2, Philadelphia, 2002, WB Saunders.)
B D
Chapter 8 Feline Cardiomyopathy
Figure 8-9. Echocardiograms from a cat with an unclassified form of cardiomyopathy. A, Right parasternal long-axis view. There is marked dilation of both left and right atria and mild dilation of
the right ventricle. LV, Left ventricle; LA, left atrium; RV, right ventricle; RA, right atrium. B, Right parasternal short-axis view shows the marked right and left atrial dilation. In addition, a thrombus is
visible within the dilated left auricle. AO, Aorta. C and D, M-mode recordings at the ventricular level and aortic level, respectively. The right ventricular wall, septal, and left ventricular wall thickness
are normal. The left ventricular chamber is only mildly dilated, and the left ventricular shortening fraction is in the low normal range (30%). The left atrium is markedly dilated.
167
168 Section II Cardiovascular Disease
A precise requirement for taurine cannot be de- Diet history should be accurately ascertained
termined for all foods because the requirement during the initial workup of any cat with myocar-
is dependent upon many factors. No commercial dial failure. Many owners have managed to for-
diet should be assumed to be taurine sufficient mulate diets with inadequate amounts of taurine
until the manufacturer has provided feeding and need to be educated to prevent recurrence.
trial data documenting that the food maintains In addition, it is likely that a small number of
normal taurine concentrations in blood and tis- cases will continue to be the result of commer-
sue during a trial of at least 6 months. cial cat foods containing inadequate amounts of
taurine, and the veterinary profession, to whom
these cats will present for diagnosis and treat-
Pathophysiology
ment, remains the most effective sentinel for de-
The hemodynamics and pathophysiology are be- tecting patterns with regard to diet and disease
lieved to be similar to idiopathic DCM as previ- occurrence.
ously outlined. Cats diagnosed with any form of myocardial fail-
In most cases, taurine deficiency is believed to ure should have plasma and whole blood taurine
be nutritionally derived, as a result of inadequate concentrations determined from blood samples
amounts of taurine in the diet. The role that tau- obtained prior to supplementation. Even a single
rine, an essential amino acid in the cat, plays in dose of taurine may make interpretation difficult
the maintenance of myocardial function remains and proper sample handling is critical for accu-
unknown. rate results.
The following guidelines should be used in han-
dling samples for taurine analysis:
Signalment and Presenting Complaints
Submit both heparinized plasma and heparin-
Signalment and presenting complaints are similar ized whole blood.
to those of other forms of cardiomyopathy. Place the sample on wet ice or centrifuge the
sample and separate plasma immediately.
Make sure the sample contains no clots or he-
Physical Examination
molysis.
The physical examination is similar to that of Store and ship samples frozen (dry ice or ice
other forms of cardiomyopathy. packs).
Funduscopic evaluation may reveal the presence Normal values:
of taurine deficiencyinduced central retinal Plasma: taurine greater than 60 nmol/ml (at
degeneration. risk when less than 30 nmol/ml). Note: Plasma
taurine concentration is very labile; 24 hours of
fasting can cause plasma concentrations to fall
Ancillary Tests
below 30 nmol/ml.
Ancillary tests do not provide a definitive diag- Whole blood: taurine greater than 200 nmol/
nosis. The results of electrocardiography and ml (at risk when less than 100 nmol/ml).
thoracic radiographs are similar to other forms of Whole blood taurine concentration is not as
myocardial disease. The echocardiographic find- labile. Fasting does not significantly affect
ings are similar to those for idiopathic DCM. values.
The primary echocardiographic abnormality is an
increase in end-systolic diameter (more than 12
Therapy
mm) with a reduced shortening fraction (less than
35%). The end-diastolic dimension is also often During the initial phase of therapy, proper
enlarged (more than 17 mm) (Figures 8-10 and supportive and symptomatic care for CHF (as
8-11). Significant LA enlargement is common. described previously under general comments
The E-point to septal separation (EPSS) is often on therapy) is essential if CHF is present. Cats
increased (> 2 mm). The right ventricle and right with documented taurine deficiency should be
atrium are variably affected. Mitral regurgitation supplemented with 250 mg every 12 hours un-
may be detected with spectral and color-flow til echocardiographically determined LV dimen-
Doppler. In some cases, a thrombus is observed sions normalize. This usually occurs within 4 to
within the body of the left atrium or in the left 6 months. Clinical improvement is usually evident
auricular appendage. within about 2 weeks.
Chapter 8 Feline Cardiomyopathy 169
Figure 8-10. Two-dimensional echocardiograms from a cat with myocardial failure associated with taurine deficiency. Right
parasternal long-axis (A) and short-axis (B) views, respectively, demonstrate marked dilation of all four cardiac chambers. LV, Left
ventricle; LA, left atrium; RV, right ventricle; RA, right atrium.
Diuretics and ACE inhibitors can be discontin- nmol/ml). Taurine supplementation can be dis-
ued when signs of CHF resolve, and radiographic continued once echocardiographic values return
improvement in cardiac size is noted. The ACE to within normal limits, and the cat is eating a diet
inhibitor should be removed first and then the with adequate amounts of taurine.
diuretic tapered over a period of 2 weeks. The Taurine concentration in plasma and whole blood
owner should be taught to monitor respiratory should be monitored periodically to be certain
rate while withdrawing heart failure medications, that the diet fed is maintaining concentrations
and clinical and radiographic evaluation should within acceptable limits. If taurine concentrations
be repeated 1 week after withdrawing medica- are depleted again, then many cats will again de-
tions to detect any decline in the cats condition. velop myocardial failure.
Digoxin is not routinely administered as a part of ther-
apy, but there is no contraindication to doing so. When
Prognosis
used initial dose should be one fourth of a 0.125 mg
tablet PO every 48 hours. Digoxin levels are taken 6 Because results of taurine analysis are not imme-
to 8 hours after the seventh dose and are used to adjust diately known and a recent dietary change may
therapy. I rarely increase the dose to more than one normalize taurine values, all cats with myocar-
fourth of a 0.125 mg tablet PO every 24 hours. dial failure should be supplemented with taurine
The diet should be altered to maintain normal and given an initially guarded-to-grave prognosis.
plasma taurine concentrations (greater than 60 In one large study, 30% of cats with myocardial
170 Section II Cardiovascular Disease
failure died within the first week after diagnosis. enlarged. There are no specific histologic or elec-
Hypothermia and thromboembolic disease were tron microscopic lesions.
associated with a poor prognosis. Taurine supple- In the past, many of these cases were classified as
mentation did not provide benefit with regard to RCM or intermediate cardiomyopathy. The echo-
survival until 2 weeks after treatment is begun. cardiographic appearance in many cases suggests
Cats that survive 1 week and respond to treat- that the hemodynamics resemble those of RCM;
ment for CHF can be upgraded to a fair progno- however, few cases have documented characteristic
sis. Catsthat survive 2 weeks and are shown to histopathologic lesions. The term intermediate sug-
be taurine deficient can be upgraded to a good gests a combination of or transition between states.
prognosis. There is no evidence that this represents a combina-
Most taurine-responsive cats have complete re- tion of or a transitional state between two forms of
versal of echocardiographic and clinical evidence cardiomyopathy. In fact, as stated previously, there
of myocardial failure after supplementation with is no evidence that these cases represent a single dis-
taurine (see Figure 8-11). Occasionally cats may ease entity or are proven to be a cardiomyopathy.
have residual mild myocardial failure (LV short- The whole blood analysis is most important.
ening fraction 25% to 30%); however, these cats
are generally asymptomatic and rarely require
any form of therapy other than maintaining nor-
Thyrotoxic Heart Disease
mal plasma taurine concentrations. Thyrotoxic heart disease is cardiac changes result-
ing from direct and indirect effects of elevations in
circulating thyroid hormone (hyperthyroidism).
Pathology
The most predominant pathologic features are
General Comments
severe LV and LA enlargement. The LV walls
may appear thin and the papillary muscles and A frequently recognized secondary cardiomyop-
trabeculations are less prominent than normal. athy that may be confused with primary myocar-
The right ventricle and right atrium may also be dial diseases in older cats
A B
Figure 8-11. M-mode echocardiograms from a cat with myocardial failure associated with taurine deficiency before (A) and
after (B) taurine supplementation and diet modification. Before therapy the left ventricle was markedly dilated, and the left ven-
tricular shortening fraction was severely reduced. Those parameters both normalized after taurine supplementation. EDD, Left
ventricular dimension at end-diastole; ESD, left ventricular dimension at end-systole.
Chapter 8 Feline Cardiomyopathy 171
Thyrotoxic heart disease or hyperthyroidism does energy economy of the heart and increases the
not cause HCM. overall work of the heart. Additionally, the thyro-
The prevalence and severity of thyrotoxic heart toxic heart, although hyperkinetic when the patient
disease has been decreasing in recent years, is at rest, has less reserve capacity available for
likely as a result of increased awareness and when increased cardiac work is necessary (e.g.,
therefore early diagnosis and treatment of exercise). This situation, placed on top of preex-
hyperthyroidism. isting cardiac disease (e.g., HCM, RCM, or DCM,
valvular disease) can lead to decompensation of a
previously well-compensated cardiac disease.
Pathophysiology
Reduced systemic vascular resistance in the pres-
The effects of thyroid hormone on the heart are ence of an increased intravascular volume (not
believed to be both direct and indirect. documented in cats) associated with significant
Direct actions increases in cardiac output are what define the
Increased protein synthesis (mitochondrial, high-output state of the cardiovascular system
ion pump, and contractile proteins) in hyperthyroid cats. This high-output state can
Alteration of myosin subtype (slow to fast (especially in the presence of underlying primary
type myosin; V3 to > V1) cardiac pathology, such as valvular insufficiency)
Less economical energy conversion from progress to result in clinically apparent signs of
chemical (adenosine triphosphate) to me- CHF in hyperthyroid cats.
chanical (force) by the myocardium Despite the reduced systemic vascular resistance
Increased rate of calcium cycling by the sar- that is part of the high-output, hyperthyroid state,
coplasmic reticulum hypertension, rather than hypotension, is ob-
Up-regulation of cardiac beta receptors served in many (87% of 39 cats in one study)
Enhanced rate of spontaneous depolarization hyperthyroid cats. Hypertension resolves in most
by sinoatrial node cells treated cases once a euthyroid state is reached.
Shortened action potential duration
Indirect actions
Signalment and Present Complaints
Enhanced metabolic demand by other tissues
results in a high-output state; the heart must Cats are generally older, with no gender or breed
increase its throughput to meet the increased predispositions.
demands of the peripheral tissues that are sim- Most cats present for routine examination or be-
ilarly stimulated to a higher metabolic state cause of signs or symptoms of hyperthyroidism
by the excess circulating thyroid hormone. (e.g., polyphagia, polyuria/polydipsia, weight loss).
Reduced systemic vascular resistance (not the Occasionally cats present with CHF or low-out-
same as hypotension) plays an important role put heart failure.
in the overall cardiac status of patients with
hyperthyroidism. Afterload is reduced while
Physical Examination
preload is increased in the presence of an in-
creased intravascular volume. Classic signs of hyperthyroidism, including evi-
In some, hypertension is a predominant find- dence of weight loss, unkempt hair coat
ing and leads to: Systolic heart murmur or gallop rhythm may be
Significant concentric hypertrophy of the present
left ventricle Sinus tachycardia is usually present
Risk of retinal detachment or hemorrhage A thyroid nodule may be palpable
The sum of these effects when there is excess
thyroid hormone (hyperthyroidism) is a heart
Ancillary Tests
that operates at a faster rate (tachycardia), is
hypertrophied, can contract faster and more Electrocardiography
powerfully (enhanced contractility), and has a Sinus tachycardia is commonly present
propensity to abnormal electrical depolarizations Tall R waves suggestive of LV hypertrophy or
(arrhythmias). dilation
Although these might at first glance sound like Variable arrhythmias, including atrial prema-
beneficial changes (bigger, faster, stronger, more ture complexes and ventricular premature com-
excitable), the thyrotoxic state greatly strains the plexes
172 Section II Cardiovascular Disease
Cardiac tumors reported in cats include: neutrophils. A viral etiology was suspected but
Lymphoma never identified.
Chemodectoma One report describes a transmissible myocarditis/
Hemangiosarcoma diaphragmitis in cats. No organism has been iso-
Metastatic pulmonary carcinoma lated, but transmission between cats by injecting
Metastatic mammary gland carcinoma. blood from infected cats into other cats does re-
Lymphoma is the most common tumor of the feline liably reproduce the disease. All cats developed
myocardium. Reported cardiac abnormalities in high fever (103.8 to 105.7 F), were lethargic,
cats with lymphoma include complete heart block, and were partially anorexic. Complete blood
pericardial effusion, and CHF. counts and chemistries were normal in all cats
Echocardiographic findings in cats with diffuse for 6 weeks except for an elevation of creatine
neoplastic infiltration of the myocardium can phosphokinase in three of seven cats. The dis-
mimic those of HCM. ease resolved on its own in these cats. Necropsy
Regression of neoplastic infiltration was reported revealed pale 1 to 3 mm discrete foci surrounded
in one cat with lymphoma following treatment by hemorrhage on ventricular myocardium and
with combination chemotherapy. on the diaphragm. No clinical signs referable to
the cardiovascular system were noticed.
The relationship of endomyocarditis to the other
Drugs, Toxins, and Physical Injury
cardiomyopathies of cats is unknown. Other re-
A large number of drugs and toxins are reported ported causes of myocarditis in cats include toxo-
to cause myocardial injury in domestic animals, plasmosis and metastatic infection from sepsis or
but very few are likely to be encountered in clinical bacterial endocarditis.
small animal practice. Of these, doxorubicin has
received the most attention in cats.
Decreased fractional shortening and increased
Summary
LV end-systolic dimensions were reported in four HCM is very common and probably represents
of six experimental cats given cumulative doses the largest percentage of cardiac diseases cur-
of doxorubicin of 170 to 240 mg/m2. However, rently diagnosed in the cat.
clinical signs of heart failure were not observed Presumed myocardial diseases that cannot be
even after a cumulative dose of 300 mg/m2, and classified into one of the known primary disor-
no cat showed electrocardiographic abnormali- ders, but that also lack common features allow-
ties during the study. As in other species, patho- ing classification as a single clinical entity, are
logic studies revealed extensive areas of myocyte increasing in frequency. Little is known about the
vacuolization and myocytolysis. Similar clinical etiology, pathophysiology, therapy, and progno-
observations have been reported in cats with ma- sis associated with these UCMs.
lignancies treated with doxorubicin. None devel- Of the secondary cardiomyopathies discussed,
oped overt heart failure, and arrhythmias were only nutritional (taurine-responsive) DCM and
only rarely observed. thyrotoxic heart disease are encountered with
With the possible exception of heat stroke and anyfrequency. Both of these disorders have
hypothermia, physical causes of myocardial beenwell classified, and both respond dramati-
damage are infrequently recognized in cats. Trau- cally to appropriate specific therapy. The other
matic myocarditis appears to be either uncom- secondary cardiomyopathies occur infrequently
mon or unrecognized in most cats that experience and are generally poorly understood. The gen-
thoracic trauma. eral approach, diagnosis, and therapy for these
disorders are similar to those for other feline
cardiomyopathies.
Infectious Myocarditis
One must recognize that the associated clinical
Infectious myocarditis is infrequently recog- and diagnostic findings frequently overlap, often
nized in cats. Liu and associates described a syn- making a definitive diagnosis difficult. Echocar-
drome of acute nonsuppurative myocarditis in diography is the one diagnostic aid that reliably
25 young cats (mean age 2.6 years). Most cats allows differentiation among the different cardio-
died unexpectedly, and necropsy revealed focal myopathies encountered in cats; however, even
or diffuse infiltration of the endocardium and with a thorough ultrasound examination, distinc-
myocardium with mononuclear cells and a few tions are still often unclear.
Chapter 8 Feline Cardiomyopathy 175
such as thromboxane that increase vascular resis- Box 9-2 Predisposing conditions for
tance. Secondary alterations in pulmonary physi- pulmonary thromboembolism
ology worsen and perpetuate derangements in gas
exchange. Release of humoral mediators such as Immune mediated hemolytic anemia
serotonin from platelets results in bronchoconstric- Neoplasia
tion and increased airway resistance. Surfactant Sepsis
function is altered leading to loss of elastic recoil Protein-losing nephropathy/enteropathy
and atelectasis, decreased pulmonary compli- Cardiac disease
Hyperadrenocorticism
ance, and increased right-to-left shunting. Work of
Central catheter use
breathing increases because of augmented alveolar Hemodialysis
dead space from nonperfused lung regions. Total parenteral nutrition
Hip replacement surgery
Trauma
Etiology
Cor pulmonale can result from disorders that im-
pact the pulmonary vasculature, such as obstruc- rapidly lysed and removed by the local fibrinolytic
tive or obliterative diseases of the pulmonary system; however, occlusion of larger pulmonary
circulation, or sustained hypoxic vasoconstric- arteries or massive showering of emboli to a large
tion associated with chronic parenchymal or circulatory volume can lead to acute right ventric-
tracheobronchial disease. Rarely, an increase in ular overload.
pulmonary blood flow will result in PH. Not all
animals with associated disorders will develop
Clinical Presentation
PH and cor pulmonale, and it is likely that ge-
netic or other influences will determine the vas- History and Clinical Signs
cular response. PH and cor pulmonale appear to Dogs or cats with PH and cor pulmonale can
be encountered more commonly in dogs than in be of any age, depending on the underlying eti-
cats. Primary PH is relatively uncommon; how- ology of elevated pulmonary artery pressures.
ever, various pulmonary conditions can lead to Generally there is a history of signs referable to
secondary PH in the dog or cat, including chronic the pulmonary system or to congestive failure.
tracheobronchial disorders, pneumonia, or inter- Animals can display any combination of signs
stitial lung disease (Box 9-1). A minority of these including lethargy, weakness, cough, respiratory
animals will develop overt clinical signs of right- distress, tachypnea, abdominal distention, and
heart failure. syncope. Historical features and clinical signs are
PTE is a secondary condition that occurs in as- not specific for PH or cor pulmonale but instead
sociation with diseases that cause blood stasis, reflect the underlying cardiopulmonary disease.
alter endothelial integrity, or increase coagulabil- PTE is generally a disorder of older animals, and
ity. PTE has been linked most commonly with history and clinical signs reflect the underlying
immune-mediated hemolytic anemia, neoplasia, disease process. Difficulty in clinical recognition
sepsis, protein losing nephropathy, cardiac disease, of this disorder is high, and animals with PTE are
and hyperadrenocorticism (Box 9-2). Clinically often presented for signs of weight loss, lethargy,
silent pulmonary embolism occurs in a majority and anorexia rather than for respiratory signs, al-
of dogs (82%) undergoing total hip replacement though tachypnea is often present on admission.
surgery. Small pulmonary thromboemboli are Secondary PTE should be suspected in an animal
with a predisposing condition that develops an
Box 9-1 Causes of cor pulmonale acute onset of tachypnea, cyanosis, and/or hypox-
emia that is refractory to oxygen therapy.
Pulmonary vascular disease
Heartworm disease
Chronic pulmonary thromboembolism
Chronic pulmonary disease Key Point
Tracheobronchial disease or collapse PTE occurs secondary to a variety of underly-
Pulmonary fibrosis/interstitial pneumonia ing conditions. Affected animals may present
Pneumonia for signs reflecting the primary condition or
Primary pulmonary hypertension for refractory respiratory distress.
178 Section ii Cardiovascular Disease
Figure 9-1. There is generalized enlargement of cardiac silhouette on the right lateral (A) and dorsoventral (B) views. Pulmo-
nary arteries are enlarged and appear to taper slowly. Numerous pleural fissure lines are identified, and there is a diffuse heavy
interstitial and peribronchial pattern identified within the lung.
Figure 9-2. Tricuspid regurgitant jet in a dog with pulmonary hypertension. Based on the modified Bernoulli equation, the right
ventricular-to-right atrial pressure gradient is 85 mm Hg. (Courtesy Dr. Fiona Campbell, University of California, Davis)
scans are rarely performed on nonanesthetized drugs require sophisticated or complicated de-
animals; however, perfusion scanning alone can livery and result in only minimal reductions
be completed without anesthesia and can assist in pulmonary artery pressures. Although these
in documentation of perfusion deficits. This is reductions are statistically significant and pro-
a safe, noninvasive technique for evaluation of vide some clinical benefit in human patients, it
PTE, although it is somewhat nonspecific be- is unclear whether these small changes in pul-
cause perfusion deficits can reflect true regions of monary arterial pressures would be beneficial in
thrombosis or simply a lung region experiencing veterinary patients.
hypoxic pulmonary vasoconstriction. An orally available nitric oxide donor silde-
nafil (Viagra), which causes accumulation of
cyclic guanosine monophosphate in vascular
Therapy
smooth muscle and resultant vasodilation, has
Currently, little is known about the optimal some efficacy in reducing pulmonary artery
therapy for either PH or PTE. In animals with pressures in both humans and experimental
cor pulmonale, cautious diuretic therapy is animals. Occasional reports in dogs suggest
warranted to reduce fluid accumulation, and that it might also be beneficial in some veteri-
judicious use of thoracocentesis or abdomino- nary patients. Supplementation with arginine
centesis can be used to improve respiration. has been investigated for use in human medi-
Excessive removal of fluid is to be avoided since cine since arginine is converted into nitric oxide
animals may develop volume contraction or through combination with molecular oxygen. A
systemic hypotension. nonselective endothelin antagonist (Bosentan)
Therapy of PH has not been well defined in vet- has been shown to be efficacious in lowering
erinary medicine. Systemic vasodilators are not pulmonary artery pressures in patients with PH,
generally effective in lowering pulmonary artery although again, the reduction in pressure was
pressures and can cause deleterious side effects quite modest. Endothelin antagonists have not
because of excessive hypotension. Standard treat- been evaluated in veterinary patients. Anti-
ment of the underlying cardiopulmonary condi- coagulants may be beneficial by reducing in situ
tion should be employed and may lessen PH. thrombosis, progressive vascular occlusion, and
Anticoagulant therapy is recommended in hu- continued proliferative vascular disease.
man patients with PH associated with PTE or to
limit in situ thrombosis that can result in progres-
sive vascular obstruction. Low molecular weight
heparin therapy is often used because of reduced
risk of bleeding due to its favorable factor X:
factor II activity. However specific information
on pharmacokinetics and pharmacodynamics
of the available products is currently lacking in
Frequently Asked
Questions
veterinary medicine. Ultra-low-dose aspirin
(< 1 mg/kg every 24 [dog] to 72 [cat] hours) can What clinical findings would support the diagnosis
be used also in an attempt to inhibit platelet ag- of cor pulmonale and how could this be confirmed?
gregation. Newer antiplatelet drugs are currently Animals with clinical signs relative to cor pulmonale
generally display respiratory abnormalities (tachy-
under investigation.
pnea, hyperpnea, and/or cough) and may also exhibit
Insight into various therapies for PH has been signs of right-heart failure (ascites, jugular venous
gained by reviewing treatment of primary PH distention, and/or subcutaneous edema). Radiographi-
in humans, which is partially mediated by al- cally, cor pulmonale is evident as right-sided heart en-
terations in endothelium-derived vasodilators largement. Right atrial enlargement and dilation of the
and constrictors and by vascular proliferation. caudal vena cava support the diagnosis. Two-dimen-
Drugs that have been employed include intra- sional echocardiography reveals eccentric dilation of
the right ventricle. With chronic PH or PH in a young
venous or inhaled prostacyclin (a breakdown
animal, right ventricular hypertrophy can be found.
product of arachidonic acid metabolism) and In the presence of tricuspid regurgitation or pulmonic
inhaled nitric oxide. These vasodilators are se- insufficiency, Doppler echocardiography can confirm
lective for the pulmonary circulation and have PH by detection of a velocity jet greater than 2.8 or
more pronounced impact on pulmonary pres- 2.2 m/sec, respectively.
sures than systemic pressures. However, these
182 Section ii Cardiovascular Disease
Glaus TM, et al: Clinical and pathological characterisa-
What tests confirm the diagnosis of PTE and provide
tion of primary pulmonary hypertension in a dog, Vet
support for institution of anticoagulant therapy?
Rec 154:786, 2004.
Unfortunately, ante-mortem diagnosis of PTE re-
Johnson L, Boon J, Orton EC: Clinical characteristics of
mains challenging, and definitive diagnosis is often
not achieved in the clinical setting. Suspicion for PTE 53 dogs with Doppler derived evidence of pulmonary
should be present in an animal with a recognized hypertension: 1992-1996, J Vet Intern Med 13:440,
predisposing condition (see Box 9-2) that develops 1999.
an acute onset of respiratory distress. Normal chest Johnson LR, Lappin MR, Baker DC: Pulmonary throm-
radiographs do not preclude the diagnosis. Support- boembolism in 29 dogs: 1985-1995, Vet Intern Med
ive evidence of PTE would include a positive d-dimer 13:338, 1999.
test, echocardiographic evidence of right ventricular Koblik PD, Hornoff W, Harnagel SH, et al: A compari-
overload, and perfusion deficits on pulmonary scin- son of pulmonary angiography, digital subtraction
tigraphy in an animal with refractory respiratory angiography, and 99mTc-DTPA/MAA ventilation-
distress. Anticoagulant therapy with low molecular perfusion scintigraphy for detection of experimental
weight heparin would often be instituted in a patient pulmonary emboli in the dog, Vet Radiol Ultrasound
with these findings. Thrombolytic therapy is rarely 30:159, 1989.
employed because of the risk of generating a sys- La Rue MG, Murtaugh RJ: Pulmonary thromboembo-
temic fibrinolytic state or creating ischemia-reperfu- lism in dogs: 47 cases (1986-1987), J Am Vet Med
sion injury. Because of the difficulty in establishing Assoc 197:1369, 1990.
a diagnosis of PTE and the morbidity and mortality Liska WD, Poteet BA: Pulmonary embolism associated
associated with this secondary complication, prophy- with canine total hip replacement, Vet Surg 32:178,
lactic anticoagulant therapy should be considered in 2003.
animals with recognized predisposing conditions.
Michelakis ED, et al: Long-term treatment with oral
What type of treatment can be considered for PH? sildenafil is safe and improves functional capac-
Aggressive management of underlying cardio- ity and hemodynamics in patients with pulmonary
pulmonary conditions should be instituted. Ani- arterial hypertension, Circulation 108(17):2066,
mals with chronic bronchitis or small airway col- 2003.
lapse often require steroids (oral or inhaled) and Nelson OL, Andreason C: The utility of plasma d-dimer
extended-release theophylline (10 mg/kg PO ev- to identify thromboembolic disease in the dog, J Vet
ery 12 hours [dog] or 15 to 19 mg/kg PO in the Int Med 17:830, 2003.
evening [cat]). Interstitial lung diseases are less likely Norris CR, Griffey SM, Samii VF: Pulmonary throm-
to respond to medical therapy. In either group of ani- boembolism in cats: 29 cases (1987-1997), J Am Vet
mals with respiratory dysfunction, supplemental oxy- Med Assoc 215:1650, 1999.
gen therapy either at home or in the hospital setting
Pyle RL, Abbott J, MacLean H: Pulmonary hypertension
can improve clinical presentation. Use of sildenafil
and cardiovascular sequelae in 54 dogs, Intern J Appl
(0.5 to 2.0 mg/kg every 8 to 12 hours) can be consid-
Res Vet Med 2:99, 2004.
ered for animals with severe PH. Blood pressure and
echocardiographic monitoring for side effects and ef- Schermerhorn T, Pembleton-Corbett JR, Kornreich B:
ficacy are recommended. Pulmonary thromboembolism in cats, J Vet Int Med
18:533, 2004.
Schober K, Baade H, Ludewig E, et al: Cor pulmonale in
terrier breed dogs with chronic-progressive, idiopathic
Suggested readings pulmonary fibrosis: 19 cases (1996-2001), Tierarztliche
Praxis Ausgabe K, Kleintiere/Heimtiere 30:180, 2002.
Bach JF, Rozanski EA, MacGregor J, et al: Retrospec- Thomas D, Steiz M, Rtanabe G, et al: Mechanism of
tive evaluation of sildenafil citrate as a therapy for bronchoconstriction produced by thromboemboil in
pulmonary hypertension in dogs, J Vet Intern Med dogs, Am J Phys 206:1207, 1964.
20(5):1132-1135, 2006. Uehara Y: An attempt to estimate the pulmonary artery
Berger M, Haimowitz A, Van Tosh A, et al: Quantitative pressure in dogs by means of pulsed Doppler echocar-
assessment of pulmonary hypertension in patients diography, J Vet Med Sci 55:307, 1993.
with tricuspid regurgitation using continuous wave
Doppler ultrasound, J Am Coll Cardiol 6:359, 1985.
Fluckiger MA, Gomez JA: Radiographic findings in dogs
with spontaneous pulmonary thrombosis or embo-
lism, Vet Rad 23:124, 1984.
Chapter 10
Heartworm Disease
Clay A. Calvert and Justin David Thomason
Heartworm Disease
Life Cycle
Heartworms invade the Mature heartworms (6-7
heart and pulmonary months) may also
arteries, reach maturity in reproduce and release
6-7 months, and shed microfilariae (heartworm
antigen into the offspring) into the
bloodstream. bloodstream.
crisis caused by obstruction of the vena cava with Box 10-1 Clinical Signs Associated with
adult worms) and occasionally when severe pul- Feline Heartworm Disease
monary arterial disease results in hemolysis due
to fibrin-thrombus related RBC trauma. Throm- Acute Signs Chronic Signs
bocytopenia is usually a consequence of these Sudden death* PIE syndrome
complications. Respiratory Coughing
Nephrotic syndrome occasionally occurs as the Pulmonary embolism Dyspnea
result of severe glomerular disease (amyloidosis Collapse; shock Cardiopulmonary
or immune complex glomerulonephritis). Mani- Hemoptysis Lethargy
festations include proteinuria, hypoalbuminemia, Dyspnea; cough Weakness
hypercholesterolemia, ascites and occasionally Pneumonitis Right-sided CHF
Dyspnea; cough Anorexia
peripheral edema and azotemia.
Neurologic Gastrointestinal
Blindness Vomiting
Cats Seizures
Clinical signs in cats are different than in dogs. The Ataxia
common signs are vomiting, collapse or syncope, Coma
asthma-like syndrome, coughing, sudden death, Circling
and occasionally central nervous system signs. Syncope
Gastrointestinal
Signs occur most often early in the infection and
Vomiting
again when young adult worms arrive in the pul-
monary arteries. Severe pulmonary complications *From severe pulmonary thromboembolism or heartworm
and death are most likely to occur whenever one occlusion of main pulmonary artery.
or more adult worm dies, either spontaneously or Pulmonary infiltrates of eosinophilia.
Congestive heart failure.
as a result of Immiticide administration.
Modified from Calvert C. Feline heartworm disease. In Fox PR,
Asthmatic signs are a common manifestation and ed: Canine and feline cardiology, New York, 1988, Churchill
often occur about 3 to 4 months post-infection. A Livingstone.
strong antibody response at this time may destroy
the developing larvae. If not, then a period of
quiescence occurs only to have asthma-like signs
recur in some cats 7 to 8 months post-infection. direct smear or a concentration test (modified Knott
Vomiting is a common, sporadic sign. It often is test or millipore filter test) in dogs with or without
not associated with eating, may include food, but clinical or radiographic findings consistent with the
mucus and bile are often the major components. disease. Testing puppies younger than 6 months of
Vomiting and coughing in a cat should increase age is not indicated.
the index of suspicion. Affected cats usually lack circulating microfi-
Sudden death related to spontaneous worm death laria, may have suggestive radiographic abnormali-
and thromboembolism is more common in cats ties, and echocardiography is very useful. A positive
than in dogs. enzyme-linked immunosorbent assay (ELISA) test
Neurologic signs, usually seizures, occur occa- for heartworm antigen, antibody or both may be
sionally when aberrant worm migration to the present.
brain occurs.
See Box 10-1. Laboratory Studies
The minimum data base varies depending on
Key Point the patients age, clinical signs, and preference
The combination of vomiting, eosinophilia, of individual clinicians. The minimum pretreat-
and hyperglobulinemia warrant a high index ment database for all dogs suspected of having
of suspicion of heartworm infection in cats. heartworm infection includes packed cell vol-
ume, blood urea nitrogen, urine specific gravity,
urine protein determination, and heartworm an-
tigen test. Thoracic radiographs should always
Diagnosis
be taken because they reveal more about disease
The diagnosis of heartworm infection in dogs is severity than any other single test.
based on immunodiagnostic antigen testing. Micro- The minimum data base for cats should include
filaria in the peripheral blood can be detected by a thoracic radiographs. Echocardiography and
Chapter 10 Heartworm Disease 187
f ecal studies for lungworms are useful for the Screening in Dogs
differential diagnosis of heartworm infection, Screening in dogs is usually recommended for
feline asthma, cardiomyopathy, bronchitis, pul- the late spring in cooler climates to maximize the
monary fibrosis, and lung parasites. A tracheal likelihood of detecting infections acquired in the
or bronchial wash may be useful for detecting previous year. In hotter climates, infections may
lung parasitic lesions, such as those produced by be acquired as late as November or early Decem-
Aelurostrongylus spp. ber and these infections are not detectable until
May or June. Run an antigen test 7 months after
the end of the previous transmission season (Fig-
Clinical Pathology
ure 10-2).
No abnormal test results are pathognomonic for
heartworm infection. Screening in Cats
Infections in cats can usually be identified by
Complete Blood Count echocardiography. Combined antibody and anti-
Eosinophilia and basophilia are the most common gen testing is recommended for cats. A negative
abnormalities in dogs. Eosinophilia is more com- antibody test weighs against the diagnosis. Al-
mon and the highest counts tend to occur with though a positive antigen test confirms infection
occult infections. Dipetalonema (Acanthocheilo- in cats, many infected cats are antigen test nega-
nema) reconditum infections produce eosinophil tive (Figures 10-3 and 10-4).
counts as high as those associated with D. immitis
infection. Immunodiagnostic Testing
Neutrophilic leukocytosis with a left shift is These tests must be performed in strict compli-
usually the result of pulmonary thrombo ance with the manufacturers instructions. False-
embolism. positive test results are usually the result of poor
Thrombocytopenia is usually present when technique. Serodiagnosis of adult heartworm an-
there is severe pulmonary arterial disease and tigens in dogs is accomplished readily by mem-
thromboembolism. brane and microwell ELISA tests and membrane
Hemoglobinuria, usually accompanied by immunochromatographic tests. Numerous spe-
thrombocytopenia, is seen with caval syndrome cific and sensitive tests are available. Test time
and with severe pulmonary thromboembolic duration is less than 30 minutes and for some
disease. tests is approximately 10 minutes. All of these
tests can be performed with plasma or serum
Serum Biochemistry and Urinalysis samples, and the majority can be run with whole
Azotemia may occur in dogs with complicated blood.
infections. Prerenal azotemia can be caused by Positive antigen test results are the result of the
dehydration or right-sided CHF. Primary azote- presence of adult female worms. The antigen is
mia can result from glomerulopathies. Increased associated with the worms reproductive tract.
hepatic enzyme activities may occur; however, The particular test employed is influenced by the
increases up to 10-fold do not affect treatment, number of tests performed daily, the amount of
complications, or survival. Hepatic failure with whole blood or serum required, and the speed of
icterus can occur in dogs with chronic right-sided results. Some tests, such as DiroCHEK (Synbiot-
CHF. ics), are very efficient for testing multiple sam-
Proteinuria is common and is most pronounced ples simultaneously.
in patients with severe infections or renal amy- Weakly positive test results should be verified by
loidosis. Mild proteinuria usually resolves after repeat testing using a different test.
Immiticide treatment. Most immunodiagnostic tests (ELISA based) are
Hypoalbuminemia occurs in some dogs with se- semi-quantitative because rapid and strong posi-
vere infections; hyperglobulinemia is common in tive test results are thought to be related to higher
dogs and cats with chronic heartworm disease. antigen concentrations. Low antigenemia indicates
Loss of albumin into the third space occurs with a low adult heartworm burden and reduced risk of
right-sided CHF and is complicated by hepatic in- post-adulticide thromboembolic complications.
sufficiency, intestinal congestion, and free-water High-antigenemia may be the result of a heavy
retention. Hyponatremia and/or mild hyperkale- worm burden and may indicate increased risk of
mia may result. thromboembolism; however, large quantities of
188 Section II Cardiovascular Disease
Diagnosis of Heartworm Infection in Dogs
Positive Negative
Start macrolide or
Run a modified Knott
diethylcarbamazine (DEC)
or filter test
therapy
Negative Positive
Perform: Perform:
Complete blood count Complete blood count
Serum chemistry panel Serum chemistry panel
Thoracic radiography Thoracic radiography
Start: Start:
Macrolide Slow kill macrolide*
Adulticidal therapy Adulticidal therapy
If milbemycin or high-dose
ivermectin (50 g/kg) is
preferred, the patient should
be observed for adverse
reaction or pretreated as
described in the text.
Figure 10-2. An algorithm approach to the diagnosis of heartworm infection (HWI). (Modified from Ettinger SE, Feldman EC:
Textbook of veterinary internal medicine: diseases of the dog and cat, ed 6, St Louis, 2005, WB Saunders.)
Antibody
Positive Negative
Figure 10-3. An algorithm demonstrating a reasonable approach to screening cats for heartworm infection.
Chapter 10 Heartworm Disease 189
Start preventative
Figure 10.4. An algorithm demonstrating a reasonable approach to diagnose HW in cats in which heartworm infection is
suspected. (Modified from Ettinger SE, Feldman EC: Textbook of veterinary internal medicine: diseases of the dog and cat, ed 6,
St Louis, 2005, WB Saunders.)
antigen released from dead worms results in a In cats, antigen tests are specific, but false-negative
quick, strong test reaction, but does not necessar- results are common. False-negative test results are
ily mean that the worm burden is high. explained by low worm burden, male-only infec-
Immunodiagnostic tests are required for diagnosis tions, and infections with young (<7 months old)
in dogs receiving monthly macrolide prophylaxis. female worms that have immature reproductive
190 Section II Cardiovascular Disease
tracts. The antigen test is usually positive if there If the lobar arteries are at least 1.5 times the
are 3 or more mature female worms. diameters of the ninth ribs, then severe (class 3)
arterial pathology has occurred.
Heartworm Antibody Test Patchy ill-defined infiltrates around the lobar ar-
Heartworm-associated antibody tests are use- teries can result from plasma leakage and inflam-
ful to rule out infections in cats. Antibodies may mation in the lung parenchyma.
appear by 2 to 3 months post-infection and are Lobar artery dilation and tortuosity are indicative
usually present by 5 months. A positive antibody of severe pathology.
test indicates exposure but not necessarily active Abrupt lobar artery branch pruning may be vis-
infection. Approximately 10% of infected cats do ible resulting from obstructed blood flow due to
not produce antibodies. myointimal proliferation and thrombus formation.
Asthma-like signs due to developing larvae often
occur months before the antigen test can become Electrocardiography
positive. The electrocardiogram (ECG) is not a component
Larvae induced antibodies can persist after the of the minimum data base although it is sometimes
larvae have been killed by a macrolide drug. helpful. The ECG is not a sensitive test for identi-
A strongly positive test result indicates pre-adult fication of mild-to-moderate right ventricular hy-
infection, live adult infection or persistent (at pertrophy. Even though the ECG will reflect severe
least 6 months) antibodies after adult heartworm hypertrophy, clinical signs and thoracic radiographic
death. Antigen testing and echocardiography are analysis provide much more clinical information.
needed to confirm the diagnosis. Intermediate ti- A right ventricular hypertrophy pattern (S waves
ters should be repeated in 1 month. in leads I, II, aVF, V2, and V4) is common in dogs
Tests that may support a diagnosis and should be with severe pulmonary hypertension and is found
evaluated include: thoracic radiographs, echocar- in 90% of dogs with overt right-sided CHF (asci-
diography, serum globulins (hyperglobulinemia), tes). However, significant pulmonary hypertension
and CBC (eosinophilia, basophilia). may exist in the absence of ECG abnormalities.
Cardiac rhythm disturbances, including atrial fibril-
Microfilaria Detection lation, can occur in dogs with severe infections.
In dogs, the incidence of occult (amicrofilaremic)
infections is greater than the incidence of false- Echocardiography
negative antigen test results. Evidence of right ventricular and pulmonary artery
Annual microfilarial detection tests are required enlargement can be detected by two-dimensional
for dogs receiving diethylcarbamazine prophy- echocardiography. Occasionally, worms may be
laxis. Otherwise, microfilarial detection tests are detected in the right ventricle, the main pulmonary
mostly indicated if the intent is to kill the micro- artery and the right/left lobar arteries (Figure 10-6).
filaria rapidly using Interceptor. Evaluate a direct Echocardiography is particularly useful in antigen
blood smear immediately after procurement of negative cats.
a diagnostic blood sample. If the direct smear is Echocardiography is the test of choice for diagno-
negative, then a concentration test is performed. sis of caval syndrome (a mass of worms is found in
The Knott test (a centrifugal concentration test) the tricuspid valve orifice and in the vena cava).
or a filter test is at least 25% more sensitive for The echocardiographic features of severe heartworm
the detection of microfilaria compared to a direct disease include right ventricular eccentric hypertro-
smear analysis. phy, septal flattening, underloading of the left ven-
tricle and left atrium (Figure 10-7), dilation of the
Radiography main pulmonary artery segment (Figure 10-8) and
A common finding in heartworm infected main arteries, and high-velocity tricuspid and pul-
dogs is dilation of the main pulmonary artery monic regurgitations (Figure 10-9). The latter two
segment at the one oclock position on the ven- findings are indicative of pulmonary hypertension.
trodorsal or dorsoventral projection. The main
pulmonary artery segment is not visible in the Key Point
cat because of its midline position. Next, evalu- Thoracic radiography is the most important
ate the lobar pulmonary arteries. The caudal diagnostic test for determining the severity of
lobar arteries are the first and most severely heartworm disease.
effected (Figure 10-5).
Chapter 10 Heartworm Disease 191
Figure 10-5. Dorsoventral (A) and lateral (B) radiographic projections of the heart in a dog with class III heartworm disease.
On the dorsoventral projection, the caudal lobar arteries are greatly enlarged (arrowheads). These same abnormalities are seen on
the lateral projection (arrows), and the right cranial lobar artery (a) is enlarged.
Sequelae of Heartworm
Infection
Key Point Parenchymal Lung Disease
Echocardiography is a sensitive test for heart- Parenchymal lung disease results from pulmo-
worm infection in cats. nary arteriolar thromboembolism with leakage of
plasma and inflammatory cells into the adjacent
192 Section II Cardiovascular Disease
Figure 10-6. Two-dimensional cardiac ultrasound study demonstrating parallel, linear echodensities (arrows) produced by
heartworms in the right heart. The dog had class III disease. RA, Right atrium; RV, right ventricle; LV, left ventricle.
Figure 10-7. Right parasternal, short-axis, two-dimensional cardiac ultrasound of the left and right ventricles. Note the severely
enlarged right ventricle. The arrowhead points to echogenic worms within the right ventricle. RV, right ventricle; LV, left ventricle.
Figure 10-8. Right parasternal, short axis, two-dimensional cardiac ultrasound of the heart base showing the severely dilated
main pulmonary artery (PA). The arrow head points to echogenic worms within the right atrium.
Chapter 10 Heartworm Disease 193
Figure 10-9. A, Color flow Doppler echocardiogram obtained from the same position as Figure 10-8. Note the aliasing color
flow pattern consistent with significant pulmonary valve regurgitation. RA, Right atrium; PA, pulmonary artery. B, Continuous
wave Doppler echocardiogram obtained through the pulmonary valve. Note the high-velocity flow pattern consistent with
pulmonary valve regurgitation and pulmonary hypertension.
Table 10-1 Classification of Heartworm Disease Severity Based on Signs, Physical Examination,
and Radiographic Findings
necessary for dogs with class 1 infection that have 2.5 mg/kg Immiticide injected intramuscularly,
low-level antigenemia; however, it is recommended once. This dose contains 0.75 mg/kg of total ar-
by the American Heartworm Society. Monthly ad- senic. The injection is given into the epaxial mus-
ministration of ivermectin (Heartgard, Merial) at culature at the level of the third to fifth lumbar
the standard prophylactic dosage will gradually kill vertebrae.
adult worms over a period of 16 to 30 months; how- The appropriate volume of the reconstituted drug
ever, pulmonary damage may continue over this is aspirated into a syringe, and then a new needle
time and resistance may develop in dogs treated in is placed on the syringe.
this manner. For dogs weighing more than 10 kg, use a 1-
inch, 22-gauge needle, and for smaller dogs, use
Treatment of Cats a 1-inch, 23-gauge needle.
Treat asthma-like signs with prednisolone (1.0 to The injection should be completed before the
2.0 mg/kg, daily for 10 days; then taper the dose needle is withdrawn, and finger pressure should
to prevent signs of disease). Do not use aspirin in be applied over the needle tract during and for a
cats. Immiticide should not be used. Each worm short time after withdrawal.
will cause pulmonary thromboembolism when it Approximately 50% (most males and some of the
dies and if multiple worms die simultaneously, se- females) of adult worms are killed.
vere pulmonary thromboembolism will occur. It is Two follow-up injections (2.5 mg/kg each) at
generally believed that 30% to 50% of cats survive a 24-hour interval are administered after 1 to 3
their infections. months. Post-treatment thromboembolism recurs,
but the severity is reduced because fewer worms
Wolbachia (Rickettseae): Is It Important? are present.
Wolbachia is a vertically transmitted endosym- Data indicate that 100% of male and 98% of fe-
biotic, gram-negative, intracellular bacterium male worms are killed by the 3 doses.
that is harbored by D. immitis larvae and adults.
It is possible that metabolic products and surface
Key Point
proteins from Wolbachia can illicit an inflamma-
tory response in the host dog or cat. The host Use the graded-kill Immiticide protocol.
is exposed to Wolbachia when larvae or adult
worms die or are killed and Wolbachia may be
expulsed from the uterus of females or the ex- Treatment of Class 3 Heartworm Disease
cretory system of either gender of D. immitis. Severe pulmonary arterial disease occurs in 10%
Organs most vulnerable to inflammation are the of infected dogs in highly endemic regions, and in
lungs and kidneys. Doxycycline may be lethal some patients, the adult worm burden is very great.
to Wolbachia and it is postulated that the admin- Extraction of adult worms from the vena cava, right
istration of doxycycline aimed at reducing Wol- atrium, right ventricle, and main pulmonary arteries
bachia numbers prior to Immiticide treatment is possible. Worm extraction is only for patients with
might reduce post-Immiticide inflammation. many worms in the right heart and pulmonary arter-
Clinical studies testing this hypothesis have not ies. These patients have a high antigen concentration,
been reported. and the high burden is confirmed by echocardiogra-
phy. The technique requires fluoroscopy and long,
Adulticide Therapy in Dogs flexible alligator forceps or a horsehair brush that is
The approved available adulticidal agent is Immiti- introduced into the right jugular vein via a surgical
cide. The following regimens have proved to be ef- approach and manipulated through the heart into the
fective. The manufacturer recommends an initial 2 pulmonary arteries. Numerous passages to grasp
dose, separated by 24 hours, regimen for dogs with and remove worms are required, and the procedure
class 1 and 2 infections. The authors do not recom- is aided by fluoroscopy. This procedure is highly ef-
mend this protocol. fective in experienced hands.
After the patient has been stabilized, treat with
Graded-Kill Immiticide Protocol Immiticide to kill any remaining worms. It is as-
We recommend this protocol for classes 1, 2, and sumed that some worms are not removed. Sub-
3 infections. This regimen kills worms gradually sequently, remaining worms can be detected by
and reduces subsequent pulmonary thromboem- echocardiography or by a positive antigen test
bolism severity. result after 4 to 6 months.
196 Section II Cardiovascular Disease
Side Effects and Efficacy of Immiticide are removed and the obstruction to blood flow is
Treatment alleviated.
Mild myositis of 1 to 3 days, duration often is ob- Clinical signs are variable, including a sys-
served after Immiticide injections. Approximately tolic heart murmur, diastolic gallop, and
one third of treated dogs experience some swell- hemoglobinuria.
ing, and a sterile seroma occurs uncommonly. Echocardiography is diagnostic.
If an injection of Immiticide causes a local re- Surgical retrieval of the worms is the only recom-
action, then consider administration of an anti- mended acute treatment.
histamine and rapid acting corticosteroid before Minimal or no sedation is used. Rather local an-
subsequent injections. esthesia is used to perform a surgical cut-down
Hepatic and renal toxicity associated with Im- on the right jugular vein. A long, flexible alliga-
miticide is uncommon; excessive dosage can tor forceps or horsehair brush is introduced and
produce noncardiogenic pulmonary edema. advanced to the heart base in order to retrieve
Confirmation of efficacy can be established af- as many worms as possible from the vena cava
ter 6 months by antigen testing. Mean antigen and right atrium with multiple passages. The
concentration is reduced to 1% of pretreatment procedure is finished when several passages
levels, indicating nearly complete elimination of fail to retrieve additional worms. This is highly
worms. effective but experience is required for optimal
results.
Drug Storage After a period of stabilization, Immiticide is ad-
Immiticide is purchased as a lyophilized powder ministered to eliminate remaining worms.
that does not require refrigeration and has a shelf
life of at least 2 years. The reconstituted drug
When to Initiate Macrolide Prophylaxis in
must be kept refrigerated.
Infected Dogs
Post-Adulticide Complications Macrolide prophylaxis should be initiated as soon
Strict patient confinement is essential for 4 to 6 as infection is confirmed. Heartgard, Revolution, or
weeks post-treatment. Reduced blood flow de- Advantage Multi can be initiated for prophylaxis
mand through the pulmonary arteries is beneficial in microfilaremic infections. Interceptor should
to diminish endothelial damage and to promote not be administered to microfilaremic dogs unless
vascular repair. rapid kill is intended. In fact, in patients that have
Thromboembolic complications may occur neither clinical signs nor obvious radiographic ab-
from several days to 4 to 6 weeks post-Immiti- normalities, it is appropriate to initiate prophylaxis
cide. Most complications occur between 1 to and wait for several months before administering
3 weeks. Immiticide. This approach eliminates migrating
Most severe thromboembolism occurs in dogs larvae that might not be killed by Immiticide.
with class 3 infections with high antigen con-
centrations. Coughing, gagging, lethargy,
Rapid Microfilaricide Therapy
anorexia, tachypnea, dyspnea, syncope, he-
moptysis, and fever are common. Thrombo- We recommend against the use of Interceptor or
cytopenia and an inflammatory leukogram are high-dose ivermectin to kill microfilaria rapidly.
usual. Eliminating the microfilaria with monthly pro-
Radiographic evidence of parenchymal lung dis- phylaxis is acceptable.
ease is always present.
controversial. Very few worms are likely to have Administer heparin at 200 units/kg SQ every 8
survived and re-treatment may not be necessary. hours.
Re-treatment is recommended for class 3 infections, Administer prednisone (1.0 mg/kg PO every 24
if clinical signs persist, and for performance dogs. hours for 3 to 10 days).
Use intranasal or cage-administered oxygen for
Adjuncts to Adulticide Therapy
dyspneic patients.
Key Point
Allergic Pneumonitis
Test for Immiticide efficacy no sooner than 6
months after the last dose. This complication occurs in 10% to 20% of patients
with occult infections. The clinical signs include
dyspnea, coughing, respiratory crackles, and exer-
Heparin cise intolerance. Thoracic radiographs contain dif-
Recommended for rapidly dropping platelet fuse interstitial-alveolar infiltrates. Eosinophilia is
counts and hemoglobinuria. common, and eosinophils predominate in tracheal
Administer 75 to 100 units/kg SQ every 8 hours, lavage cytology. The syndrome responds well to oral
for several days up to 1 week. prednisone (1 to 2 mg/kg every 24 hours for sev-
Combine with strict cage confinement. eral days). Stop prednisone therapy after 3 to 7 days
and begin Immiticide therapy as soon as dyspnea,
Corticosteroids coughing, and pulmonary infiltrates have resolved.
Reduce parenchymal inflammatory disease in
the lungs but promote thrombosis and reduce
Pulmonary Eosinophilic Granulomatosis
pulmonary arterial blood flow if used for longer
than 10 to 14 consecutive days. Do not use corti- This uncommon complication of occult heart-
costeroids routinely, but only as needed to control worm disease probably results from the granulo-
sequelae. matous inflammation known to be associated with
occult infections. Prednisone (2 mg/kg PO every
Oxygen 24 hours for 7 to 14 days; then gradually taper
The only effective means of dilating the pulmo- dose) with azathioprine (50 mg/m2 PO every 24
nary arteries. hours for 7 days; then 25 mg/m2 every 24 hours
For class 3 infections associated with dyspnea, for 7 days; then 25 mg/m2 every 48 hours) may in-
orthopnea, or CHF. duce partial or complete remission. Relapses are
Administer intra-nasally or by oxygen cage. common even in the face of medical therapy. The
prognosis is guarded, and surgical excision of lo-
bar lesions may be required. Adulticide treatment
Treatment of Sequelae should be delayed until remission is attained.
Pulmonary Thromboembolism
Feline AsthmaLike Syndrome
This common complication of moderate to
severe pulmonary arterial disease can occur Treat asthma-like signs in cats with prednisolone
before adulticide therapy, but is most common 7 (1.0 to 2.0 mg/kg PO daily for 10 days; then taper
to 21 days after adulticide therapy. In dogs, clini- the dose to prevent signs of disease).
cal signs include coughing, dyspnea, fever, and
hemoptysis.
A regenerative leukocytosis with thrombocytope-
Prevention
nia usually is present. Amicrofilarial examination always is indicated be-
Positive d-dimers (>500mg/dl) may be a sen- fore initiation of drugs that can be associated with
sitive indicator. However, in the authors an acute adverse reaction. These drugs are Intercep-
experience, negative d-dimers do not exclude tor and diethylcarbamazine. Prevention should be
thromboembolism. in place whenever the average daily temperature
Thoracic radiographs reveal severe pulmonary exceeds about 57 F. Year-round prevention is prac-
arterial disease with periarterial parenchymal ticed in hotter climates, even though transmission
disease of variable severity. is uncommon in December and January in the
Initiate cage confinement for 5 to 10 days. continental United States.
198 Section II Cardiovascular Disease
Start as early as 6 to 8 weeks of age. In cooler cli- It is not as effective as ivermectin at preventing
mates, start puppies on prophylaxis as soon after the maturation of larvae when monthly adminis-
8 weeks of age as dictated by seasonal risk. tration is started 4 months post-L3 inoculation.
Heartgard, Interceptor, Revolution, and Advan- It also controls hookworm, roundworm, and
tage Multi should be started within 1 month of whipworm infestations.
the transmission season. These drugs kill migrat- One dose of Interceptor at the prophylactic dos-
ing larvae during the first 6 to 8 weeks after L3 age will kill most microfilaria within 24 hours. If
inoculation. the microfilaria concentration is high, an adverse
Successful prophylaxis is confirmed by a nega- reaction is likely.
tive antigen test result one year after initiation.
Macrolides are safe for collies when prescribed
Moxidectin
according to the label.
Macrolide prophylaxis not only interferes with lar- A topical solution formulation (Advantage Multi)
val embryogenesis, which reduces the circulating is an effective once-a-month heartworm preven-
levels of microfilaria, but also gradually kills exist- tative agent for dogs and cats. Advantage Multi
ing microfilaria over a period of 6 to 8 months. also controls fleas, hookworms, roundworms,
whipworms, and ear mites.
Key Point
Key Point
In all studies to date, owner administration
compliance has been poor. All macrolide preventive drugs eliminate micro-
filaria, either quickly or slowly. For this reason,
chronic dosing with Heartgard, Revolution, In-
terceptor, or Advantage Multi leads to occult
Ivermectin status in infected dogs. All monthly prophylac-
Ivermectin (Heartgard), at a dosage of 6 to 12 tic drugs can be administered without prior
micrograms/kg given monthly, is an effective pre- testing and fear of adverse reactions.
ventive drug. A chewable formulation of Ivermec-
tin plus pyrantel pamoate (Heartgard Plus) is an
effective heartworm preventive that also controls
Diethylcarbamazine
ascarid and hookworm infestations. Drug reac-
tions are rare at the recommended dosage. Diethylcarbamazine (2.5 to 3.0 mg/kg, PO) given
The reach-back larvacidal action is 100% at daily is an effective prophylactic drug. If the
1 month and nearly 100% at 2 months. owner skips more than a few days of treatment,
If initiated 4 months following L3 inoculation do not reinstitute preventive treatment before per-
and continued for at least 1 year, the likelihood of forming a microfilarial concentration test. Dieth-
developing infection is reduced by at least 98%. ylcarbamazine has been largely supplanted by the
When administration is begun 5.5 months post-L3 macrolide drugs. The duration of action of dieth-
inoculation, the subsequent adult worm burden is ylcarbamazine is short because the drug affects
reduced by about 50%. the L3-L4 (larval) molt 9 to 12 days postinfection.
When administration is begun 6.5 months post- Begin therapy before mosquito season and con-
L3, the subsequent adult worm burden is reduced tinue for 2 months after the first frost (or year-
by about one third. round in regions that have mosquitoes all year).
Heartgard Plus kills adult heartworms slowly Combination diethylcarbamazine and oxibenda-
over a 16- to 30-month period and microfilariae zole (Filaribits Plus) controls intestinal helminths.
over a period of 6 to 8 months. An occasional side effect of oxibendazole is in-
A dose of 24 g/kg administered monthly is an creased liver enzyme activity, icterus, and hepatic
effective heartworm prophylaxis in cats, and it insufficiency, which is reversible after the drug is
controls hookworms. discontinued.
Key Point
Milbemycin
Never initiate diethylcarbamazine treatment
Milbemycin (Interceptor), at a dosage of 0.5 to 0.99 in microfilaremic dogs because a severe reac-
mg/kg, is an effective once-a-month preventive tion may occur.
agent for heartworm disease in dogs and cats.
Chapter 10 Heartworm Disease 199
Missed Doses of Oral How likely is it that a cat will survive heartworm
Macrolide Prophylactic infection?
Drugs Estimates are that mortality is about 50% whether or
not Immiticide is administered.
One dose of any macrolide will kill all lar- What is the most practical method to rule out
vae that have infected a dog in the previous heartworm infection in cats?
month. A negative antibody test is associated with a high
One dose of Heartgard, Interceptor or Revolution likelihood that infection is absent. If there is still con-
will kill virtually all larvae that have infected a cern, then echocardiography is indicated.
dog during the prior two months. Why is it unnecessary to kill microfilaria quickly?
Microfilaria will be eliminated in 6 to 8 months with
Heartgard, Interceptor, and Revolution will pre-
macrolide prophylaxis and the likelihood of the in-
vent almost all infections from maturing after fected dog being responsible for spread during this
three consecutive doses are missed, providing period is low.
that at least 12 consecutive subsequent monthly What is the proper course of action if 3 consecutive
doses are administered. prophylactic doses are missed?
Administer Heartgard, Interceptor or Revolution for
at least 12 consecutive months and the likelihood of
Macrolide Efficacy Against maturation of heartworm larvae is extremely low. In
Adult Heartworms fact, if the infection is only about 2 months old, one
dose of any of these preventatives will stop almost all
Heartgard will kill almost all adult heartworms if infections.
administered every month for 30 months. Is Heartgard recommended as an adulticide
We rarely recommend Heartgard for adulticide treatment?
treatment because progressive pulmonary pathol- No. Almost all dogs with adult heartworm infection
ogy can occur and resistance is a possibility. should be treated with Immiticide. The slow kill-rate
of Heartgard against adults may allow progressive
pulmonary pathology and resistance is possible.
Retesting Dogs Receiving
Macrolide Prophylaxis
Macrolide prophylactic drugs are highly effica-
cious, and therefore annual retesting often is not
performed; however, we recommend annual re- Suggested Readings
testing because: Atkins C: Canine heartworm disease. In Ettinger SJ Feld-
Owner compliance has been proven to be poor in man EC, eds: Textbook of veterinary internal medi-
all regions examined. cine, Philadelphia, 2005, WB Saunders.
Inadequate dosing is likely in growing puppies. Atkins C: Feline heartworm disease. In Ettinger SJ, Feld-
man EC, eds: Textbook of veterinary internal medi-
cine, Philadelphia, 2005, WB Saunders.
Frequently Asked Questions Heartworm disease. In Kahn CM, ed: The Merck manual.
Whitehouse Station, NJ, 2005, Merck and Co.
Is Immiticide an effective adulticide in cats and should
Heartworm disease, In Birchard SJ, Sherding RG, eds:
treatment be attempted?
Saunders manual of small animal practice, St. Louis,
An Immiticide dosage schedule that is both safe and
2006, WB Saunders.
effective in cats has not been developed. Dying worms,
whether the result of Immiticide or natural death, will
always cause pulmonary thromboembolism which
may be fatal. Immiticide dosages have been investi-
gated but some were too low to kill worms and others
were high enough to cause acute pulmonary toxicity
(acute respiratory distress syndrome).
Chapter 11
Pericardial Disorders
and Cardiac Tumors
Anthony H. Tobias and Elizabeth A. McNiel
sociated with pericardial effusions (abnormal accu- Males and females were nearly equally repre-
mulations of fluid within the pericardial sac) leading sented (46 [53%] males to 41 [47%] females).
to cardiac tamponade (significant compression of Pericardial effusions were most frequently di-
the heart by accumulating pericardial contents). agnosed in Golden Retrievers (23 [26%] of the
Most pericardial effusions in dogs are associated 87 cases), and this was the only breed that was
with cardiac tumors. Similarly, most cardiac tumors overrepresented when compared to the general
are associated with pericardial effusions. Conse- hospital population (odds ratio=4.4; 95%
quently, cardiac tamponade typically dominates the confidence interval 2.7 to 7.0).
clinical presentation in dogs with cardiac tumors.
Pericardial effusions in cats occur most commonly
Chief Complaints and History
s0040
are usually mild and incidental manifestations of effusions are nonspecific and have an acute onset.
underlying disease, rather than the primary cause Presenting signs in the UMVMC study population
for the presenting signs. Consequently, the ensu- included:
ing discussion pertains primarily to dogs. Lethargy (53%)
u0030
Vomiting (30%)
Incidence and Signalment
s0030
Symptomatic pericardial effusions most commonly ical signs ranging from subtle to hemodynamic
occur in older and larger dogs. In the UMVMC collapse (severe clinical tamponade).
200
Chapter 11 Pericardial Disorders and Cardiac Tumors 201
In the UMVMC study population, muffled heart Low voltage QRS complexes (R waves < 1 mV
sounds were the most common physical examina- in all limb leads) are present in approximately
tion abnormality, occurring in 71% of the cases. half of the cases (Figure 11-2, A, B).
Other physical examination findings included: Electrical alternans, a beat-to-beat variation in
Depression (63%). the contour and amplitude of the QRS and ST-T
Weak pulses (62%). complexes (Figure 11-2, C), is strongly sugges-
Abdominal distention with a fluid wave due to tive of a pericardial effusion. Electrical alternans
ascites (43%). Ascites, when present, is usu- is present in up to approximately 20% of dogs
ally mild, and consequently not recognized by with pericardial effusions.
owners in about half of the dogs in which it is
detected on physical examination. Pericardial fluid analysis
s0090
Thorough physical examination usually discloses Pericardial effusions in dogs irrespective of cause
u0070
Thoracic radiographic features that support a di- dial effusions in dogs, are rarely identified on
p0020
tracheal elevation and widening of the caudal dramatic mesothelial proliferation, and exfoliated
vena cava mesothelial cells often have characteristics that
Overlap of the cardiac silhouette and diaphragm mimic malignancy. Cytology must be interpreted
and bilateral contact between the pericardial very cautiously.
sac and the costal margins However, some of the less common causes of peri-
p0040
A sharply delineated edge to the cardiac silhouette cardial effusion, such as infectious pericarditis and
because the distended pericardial sac undergoes lymphosarcoma, are diagnosed primarily on the
little, if any, motion during systole and diastole basis of pericardial fluid cytology. Consequently,
Lung fields that show no evidence of left-sided the authors submit pericardial fluid for analysis
congestive heart failure (i.e., no cardiogenic in all cases with pericardial effusions, despite the
pulmonary edema, Figure 11-1) generally low diagnostic yield of this test.
However, these typical radiographic findings are b0010
only present in more chronic cases with large volume Key Point
pericardial effusions. With smaller pericardial effu- Cytologic examination of pericardial effusates
sions, the cardiac silhouette is variably enlarged, and is unreliable in distinguishing neoplastic vs.
it is not necessarily globoid. Also, pericardial effu- non-neoplastic (i.e., inflammatory) etiologies
sions in dogs are frequently accompanied by pleural in the large majority of cases of pericardial ef-
effusions that may obscure the cardiac silhouette. fusion in the dog.
Despite these limitations, thoracic radiographs are
p0030
cilitating a diagnosis of pericardial effusion in many Echocardiography is the most sensitive and spe-
p0050
cases, thoracic radiographs may demonstrate the cific noninvasive method to confirm the presence
presence of abnormalities such as pulmonary metas- of pericardial effusion.
tases, or radiopaque intrapericardial foreign bodies. With two-dimensional echocardiography, peri-
u0080
Most dogs with pericardial effusions have either pleural effusion, the pericardium is well visual-
u0060
a normal sinus rhythm or a sinus tachycardia. ized with anechoic fluid on either side.
Ventricular arrhythmias are fairly common and The heart may show swinging motions within the
supraventricular arrhythmias occasionally occur. pericardial fluid.
202 Section II Cardiovascular Disease
f0010
Figure 11-1. Thoracic radiographs from a dog with pericardial effusion. A, The lateral projection shows a markedly enlarged
cardiac silhouette, tracheal elevation, and overlap of the cardiac silhouette and diaphragm. B, The ventrodorsal projection shows
bilateral contact between the pericardial sac and the costal margins. The edge of the cardiac silhouette is sharply delineated, and
the lung fields are clear of any infiltrate that would indicate the presence of left-sided congestive heart failure.
The various heart chambers may appear small systole for a variable period before normalizing
and the walls may show thickening or pseudohy- (Figure 11-3, A).
p0060
The right atrial free wall is normally rounded lar diastolic collapse is characterized by inward
throughout the cardiac cycle, reflecting the nor- motion of the right ventricular free wall (Figure
mal positive right atrial transmural pressure. Any 11-3, B). This may range from transient and local-
inversion or collapse of the right atrial free wall ized concavity of the right ventricular free wall, to
provides indirect evidence of elevated intraperi- virtual complete right ventricular chamber oblitera
cardial pressure and transient reversal of trans- tion throughout diastole.
mural pressure (echocardiographic evidence of In addition to confirming the presence of pericar-
p0080
cardiac tamponade). Right atrial inversion occurs dial effusion and cardiac tamponade, echocardiog-
in late diastole and continues into ventricular raphy is the noninvasive procedure of choice to
Chapter 11 Pericardial Disorders and Cardiac Tumors 203
f0020
Figure 11-2. Electrocardiograms (lead II) from dogs with pericardial effusion. Calibration square wave is 1mV in amplitude.
A, Before pericardiocentesis, the complexes are low voltage (R wave <1 mV) and heart rate is 140 beats per minute (bpm).
B, After pericardiocentesis, R wave amplitude is almost 2 mV and heart rate is 100 bpm. C, Beat-to-beat variations in amplitude
and contour of the QRS and ST-T complexes that characterize electrical alternans. (Modified from Tobias AH: Pericardial disorders.
In Ettinger SJ, Feldman EC, eds: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, WB Saunders.)
detect associated intrapericardial masses such as cavitary appearance, and the tumors are occa-
hemangiosarcoma and heart base tumors. Whereas sionally cystic (see Figure 11-4).
histopathology is necessary to confirm and de- Hemangiosarcoma, when present, is usually
finitively identify a tumor, the echocardiographic demonstrated while imaging from the right
location and characteristics of an intrapericardial parasternal long- and short-axis views. How-
or myocardial mass provides important informa- ever, these tumors may be small and elusive.
tion about the probable tumor type. Imaging from the left parasternal locations to
The following echocardiographic features are provide alternate imaging planes, especially of
p0090
consistent with a diagnosis of hemangiosarcoma: the right auricle, is necessary to demonstrate the
Hemangiosarcoma most commonly arises from presence of hemangiosarcoma in some cases.
u0090
the wall of the right atrium or auricle, protrudes Hemangiosarcoma involving the wall of the left
into the pericardial space, and moves with the ventricle has been described.
right auricle or atrium (Figure 11-4). The following echocardiographic features are
p0100
These tumors may also protrude into the right characteristic for heart base tumors:
atrial chamber, spread to involve other areas of the Heart base tumors are usually associated with
u0100
heart base and pericardium, and involve the right the ascending aorta (Figure 11-5, A).
atrioventricular groove (see Figure 11-3, A). They vary from small ovoid structures attached to
Hemangiosarcoma typically contains small hy- the ascending aorta, to very extensive masses that
poechoic spaces, giving the tumor a mottled or surround the aorta and main pulmonary artery.
204 Section II Cardiovascular Disease
f0030
Figure 11-3. Echocardiographic tamponade in a dog with pericardial effusion (PE). The images were recorded from the right
parasternal location. A, Late diastolic inversion of the right atrium (arrow). The mass at the atrioventricular groove was confirmed
as hemangiosarcoma by surgical biopsy. B, Diastolic inversion of the right ventricular wall (arrow). RV, Right ventricle.
Tumor indentation or invasion of the atria and ma- Benign intrapericardial cyst.
jor blood vessels may be seen (Figure 11-5, B). Intrapericardial thrombi associated with left
Heart base tumors tend to have a more homog- atrial perforation. Left atrial perforation is
enous appearance than the mottled or cavitary suspected when signs of acute tamponade de-
appearance of hemangiosarcoma. velop in smaller breed dogs with significant
Heart base tumors are usually, but not invari- mitral regurgitation.
ably, associated with pericardial effusions.
Echocardiography may also demonstrate:
Initial Patient Stabilization:
s0110
pericardial sac in cases with peritoneoperi- dial fluid as possible is necessary for initial pa-
cardial diaphragmatic hernia. tient stabilization in any case with a pericardial
Chapter 11 Pericardial Disorders and Cardiac Tumors 205
b0020
Key Point The catheter is then advanced over the needle into
the pericardial space (Figure 11-6, C), the needle
The presence of pericardial fluid greatly facili- is removed, the extension tube is connected to the
tates the detection of intrapericardial masses,
catheter (Figure 11-6, D), and a small amount of
and this is particularly relevant to the diagno-
sis and delineation of hemangiosarcoma and fluid is aspirated (Figure 11-6, E).
heart base tumors. Pericardial fluid forms an The gross appearance of pericardial fluid is almost
echolucent zone around the right atrium and invariably indistinguishable from blood. To con-
auricle and the ascending aorta, the locations firm that the catheter is in the pericardial space,
at which these tumors most commonly occur. an aliquot of fluid is placed in an activated clotting
In the absence of pericardial fluid, these loca- time tube. Blood will normally clot in an activated
tions are obscured by lung interference. Con- clotting time tube within 60 to 90 seconds. In con-
sequently, whenever the clinical condition of trast, sanguinous effusions in body cavities are rap-
the patient permits, pericardiocentesis should idly depleted of clotting factors and thrombocytes,
be deferred until a thorough echocardio- and pericardial fluid will consequently not clot. If
graphic examination has been completed.
no clots form within the activated clotting tube af-
ter 3 to 5 minutes, samples are collected for fluid
analysis and culture, and all of the pericardial fluid
e ffusion that is causing significant hemodynamic is aspirated. The catheter is then removed.
compromise (clinical cardiac tamponade). Ventricular arrhythmias are common during peri-
The authors preferred approach is to restrain the cardiocentesis and ECG monitoring during the
u0110
the risk of lacerating a coronary blood vessel dur- pericardiocentesis results in rapid and marked he-
ing the procedure. modynamic improvement. Clinical signs, pulse
Dogs usually tolerate the procedure without seda- quality, and mucous membrane perfusion im-
tion, but mild sedation is necessary in some cases. prove, and heart rate decreases. However, ventric-
The authors usually use a 14- or 16-gauge over- ular and supraventricular arrhythmias (including
the-needle catheter system to perform pericardio- atrial fibrillation) are common both during and
centesis in dogs. Two small side holes are made following pericardiocentesis. These arrhythmias
near the tip of the catheter to avoid any blockages seldom require therapy and usually resolve spon-
and aspirating the myocardium against a single taneously. Nevertheless, we prefer to hospitalize
end hole during the procedure. and monitor cases for 12 to 24 hours following
The catheter system is coupled to a large volume pericardiocentesis and to provide supportive care
syringe via an extension tube and a three-way as indicated.
stopcock.
The right thorax is shaved and the ideal location
to perform the procedure is determined by echo- Specific Causes of
s0120
are infiltrated with local anesthetic, and the area Hemangiosarcoma, a highly malignant neoplasm
p0130
cardium, fluid flows into the extension tube and diagnosed either by echocardiography, or echo-
syringe. cardiography and histopathology in 53 of 87 dogs
206 Section II Cardiovascular Disease
f0040
Figure 11-4. Echocardiographic images from a dog with cardiac hemangiosarcoma recorded in the short-axis view from the right
parasternal location. A, A cavitary and cystic mass (arrow) is associated with the right auricle (RA). B and C, The mass moves back and
forth with right auricular motion during different phases of the cardiac cycle. AO, Aorta; PE, pericardial effusion.
Chapter 11 Pericardial Disorders and Cardiac Tumors 207
f0050
Figure 11-5. Echocardiographic images from a dog with a heart base tumor recorded from the left cranial parasternal location.
A, A large homogeneous mass (arrow) is attached to the caudal aspect of the aorta (AO). B, The tumor has infiltrated the main
pulmonary artery (PA). LVOT, Left ventricular outflow tract; LA, left atrium.
(61%) in the study population with pericardial ef- (odds ratio, 5.3; 95% confidence interval, 2.9 to
fusion. Cardiac hemangiosarcoma with pericardial 9.4), which is consistent with data from the Veteri-
effusion was nearly three times more prevalent nary Hospital of the University of Pennsylvania.
than the second most common form of pericardial Treatment for all forms of hemangiosarcoma is
p0150
(2.1) years, and their average weight was 32.0 time of diagnosis, cardiac hemangiosarcoma usu-
(12.2) kg. ally has metastasized, and it should be considered
There was no sex predisposition. Although males a systemic disease.
outnumbered females (31 [58.5%] males: 22 Many owners of dogs with cardiac hemangiosar-
u0130
[41.5%] females), this was not significantly dif- coma elect palliation with pericardiocentesis alone.
ferent from the sex distribution among dogs in Pericardiocentesis is predictably associated with
the general hospital population. marked clinical improvement, but clinical signs of
A total of 16 of the 53 dogs (30%) were Golden tamponade typically recur within a few days, often
Retrievers, and the breed was over-represented resulting in death or prompting euthanasia.
208 Section II Cardiovascular Disease
A B
C D
f0060
Figure 11-6. Pericardiocentesis in a dog. A, A small skin incision is made after local anesthetic has been administered. B, An over-
the-needle catheter system with 2 side holes is advanced towards the pericardium. Slight negative pressure is applied via a syringe
coupled to the needle by extension tubing. C, Pericardial fluid flows into the extension tubing, and the catheter is advanced over
the needle into the pericardial space. D, The extension tubing is removed from the needle and coupled to the catheter. E, Pericardial
effusion is aspirated. The gross appearance of pericardial effusion is almost invariably sanguinous, irrespective of cause.
In the UMVMC study population, median sur- of tumor resection, pericardectomy, chemotherapy,
vival time for 30 dogs with cardiac hemangio- and splenectomy in cases with splenic metastases.
sarcoma that were treated by pericardiocentesis A recent retrospective study from the University of
alone on one or more occasions was just 11 days Pennsylvania reported on 23 cases in which tumor
(range, 0 to 208). resection was performed. In addition, pericardec-
More aggressive approaches to the treatment of car- tomy was performed in 21 of the dogs, 3 had sple-
p0160
diac hemangiosarcoma include various combinations nectomies, and 8 received adjuvant chemotherapy.
Chapter 11 Pericardial Disorders and Cardiac Tumors 209
Median survival time from time of surgery for metastases occur in both dogs and cats. The bio-
u0140
all 23 cases was 56 days (range, 0 to 229), once logic behavior of ectopic thyroid tumors at the
again emphasizing the extremely poor progno- heart base is less well described, and both ecto-
sis associated with cardiac hemangiosarcoma. pic thyroid adenomas and adenocarcinomas with
Adjuvant chemotherapy following tumor resec- metastases have been reported.
tion may prolong survival in dogs with cardiac Complete surgical resection of heart base tumors
p0200
hemangiosarcoma, especially with protocols that is seldom possible because the tumors are highly
include doxorubicin. However, the data are not vascular, located close to major blood vessels,
compelling and the survival advantage is small. and usually extensive by the time of diagnosis.
Nevertheless, management of cardiac heman- However, palliation with pericardectomy alone
giosarcoma should always include consultation often results in prolonged survival with an excel-
with an oncologist to take advantage of continu- lent quality of life.
ally emerging modalities for the treatment of this In a recent retrospective study in dogs with aor-
u0160
highly malignant tumor. tic body tumors in which surgery was performed,
only pericardectomy had a significant effect on
Heart Base Tumors survival, and the survival advantage was remark-
s0150
The term heart base tumor is used to designate any able. Median survival time among dogs following
p0170
mass located at the base of the heart in associa- pericardectomy was 730 days, whereas median
tion with the ascending aorta and main pulmonary survival time among those that did not have a
artery. Most heart base tumors in dogs are aortic pericardectomy was only 42 days.
body tumors, although 5% to 10% of heart base
tumors in dogs are thyroid tumors (both adeno- Mesothelioma
s0160
mas and adenocarcinomas) that arise from ectopic Mesothelioma, a diffuse neoplasm of the peri-
p0210
thyroid tissue at the base of the heart. Aortic body cardium and other serosal surfaces is emerging
tumors have occasionally been reported in cats. as an increasingly important cause of pericardial
Heart base tumors were diagnosed either by echo- effusion. Mesothelioma was confirmed in 4 of 87
p0180
cardiography, or echocardiography and histopa- dogs (5%) in the UMVMC study population of
thology in 6 of the 87 dogs (7%) with pericardial dogs with pericardial effusion.
effusion in the UMVMC study population, which Average age among the affected cases at time of
u0170
is consistent with a recent review of the epidemi- presentation was 9.5 (2.2) years, average weight
ology of cardiac tumors in dogs. Despite being the was 37.5 (11.1) kg, and males and females were
second most common cardiac tumors in dogs, the equally represented.
incidence of aortic body tumors is approximately No breed predisposition has been reported, and
10-fold lower than cardiac hemangiosarcoma. affected breeds in the UMVMC population were
English Bulldogs, Boxers, and Boston Terriers Akita, Golden Retriever, Labrador Retriever, and
u0150
induces hyperplasia and neoplasia of chemore- mesothelioma in the UMVMC study population
ceptors, which may explain the predisposition of followed a characteristic pattern.
brachycephalic breeds to aortic body tumors. Presenting and clinical signs were no differ-
Among the predisposed breeds, males may be at ent from other cause of pericardial effusion.
u0180
increased risk for developing aortic body tumors, In all four cases, a provisional diagnosis of
but differences in sex predisposition are not sta- idiopathic pericardial effusion was made af-
tistically significant in all studies. ter various diagnostic procedures, including
The age range at time of diagnosis of aortic echocardiography and pericardial fluid anal-
body tumors is 6 to 15 years, with an average of ysis failed to disclose a cause for the pericar-
10 years. dial effusion.
Between 5% and 10% of tumors at the heart base Pericardiocentesis was performed, and this was
are ectopic thyroid tumors. repeated 31 to 133 days later, when the dogs
Aortic body tumors tend to be slow-growing developed recurrent effusions with clinical
p0190
cases, and histopathology of the excised peri- Cardiac lymphosarcoma, rhabdomyosarcoma, and
p0250
cardia was consistent with idiopathic pericardi- fibrosarcoma with pericardial effusion have been
tis in three cases and mesothelioma in one. reported in both dogs and cats. Cardiac lympho-
Severe and unremitting pleural effusions re- sarcoma is diagnosed in approximately 1% of dogs
quiring repeated thoracocentesis began 48 to with pericardial effusion, whereas rhabdomyo-
148 days following pericardectomy. sarcoma and fibrosarcoma are rare. Among the
Intracavitary cisplatin was administered in 2 various cardiac tumors, cardiac lymphosarcoma
dogs, but this did not appear to significantly is unique because cytology of the pericardial fluid
change the course of the disease. establishes the diagnosis in many cases and the tu-
Thoracocentesis was necessary every 2 to 3 mor is amenable to combination chemotherapy.
weeks until death or euthanasia, and median sur-
vival time from the initial episode of pericardial
Infections
s0180
throughout the thoracic cavity was confirmed sionally associated with pericardial effusions in
on post-mortem examination. small animals.
The signalment and clinical course among Most cases of pericardial effusions due to bacterial
p0230 u0190
cases with pericardial effusion due to meso- infections are thought to arise as a consequence of
thelioma in the UMVMC study population are intrapericardial foreign body penetration, usually
strikingly similar to those described by others. by migrating foxtails (Hordeum spp.). In contrast
It is extremely difficult to distinguish between to most other causes of pericardial effusion, peri-
idiopathic pericardial effusion and pericar- cardial fluid cytology and culture is crucial for
dial effusion due to mesothelioma, even with the diagnosis of infectious cases. In the largest
pericardial histopathology and immunohisto- series of bacterial pericarditis reported in dogs
chemistry. However, accumulations of signifi- (5 cases), treatment involved pericardectomy
cant amounts of pleural effusion within 4 to 6 and removal of any foreign bodies, chest drain-
months of pericardectomy increase the index age, and antibiotic therapy for up to 6 months.
of suspicion for mesothelioma. All dogs recovered without complications, sug-
In addition to being a diagnostic challenge, gesting that dogs with bacterial pericarditis have
p0240
mesothelioma is difficult to treat. However, a good prognosis when treated aggressively with
long-term survival has been reported in a dog a combination of surgical and medical therapy.
in which a histopathological diagnosis of peri- Systemic coccidioidomycosis in dogs is occa-
cardial mesothelioma was made following sionally associated with pericardial disease. In
pericardectomy for recurrent pericardial effu- most cases the fungal infection results in effu-
sion. Treatment in that case was initiated 48 sive-constrictive or constrictive pericarditis. Coc-
hours after surgery with intracavitary cisplatin cidioidomycosis should be considered especially
and intravenous doxorubicin, and the dog was in dogs with pericardial disease that reside in or
free of disease 27 months later. have a travel history that includes areas where
the soil fungus Coccidioides immitis is endemic,
such as the southwestern United States. Treat-
ment involves pericardectomy, chest drainage,
b0030
fusion. Affected cases have a history consistent Idiopathic pericardial effusion is a diagnosis
p0270
with acute pericardial effusion, and a loud left of exclusion. It is made in cases with pericar-
apical murmur is usually apparent despite muf- dial effusion where no intrapericardial masses
fling of the heart sounds. Echocardiography dis- are identified after thorough echocardiographic
closes intrapericardial fluid, a mobile thrombus evaluation, and the results of ancillary tests such
caudal to the left ventricle, and substantial mitral as pericardial fluid analysis fail to disclose an
regurgitation. We have diagnosed left atrial per- etiology. Pericardial histopathology and immu-
foration in several dogs following an episode of nohistochemistry from dogs with idiopathic peri-
weakness or collapse. In many of these cases, the cardial effusion demonstrate changes consistent
dog is either recovering or clinically normal by with pericarditis of undetermined etiology.
the time of their echocardiogram, and relatively As with any diagnoses of exclusion, a diagnosis
p0280
little pericardial fluid and only mild echocardio- of idiopathic pericardial effusion should be made
graphic evidence of tamponade is demonstrated. cautiously.
In such cases, we provide no therapy other than Small intrapericardial tumors may elude detec-
u0220
congestive heart failure medications if appro- tion, especially in cases where echocardiogra-
priate (i.e., for cases with left-sided congestive phy is performed following pericardiocentesis.
heart failure due to mitral regurgitation). Repeat Mesothelioma does not result in appreciable
echocardiograms 7 to 10 days later have demon- thickening of the pericardium on echocardiog-
strated complete resolution of both the pericar- raphy. Routine cytology of pericardial effusion
dial effusion and the intrapericardial thrombus. does not distinguish between idiopathic pericar-
On the other hand, pericardiocentesis is required dial effusion and mesothelioma. Consequently,
for cases with left atrial perforation that are he- mesothelioma should always be considered as
modynamically compromised as a result of tam- an important differential diagnosis for idio-
ponade. Furthermore, the possibility of continued pathic pericardial effusion.
hemorrhage exists, necessitating blood transfu- Idiopathic pericardial effusion has not been re-
sion and thoracotomy to remove larger clots from ported in cats.
the pericardial space and to repair the left atrium. Idiopathic pericardial effusion was diagnosed in
p0290
The prognosis in such cases is grave. 8 of 42 dogs (19%) with pericardial effusion in a
Pericardial effusions secondary to coagulation retrospective study from the Veterinary Teaching
disorders are rare causes of clinically significant Hospital, Colorado State University. Idiopathic
tamponade. A single case of pericardial effusion pericardial effusion was provisionally diagnosed
and cardiac tamponade secondary to anticoagulant in 24 of 87 dogs with pericardial effusion in the
rodenticide toxicity has been reported in a dog. UMVMC study population, but mesothelioma
Pericardial effusions secondary to disseminated was subsequently confirmed in 4 of these cases.
intravascular coagulation, warfarin toxicity, and Thus, 20 of the 87 cases (23%) with pericardial
other coagulopathies have been reported in cats. effusion were finally diagnosed as having idio-
pathic pericardial effusion, which is similar to
the Colorado State University data.
Miscellaneous
s0200
Pericardial effusion is frequently detected in both pericardial effusion in the UMVMC study pop-
u0210
dogs and cats with congestive heart failure, but ulation was 9.4 (2.2) years, average weight
usually not in sufficient quantity to cause signifi- was 28.9 (14.5) kg, and there was no apparent
cant hemodynamic compromise. sex predisposition (11 [55%] males to 9 [45%]
Pericardial effusion secondary to uremia has been females).
recognized in small animals. Five of the 20 dogs (25%) were Golden Retriev-
A case of cholesterol-based pericardial effusion ers, and the breed was over-represented (odds
has been reported in a dog with hypothyroidism. ratio, 4.2; 95% confidence interval, 1.6 to 11.2).
212 Section II Cardiovascular Disease
We have frequently treated first episodes of idio Echocardiography is the method of choice to de-
p0300
pathic pericardial effusion by pericardiocente- tect cardiac tumors, and the procedure should be
sis alone, followed by pericardectomy in cases performed before pericardiocentesis whenever
that develop recurrent effusions. However, the the clinical condition of the patient permits.
UMVMC data show that: Pericardiocentesis provides initial patient stabili-
Tamponade recurs in approximately one third zation. Pericardiocentesis alone is rarely, if ever,
u0240
gical or minimally invasive thoracoscopic pericardec- grave to excellent. Pericardectomy forms part or
tomy with the initial episode of idiopathic pericardial all of the therapy in virtually all cases that have
effusion. Although pericardectomy is by no means prolonged, disease-free survival.
devoid of morbidity and mortality, it is an extremely
successful procedure for idiopathic pericardial ef-
fusion. Pericardectomy avoids the risk of recurrent
life-threatening cardiac tamponade and the potential
for developing effusive-constrictive and constrictive
Frequently Asked Questions
b0040
Pericardial effusions causing clinical tamponade Commonly, dogs with significant pericardial effusion
present with three cardinal signs, historically referred
are common in dogs and Golden Retrievers are
to as Becks triad. These signs include muffled heart
over-represented. sounds, weak femoral pulses, and jugular venous
Chief complaints, histories, and physical exami- distension. Careful examination of dogs suspect for
nation findings in dogs with pericardial effusions pericardial effusion usually reveals the presence of all
are diverse and often vague. three components of the triad. Successful inspection
Whereas thoracic radiography and electrocardi- of the jugular veins sometimes necessitates shaving
ography may be helpful to diagnose the presence the hair from the patients jugular groove in order to
properly visualize the vein. Inspection of the jugular
of pericardial effusion, echocardiography is the
vein should be done with the patient standing. The
most sensitive and specific procedure to confirm finding of jugular venous distension is a quick and
its presence. reliable way to help distinguish cardiac versus non-
The great majority of dogs with pericardial effu- cardiac causes of abdominal effusion that is often
sion have an associated cardiac tumor, of which overlooked.
hemangiosarcoma is the most common.
Chapter 11 Pericardial Disorders and Cardiac Tumors 213
Churg A, Colby TV, Cagle P, et al: The separation of
What are the advantages and disadvantages of surgi-
benign and malignant mesothelial proliferations, Am
cal versus thorascopic pericardectomy?
J Surg Path 24:1183, 2000.
Surgical pericardectomy using a median sternotomy
allows for complete resection of the ventral two thirds Closa JM, Font A, Mascort J: Pericardial mesothelioma
of the pericardial sac. The surgical approach allows in a dog: long-term survival after pericardiectomy in
for visual inspection of the heart base and right heart combination with chemotherapy, J Small Anim Pract
in an attempt to identify small tumors that may have 40:383, 1999.
been undetected during cardiac ultrasound. The dis- Cobb MA, Brownlie SE: Intrapericardial neoplasia in 14
advantages of the surgical approach include increased dogs, J Small Anim Pract 33:309, 1992.
invasiveness, morbidity, cost, and length of hospital Constantino-Casas P, Rodriguez-Martinez HA, Guter-
stay as opposed to thorascopy. Thorascopy is best rez Diaz-Ceballos ME: A case report and review: the
performed in larger dogs and enables the operator to gross, histological, and immunohistochemical char-
cut a window into the lateral or apical pericardial acteristics of a carcinoma of ectopic thyroid in a dog,
surface. A lesser amount of pericardium is removed Br Vet J 152:669, 1996.
during the thorascopic technique as opposed to the Day MJ, Martin MWS: Immunohistochemical character-
subtotal pericardectomy, but resealing of the peri- ization of the lesions of canine idiopathic pericarditis,
cardium after window procedures is rare. The main J Small Anim Pract 43:383, 2002.
disadvantage of the thorascopic procedure is the lim- Dunning D, Monnet E, Orton EC, et al: Analysis of
ited ability to inspect the heart base and right heart for prognostic indicators for dogs with pericardial ef-
small tumors that may have been undetected during fusion: 46 cases (1985-1996), J Am Vet Med Assoc
cardiac ultrasound. Biopsy of the pericardial tissue 212:1276, 1998.
can be accomplished using either technique.
Ehrhart N, Ehrhart EJ, Willis J, et al: Analysis of factors
affecting survival in dogs with aortic body tumors,
Vet Surg 31:44, 2002.
Fine DM, Tobias AH, Jacob KA: Use of pericardial fluid
s0240
Box 12-1 C
lassification of Congenital Defects According to Pathophysiology
Canine Feline
Defects primarily causing volume overload Defects primarily causing volume overload
Systemic to pulmonary (left-to-right) shunting
Common Common
Patent ductus arteriosus Ventricular septal defect
Ventricular septal defect Patent ductus arteriosus
Uncommon Atrial septal defect
Atrial septal defect Endocardial cushion defect
Endocardial cushion defect Uncommon
(Pseudo) truncus arteriosus Truncus arteriosus
Valvular regurgitation Valvular regurgitation
Common Common
Mitral dysplasia Mitral dysplasia
Tricuspid dysplasia Tricuspid dysplasia
Uncommon
Pulmonic insufficiency
Aortic insufficiency
Miscellaneous cardiac and vascular defects Miscellaneous cardiac and vascular defects
Common Common
Peritoneopericardial diapharagmatic hernia Peritoneopericardial diapharagmatic hernia
Persistent right aortic arch Endocardial fibroelastosis
Persistent left cranial vena cava Uncommon
Uncommon Persistent right aortic arch
Endocardial fibroelastosis
Pericardial defects
Anomalous pulmonary venous return
Double aortic arch
Retroesophageal left subclavian artery
Situs inversus
Chapter 12 Congenital Heart Disease 217
From Ettinger SE, Feldman EF: Texbook of veterinary internal medicine, ed 6, St Louis, 2005, WB Saunders.
*At times a diastolic murmur of aortic regurgitation may also be present.
Mitral stenosis and tricuspid stenosis are rare but may cause diastolic murmurs over the affected valve and ventricle.
PMI, Point of maximum intensity.
transcatheter occlusion of PDA using a Gianturco tion, the ductus is permanently closed by fibrous
coil or similar device. Surgical correction or pal- contracture, which produces the ligamentum ar-
liation is possible for certain defects. teriosum. Failure of the ductus to close is termed
Medical treatment is primarily for the control patent ductus arteriosus (PDA) or persistent duc-
or prevention of complications, such as conges- tus arteriosus.
tive heart failure, arrhythmias, and endocarditis,
rather than for correction of the defect. Medical
Pathophysiology
therapy is discussed briefly in this chapter.
The consequences of a PDA depend primarily
on the diameter of the ductus and the pulmonary
Innocent (Functional) vascular resistance.
Murmur When pulmonary vascular resistance is normal,
Not all young dogs and cats with heart murmurs blood continually shunts from the aorta (high
have congenital heart disease. Innocent, or func- resistance) into the pulmonary circulation (low
tional, murmurs are created by mild turbulence resistance). Shunting in this fashion (systemic
within the heart and great vessels and usually di- to pulmonary) is referred to as left-to-right and
minish in intensity or resolve by 4 to 5 months represents the most common pattern in PDA
of age. The following characteristics of innocent (Figure 12-1).
murmurs help differentiate them from pathologic When pulmonary vascular resistance increases
murmurs. and exceeds systemic vascular resistance, blood
Innocent murmurs are systolic in timing, usually will shunt from the pulmonary artery into the
occurring early in systole and of short duration aorta (so-called right-to-left or reversed PDA).
(ejection-type). They are soft (i.e., grade III/VI Failure of ductal closure is due to an abnormal
or less in intensity) and often have a low-pitched, amount of elastic fibers compared to contractile
vibrating, or musical quality. smooth muscle fibers (so-called extension of the
Innocent murmurs are usually loudest along the noncontractile wall structure of the aorta into the
left sternal border and are poorly transmitted. ductus arteriosus). Varying amounts of normal
Their intensity may vary with changes in posi- smooth muscle causes varying degrees of ductal
tion, with the phase of respiration, with exercise, closure; this creates a structure that ranges from
and from day to day. a funnel-shaped ductus that narrows on the pul-
The most important characteristic of the innocent monary artery side of the ductus (Figure 12-2)
murmur is that it is heard in the absence of any to a tubelike structure without narrowing.
other demonstrable evidence of cardiovascular Blood flow through the ductus is also dependent
disease (e.g., lack of clinical signs or radiographic upon ductal diameter. With a small ductus, the
abnormalities). volume of blood shunted is restricted and there
Loud systolic murmurs (grade IV/VI or greater), may be no hemodynamic effects. In cases with
precordial thrills, and diastolic murmurs are in- a large ductus and significant shunting, one of
dicative of cardiac disease and should prompt two major consequences usually occurs. In most
further diagnostics. cases, volume overloading of the left atrium and
left ventricle results in eventual left-sided fail-
ure. In the largest of shunts, the excessive pul-
Specific Defects monary blood flow induces dramatic increases
in pulmonary vascular resistance, pulmonary
Patent Ductus Arteriosus
hypertension and shunt reversal (Eisenmengers
In fetal circulation, the ductus arteriosus serves physiology).
to shunt maternally oxygenated blood into the
Diagnosis
aorta, thereby bypassing the nonfunctional lungs.
Shortly after birth, several factors contribute to Etiology and Breed Disposition
effect closure of the ductus. Pulmonary vascu- PDA occurs in both the dog and cat, with higher
lar resistance drops dramatically, vasodilatory frequency in the dog. There is also a higher fre-
prostaglandin levels decrease, and oxygen ten- quency in the female.
sion increases, resulting in a marked increase in Breeds predisposed or at increased risk include
pulmonary blood flow and vasoconstriction of Bichon Fris, Chihuahua, Cocker Spaniel, Collie,
the ductus. Following closure by vasoconstric- English Springer Spaniel, German Shepherd,
Chapter 12 Congenital Heart Disease 219
Dilation Aorta
pulmonary
flow Venous
LA return
PA
PDA
Dilation
RA LVDP
S1 S2 S1 LV
Patent ductus
arteriosus
L R shunt RV
Figure 12-1. Pathophysiology and genesis of clinical findings in PDA. (Modified from Fox PR, Sisson D, Moise N, eds: Textbook
of canine and feline cardiology: principles and clinical practice, ed 2, Philadelphia, 1999, WB Saunders.)
Physical Examination
Palpation
Water-hammer, or bounding, arterial pulses are
usually present in animals with left-to-right shunt-
ing PDA. This type of pulse represents a widened
pulse pressure secondary to the loss of diastolic
pressure through the ductus, and elevation of sys-
Figure 12-2. Postmortem specimen from a young German tolic blood pressure from the volume-overloaded
shepherd of the transverse and proximal descending aorta on left ventricle. Usually, the larger the ductus (and
top, the pulmonary artery branches ventrally, and a left-to- therefore the shunt), the more prominent the arte-
right shunting patent ductus arteriosus between them. The
aortic end of the PDA is wide open. The pulmonary artery
rial pulse.
end is partially constricted. This results in a funnel shape to In the majority of cases, a precordial thrill can
the PDA. (From Kittleson MD, Kienle RD, eds: Small animal be palpated over the cranial left-heart base and
cardiovascular medicine, St Louis, 1998, Mosby. Courtesy Dr. the left apical impulse is prominent. In cases
Mark Rishniw.)
with right-to-left shunting, there is no precor-
dial thrill, and the right apical impulse is more
Keeshond, Labrador Retriever, Maltese, New- prominent.
foundland, Poodle, Pomeranian, Shetland Sheep-
dog, and Yorkshire Terrier. General
The defect has been shown to be inherited in the Caudal cyanosis is an important physical find-
miniature poodle, transmitted as a polygenic trait. ing in animals with right-to-left shunting PDA.
Owing to the location of the ductus (distal to
History and Clinical Signs the arteries supplying the head and forelimbs),
Clinical signs are related to the degree of shunt- cyanosis is limited to the caudal half of the body.
ing and may range from none to severe conges- This differential cyanosis is best appreciated by
tive heart failure. examining caudal mucous membranes, although
Depending on the degree of heart failure, owners occasionally cyanosis of the skin caudal to the
may report signs such as cough, labored breath- costal arch can be seen.
ing, exercise intolerance, and collapse. Reports of Polycythemia (packed cell volume greater than
seizures and cyanosis are suggestive of a right- 60) is usually present in cases with right-to-left
to-left shunting PDA. shunts.
220 Section ii Cardiovascular Disease
Figure 12-3. Patent ductus arteriosus (lateral projection) in a 3-month-old poodle. There is generalized heart enlargement, en-
gorgement of the right cranial lobar artery (white arrows), and engorgement of the right cranial lobar vein (black arrows). Vascular
engorgement, perivascular congestion, and alveolar edema are seen in the caudal lung lobes.
Figure 12-4. Patent ductus arteriosus (dorsoventral projection) in a 3-month-old poodle. There is generalized heart enlarge-
ment, an aneurysm-like bulge of the descending aorta (open arrow), a bulge of the main pulmonary artery (curved arrow), and
enlargement of the left auricle (straight arrow). Alveolar infiltrate due to pulmonary edema is present in the caudal lung lobes.
222 Section ii Cardiovascular Disease
transcatheter occlusion. This procedure employs transvalvular blood velocity without other struc-
delivery of a Gianturco coil, resulting in emboli- tural abnormalities.
zation of the ductus.
Coils are composed of prothrombotic poly-Dacron
Pathophysiology
fibers. The size of the coil selected is based on the
approximate size of the ductus (as determined by Stenosis of the left ventricular outflow tract re-
angiography or echocardiography). The device(s) sults in pressure overload of the left ventricle
are delivered from a catheter passed up the fem- (Figure 12-6). The left ventricle responds to this
oral artery and into the ductus (Figure 12-5). chronic pressure overload by undergoing con-
Multiple coils may be needed for full occlusion centric hypertrophy. As blood is forced through
of the ductus. the stenotic area, its velocity increases, result-
Advantages ing in turbulence, a systolic ejection murmur,
Less invasive procedure with short hospitaliza- and a post-stenotic dilation of the aorta. The
tion period. velocity of blood through the lesion is directly
Little need for post-operative analgesia. proportional to the severity of stenosis. Left
Disadvantages ventricular hypertrophy increases the myocar-
Difficult to catheterize femoral artery of very dial oxygen demand.
small dogs due to size constraints. Myocardial hypertrophy, decreased capillary
Ineffective in patients with large, tubular PDA. density, and increased wall tension all contribute
Requires fluoroscopy. to produce myocardial hypoxia/ischemia. Focal
areas of myocardial infarction and fibrosis, par-
Medical management ticularly involving the papillary muscles and
In cases deemed unacceptable anesthetic-surgical subendocardium, have been commonly observed
candidates, medical management of congestive in patients with severe stenosis. These cases are
heart failure is indicated (see Chapter 15). prone to sudden death, presumably from fatal
There are no drugs currently effective for closing ventricular arrhythmias induced by hypoxia.
the patent ductus in dogs and cats. Infrequently, left-sided heart failure develops.
The presence of aortic/subaortic stenosis may
increase the risk of the development of infective
Aortic Stenosis endocarditis.
Anatomy Diagnosis
Aortic stenosis is a narrowing or reduction of Etiology and Breed Predisposition
the left ventricular outflow tract dimension at the A polygenic inheritance pattern has been iden-
subvalvular (fibrous ring or muscular), valvular, tified in the Newfoundland, which is most con-
or supravalvular level. sistent with an autosomal dominant mode of
The subvalvular form (subaortic stenosis) is the transmission with modifying genes.
most common form in the dog. With this defect, Other commonly affected breeds include Bouvier
a fibrous band or ring located just below the de Flanders, boxer, English bulldog, German
aortic semilunar valves impedes left ventricular Shepherd, German shorthair pointer, golden re-
emptying. triever, great Dane, rottweiler, and samoyed.
Fixed valvular and supravalvular stenosis have Bull terriers are predisposed to valvular aortic
been reported in the cat. stenosis characterized by thickened aortic valve
Some patients demonstrate a dynamic subaortic leaflets and a hypoplastic annulus.
stenosis associated with systolic anterior motion
of the anterior mitral valve leaflet. This condition History and Clinical Signs
has been described in patients with fixed aortic/ In mildly to moderately affected cases, there are
subaortic stenosis, hypertrophic cardiomyopa- often no clinical signs, and the suspicion of aortic
thy, mitral valve dysplasia, and other conditions stenosis occurs when a murmur is detected dur-
that cause hypertrophy of the interventricular ing routine examination.
septum. In severe cases, owners may report failure to
Some breeds (boxers, bull terriers, golden retriev- thrive, exercise intolerance, collapse, and labored
ers) have mildly decreased left ventricular outflow breathing. In some cases, the first clinical sign is
tract dimensions that result in mild elevations of sudden death.
224 Section ii Cardiovascular Disease
Figure 12-5. Serial angiocardiograms obtained during a PDA coil embolization procedure. Note the catheter access is via a femoral
artery (right femoral artery) and the placement of one coil completely occludes contrast (and blood) flow across the ductus arteriosus.
Chapter 12 Congenital Heart Disease 225
Aorta
PA
1 2
Dilation
LA LAP AS
LV
RA
LVP
RV 1 2 1
AS AR
Subaortic LVH
stenosis
Figure 12-6. Pathophysiology and genesis of clinical signs in congenital subaortic stenosis. (From Fox PR, Sisson
D, Moise NS, eds: Textbook of canine and feline cardiology: principles and clinical practice, ed 2, Philadelphia, 1999,
WB Saunders.)
Figure 12-7. Aortic stenosis (lateral projection). There is marked enlargement of the aortic arch cranial to the heart base (arrows).
Figure 12-8. Aortic stenosis (dorsoventral projection). The enlarged aortic arch extends to the heart base (arrows). The left
auricle (open arrow) extends beyond the cardiac border, and there is slight left ventricular enlargement.
or advanced cases, the papillary muscles and myo- provides reliable data regarding severity. The ve-
cardium become hyperechoic (bright) secondary to locity of blood (m/s) through the stenosis, mea-
calcium deposition, ischemia and/or fibrosis. sured by Doppler echocardiography, provides a
Doppler echocardiography allows measurement reliable and noninvasive measure of the pressure
of blood flow velocity through the defect and gradient across the stenosis. The pressure gradient
Chapter 12 Congenital Heart Disease 227
(in mm Hg) can be readily derived with the modi- Balloon Dilation
fied Bernoulli equation: As in PS, balloon valvuloplasty may be effective
in alleviating outflow obstruction. This technique
Pressure gradient = 4 (maximum velocity) 2 has much less morbidity than corrective surgery
because it requires insertion of an arterial cath-
Pressure gradients between 80 to 100 mm Hg eter rather than a thoracotomy.
represent moderate stenosis; pressure gradients Studies have documented significant reduc-
greater than 100 mm Hg are consistent with se- tions (50%) in pressure gradients immediately
vere stenosis. following balloon dilation. However, although
short-term (2 to 3 months) effects are favorable,
Cardiac Catheterization there does not appear to be a long-term survival
Cardiac catheterization may be used to confirm benefit.
the diagnosis, but this procedure is usually un-
necessary since the advent of echocardiography. Medical Management
Cardiac catheterization and angiography are oc- Beta blockers (propranolol, atenolol) are used to
casionally used when multiple cardiac defects are reduce myocardial oxygen demands. They appear
suspected. to be of some benefit in reducing the frequency of
Angiography will illustrate the stenosis and arrhythmias.
poststenotic dilation. Pressure measurements ob- Antibiotics should be administered when bactere-
tained during selective catheterization are used mia is suspected or likely (e.g., dental procedures)
to determine the gradient across the stenosis. to reduce the chance of endocarditis developing.
Unlike echocardiography, general anesthesia is Treatment with various cardiac drugs, diuretics,
required, which can significantly lower pressure low-salt diets, and rest is usually of some benefit
gradients. in those severe cases that have developed conges-
tive heart failure.
Natural History
Pulmonic Stenosis
The clinical manifestations of aortic/subaortic
stenosis are variable. Up to 25% of dogs with se- PS is the third most commonly reported con-
vere stenosis may die suddenly during the first 3 genital defect in the dog. Obstruction to the ejec-
years of life. In others, congestive heart failure tion of blood from the right ventricle may occur
may develop. A serious, but rare complication at the following levels. The latter two types are
is the development of infective endocarditis, re- uncommon.
sulting in metastatic infection and aortic insuf- Valvular (pulmonic valve dysplasia)
ficiency. Cardiac arrhythmias are common in Subvalvular
affected dogs. Other affected individuals may Supravalvular
228 Section ii Cardiovascular Disease
Aorta
S1 S2
Dilated PA
LA
a wave
RA
RAP
LV Pulmonic
o
2 TR stenosis
RVSP
S1 S2
Figure 12-9. Pathophysiology and genesis of clinical signs in pulmonic stenosis. (Modified from Fox PR, Sisson D, Moise NS,
eds: Textbook of canine and feline cardiology: principles and clinical practice, ed 2, Philadelphia, 1999, WB Saunders.)
Chapter 12 Congenital Heart Disease 229
It can be difficult to differentiate between the A post-stenotic dilation of the main pulmonary
murmurs of subaortic/aortic stenosis and PS. artery is usually evident.
Doppler echocardiography provides a sensitive
Diagnostic Testing
and noninvasive method to determine the sever-
Electrocardiogram ity of stenosis by estimating the pressure gradient
Signs of right ventricular hypertrophy are pres- across the obstruction in a similar manner as with
ent in almost all cases. There are deep S waves aortic stenosis: mild (less than 50 mm Hg), mod-
present in leads I, II, and III, and a right shift of erate (50 to 80 mm Hg), and severe (greater than
the mean electrical axis in the frontal plane (more 80 mm Hg).
than 120 degrees).
Ventricular arrhythmias may be present. Atrial Other Diagnostic Techniques
fibrillation may be present in severe cases. Cardiac catheterization may be used to confirm
the diagnosis of PS, but this procedure is usually
Thoracic Radiographs unnecessary since the advent of echocardiogra-
The primary radiographic features (Figures 12-10 phy. Cardiac catheterization and angiography are
and 12-11) include the following: occasionally used when multiple cardiac defects
Right ventricular enlargement and right atrial are suspected.
enlargement Cardiac catheterization and angiography are per-
Enlargement of the main pulmonary segment formed routinely prior to an interventional pro-
Decreased pulmonary vascularity; pulmonary ar- cedure such as balloon valvuloplasty. Selective
teries smaller than normal coronary angiography is required to rule out the
presence of an anomalous left main coronary ar-
Echocardiography tery in English bulldogs and Boxers if surgery or
Echocardiography has proven to be highly sensi- balloon valvuloplasty is considered.
tive in the diagnosis and determination of severity
of PS.
Differential Diagnosis
Characteristic findings include the following:
Right ventricular dilation and hypertrophy of the Atrial septal defect: The right ventricular volume
right ventricular wall and interventricular sep- overload associated with a left-to-right shunting
tum. Owing to increased pressures within the atrial septal defect may result in a systolic ejection
right ventricle, the septum is typically flattened murmur over the pulmonic valve. Such murmurs
(Figure 12-12). are usually softer than those associated with PS.
The right ventricular outflow tract is often di- Innocent or physiologic murmurs: These murmurs
lated, and in cases of valvular stenosis, the pul- are usually much softer than typical PS murmurs and
monic valve cusps are thickened and immobile. do not typically persist beyond 6 months of age.
Figure 12-10. Pulmonic stenosis (lateral projection) in a 2-month-old mixed-breed dog. There is increased sternal contact of
the right heart, due to right-heart enlargement, and normal to slightly diminished pulmonary vasculature.
230 Section ii Cardiovascular Disease
Figure 12-11. Pulmonic stenosis (dorsoventral projection) in a 2-month-old mixed-breed dog. There is marked right-heart
enlargement and prominence of the main pulmonary artery (arrows).
Figure 12-12. Right parasternal short-axis 2-dimensional echocardiogram obtained from a West Highland white terrier with
severe pulmonic stenosis. Note the severely thickened right ventricle. RV, right ventricle; LV, left ventricle.
Natural History
with moderate to severe PS may develop signs
Uncomplicated survival to adulthood may oc- of right-sided congestive heart failure, cardiac
cur in dogs with mild to moderate PS. In gen- arrhythmias, exertional syncope, and/or sudden
eral, the natural history correlates well with death. Concurrent tricuspid valve dysplasia in-
disease severity (pressure gradient) and the creases the risk of the development of conges-
degree of right ventricular hypertrophy. Dogs tive heart failure.
Chapter 12 Congenital Heart Disease 231
Pulmonary
flow
O2 sat.
Venous return
LA
L R shunt
S1 S2 RA
LVDP
Ventricular
RV septal defect
VSD
+/- RVH
S1 S2
Figure 12-13. Pathophysiology and genesis of clinical findings in VSD. (Modified from Fox PR, Sisson D, Moise NS, eds: Text-
book of canine and feline cardiology: principles and clinical practice, ed 2, Philadelphia, 1999, WB Saunders.)
Chapter 12 Congenital Heart Disease 233
Figure 12-14. Ventricular septal defect. A routine examination of a 3-month-old Doberman revealed a grade 2 systolic murmur
over the mitral and aortic valve areas. There were a weak pulse and a split R wave. A to C, The plain lateral radiograph shows
fluid in an interlobar fissure and increased pulmonary vascular markings. The right heart cannot be evaluated on the lateral view
because of the fluid. The lateral and dorsoventral views show left ventricular enlargement. A thymic sail is seen. Selective cath-
eterization of the left ventricle and angiocardiography show simultaneous filling of the left and right ventricles. The aorta and the
pulmonary arteries are also seen. Continued
234 Section ii Cardiovascular Disease
D E
F G
Figure 12-14, contd. D, A 4-month-old German shepherd puppy presented for vaccination. A murmur was auscultated, and a
pronounced precordial thrill was palpated. A 1-cm septal defect is seen high in the interventricular septum (arrow). Diagnosis: inter-
ventricular septal defect. ra, right atrium; rv, right ventricle; la, left atrium; lv, left ventricle. E, A Staffordshire bull terrier presented for
vaccination. A murmur was auscultated, and a palpable thrill was felt on the thoracic wall. A small interventricular septal defect (proved
at autopsy) is seen between the left and right ventricles. The edges of the septal defect are thickened and hyperechoic. The defect was
visible only when the image orientation was optimized for the left ventricular outflow tract. Diagnosis: interventricular septal defect.
(From Kealey JK, McAllister H: Diagnostic radiology and ultrasonography of the dog and cat, ed 3, Philadelphia, 2000, WB Saunders.)
Figure 12-15. Right parasternal long-axis-2 dimensional echocardiogram obtained from a 9-week-old golden retriever puppy
with a right sided systolic murmur. Note the aliased color flow pattern crossing the interventricular septum. This finding is consis-
tent with a left to right shunting ventricular septal defect. RV, right ventricle; LV, left ventricle; LA, left atrium.
locations and are often prohibitively expensive. The right ventricular hypertrophy is secondary to
Reduction of the shunt can be accomplished by the obstruction in right ventricular outflow. The
pulmonary artery banding, a technique result- PS may be valvular, infundibular, or both.
ing in elevation of the right ventricular systolic
pressure. As right ventricular pressure increases,
Pathophysiology
the shunt volume decreases, and the pulmonary
circulation is spared the deleterious effects of The hemodynamic consequences of tetralogy of
chronic volume overload. Fallot depend primarily on the severity of the PS
and the size of the VSD.
Medical Management The direction and magnitude of the shunt through
In patients where surgical correction or palliation the septal defect are dependent upon the degree
is not an option, medical management of con- of right ventricular obstruction. If the PS is mild,
gestive heart failure may be required. Treatment and right ventricular pressures are only modestly
should be tailored to the type and degree of fail- elevated, then blood will shunt primarily from
ure (see Chapter 15). Animals with VSD should left to right. Pathophysiologically, these cases
receive antibiotic prophylaxis prior to proce- are similar to VSD cases with pulmonary artery
dures likely to produce bacteremia (e.g., dental banding (i.e., the mild right ventricular obstruc-
cleaning). tion protects the pulmonary vasculature from ex-
cessive shunting).
Prognosis When PS is severe, the elevated right ventricu-
Prognosis is excellent for animals with small lar pressures will result in right-to-left shunting.
defects or for those with surgically corrected de- Consequences include reduced pulmonary blood
fects. Cases with moderate to large defects have a flow (resulting in fatigue and shortness of breath)
variable clinical course and prognosis, depending and generalized cyanosis (resulting in weakness).
on shunt volume. Owing to the shunting of venous blood into the
aorta and consequent hypoxemia, the kidneys are
stimulated to release erythropoietin. Chronic el-
Tetralogy of Fallot evations in erythropoietin result in polycythemia.
Tetralogy of Fallot is the most common cyanosis- The increased blood viscosity associated with
producing defect and results from a combination of polycythemia can have significant hemodynamic
PS, high VSD, right ventricular hypertrophy, and effects, resulting in sludging of blood and poor
varying degrees of dextroposition and overriding of capillary perfusion. Animals with severe polycy-
the aorta. themia may seizure.
236 Section ii Cardiovascular Disease
Echocardiography
Echocardiography will confirm the diagnosis,
Atrioventricular Valve
with malposition of the aortic root, right ventricu-
Dysplasia
lar hypertrophy, and VSD. Congenital malformation of the mitral and tri-
Routine contrast echocardiography will dem- cuspid valves has been reported in dogs and cats.
onstrate right-to-left shunting at the level of the Malformation of the valve may result in a range
VSD. Flow through the defect can also be deter- of hemodynamic consequences including valvu-
mined by Doppler echocardiography. lar regurgitation, mitral or tricuspid stenosis, and
dynamic left ventricular outflow obstruction. Con-
Cardiac Catheterization genital malformation of the mitral valve complex
Selective angiocardiography of the right ventricle (mitral valve dysplasia) is a common congenital
demonstrates simultaneous filling of the aorta and cardiac defect in the cat. In addition, several canine
pulmonary artery in cases with right-to-left shunts. breeds are predisposed including bull terriers, Ger-
Nonselective angiocardiography may support a man shepherds, and Great Danes. Tricuspid valve
diagnosis of tetralogy of Fallot, but this technique dysplasia has been shown to have a genetic basis in
is much less sensitive than echocardiography. Labrador retrievers.
Chapter 12 Congenital Heart Disease 237
Figure 12-16. Echocardiogram from a dog with tricuspid valve dysplasia. Note the severely thickened tricuspid valve leaflets
(arrow). RV, right ventricle; LA, left atrium; RA, right atrium.
238 Section ii Cardiovascular Disease
Suggested Readings
Bonagura JD, Lehmkuhl LB: Congenital heart disease.
In Fox PR, Sisson D, Moise NS, eds: Textbook of ca-
nine and feline cardiology, Philadelphia, 1999, WB
Saunders.
Chapter 13
Cardiovascular Effects
of Systemic Diseases
Francis W. K. Smith, Jr., Donald P. Schrope, and Carl D. Sammarco
Introduction
nonfunctional adenocarcinomas that dont
Many systemic diseases are capable of profoundly cause hyperthyroidism. Iatrogenic hyperthy-
affecting cardiovascular structure and function (Box roidism can result from over supplementation
13-1). The veterinarian may detect cardiovascular of thyroxin in hypothyroid dogs.
abnormalities as the predominant clinical sign or sys-
temic disease manifestations may overshadow cardiac
Cardiac Pathophysiology
abnormalities. Although cardiovascular manifestations
may sometimes be of no clinical significance, at other Direct Effects
times they may constitute the major medical concern. Positive inotropic effects (i.e., increased contractil-
Detection of cardiovascular involvement may be based ity) result from an increased sodium-potassium
on clinical signs, radiographic changes, electrocardio- exchanging adenosine triphosphatase (Na+, K+-
graphic (ECG) or echocardiographic abnormalities, or ATPase) activity, increased mitochondrial protein
laboratory findings. Emphasis in this chapter is given synthesis, and increased synthesis and enhanced
to diseases having the greatest cardiovascular effects contractile properties of myosin. Thyroid hormone
or incidence in practice. The focus of discussion is the favors the production of the alpha heavy chain myo-
cardiovascular effects and their treatment. sin isoenzyme, which has the fastest ATPase activity,
but is less efficient at converting ATP to mechanical
Box 13-1 C
lassification of Important perfusion and oxygen delivery requires greater
Systemic Disorders That Affect cardiac output. Peripheral vasodilation increases
the Heart tissue perfusion and decreases afterload. As blood
volume increases, increased venous return to the
heart and increased preload result. The combina-
Endocrine
tion of increased preload, increased contractil-
Thyroid gland
Hyperthyroidism ity, increased heart rate, and decreased afterload
Hypothyroidism results in increased cardiac output. Chronic vol-
Adrenal gland ume overload and high metabolic rate can result
Hyperadrenocorticism in heart failure even though the cardiac output
Hypoadrenocorticism is still greater than normal. This is referred to as
Pheochromocytoma high-output heart failure.
Pituitary
Hypertension is a frequent although usually not
Acromegaly (hypersomatotropism)
Pancreas severe sequela of hyperthyroidism in cats, with
Diabetes mellitus (hyperglycemia) one study showing an incidence of mild to mod-
erate hypertension in 73% of cases. This occurs
Metabolic
Hypercalcemia in spite of peripheral vasodilation, and probably
Hypocalcemia reflects the increased stroke volume and heart rate
Hyperkalemia which increases cardiac output in these animals.
Hypokalemia Blood pressure is a function of cardiac output and
Hypoglycemia systemic vascular resistance.
Uremia The combination of volume and pressure over-
Anemia
load alters myocardial protein synthesis and deg-
Neoplastic and infiltrative heart diseases radation, which results in myocardial hypertrophy
Physical and chemical agents and chamber dilation. These changes are most
Hyperpyrexia (heat stroke)
notable in the left heart. In rare cases, hyperthy-
Hypothermia
Carbon monoxide roid cats with congestive heart failure develop a
Toad poisoning cardiomyopathy of overload that resembles di-
Oleander toxicity lated cardiomyopathy.
Chocolate (theobromine) toxicity
Doxorubicin cardiotoxicity
Infectious/inflammatory myocardial diseases Key Point
Bacterial (Lyme disease)
The net effects of hyperthyroidism on the
Viral (parvovirus)
cardiovascular system are enhanced cardiac
Mycotic
contractility, tachycardia, cardiomegaly, left
Protozoal (trypanosomiasis)
ventricular hypertrophy, high cardiac output,
Miscellaneous systemic hypertension, and occasionally high-
Systemic lupus erythematosus (SLE) output heart failure.
Neurologic disease
Gastric dilatation-volvulus (GDV)
Pancreatitis Diagnosis
Traumatic myocarditis
History and Physical Examination
Historical findings and clinical signs include
weight loss, polyphagia, unkempt hair coat,
increased in hyperthyroid animals. However, this polydipsia, diarrhea, nervousness, hyperactivity,
does not always explain or result in an increased vomiting, tremor, polyuria, lethargy, aggression,
responsiveness to catecholamines. Postreceptor ef- decreased appetite, weakness, episodic panting,
fects of thyroid hormone are probably mediated by and bulky, foul-smelling stool.
changes in intracellular G protein populations that Cardiovascular abnormalities that may be present
result in an enhanced response to adrenergic ago- on physical examination include tachycardia, pre-
nists. Circulating catecholamine levels are normal. mature heart beats, gallop rhythm, apical systolic
Hyperthyroidism results in an increased meta- murmur, accentuated heart sounds, forceful pre-
bolic rate, and consequently an increased tissue cordial beat, strong femoral pulses, jugular venous
oxygen demand. The need for increased tissue distention, and dyspnea when stressed.
242 Section II Cardiovascular Disease
Noncardiac findings can include thinness, pal- day and may dip into the normal range in mildly
pable thyroid gland, hyperactivity, dehydration, hyperthyroid animals.
easily stressed, small kidneys, depression, weak-
ness, and ventral flexion of the neck. Specialized Diagnostic Tests
Additional diagnostic tests may occasionally be
Electrocardiography needed to confirm the diagnosis of hyperthy-
ECG findings in hyperthyroid cats are sinus tachy- roidism in cats with normal resting T4 values on
cardia (42%), right bundle branch block (7%), tall repeated assessment.
R waves in lead II (22%), left anterior fascicular Free T4 by Equilibrium Dialysis
block (4%), ventricular premature complexes Cats with mild hyperthyroidism and normal T4
(1%), atrial premature complexes (5%) atrial levels often have a high free T4 level, whereas
tachycardia or atrial fibrillation (2%). Ventricu- cats with nonthyroidal illness often have a normal
lar tachycardia, ventricular bigeminy, ventricular free T4 (specificity and sensitivity > 90%).
pre-excitation and atrioventricular (AV) block Not recommended as a screening test for hyper-
have also been described. thyroidism, as some cats with nonthyroidal ill-
Sinus tachycardia and increased R wave volt- ness will have a high free T4 level.
age resolve with treatment of hyperthyroidism. T3 Suppression Test
Atrial and ventricular premature contractions Administer triiodothyronine (T3) at 25 g PO
(APCs and VPCs) may decrease in frequency every 8 hours for seven doses for a cat. Collect
or become abolished. Conduction disturbances blood for a T4 determination prior to the first dose
may or may not resolve. If arrhythmias or R wave of T3 and 2 to 4 hours after the last dose.
amplitude changes persist after hyperthyroid- A normal cats T4 level will suppress to less than
ism is controlled, the patient should be evalu- 1.5 g/dL. Values between 1.5 to 2 g/dL are non-
ated for idiopathic cardiomyopathy or systemic diagnostic whereas values greater than 2 g/dL
hypertension. support diagnosis of hyperthyroidism. T3 values
can be measured concurrently to assess owner
Radiography compliance. T3 values should rise regardless of
Mild to severe cardiomegaly is seen in 50% of the cats thyroid status.
cases. Thyroid-Releasing Hormone
Evidence of congestive heart failure (pulmonary Response Test
edema or pleural effusion) is reported in fewer To perform the thyroid-releasing hormone (TRH)
than 5% of cases. response test, inject 0.1 mg/kg of TRH and ob-
tain blood samples before and 4 hours after TRH
Echocardiography injection.
Common findings in hyperthyroidism include In normal cats, the post-TRH T4 is at least 60%
left atrial enlargement, left ventricular wall and greater than baseline. A hyperthyroid cats T4 levels
septal hypertrophy, increased aortic amplitude, change less than 50% following TRH administration.
hyperkinetic left ventricular wall and septum, left Values between 50% and 60% are not diagnostic.
ventricular dilation (eccentric hypertrophy), and The TRH response test takes less time to perform
increased fractional shortening. than the T3 suppression test and does not depend
A dilated form of cardiomyopathy occasion- on the owners ability to medicate the cat. TRH
ally develops and is characterized by left atrial can cause vomiting, salivation, tachypnea, and
and ventricular dilation and low fractional defecation following the injection. TRH is sub-
shortening. stantially more expensive than T3.
Results not superior to repeated assessment of
Clinical Pathology total T4 coupled with free T4 by equilibrium
Elevated serum values for alkaline phosphatase, dialysis, if necessary.
aspartate aminotransaminase, and alanine amino- Thyroid Imaging
transaminase are common. Thyroid imaging with radioactive technetium
Mild azotemia is present in approximately 34% 99mwill identify the affected gland(s). This im-
of cases. aging study is recommended prior to surgery in
The thyroxine (T4) value is usually elevated and any hyperthyroid cat with nonpalpable thyroid
is the diagnostic screening test of choice; how- glands, because the thyroid glands can migrate
ever, thyroid hormone levels fluctuate during the into the chest, rendering them inoperable.
Chapter 13 Cardiovascular Effects of Systemic Diseases 243
assessing thyroid status in any animal with nor- Cortisol has a positive inotropic effect on the
mal renal function that develops digoxin toxic- heart.
ity on reasonable doses of digoxin. Ideally the Cortisol affects the distribution and elimination
digoxin level on a sample obtained 8 hours post- of body water.
dose should be between 0.5 to 1 ng/dL. Cortisol is important in helping the body deal
with stress. This is why so many addisonian cri-
ses follow stress, and why glucocorticoid supple-
Prognosis
mentation must be increased during periods of
There are few complications in the treatment of stress.
hypothyroidism.
Cardiovascular Effects of Aldosterone
Aldosterone acts on the distal renal convoluted
Hypoadrenocorticism tubule and collecting duct to enhance sodium
(Addisons Disease) retention and potassium elimination. Aldoste-
Hypoadrenocorticism is a potentially life-threat- rone deficiency results in hyponatremia and
ening endocrinopathy that is uncommon in dogs hyperkalemia.
and rare in cats. The disease is more common in Hyponatremia decreases plasma osmotic pres-
female dogs and usually occurs in young to mid- sure, causing fluid shifts out of the vascular com-
dle-aged animals. Approximately 76% of cases partment. This contributes to hypovolemia and
occur before 7 years of age, with an age range of hypotension.
5 weeks to 16 years. Hyperkalemia alters cardiac conduction, result-
Primary hypoadrenocorticism (Addisons dis- ing in numerous arrhythmias. The cardiac effects
ease) results from destruction of the zona glomer- of hyperkalemia are aggravated by low sodium,
ulosa and zona fasciculata of the adrenal gland. low calcium, and acidosis.
These areas of the adrenal gland produce aldo-
sterone and cortisol, respectively. Destruction
is generally immune mediated, but also can oc- Key Point
cur secondary to infection, neoplasia, infarction,
Net cardiovascular effects of hypoadrenocorti-
and drugs such as o,p-dichlorodiphenyldichlo- cism are hypovolemia, systemic hypotension,
roethane (o,p-DDD) (Lysodren, [mitotane]). altered cardiac conduction, and depressed
Secondary hypoadrenocorticism results from de- myocardial function. These changes can be
creased production or release of adrenocorticotropic fatal if not rapidly diagnosed and aggressively
hormone (ACTH) from the pituitary gland. Second- treated.
ary adrenal insufficiency may occur following acute
withdrawal of long-term, high-dose glucocorticoid
therapy that has suppressed the hypothalamic-pi-
Diagnosis
tuitary-adrenal axis. These patients have normal
mineralocorticoid activity, so electrolyte values are History and Physical Examination
normal. Cortisol values are depressed. A history of waxing and waning of clinical signs,
Adrenal destruction occurs gradually, so basal with more severe signs during periods of stress,
hormone levels remain normal. It is only when generally is present.
the animal is stressed and the adrenal reserve is Patients often present with history of anorexia,
inadequate that signs develop. Eventually, the vomiting, diarrhea, depression, weakness, and
destruction proceeds to the point that basal hor- cardiovascular collapse. Other signs include
mone levels are depressed and clinical signs are weight loss, polyuria, polydipsia, melena, and
present without stress. shivering.
Transient improvement after intravenous fluid
therapy or corticosteroid administration followed
Cardiac Pathophysiology
by subsequent relapse days or weeks later can
Cardiovascular Effects of Cortisol occur.
Cortisol is important in maintaining vascular Findings on physical examination include de-
integrity and responsiveness to catecholamines. pression, weakness, dehydration, hypothermia,
Cortisol deficiency predisposes animals to slow capillary refill time, shaking, bradycardia,
hypotension. and weak femoral pulses.
Chapter 13 Cardiovascular Effects of Systemic Diseases 247
A B
Figure 13-1. A, Hyperkalemia in a dog in cardiovascular collapse, consistent with an Addisonian crisis. P waves are absent (atrial
standstill), and T waves are tall and peaked. Serum potassium was 8.4 mEq/L. B, After institution of therapy, P waves are present,
and the T wave is of smaller amplitude. Serum potassium is now 4.8 mEq/L. (From Tilley LP: Essentials of canine and feline elec-
trocardiography: interpretation and treatment, ed 3, Malvern, Penn, 1992, Lea & Febiger.)
Electrocardiography Radiographs
ECG changes vary with the magnitude of the Approximately 80% of untreated dogs have one
hyperkalemia and are aggravated by hyponatre- or more radiographic abnormalities. Abnormali-
mia, hypocalcemia, and acidosis. The follow- ties in order of reported frequency include narrow
ing ECG findings are seen with experimentally caudal vena cava, microcardia, narrow cranial lo-
induced hyperkalemia (Figure 13-1): bar pulmonary artery and microhepatica. These
Peaking of the T wave with a narrow base is the changes are the result of hypovolemia and rapidly
earliest ECG abnormality and may be observed resolve with steroid and volume replacement.
when serum K+ exceeds 5.7 to 6.0 mEq/L.
P wave morphology is altered, its amplitude Clinical Pathology
reduced, intra-atrial conduction delayed, and A low-grade normocytic, normochromic nonre-
PR interval prolonged when serum K+ exceeds generative anemia is present in 25% of cases, but
7.0 mEq/L. may be masked by the effects of hemoconcentra-
P waves become unrecognizable (atrial standstill) tion. Eosinophilia and lymphocytosis may also
at plasma K+ levels greater than 8.5 mEq/L. be present.
The QRS widens uniformly at plasma K+ levels A serum chemistry profile frequently reveals
greater than 9 mEq/L. azotemia, hyponatremia, and hyperkalemia. A
Sinoatrial exit block or junctional rhythms with sodium: potassium ratio of less than 27 supports
and without escape complexes may be present. hypoadrenocorticism, but is not pathognomonic
Ventricular fibrillation and ventricular asystole may for the disease. Hypercalcemia and hypoglyce-
occur at plasma K+ levels greater than 10 mEq/L. mia are not uncommon.
In clinical cases, ECG changes do not correlate Mild-to-moderate metabolic acidosis is common
as closely with potassium concentrations as during a crisis.
they do in published experimental studies. It is unusual for a dog with untreated Addisons
The rhythm with atrial standstill secondary to disease to have a urine specific gravity greater
hyperkalemia is generally slow and may be reg- than 1.030, and it is often less than 1.020.
ular or irregular. It is a sinoventricular rhythm. In patients with secondary hypoadrenocorti-
The sinus node continues to fire, and impulses cism, sodium and potassium levels are normal.
are transmitted to the AV node and ventricles The other abnormalities described above may be
by internodal pathways. P waves are absent be- present.
cause atrial myocytes are not activated.
Specialized Diagnostic Tests
Key Point
A tentative diagnosis is frequently obtained from
Hyperkalemia is the most common cause of the history and results of the complete blood
atrial standstill. Atrial standstill also occurs count and serum chemistry profile. However,
with fibrous replacement of atrial muscle cells
there are numerous causes of hyperkalemia, and
secondary to severe atrial distention (valve
acid-base and electrolyte changes associated
disease, cardiomyopathy) in dogs and cats,
with cardiac arrest, and secondary to an atrial with severe gastrointestinal disease and renal
myopathy in dogs, a condition most com- failure can cause an abnormal sodium: potassium
monly seen in English springer spaniels. ratio that would erroneously suggest Addisons
disease.
248 Section II Cardiovascular Disease
An ACTH response test is helpful in confirming ml/kg slowly IV over 10 to 15 minutes. Monitor
Addisons disease and essential for document- the ECG while administering calcium. Calcium
ing secondary hypoadrenocorticism. will temporarily correct rhythm disturbances by
countering the effect of potassium on the conduc-
tion tissue. Calcium has no effect on serum po-
Therapy
tassium levels. Calcium overdose can also cause
Addisonian Crisis Therapy severe cardiac disturbances, so careful monitor-
Patients that present with cardiovascular collapse ing is required.
and atrial standstill require aggressive therapy.
Therapy is directed at rapidly correcting hypovo- Maintenance Therapy
lemia, correcting rhythm disturbances, correcting Mineralocorticoid replacement is initiated with
electrolyte imbalances, and replacing mineralo- either fludrocorticosterone acetate at 0.02 mg/
corticoids and glucocorticoids. kg/day given orally or DOCP at 2.2 mg/kg every
Volume replacement and correction of hyponatre- 25 days given IM. These dosesand dose inter-
mia and hypochloremia is initially achieved with val for DOCPare adjusted as needed to main-
rapid infusion of 0.9% saline at 60 to 80 ml/kg/ tain normal electrolyte balance. Therapy must be
hr for 1 to 2 hours and then modified according to individualized to the patient. A large trial with
patient needs. The ACTH response test can be per- DOCP showed a dose and interval range of 1.5 to
formed while saline is being administered. 2.2 mg/kg every 25 to 30 days.
Glucocorticoid deficiency is corrected with ei- Glucocorticoid replacement is achieved with ei-
ther methylprednisolone sodium succinate ther prednisone at 0.2 mg/kg PO every 24 hours
(1 to 2mg/kg IV) or dexamethasone sodium or cortisone at 1.0 mg/kg PO every 24 hours.
phosphate (0.5 to 2 mg/kg IV) and then repeated Some patients receiving fludrocorticosterone ac-
every 2 to 6 hours. After the initial high dose of etate or DOCP do not need glucocorticoid sup-
a rapidly acting water-soluble glucocorticoid has plementation except during periods of stress.
been administered, glucocorticoid therapy can be
continued with dexamethasone at a dosage of Prognosis
0.05 to 0.1 mg/kg PO every 12 hours added to Excellent prognosis with therapy
the IV fluids. Once the patient is stable, switch to Many dogs appear to do better with a small daily
oral prednisone. It should be noted that predniso- maintenance dose of prednisone or cortisone.
lone interferes with cortisol assays, so ideally it During illness or other stressful periods, however,
should be started after the ACTH response test larger doses of glucocorticoids are necessary to
is performed. Dexamethasone has no mineralo- avoid relapse into acute adrenal crisis.
corticoid effects and does not interfere with the
cortisol assay.
Hyperadrenocorticism
Mineralocorticoid deficiency is initially corrected
(Cushings Disease)
(after the ACTH response test is performed) with
desoxycorticosterone pivalate (DOCP) at 2.2 Hyperadrenocorticism is a common endocri-
mg/kg IM or fludrocortisone acetate (Florinef) nopathy in older dogs and is rarely reported in
at 0.02 mg/kg/day PO if the dog is not vomiting cats. The syndrome is associated with exces-
Hyperkalemia is corrected in several different sive levels of cortisol that result from excess
ways. pituitary ACTH or excess ACTH from ectopic
Saline infusion results in rapid dilution of potas- nonendocrine tumors, functional adrenocortical
sium and is often the only treatment needed. adenoma, or carcinoma. Iatrogenic Cushings
Severe hyperkalemia associated with significant syndrome occurs with excessive glucocorticoid
cardiac conduction abnormalities often requires administration.
more aggressive therapy. Treatment options include Pituitary-dependent hyperadrenocorticism ac-
sodium bicarbonate (1 to 2 mEq/kg) given slowly counts for 80% to 85% of cases of hyperadre-
IV over 5 minutes or a combination of regular in- nocorticism. It is a disease of middle-aged and
sulin (0.5 U/kg IV) and 50% dextrose (1 g/kg IV). older dogs (usually older than 6 years), although
Dextrose can also be administered alone, as it will a few cases have been diagnosed under 1 year
stimulate endogenous insulin secretion. of age. There is no sex predilection. Poodles,
If life-threatening cardiac arrhythmias are noted, dachshunds, and beagles may be at increased
administer calcium gluconate (10%) at 0.5 to 1 risk.
Chapter 13 Cardiovascular Effects of Systemic Diseases 249
Dogs with functional adrenocortical tumors The triad of mitral/tricuspid insufficiency, respi-
tend to be older, ranging from 6 to 16 years of ratory disease, and Cushings syndrome may cre-
age with a mean age of 11 years. Females are af- ate intractable dyspnea due to cardiopulmonary
fected more frequently. German shepherds, toy failure.
poodles, dachshunds, and terriers are most com-
monly affected.
Diagnosis
Hyperadrenocorticism rarely produces signifi-
cant cardiac disease; however, signs and side History and Physical Examination
effects of hyperadrenocorticism can mimic car- The major historical features are systemic mani-
diac disease. Systemic effects of hyperadreno- festations of hypercortisolism; they include poly-
corticism can also exacerbate underlying cardiac dipsia, polyuria, polyphagia, panting, alopecia,
disease. anestrus, exercise intolerance, and lethargy.
Findings on physical examination may include
abdominal enlargement, hepatomegaly, muscle
Pathophysiology
weakness, testicular atrophy, symmetric alopecia,
Systemic Hypertension skin atrophy, hyperpigmentation, calcinosis cutis,
Hypercortisolism increases vascular resistance bruising, and obesity.
by increasing smooth muscle sensitivity to cat- ECGs show no characteristic changes. ECG
echolamines and increasing production of an- evidence of left ventricular enlargement is often
giotensinogen. Mineralocorticoid properties of present in cushingoid dogs with mitral valvular
cortisol enhance the renal resorption of sodium insufficiency.
and secondary fluid retention, resulting in an in-
creased vascular volume. Hypertension is present Radiography
in 57% to 82% of cushingoid dogs. Hypercortisolism causes changes on thoracic ra-
Systemic hypertension may cause myocardial diographs that include calcification of the tracheal
hypertrophy. and bronchial rings and osteoporosis of the tho-
Many affected dogs have coexisting AV valvular racic vertebrae. Metastatic pulmonary lesions are
insufficiency and its associated cardiac changes. seen infrequently with adrenal tumors.
Hypertension might exacerbate underlying car- Radiographic changes associated with pulmonary
diac problems. thromboembolism include hypoperfusion of the
infarcted lung lobes, overcirculation within the
Pulmonary Thromboembolism normal lung lobes, pleural effusion, and blunting
Patients with hyperadrenocorticism are predis- and thickening of the pulmonary arteries. Tho-
posed to pulmonary thromboembolism, with racic radiographs may be normal.
most cases diagnosed while the animal is being Echocardiography is rarely part of the workup of
treated for Cushings disease. Factors causing Cushings disease.
thromboembolism with Cushings disease in-
clude obesity, high hematocrit, hypertension, and Clinical Pathology
increased levels of clotting factors. The excessive production of cortisol may result
Pulmonary thromboembolism should be sus- in neutrophilia, lymphopenia, eosinopenia, and
pected in any cushingoid patient with a history of erythrocytosis (females).
acute onset of dyspnea or cyanosis. Chemistry abnormalities include fasting hy-
perglycemia, high serum alkaline phosphatase
Panting and Dyspnea (sometimes extremely elevated), high alanine
Altered ventilation mechanics are often present aminotransferase, high cholesterol, lipemia, and
owing to weakness in the muscles of respiration, low blood urea nitrogen.
increased thoracic fat deposition (decreasing Urinalysis shows specific gravity less than 1.015
chest wall compliance), and increased diaphrag- and often less than 1.008. Proteinuria, glycosuria,
matic abdominal pressure resulting from adi- and bacterial cystitis are sometimes noted.
pose tissue and hepatomegaly. Mild respiratory
distress or rapid respiratory rate at rest often Specialized Diagnostic Tests
results. A urine cortisol:creatinine ratio is a quick screen-
Many cushingoid dogs have variable degrees of ing test for Cushings disease. This test has a
lower airway disease or parenchymal disease. high sensitivity, but low specificity for Cushings
250 Section II Cardiovascular Disease
d isease. The ACTH response test and low-dose Management of pulmonary embolism and sys-
dexamethasone suppression tests are the standard temic hypertension, if present, is undertaken
tests used to confirm the diagnosis. through standard therapeutic protocols (see Chap-
A high-dose dexamethasone suppression test or ters 9 and 15).
serum ACTH level is used to try to differentiate
between adrenal tumors and pituitary-dependent
Prognosis
Cushings disease.
Ultrasound or computed tomography scan can Excellent prognosis is confirmed with resectable,
be used to try to differentiate pituitary-dependent benign adrenal tumors.
Cushings disease from adrenal tumors in patients Nonresectable or metastatic adrenal adenocarci-
that do not suppress with the high-dose dexa- nomas have a poor prognosis.
methasone suppression test. Chemotherapy with o,p-DDD (Lysodren) or
ketoconazole for pituitary-dependent hyperadre-
nocorticism has potential side effects, but most
Therapy
treated dogs respond well to therapy. Average
Pituitary-Dependent Hyperadrenocorticism survival in one study was 2 years, with a range
Chemotherapy using mitotane (Lysodren) is the of 18 days to 7 years. Clinical experience with
standard treatment. Lysodren selectively, and trilostane is not as extensive as with o,p-DDD,
usually reversibly, destroys the zona fasciculata but side effects with trilostane are negligible and
(cortisol) and zona reticularis (sex hormones) of therapy appears to be efficacious in most dogs.
the adrenal gland. The zona glomerulosa (aldo- Systemic hypertension generally resolves with
sterone) is occasionally affected. control of hypercortisolism.
Ketoconazole (Nizoral) can be substituted in ani-
mals that do not tolerate Lysodren. Ketoconazole
Hypersomatotropism
blocks an enzymatic step that is necessary for the
(Acromegaly) In Cats
production of cortisol.
Trilostane (Vetoryl) inhibits adrenal steroido- Acromegaly is a syndrome associated with high
genesis through enzyme inhibition and can also levels of growth hormone (hypersomatotropism).
be substituted for Lysodren. This drug is not cur- In cats, acromegaly occurs secondary to a pitu-
rently approved by the FDA but is licensed for itary tumor. It is a rare endocrinopathy that is
use in dogs in Europe. seen in middle-aged to old cats (mean age: 10
Hypophysectomy and bilateral adrenalectomy years; median age: 9 years; range: 4 to 17 years).
with replacement hormone therapy are rarely It is most common in males and rarely seen in
used alternatives to medical management. females.
In dogs, hypersomatotropism is associated with
Adrenocortical Tumor progestogen treatment or endogenous progesto-
Surgical removal of the affected adrenal gland(s) gens that are produced during diestrus. It does ot
is recommended if possible. cause clinically significant cardiac problemsin
dogs. The syndrome is seen in females and is
Key Point reversible with discontinuation of progestogen
There is a high morbidity associated with sur- therapy or resolves spontaneously with the end of
gery. Ideally, the patient is stabilized first by diestrus.
decreasing cortisol synthesis with ketocon-
azole.
Cardiovascular Pathophysiology
The trophic effect of growth hormone results
If the tumor is inoperable or metastasis is identi- in generalized organomegaly, including the
fied, manage the patient with either mitotane or heart. Cardiac changes are those of myocardial
ketoconazole. Very high doses of mitotane are hypertrophy, interstitial fibrosis, myocytolysis
usually required in patients with adrenal tumors. and intramural arteriosclerosis. Heart failure is a
Many dogs with adrenal tumors respond poorly common sequela of acromegaly in cats.
to medical management. Systemic hypertension is seen frequently in hu-
Replacement steroid therapy is necessary both mans with acromegaly. Systemic hypertension
during and after surgery. is sometimes present in cats with acromegaly
Chapter 13 Cardiovascular Effects of Systemic Diseases 251
and is usually accompanied by evidence of renal Supportive medical care includes high doses of
insufficiency. insulin for insulin-resistant diabetes mellitus and
diuretics for congestive heart failure.
Diagnosis
Prognosis
History and Physical Examination
Most cats present with a history of polyuria, poly- Survival in cats with acromegaly ranges from 4 to
dipsia, and weight gain. 60 months (generally 1.5 to 3 years) from time of
Cardiac abnormalities noted on physical exami- diagnosis.
nation may include a systolic murmur, gallop Most cats die or are euthanized owing to severe
rhythm, and signs of congestive heart failure congestive heart failure, renal failure, or expand-
(dyspnea, cyanosis, muffled heart sounds, or ing pituitary tumor.
crackles). Note: Hypersomatotropism without acromegaly has
Other abnormalities include hepatomegaly, neph- been associated with hypertrophic cardiomyopathy
romegaly, large head, arthritis, prognathism, pot in some cats. A total of 31 cats with hypertrophic
belly, large tongue, and circling. cardiomyopathy were shown to have growth hor-
ECG abnormalities have not been observed in mone levels that were four times the control levels.
these patients. None of the cats that were examined postmortem
Radiographs of the thorax usually demonstrate had pituitary tumors, and none demonstrated hy-
cardiomegaly and, less commonly, pulmonary perinsulinism or diabetes mellitus.
edema or pleural effusion.
Echocardiograms generally reveal hypertrophy
Pheochromocytoma
of the intraventricular septum and left ventricular
free wall. These tumors of adrenal medullary origin are
uncommonly detected in dogs. They are typi-
Clinical Pathology cally seen in old dogs (mean age, 11 years, with
The hemogram is generally unremarkable, but range of 1 to 16 years) and extremely rare in
some cats have erythrocytosis. cats.
All cases are hyperglycemic and glucosuric. Most Pheochromocytomas are catecholamine-produc-
cats are also hyperproteinemic, azotemic, and ing tumors derived from chromaffin cells.
hyperphosphatemic. Hypercholesterolemia, high In addition to important effects on the cardiovas-
alanine aminotransferase, high serum alkaline phos- cular system, catecholamines have significant
phatase, and ketonuria are seen less frequently. metabolic effects, stimulating glycogenolysis and
gluconeogenesis.
Specialized Diagnostic Tests
A commercially available validated growth hor-
Cardiac Pathophysiology
mone assay is not currently available for cats.
Insulin-like growth factor I level was high in two The cardiovascular effects of pheochromocyto-
cats with acromegaly that were tested. This test is mas result from the alpha-1, beta-1, and beta-2
commercially available. effects of norepinephrine and epinephrine. Stim-
Computed tomography can be used to identify ulation of alpha and beta-adrenergic receptors
the pituitary tumor. generally causes opposite effects. The dominant
Evaluate blood pressure in any suspected or con- effect varies with relative receptor density and
firmed cases. activation thresholds. For example, in vascular
smooth muscle, alpha adrenergic effects predomi-
nate. Thus, hypertension results when both alpha-
Therapy
and beta-adrenergic receptors are stimulated.
Treatment options include hypophysectomy, ra- Beta-1 adrenergic effects include sinus tachycar-
diation therapy, and medical management with dia, increased cardiac conduction velocity, and
bromocriptine or octreotide (a somatostatin ana- increased contractility.
logue). Hypophysectomy has not been reported in Beta-2 adrenergic effects on the cardiovascular
cats. Radiation therapy is difficult to obtain and system include venous and arteriole vasodilation.
has only resulted in transient improvement to date. Alpha-1 adrenergic effects on the cardiovas-
Medical management is generally unsuccessful. cular system include venous and arteriole
252 Section II Cardiovascular Disease
Diagnosis Therapy
History and Physical Examination Alpha- and beta-adrenergic blocking drugs may
Historical observations include weakness, col- help control hypertension and arrhythmias, respec-
lapse, anorexia, vomiting, weight loss, panting, tively. Always start with an alpha-adrenergic blocker
dyspnea, lethargy, diarrhea, whining, pacing, such as phenoxybenzamine (0.2 to 1.5 mg/kg PO
polyuria, polydipsia, shivering, and epistaxis. every 12 hours). If a hypertensive crisis is identi-
Abnormalities noted on physical examination fied, administer phentolamine at 0.02 to 0.1 mg/kg
include lethargy, tachypnea and dyspnea, ar- IV, followed by an intravenous infusion. If tachyar-
rhythmias, systolic murmur, pulmonary crackles, rhythmias remain a problem, then add a beta blocker
tachycardia, weak pulses, pale mucous mem- such as propranolol. Using a beta blocker without
branes, and muscle wasting. alpha blockade can result in severe hypertension.
Other physical findings are emaciation, periph- Surgical tumor removal is the only definitive
eral edema, ascites, and abdominal mass. treatment. This should be attempted after medi-
Many signs and physical findings are reported to cal stabilization in patients without metastasis.
be episodic because of the episodic release of cat-
echolamines by the tumor.
Prognosis
Electrocardiography Dogs with inoperable lesions have a poor progno-
Nonspecific ST segment and T wave changes sis. Long-term alpha- and beta- adrenergic block-
may be noted. ers may be used in these instances.
Arrhythmias can occur, especially ventricular
premature complexes and paroxysmal ventricular
Diabetes Mellitus
tachycardia.
Diabetes mellitus causes devastating cardiovascu-
Radiography lar problems in humans. The cardiovascular sys-
Generalized cardiomegaly and pulmonary edema tems of dogs and cats are relatively immune to the
can develop, probably owing to sustained chronic effects of hyperglycemia. Recent studies reported
hypertension. hypertension (defined as a pressure higher than
Adrenal tumors can be identified in one third of 160 mm Hg systolic, 100 mm Hg diastolic, and
the cases. 120 mm Hg mean) in 46% of 50 dogs with diabe-
tes. Subclinical reduction of myocardial contractil-
Clinical Pathology ity has also been reported
No consistent abnormalities are present on the
hemogram or chemistry profile.
Cardiac Pathophysiology
Demonstration of elevated 24-hour urinary ex-
cretion of vanillylmandelic acid, total metaneph- Systemic hypertension in diabetic dogs is associ-
rines, fractionated catecholamines, and plasma ated with the duration of disease and an increased
catecholamines is diagnostic in humans. urine albumin to creatinine ratio. Severity of
mean and diastolic hypertension correlated with
Special Diagnostic Tests duration of disease. In humans, severity of hy-
Abdominal ultrasound may be helpful as a local- pertension correlates with degree of glycemic
izing procedure. The presence of an adrenal mass control. This association has not been reported in
on ultrasound with no evidence of Cushings dis- dogs. Hypertension is rarely reported in cats with
ease is highly suggestive. diabetes.
Chapter 13 Cardiovascular Effects of Systemic Diseases 253
Ruptured urinary tract and urethral obstruction ECG changes are manifested in delayed and
Translocation from intracellular to extracel- abnormal repolarization, increased automaticity,
lular space (metabolic acidosis, rapid release and increased duration of the action potential.
from tissue during severe injury such as aortic
thromboembolism)
Diagnosis
History and Physical Examination
Diagnosis, Therapy, and Prognosis
Muscle weakness may be mild or present as pro-
ECG changes caused by hyperkalemia are depen- found weakness and depression.
dent on magnitude and also rate of development Ventroflexion of the head is frequently seen in
of hyperkalemia (see p. 247). symptomatic cats.
Polyuria and polydipsia may occur.
Key Point
Electrocardiography
Majority of patients with clinically signifi-
cant hyperkalemia will have bradycardia but QT interval prolongation and U waves may occur.
uncommonly tachycardia can also develop ST segment may become depressed (Figure
(Figure 13-2). 13-3), with a gradual blending of T waves and
what appears to be a tall U wave.
Ventricular and supraventricular arrhythmias may
Identification and treatment of the underlying occur.
cause of hyperkalemia are essential. See Hypo- Clinical pathology may be reflective of the
adrenocorticism (Addisons Disease). underlying disease process contributing to hy-
pokalemia. Urine concentrating ability may be
impaired.
Disorders Associated
with Hypokalemia Therapy
When severe potassium loss has occurred, severe Treat the primary disease process.
muscle weakness or paralysis may develop. Parenteral replacement with potassium chloride
Clinical causes of hypokalemia include the is recommended when potassium loss is severe
following: and the animal is symptomatic for hypokalemia
Decreased intake (anorexia, especially when (Table 13-1).
combined with potassium-deficient fluid
Key Point
administration)
Excessive gastrointestinal loss When administering potassium chloride, do
Chronic vomiting not exceed 0.5 mEq/kg/hr.
Severe diarrhea
Overuse of enemas, laxatives, or exchange Parenteral administration may initially decrease
resins the serum K+ level. This effect is minimized by
Excessive urinary loss avoiding dextrose-containing fluids, adminis-
Renal (renal tubular acidosis, postobstructive tering K+ at correct rate and concentration, and
diuresis, chronic pyelonephritis) starting oral potassium gluconate supplementa-
Drugs (diuretics, amphotericin B) tion early.
Secondary hyperaldosteronism (liver failure, Return to alimentation and treatment of the pri-
congestive heart failure, nephrotic syndrome) mary disease responsible for hypokalemia will
Extracellular to intracellular transfer replace potassium deficits. Therefore, prolonged
Metabolic alkalosis oral maintenance therapy is rarely indicated
Insulin and glucose administration except when ongoing excessive loss of potassium
Hyperinsulinism (insulinoma) owing to diuretic administration or polyuric renal
Ketoacidotic diabetes mellitus disease is present.
Hypokalemia markedly increases the likeli-
hood of toxicity when digitalis is being admin-
Cardiac Pathophysiology
istered. Serum potassium should be promptly
Severe hypokalemia causes hyperpolarization of checked and corrected when digitalis toxicity
nerve and muscle fiber membranes. is suspected.
Chapter 13 Cardiovascular Effects of Systemic Diseases 255
Figure 13-2. A, Hyperkalemia in cat with urinary obstruction resulting in a wide-complex bradycardia. B, Same cat developed
wide complex tachycardia as treatment with insulin and dextrose was initiated. Normal sinus rhythm developed as treatment was
continued.
Figure 13-3. ST segment depression in a dog with hypokalemia (serum potassium 3.3 mEq/L) secondary to respiratory alkalosis.
(From Tilley LP: Essentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Malvern, Penn: 1992,
Lea & Febiger.)
256 Section II Cardiovascular Disease
Skeletal survey radiographs may exhibit isolated Preexisting dehydration should be corrected
bony lesions that could account for hypercalce- and hydration maintained.
mia. Osteopenia, metastatic calcification, or focal Administration of 0.9% saline should be
bony lesions may be present. used to enhance the renal excretion of
calcium.
Electrocardiography Furosemide (5 mg/kg IV bolus initially then 2 to
The characteristic ECG finding is a short QT in- 4 mg/kg PO every 8 to 12 hours thereafter) and/
terval. In extreme cases, the ST segment may fuse or sodium bicarbonate (1 mEq/kg IV every 10
with the upstroke of the T wave. to 15 minutes, up to 4 mEq/L maximum dose)
may also help in cases of moderate-to-severe
hypercalcemia.
Key Point Glucocorticosteroids may limit bone resorp-
ECG changes do not correlate closely with se- tion, decrease intestinal calcium absorp-
rum calcium concentration. tion, increase renal calcium excretion, and
be cytolytic in certain neoplasms. Admin-
istration may interfere with diagnosis of
With severe hypercalcemia, bradycardia may neoplasia.
occur. Definitive treatment is directed at the underlying
Hypercalcemia may predispose to arrhythmias of etiology.
digitalis intoxication.
ECG changes resolve after normalization of se-
Prognosis
rum calcium.
The prognosis depends on early detection, abil-
Clinical Pathology ity to establish a definitive diagnosis, and success
Hypercalcemia often causes diminished urinary of treatment. The prognosis of many causes of
concentrating ability. The urine is usually hypos- hypercalcemia is guarded to poor.
thenuric or isosthenuric.
Renal failure with azotemia may develop from
Disorders Associated with
progressive structural and functional alterations
Hypocalcemia
in the kidney.
Hypophosphatemia or hyperphosphatemia may Hypocalcemia, although infrequently encoun-
be recorded, depending on the presence or ab- tered, can cause profound clinical signs. It occurs
sence of renal failure and the underlying etiology when serum calcium concentration is less than 8
of hypercalcemia. mg/dL in the dog and less than 7 mg/dL in the cat
Serum alkaline phosphatase may be elevated if (ionized calcium less than 5 in dogs and less than
severe bone disease or concomitant hepatic dis- 4.5 in cats).
ease is present. The following conditions may be associated with
A hemogram may be normal, display hemo- hypocalcemia:
concentration or anemia, or occasionally show Renal failure
evidence of leukemia (when this disease is asso- Eclampsia (puerperal tetany)
ciated with the underlying etiology). Canine acute pancreatitis
Bone marrow evaluation may be unremarkable Hypoparathyroidism
or disclose evidence of lymphoma, leukemia, or Idiopathic
multiple myeloma. Postoperative (during bilateral thyroid surgery)
Ethylene glycol toxicity
Hyperphosphatemia
Therapy
Hypocalcemia due to hypoalbuminemia, where
Initial treatment is directed at reducing the sys- calcium values are not adjusted for serum pro-
temic effects of hypercalcemia. tein concentration
258 Section II Cardiovascular Disease
Figure 13-4. Prolonged QT interval in a dog with severe hypocalcemia (2.2 mg/dL) secondary to ethylene glycol toxicity.
(From Tilley LP: Essentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Malvern, Penn: 1992,
Lea & Febiger.)
In treatment of postoperative parathyroid insuf- Insulin overdose for the treatment of diabetes
ficiency, care must be taken to detect recovery mellitus.
of parathyroid function in order to avoid vitamin Nonpancreatic tumors
Dassociated hypercalcemia. Glycogen storage diseases
Neonatal/juvenile hypoglycemia
Septic shock
Prognosis
Addisons disease
For most causes of hypocalcemia that are carefully Hepatic disease
managed, the prognosis is good to excellent.
Cardiac Pathophysiology
Disorders Associated Irrespective of the etiology, hypoglycemia trig-
with Hypomagnesemia gers catecholamine release, which causes tachy-
and Hypermagnesemia cardia, increases in myocardial oxygen demand,
Abnormalities in magnesium levels rarely af- and, potentially, arrhythmias.
fect cardiac function directly, but they may po-
tentiate problems caused by other electrolyte
Diagnosis
derangements.
Causes of hypomagnesemia are very similar to History and Physical Examination
causes of hypokalemia. Clinical manifestations of hypoglycemia range
from lethargy to episodic weakness and seizures.
Cardiac Pathophysiology
Electrocardiography
Abnormalities of magnesium have minimal ECG findings can include:
effects on the ECG with normal calcium and ST depression
potassium levels. T wave flattening
Hypomagnesemia will exacerbate problems due QT prolongation
to hypocalcemia. Supraventricular and/or ventricular arrhythmias
Hypomagnesemia predisposes to digitalis- ECG changes usually resolve with correction
induced arrhythmias. of hypoglycemia
Hypomagnesemia prevents correction of
hypokalemia. Laboratory Findings
A low blood glucose level (less than 60 mg/dL)
is usually present. A fasting blood glucose level
Diagnosis
may be needed to confirm hypoglycemia.
Consider hypomagnesemia with conditions that Elevated insulin levels or amended insu-
lead to hypokalemia. lin: glucose ratio may be demonstrated with
Consider hypomagnesemia when there is diffi- insulinomas.
culty correcting hypokalemia.
Therapy
Therapy
Hypoglycemic crisis, regardless of cause, is man-
Treat the underlying disease process. aged by slow, intravenous administration of 50%
Parenteral replacement if there is evidence of car- dextrose to effect. A slow IV bolus of 0.5 to 1.0
diac complications or if there is difficulty correct- mg/kg could be considered.
ing hypokalemia. Magnesium sulfate at 0.75 to Treat underlying disease or improve diabetic
1.0 mEq/kg/day in 5% dextrose in water (D5W) regulation.
as a constant rate infusion could be considered.
Prognosis
Hypoglycemia Resolution of neurologic signs due to hypoglyce-
Hypoglycemia may be caused by: mia is usually abrupt and virtually complete.
Hyperinsulinism due to a functional islet cell Prolonged, untreated hypoglycemia may result
pancreatic carcinoma. in cerebrocortical hypoxic damage. Lack of
260 Section II Cardiovascular Disease
Electrocardiography
Cardiac Pathophysiology
Nonspecific ECG abnormalities may be attrib-
Hypertensive cardiovascular disease, electrolyte uted to hypertension, anemia, electrolyte abnor-
imbalance, fluid overload, and anemia can con- malities, and pericarditis.
tribute to the production of cardiac disturbances. Conduction defects or arrhythmias may occur.
Renal failure can cause elevations or reductions
of potassium and calcium; associated changes Echocardiography
may register on the ECG. Echocardiography may show changes consistent
Systemic hypertension is a common sequela of with hypertension and chronic anemia.
chronic renal failure in dogs and cats and is re-
ported in 50% to 93% of dogs and 65% of cats. Clinical Pathology
Pericardial effusion is reported as an uncommon Clinical pathology may reveal abnormalities in
sequela of uremia in cats and dogs. The effusion the hemogram, urinalysis, and biochemistry pro-
may occur secondary to uremic serositis. file consistent with uremia (increased blood urea
Pulmonary thromboembolism may occur as- nitrogen, creatinine, and phosphorus, nonregen-
sociated with protein-losing glomerulopathy. erative anemia, and isosthenuria).
(Figure 13-5)
Uremic pneumonitis can uncommonly cause
Therapy
noncardiogenic pulmonary edema.
Treatment is directed at managing uremia and
Key Point its underlying causes. Therapy generally in-
cludes parenteral fluids, protein and phosphorus
Uremic toxins have a cardiodepressant effect. restriction, phosphate binders, and sometimes
calcitriol and erythropoietin.
Management of severe azotemia in patients with
concurrent heart disease is extremely challenging
and often frustrating.
Azotemia identified while treating congestive heart
failure may be prerenal and/or renal in origin.
Rehydrate cautiously.
Consider low-sodium fluids (half-strength
Ao
saline)
PA
Consider reduced administration rates (start
at maintenance rate)
May take 48 hours to see improvement in
azotemia.
Monitor clinically and radiographically for de-
velopment of congestive heart failure.
Reduce doses or avoid cardiac drugs elimi-
nated by the kidneys. If using ACE inhibitors
Figure 13-5. Right parasternal short-axis view at the base
of the heart in a dog with protein-losing nephropathy. A well or digoxin, monitor kidney function and elec-
circumscribed thrombus can be seen at the bifurcation of the trolytes frequently. Monitor digoxin levels
pulmonary artery. Ao, Aorta; PA, pulmonary artery. periodically. Pimobendan, or hydralazine
Chapter 13 Cardiovascular Effects of Systemic Diseases 261
and nitroglycerin can be substituted for ACE anemia is usually well tolerated because of
inhibitors. compensatory mechanisms that include in-
Monitor and control hypertension, electrolyte, creased cardiac output, redistribution of
and acid-base disturbances. blood flow, and decreased oxygen affinity of
red blood cells.
Uncommonly the volume overload can result
Prognosis
in congestive heart failure. In many of these
Resolution of the uremic state may improve ECG cases, pre-existing subclinical heart disease
abnormalities but arrhythmias may persist. may be a factor.
The development of congestive heart failure in the Pulmonary thromboembolism may occur
face of severe azotemia carries a poor prognosis. with autoimmune hemolytic anemia.
Anemia Diagnosis
Anemia is a sign of a disease, not a disease History and Physical Examination
entity. Chronic anemia produces variable symptoms that
Evaluation should emphasize history (drug or may include fatigue and mild exertional dyspnea.
toxin exposure), clinical signs related to other In rare situations chronic anemia can lead to
disorders complicated by anemia (fever, leth- syncope.
argy, bleeding, weight loss), physical examina- Acute anemia may present with collapse, weak-
tion (petechiae, lymphadenopathy), and clinical ness, lethargy, stupor, and dyspnea.
pathology. Physical exam may reveal precordium that is hy-
Symptoms of reduced cardiac reserve associated perkinetic, bounding or pistol shot arterial pulses,
with anemia depend on the severity of anemia, pale or icteric mucous membrane color, and pro-
rate of anemia development, and on the presence longed capillary refill time.
and extent of underlying cardiac disease. A soft, systolic murmur at the left apex, generally
grade I to III/VI, is common with severe anemia.
Heart sounds may be accentuated.
Cardiac Pathophysiology
The combination of tissue hypoxia and reduced Radiology
blood viscosity leads to decreased systemic Thoracic radiographs may display cardiac en-
vascular resistance. The body responds to de- largement, but this will vary depending on the
creased systemic vascular resistance by increas- presence and extent of previously existing heart
ing sodium and water retention resulting in an disease.
increased stroke volume and cardiac output. Uncommonly cardiac changes can result in evi-
Tissue hypoxia may also result in sinus dence of pulmonary venous congestion, pulmo-
tachycardia. nary edema, and/or pleural effusion.
When anemia is associated with increased viscos-
ity (multiple myeloma or macroglobulinemia), Electrocardiography
cardiac output may fail to rise. Sinus tachycardia is often present. The heart
Physiologic consequences depend on the devel- rate varies with the rate of onset and degree of
opmental rate of anemia. anemia.
With acute blood loss (i.e., hemorrhage), hypo- Ventricular premature complexes may be seen.
volemic shock may predominate. Evidence of left ventricular enlargement (wide
Acute blood loss leads to volume depletion and QRS complex and/or tall R waves) may be
a resultant decrease in cardiac output. Addition- present.
ally, acute anemia can lead to myocardial hy-
poxia and resultant depressed cardiac function. Echocardiography
With chronic anemia blood volume is main- May show evidence of left ventricular, left atrial,
tained but cardiac output may rise as described right ventricular, and/or right atrial dilation.
previously. Hyperdynamic cardiac function (increased frac-
The augmented stroke volume associated tional shortening, decreased end-systolic left
with the increased cardiac output may result ventricular diameter) is usually seen in the pres-
in cardiac dilation and hypertrophy. Chronic ence of volume overload.
262 Section II Cardiovascular Disease
Heart Diseases
Hemangiosarcoma * Ao
Diagnosis
History and Physical Examination
Cardiac involvement may not always lead to
clinical signs. Signs depend on the site and extent
of metastasis. Resultant cardiac dysfunction may
cause signs of congestive heart failure, weakness,
and/or syncope.
Pericardial effusion and tamponade may lead to
similar clinical signs.
Possible physical findings include muffled heart
sounds on auscultation, jugular venous disten-
Figure 13-8. Transverse section through the heart of a dog
tion, ascites, weakness (often acute), hypokinetic
diagnosed with cardiac lymphoma. Multiple pale nodules pulses, tachypnea, weight loss, and pale mucous
can be seen in the left and right ventricular myocardium. Ao, membranes.
Aorta; LV, left ventricle; LA, left atrium.
Radiography
More common in dogs over 6 years old; no gen- Radiographic evidence of a cardiac mass is un-
der predilection; increased incidence in boxers commonly seen (Figure 13-11).
and Boston Terriers. Cardiac enlargement and rounding of the cardiac
Metastasis is uncommon, but can appear in lungs, silhouette may be observed if pericardial effusion
liver, lymph nodes, and bone. is present.
Dilation of the caudal vena cava may present sec-
ondary to cardiac tamponade or obstruction to
OTHER ETIOLOGIES blood flow within the lumen of the right heart.
Lymphoma is the most common tumor that me- In general, the diameter of the caudal vena cava
tastasizes to the heart in cats but also can be seen should be less than the length of the vertebra
in dogs. (Figures 13-8 and 13-9) above the carina.
Ectopic thyroid carcinomas occur at the heart base Pneumopericardiography or angiocardiogra-
and, rarely, in the right ventricular outflow tract. phy may assess the thickness and any irregu-
Cardiac myxomas are rare but are more com- larities of the pericardium, epicardium, and
mon in the right heart (right atrial lumen). (Fig- endocardium.
ure 13-10) The use of magnetic resonance imaging may
Rarely, cardiac fibroma, fibrosarcoma, and rhab- allow visualization of a cardiac mass.
domyosarcoma are diagnosed in young dogs.
Infiltrative myocardial disease (e.g., amyloido- Electrocardiography
sis, hypereosinophilic syndrome) involving non- Reduced QRS voltage on the ECG and electrical
neoplastic cells is rare in dogs and uncommon in alternans occur in many, but not all, cases with
cats. pericardial effusion.
Atrial or ventricular arrhythmias, conduction dis-
turbances, and complete heart block can occur.
Cardiac Pathophysiology
Tumors from other tissues gain access to the heart Echocardiography
by invasive growth from adjacent structures or Echocardiographic evidence of pericardial effu-
spread by hematogenous or lymphatic vessels. sion may be demonstrated. Diastolic right atrial
The relative infrequency of cardiac metastasis or right ventricular collapse signifies pericardial
has been attributed to metabolic peculiarities of tamponade. Dilation of the abdominal vena cava
striated muscle, rapid coronary blood flow, effer- and/or hepatic veins is also typically seen with
ent lymphatic drainage from the heart, and the tamponade.
vigorous kneading action of the myocardium. Two-dimensional echocardiography may facili-
Myocardial neoplasia may cause congestive heart tate identification of cardiac neoplasia. Unfortu-
failure owing to diastolic dysfunction, obstruc- nately due to the elusive nature of some cardiac
tion to ventricular inflow or outflow, pericardial masses, the lack of a mass on echocardiogram
tamponade, or arrhythmias. does not rule out neoplasia.
264 Section II Cardiovascular Disease
LV Ao
A LV B
LA
Figure 13-9. Right parasternal long-axis (A) and short-axis (B) views in a cat with cardiac lymphoma confirmed on histopathol-
ogy. Note the marked thickening of the left ventricular and left atrial myocardium. Ao, Aorta; LV, left ventricle; LA, left atrium.
Therapy
Pericardiocentesis may offer temporary relief
from cardiac tamponade.
If recurrent pericardiocentesis is necessary, then
partial pericardectomy via thoracotomy, or a
pericardial window via thoracoscopy could be
considered.
Surgery would likely improve the patients qual-
ity of life but may not prolong life.
Other than standard thoracotomy concerns and
risks, the main complication with surgery is on-
going hemorrhage from the tumor. This can result
in hemothorax.
Animals with myocardial infiltration of tumors
sensitive to chemotherapy or radiotherapy may
respond favorably, but this is uncommon.
Congestive heart failure and arrhythmias result-
Figure 13-10. Right parasternal long-axis view in a dog.
ing from cardiac neoplasia can be difficult to
A large, well-circumscribed mass effect (*) is seen filling the
majority of the right atrial lumen. The mass was confirmed as treat.
a myxoma on histopathology. Surgical resection or debulking of cardiac masses
is uncommonly possible.
Masses confined to the right atrial appendage can
Whenever safely possible, an echocardiogram periodically be removed with resection of the
should be performed while pericardial fluid is appendage.
present. The fluid can be helpful in identifying a Some intraluminal cardiac masses can be re-
mass. moved using cardiac bypass or inflow occlusion.
Pericardiocentesis may detect cytologic evidence Studies with long-term follow-up with such pa-
of neoplasia. The majority of the time, though, tients are not available.
fluid analysis will come back as nonspecific hem-
Prognosis
orrhagic effusion.
Uncommonly, biopsy of the tumor is possible Hemangiosarcoma
without thoracotomy using techniques such as Surgical resection may be possible, but distant
myocardial biopsy or thoracoscopy. microscopic metastasis is almost always present.
Chapter 13 Cardiovascular Effects of Systemic Diseases 265
Figure 13-11. Lateral (A) and ventrodorsal (B) radiographs in a Boxer with a large heart base mass. A bulge in the area of the
cranial waist of the cardiac silhouette can be seen on the lateral. A similar bulge can be seen on the ventrodorsal projection at the
2 oclock position on the cardiac silhouette.
Poor response to chemotherapy in general al- Radiation therapy may be beneficial in some cases,
though a combination of surgical resection and but general response to chemotherapy is poor.
chemotherapy may improve the prognosis to
some degree. Key Point
Pericardectomy may improve quality of life.
In general, long-term prognosis with cardiac
cancer is poor owing to difficulty in surgical
Chemodectoma resection, minimal response to chemotherapy
Debulking surgery is an option, but complete re- and radiation therapy, and detrimental side
section of the tumor is rarely possible. effects of chemotherapy and radiation thera-
Pericardectomy may improve quality of life. py on the heart.
266 Section II Cardiovascular Disease
Nonsteroidal anti-inflammatory drugs or anti- 82.4 to 89.6 F) and severe (lower than 28 C or
pyretics (e.g., aspirin, flunixin meglumine) are 82.4 F).
contraindicated. The use of glucocorticoids re- Signs include lethargy, ataxia, stupor, shivering
mains controversial, but they are often used when and bradycardia. Cardiopulmonary arrest may
cerebral edema is suspected. occur with severe hypothermia.
When malignant hyperthermia is anesthetic re-
lated, all inhalation agents and relaxants should Electrocardiography
be discontinued. Hyperventilation with 100% Mild hypothermia results in prolongation of the
oxygen should be started. PR interval, QRS duration, and QT interval; atrial
For malignant hyperthermia, dantrolene, 2 mg/kg premature complexes; and inverted T waves.
IV up to 10 mg/kg IV has been used in the dog. Moderate hypothermia produces atropine-resis-
No proven efficacy is known. Its use is based on tant bradycardia and ventricular arrhythmias.
experience from humans, horses, and pigs. Dan- Severe hypothermia may cause cardiac arrest sec-
trolene exhibits muscle relaxation activity by ondary to ventricular fibrillation or asystole.
direct action on muscle.
Administer mannitol (0.25 to 2 gm/kg of a 20%
Therapy
solution over 15 to 20 minutes) if cerebral edema
is suspected or if stupor or coma develops. Treatment initially involves warming the patient.
The patient should be monitored for several days Active external warming with warm-water blan-
for the development of complications, such as re- kets is recommended for mild to moderate hypo-
nal failure and DIC. thermia. External warming causes vasodilation of
skin vessels, which may initially transfer cooled
blood to the body core, further lowering internal
Prognosis
temperature. This is rarely a significant clinical
The prognosis for heat stroke is guarded to good complication with mild to moderate hypothermia.
if detected and treated early. Internal (core) warming is recommended if the
Malignant hyperthermia is rare, but seems to of- rectal temperature is less than 30 C (86 F)
fer a worse prognosis. or the cardiovascular status is unstable. This is
Coagulopathy and renal failure confer a worse accomplished by peritoneal dialysis with dialy-
prognosis. sate fluids warmed to 45 C (113 F).
Appropriate supportive care (e.g., intravenous
fluids, ventilation) must be administered. Se-
Hypothermia vere hypothermia can cause cardiopulmonary
Lowering of body temperature can occur acciden- collapse. Keep these patients well oxygenated,
tally, owing to deep cooling from external cold, drugs, and administer warmed intravenous fluids.
or interference with thermoregulatory centers during Cardiac output and ECG abnormalities improve
anesthesia. Physiologic consequences of hypother- after warming.
mia depend on the extent and duration of exposure. Evaluation of the patient for underlying systemic
disorders that could have predisposed it to hypo-
thermia should be made once normothermia has
Cardiac Pathophysiology
been achieved.
Cardiac dilation with epicardial and subendocardial
hemorrhage can result from severe hypothermia.
Carbon Monoxide TOXICITY
Microinfarcts can occur in myocardial tissue.
Lesions may result from circulatory collapse, he- Carbon monoxide is a colorless, odorless, taste-
moconcentration, sludging of blood in capillar- less, toxic gas that has the molecular formula CO.
ies, or decreased cellular metabolism. CO is produced by the incomplete combustion of
the fossil fuelsgas, oil, coal and wood used
in boilers, engines, oil burners, gas fires, water
Diagnosis
heaters, solid fuel appliances and open fires. CO
History and Physical Examination is a commercially important chemical. It is also
Signs vary with the degree of hypothermia (re- formed in many chemical reactions and in the
duction in core temperature), mild (32 to 35C thermal or incomplete decomposition of many
or 89.6 to 95 F), moderate (28 to 32 C or organic materials.
268 Section II Cardiovascular Disease
involved in the pathogenesis. The heart rate at the The mechanism for cardioprotection is not under-
time of drug administration may also determine stood. One suggested mechanism is dexrazoxane
the degree of cardiac toxicity, with slower heart prevents the formation of the free radicals and
rates associated with less toxicity. subsequent lipid peroxidation that occurs from
Histologic lesions consist of myocyte vacuoliza- free iron and iron associated with the doxorubi-
tion, myocytolysis, and, occasionally, interstitial cin-iron complex.
fibrosis. It is FDA approved for use in women with doxo-
rubicin administration against metastatic breast
cancer.
Diagnosis
It has been shown in studies to protect mice, rats,
History and Physical Examination hamsters, pigs and dogs.
Clinical signs and physical findings are associ- It appears to prevent cardiotoxicity, but does
ated with dilated cardiomyopathy and include not protect against other toxic effects by
exercise intolerance, dyspnea and coughing, hep- anthracyclines.
atomegaly, and ascites. Congestive heart failure Dexrazoxane ameliorates anthracycline extrava-
usually develops acutely. sation lesions.
The recommended dose ratio of dexrazoxane to
Electrocardiography doxorubicin is 10:1. It is given as an infusion
In dogs, ECG abnormalities include ST segment over 15 minutes, 30 minutes prior to using
and T wave changes, decreased QRS voltages, doxorubicin.
intraventricular conduction abnormalities, and Expense of the drug limits its routine use.
atrial and ventricular arrhythmias. ECG changes
are rare in cats treated with doxorubicin.
ECG changes can occur acutely during drug ad-
t Infectious/Inflammatory
ministration. In this situation, stopping the drip Diseases
and then reinstituting it at a slower rate may re-
solve the problem. The heart can be involved in an inflammatory pro-
cess owing to many infectious agents. Myocardial
Radiography cells, interstitium, or vessels may be affected.
With dilated cardiomyopathy, radiography may
show cardiomegaly, pulmonary edema, pleural
Cardiac Pathophysiology
effusion, hepatomegaly, and ascites.
Myocardial injury can occur from direct myo-
Echocardiography cardial invasion of an infectious agent, from a
The most consistent abnormalities with doxorubicin myocardial toxin produced by the agent, or from
cardiotoxicity are increased left ventricular end-sys- a secondary immune-mediated reaction.
tolic internal dimensions and decreased fractional Important causes of myocardial injury in small
shortening. As cardiac function deteriorates, pro- animals include the following:
gressive left atrial enlargement can be seen. Bacterial myocarditis
Pyogenic bacteria originate in septicemic
states or from other septic foci.
Therapy
Clinical signs range from subclinical and
If congestive heart failure develops, the patient nonspecific (weight loss, lethargy) to ap-
should be treated accordingly. Unfortunately, parent and specific (arrhythmias, conges-
the therapeutic response is poor. An ECG is rec- tive heart failure).
ommended prior to each doxorubicin treatment, Viral myocarditis has been associated with
especially in dogs. If arrhythmias develop, doxo- canine parvovirus and distemper virus in
rubicin treatment should be discontinued. An dogs, and with suspected but not yet identi-
echocardiogram is recommended after the third fied viral pathogens in cats. Clinical abnor-
cycle in dogs or fifth cycle in cats, and every malities include cardiomegaly, arrhythmias,
one to three cycles thereafter. Doxorubicin treat- and nonspecific ECG abnormalities. The
ment should be discontinued if contractility is severity of the cardiac changes ranges from
impaired. congestive heart failure with canine parvo-
Protection from cardiomyopathy has been dem- virus to subclinical myocarditis with canine
onstrated with dexrazoxane (Zinecard). distemper virus.
Chapter 13 Cardiovascular Effects of Systemic Diseases 271
Fungi and algae can infect the heart second- Specialized Diagnostic Tests
ary to a disseminated disease process, often Commercial test kits are available, but titers
in conjunction with reduced host defense. should be interpreted in view of the history, physi-
Protozoal myocarditis can occur in dogs cal examination, and clinical signs. False-positive
with canine trypanosomiasis (Trypanosoma and false-negative titers are not uncommon.
cruzi) or in dogs and cats with toxoplasmosis
(Toxoplasma gondii).
Therapy
Trypanosomiasis is discussed later.
Toxoplasmosis can produce signs domi- Antibiotics are the treatment of choice for bor-
nated by the extent and severity of multior- reliosis. Tetracycline, doxycycline, ampicillin,
gan system involvement. or amoxicillin appear to be the most effective
first-line agents.
Humans with cardiac involvement are often
Therapy
treated with IV ceftriaxone or cefotaxime.
Treatment is often supportive and usually focused A 5- to 7-day course of anti-inflammatory doses
on the most prominent systemic manifestation of of corticosteroids may be helpful for heart block
the disease process. that does not rapidly resolve with appropriate an-
tibiotic therapy.
Borreliosis (Lyme Disease)
Trypanosomiasis
Borreliosis is caused by the spirochete Borrelia
(Chagas Disease)
burgdorferi. Transmission is by ticks of the Ixodes
species. The incidence of cardiac involvement is Trypanosomiasis is a rare disease caused by the
unknown in animals. In humans, 10% of patients protozoan T. cruzi. It usually occurs in young
with borreliosis have cardiac involvement. Bor- dogs in the southeastern United States. Transmis-
reliosis in animals is usually acute and cured by sion is via the bite of a reduviid bug.
antibiotics. However, the prognosis may be poor
if second-stage disease involving the heart, kid-
Cardiac Pathophysiology
neys, or central nervous system (CNS) develops.
During the acute stage (2 to 4 weeks after infection),
cardiac damage occurs when trypomastigotes rup-
Cardiac Pathophysiology
ture from myocardial cells. This causes myocardial
Spirochetes have been isolated from myocardial failure, conduction disturbances, and arrhythmias.
biopsies in humans. If animals survive the acute stage, they may re-
DCM has been reported in a few humans with main asymptomatic for months. During this
Lyme disease. Cardiac damage may involve an time, myocardial degeneration occurs, and DCM
immune-mediated mechanism. develops. Myocardial damage during this stage
may be related to immune mechanisms or to the
release of toxic parasitic products.
Diagnosis
History and Physical Examination
Diagnosis
Ticks may be found on dogs, or owners may re-
port recent exposure to ticks in endemic areas. History and Physical Examination
Although nonspecific, clinical signs include an- Clinical signs during the acute stage are related
orexia, depression, and lameness. to left- and (mainly) right-heart failure. Collapse
Physical examination reveals fever, joint pain, and sudden death may be noted in a previously
and lymphadenopathy. healthy dog. Gastrointestinal signs of anorexia
and diarrhea are also common. The lymph nodes
Electrocardiography will be enlarged during the acute stage.
The most common ECG finding in humans is AV Clinical manifestations during the chronic
block. stage are associated with dilated cardiomyopa-
Ectopic beats and ST segment abnormalities have thy, with signs of right-sided heart failure often
also been reported in humans. predominating. Various cardiac arrhythmias
AV block secondary to B. burgdorferi in the dog also occur. The cardiomyopathy is not curable
has been reported in one case. and responds poorly to treatment.
272 Section II Cardiovascular Disease
Figure 13-12. Accelerated idioventricular rhythm. Beats 7 through 13 and the last four beats on the right are ventricular in
origin. These beats represent an accelerated ventricular rhythm. Beats 6 and 14 are fusion beats, a hybrid of the sinus beat and
the ventricular focus.
rhythm. As the underlying sinus rate slows, the Sudden death associated with cardiac complica-
ventricular rate may slow also (Figure 13-12) tions can occur.
ST segment and T wave changes may be evident.
Electrocardiography
Radiography Atrial and ventricular arrhythmias and ST seg-
The stomach is gas-filled, distended, and often ment changes have been reported.
rotated.
The cardiac silhouette may be small owing to de- Radiography
creased venous return. Abdominal radiographs may reveal an increased
density, calcification, or gas in the area of the
pancreas.
Treatment
Treatment should be directed toward gastric de- Clinical Pathology
compression and shock therapy. Leukocytosis, hyperglycemia, high liver en-
Any arrhythmias should be treated as needed. zymes, and high amylase and lipase in serum and
peritoneal fluid are common findings in animals
with pancreatitis.
Pancreatitis
Pancreatitis is a disease most frequently diag-
Therapy
nosed in middle-aged, obese dogs and cats. Al-
though many factors have been associated with It is important to decrease pancreatic secretions
pancreatitis, the etiology is often unknown. by withholding food and water.
Supportive care should include fluid and electro-
lyte replacement along with antibiotics.
Cardiac Pathophysiology
Cardiac arrhythmias should be treated as needed,
A myocardial depressant factor is released from although most arrhythmias will resolve spontane-
the pancreas, which can result in decreased myo- ously with resolution of the underlying disease.
cardial contractility and arrhythmias.
Activated pancreatic enzymes may also damage
Traumatic Myocarditis
the myocardium directly or play a role in throm-
bus formation, resulting in myocardial ischemia. The term traumatic myocarditis is a catchall phrase
Acid-base and electrolyte imbalances may also for arrhythmias that may occur following blunt
contribute to arrhythmias. trauma. The arrhythmias seen following blunt
trauma include supraventricular tachycardia, ven-
tricular arrhythmias, or bradyarrhythmias. The
Diagnosis
trauma does not have to occur directly to the chest.
History and Physical Examination
Clinical signs are nonspecific and include vomit-
Cardiac Pathophysiology
ing, diarrhea, anorexia, and depression.
Physical examination may reveal abdominal pain, Blunt trauma mechanisms include the following:
fever, dehydration, and shock. (1) unidirectional force, (2) bidirectional force
Chapter 13 Cardiovascular Effects of Systemic Diseases 275
(compressive), (3) indirect force, (4) decelerative total dose given over a 20-minute period should
force, and (5) concussive force. not exceed 20 mg/kg. The constant-rate infusion
The actual mechanism for the cause of the ar- for procainamide is 20 to 50 g/kg/min. Alterna-
rhythmias is not known. Direct damage to the tively, oral or intramuscular dosing could be initi-
heart from the trauma does not have to occur to ated following the IV dose if the dog is receiving
result in the arrhythmias. Autonomic imbalance nothing by mouth.
or reperfusion of ischemic tissue may have a Other therapies such as beta blockers or magne-
role. sium (IV) have been suggested.
Diagnosis Prognosis
Various arrhythmias, both atrial and ventricular, Fortunately, the arrhythmias are generally not
may be seen following trauma. The most com- lethal. They have a tendency to resolve over the
mon appears to be an AIR. The terminology for next 3 to 5 days, as the patient improves clini-
this arrhythmia is still in dispute. Other terms cally. Generally, progression of the underlying
for this ventricular rhythm are slow ventricular disorders, and not the arrhythmia, causes the
tachycardia, fast idioventricular rhythm, or idio- patients demise.
ventricular tachycardia. If the patient requires antiarrhythmic therapy,
The features of AIR are a wide, bizarre com- this is usually discontinued prior to discharge, or
plex rhythm, typically with a rate similar to the within several days of discharge.
underlying sinus rate. As the sinus rate slows,
the ventricular rate may capture the heart
rhythm. Commonly, fusion beats are seen as the
Frequently Asked Questions
rhythm waxes between the sinus and the ven-
tricular rhythm. As the underlying sinus rate How useful is the ECG in diagnosing electrolyte
slows, the ventricular rate may slow also (see disturbances and what changes would you expect to
Figure 13-12). see?
The ECG can be helpful in raising suspicion regard-
ing the presence of some electrolyte abnormalities,
Therapy most notably hyperkalemia, but it is not a very sensi-
tive test for detecting electrolyte abnormalities. One
The main goal of therapy is supportive care for of the reasons that the ECG is not very sensitive is that
the underlying disease: fluid therapy, control of the morphology of the ECG complexes is influenced
hemorrhage, oxygen therapy, analgesia, and cor- by several electrolytes (e.g., sodium, potassium, cal-
rection of electrolyte imbalance. cium) and further influenced by the patients acid
base status. As potassium levels rise above normal,
Therapy for the ventricular arrhythmias may be
T waves become peaked with a narrow base, P wave
necessary only if the tachycardia is persistent and amplitude decreases, and the P-R interval prolongs.
the clinician feels it has a role in the patients hy- If potassium is very high, QRS complexes widen and
potension. If therapy is felt to be necessary, then P waves disappear (atrial standstill) and with further
lidocaine by intravenous route is recommended elevation in potassium, conduction delays lead to ven-
at 2 to 4 mg/kg as a bolus. The maximum dose tricular fibrillation and ventricular asystole. Hypoka-
to be given over a 10-minute period is 10 mg/kg. lemia produces prolonged QT intervals, U waves, and
ST segment depression, with possible ventricular and
Lidocaine can cause nausea, vomiting, hypoten-
supraventricular arrhythmias. Hypocalcemia may
sion, and seizures. If this suppresses the arrhyth- cause QT interval prolongation, whereas hypercal-
mias, then a constant-rate infusion of lidocaine cemia may shorten the QT segment and with severe
can be given at 40 to 100 g/kg/min. A repeat 4- hypercalcemia, bradycardia may develop.
to 8-mg bolus of lidocaine may be needed once, A patient presents with a ventricular arrhythmia. What
after starting the lidocaine infusion, if more than systemic disturbances should be considered?
10 minutes elapses after injection of the original VPCs may be seen with a variety of noncardiac condi-
test bolus. It is not unusual for the constant-rate tions including pancreatitis, GDV, traumatic myocar-
infusion of lidocaine to lose its effect after several ditis, splenic disease and neoplasia, cardiac masses,
hours. hypokalemia, trypanosomiasis, shock, heat stroke and
pyrexia. Drugs and plant toxins such as doxorubicin,
If lidocaine is not effective, then procainamide
methylxanthines (chocolate, theophylline), digoxin,
may be tried. The intravenous dose of procain- sympathomimetics, oleander can all cause VPCs.
amide is 2 to 3 mg/kg over 2 to 3 minutes. The
Continued
276 Section II Cardiovascular Disease
Kienle RD, Bruyette D, Pron PO: Effects of thyroid hor-
A dog presents with echocardiographic evidence of
mone and thyroid dysfunction on the cardiovascular
myocardial failure based on depressed indices of sys-
tolic function (stroke volume, fractional shortening). system, Vet Clin North Am 24:495, 1994.
What needs to be considered in addition to idiopathic King JM, Roth L, Haschek WM: Myocardial necrosis
dilated cardiomyopathy? secondary to neural lesions in domestic animals, J Am
Systolic function can be depressed secondary to several Vet Med Assoc 180:144, 1982.
systemic diseases, nutritional deficiencies and toxic Kintzer PP, Peterson ME: Primary and secondary canine
insults. Systemic abnormalities associated with de- hypoadrenocorticism, Vet Clin North Am 27:349,
pressed myocardial function include hypothyroidism, 1997.
pancreatitis, sepsis and shock and trypanosomiasis. Loar AS, Susaneck SJ: Doxorubicin-induced cardiotox-
Taurine and l-carnitine deficiencies can lead to dilated icity in five dogs, Semin Vet Med Surg 1:68, 1986.
cardiomyopathy. Adriamycin toxicity leads to myocar- Melian C, Stefanacci J, Peterson ME, Kintzer PP:
dial failure. Note that in some animals, especially large Radiographic findings in dogs with naturally-occur-
breed dogs, fractional shortening may be slightly be- ring primary hypoadrenocorticism, J Am Anim Hosp
low normal values established for smaller breeds and Assoc 35(3):208-212, 1999.
represent a normal variant. Mount ME: Toxicology. In Ettinger SJ, ed: Textbook
A cat presents with left ventricular hypertrophy on the of veterinary internal medicine, ed 3, Philadelphia,
echocardiogram. What systemic disturbances need to 1989, WB Saunders.
be considered along with idiopathic hypertrophic car- Muir WM: Gastric dilatation-volvulus in the dog, with
diomyopathy? emphasis on cardiac arrhythmias, J Am Vet Med As-
Consider the possibility of systemic hypertension, acro- soc 180:739, 1982.
megaly, hyperthyroidism or infiltrative processes such as Nichols R: Complications and concurrent disease as-
lymphoma. Dehydration causes a reduction in the size sociated with canine hyperadrenocorticism, Vet Clin
of the left ventricular lumen and as a result can give the North Am 27:309, 1997.
impression of left ventricular hypertrophy. OKeefe DA, Sisson DD, Gelberg HB, et al: Systemic
toxicity associated with doxorubicin administration in
cats, J Vet Intern Med 7:309, 1993.
Palumbo ME, Perri SF: Toad poisoning. In Kirk RW, ed:
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Appel MJ: Lyme disease in dogs and cats, Compend Peterson ME, Taylor RS, Greco DS, et al: Acromegaly in
Cont Ed 12:617, 1990. 14 cats, J Vet Intern Med 4:192, 1990.
Atkins C: The role of non-cardiac disease in the develop- Rosenthal DS, Braunwald E: Hematologic-oncologic
ment and precipitation of heart failure, Vet Clin North disorders and heart disease. In Braunwald E, ed: Heart
Am Small Anim Pract 21:5, 1991. disease, ed 4, Philadelphia, 1992, WB Saunders.
Atkins CE: Cardiac manifestations of systemic and meta- Ruslander D: Heat stroke. In Kirk RW, ed: Current veter-
bolic disease. In Fox PR, Sisson D, Moise NS, eds: inary therapy XI, Philadelphia, 1992, WB Saunders.
Textbook of canine and feline cardiology, Philadelphia, Sennello KA, Schulman RL, Prosek R, Siegel AM:
1999, WB Saunders. Systolic blood pressure in cats with diabetes mellitus,
Barr SC: American trypanosomiasis in dogs, Compend J Am Vet Med Assoc 223(2):198-201, 2003.
Cont Ed 13:745, 1991. Sisson D, OGrady MR, Calvert CA: Myocardial diseases
Carson TL: Toxic gases. In Kirk RW, ed: Current veteri- of dogs. In Fox PR, Sisson D, Moise NS, eds: Text-
nary therapy IX, Philadelphia, 1986, WB Saunders. book of canine and feline cardiology, Philadelphia,
Chew DJ, Nagode LA, Carothers M: Disorders of calcium: 1999, WB Saunders.
hypercalcemia and hypocalcemia. In DiBartola SP, ed: Struble AL, Feldman EC, Nelson RW, Kass PH: System-
Fluid therapy in small animal practice, Philadelphia, ic hypertension and proteinuria in dogs with diabetes
1992, WB Saunders. mellitus, J Am Vet Med Assoc 213(6):822-825, 1998.
DiBartola SP, deMorais HSA: Disorders of potassium: Tilley LP, Bond BR, Patnaik AK, Liu S-K: Cardiovascu-
hypokalemia and hyperkalemia. In DiBartola SP ed: lar tumors in the cat, J Am Anim Hosp Assoc 17:1009,
Fluid therapy in small animal practice, Philadelphia, 1981.
1992, WB Saunders. Williams GH, Lilly LS, Seely EW: The heart in endocrine
Feldman EC, Nelson RW: Canine and feline endocrinology and nutritional disorders. In Braunwald E, ed: Heart
and reproduction, ed 3, St Louis, 2004, WB Saunders. disease, ed 5, Philadelphia, 1997, WB Saunders.
Fisch C: Electrolytes and the heart. In Hurst JW, ed: The Yates RW, Weller RE: Have you seen the cardiopulmo-
heart, ed 5, New York, 1982, McGraw-Hill. nary form of parvovirus infection? Vet Med April
Hooser SB, Beasley VR: Methylxanthine poisoning 1988, p 380.
(chocolate and caffeine toxicosis). In Kirk RW, ed:
Current veterinary therapy IX, Philadelphia, 1986,
WB Saunders.
Chapter 14
Systemic Hypertension
Rosemary A. Henik and Scott A. Brown
Introduction
Hypertension may exist transiently due to fear or This practice may occasionally identify a hy-
excitement, or be sustained and pathologic. Small pertensive cat with subclinical kidney disease;
animal patients most commonly have secondary however, it should be realized that the risk of a
hypertension, with an underlying disease triggering false positive result (i.e., high BP measurement)
increased blood pressure (BP). A diagnosis of sys- increases when the prevalence of a disease is low
temic hypertension is established when reliable BP (as in a healthy population).
measurements demonstrate a sustained elevation of BP measurement is advised in all cats with:
systolic (= 160 mm Hg) or diastolic (= 120 mm Hg) Kidney disease
BP. The prevalence of idiopathic, hypertension in Endocrinopathy
dogs and cats is unknown. Compatible ocular signs (e.g., hemorrhage, de-
tachment, retinal vessel tortuosity)
Neurologic signs (e.g., nystagmus, head tilt,
Population at Risk other cranial nerve signs, or seizures)
A cardiac murmur or gallop
Cats
Radiographic cardiomegaly
Chronic kidney disease, with or without protein- Echocardiographically determined cardiac wall
uria, and hyperthyroidism are the two most com- hypertrophy (although this is not a consistent
mon causes of hypertension in cats. Although change in hypertension)
effective resolution of hyperthyroidism may
reduce BP, some cats will become hypertensive
Dogs
only after therapy for this endocrinopathy.
Occasionally, diseases such as hyperaldosteron- Chronic glomerular disease or tubulointerstitial
ism, pheochromocytoma, or other endocrine dis- disease associated with proteinuria are most
eases may also be associated with hypertension. commonly associated with hypertension in dogs.
Many cats that are not hypertensive initially will Endocrine diseases including hyperadrenocor-
become hypertensive when fluid therapy, ste- ticism, diabetes mellitus, pheochromocytoma,
roids, erythropoietin, or vasoconstricting drugs and hyperaldosteronism may be associated with
are given. hypertension.
Some clinicians are incorporating the routine Metabolic abnormalities including obesity or
measurement of BP into geriatric wellness exams. hypercholesterolemia may result in hypertension.
277
278 Section II Cardiovascular Disease
Key Point
Chronic kidney disease and endocrinopathies
are most commonly associated with systemic
hypertension in cats and dogs.
Congestive heart failure secondary to systemic amplitude and frequency, and the auscultatory
hypertension is rare. technique is difficult in dogs and cats.
Doppler flow meters detect blood flow as a
change in the frequency of reflected sound (Dop-
Measurement of Blood pler shift) due to the motion of underlying red
Pressure blood cells. BP is read by the operator from an
aneroid manometer connected to the occluding
Patient Selection
cuff placed proximal to the Doppler transducer.
Currently there is no evidence to suggest that BP Devices utilizing the oscillometric technique
should be measured in all animals. detect pressure fluctuations produced in the oc-
BP should be measured in those animals that cluding cuff resulting from the pressure pulse.
present with clinical signs attributable to high Machines using the oscillometric technique gen-
systemic arterial BP, such as blindness, hyphema, erally determine systolic, diastolic, and mean ar-
seizures, ataxia, or sudden collapse (signs com- terial pressures as well as pulse rate.
patible with cerebral vascular hemorrhage, Another device for measuring BP indirectly is the
edema, or stroke). photoplethysmograph, which measures arterial
Animals with azotemic kidney disease, hyperad- volume by attenuation of infrared radiation, and
renocorticism, hyperthyroidism, pheochromocy- is designed for use on the human finger. It can be
toma, mineralocorticoid-secreting tumor, marked employed in cats and small dogs weighing less
obesity, or cardiac hypertrophy should also be than 10 kg.
evaluated for hypertension. We have evaluated the ultrasonic Doppler and
oscillometric methods in conscious dogs and
cats. In both species, the oscillometric devices
Methods
tend to underestimate BP by increasing amounts
BP may be measured by either direct or indirect as pressure increases. Another problem with
methods. Direct BP measurement is the gold the oscillometric devices is the excessive time
standard, but is technically difficult in unsedated required to obtain readings in cats. The major
dogs and cats, may be painful to the patient, and limitation of the Doppler technique is the im-
may be associated with hematoma formation and precise discrimination of the sounds designat-
other complications. ing the diastolic, and therefore mean, pressures.
The indirect techniques are more applicable to Owing to this fact, the Doppler method of BP
a clinical setting, as they require less restraint measurement may be unreliable for the routine
and are technically easier to perform. Indirect diagnosis and surveillance of patients with dia-
techniques of BP measurement include the aus- stolic hypertension.
cultatory, ultrasonic Doppler, oscillometric, and On the basis of our studies in conscious animals,
photoplethysmographic methods. devices using the Doppler principle are recom-
All of the indirect techniques employ an inflat- mended for use in cats; either the oscillometric
able cuff wrapped around an extremity. The or the Doppler devices are recommended in dogs.
pressure in the cuff is measured with a manom- For comparative purposes, the same device should
eter or pressure transducer. A squeeze bulb is be used each time in an individual animal.
used to inflate the cuff to a pressure in excess
of systolic BP, thereby occluding the underly-
ing artery. As the cuff is gradually deflated,
Key Point
changes in arterial flow are detected by one
of several means; the value for cuff pressure Doppler is the preferred method of measure-
at various levels of deflation is then correlated ment in unsedated cats; the oscillometric
with systolic, diastolic, or mean BP. This de- technique may be used in dogs.
tection method varies among different indirect
methods.
For the auscultatory method, a stethoscope is
Cuff Size and Placement
placed over the artery distal to the cuff, and the
listener hears a tapping sound when the inflation A complete range of pediatric cuff sizes should
pressure falls below systolic pressure. In animals, be available for an optimal patient limb circum-
the arterial (Korotkoff) sounds are low in both ference to cuff width ratio.
280 Section II Cardiovascular Disease
Figure 14-2. Demonstration of the technique to obtain Figure 14-3. Demonstration of cuff placement over the cra-
systemic blood pressure measurements using a Doppler trans- nial tibial artery in a dog. The oscillometric unit is most reliable
ducer in a cat. in medium- and large-breed dogs.
of indirectly measured BP, or with clinical If an agent or combination of agents is in-
abnormalities directly attributable to hyperten- completely effective, the dosage(s) may be
sive injury, should be considered candidates for increased, or additional agents may be added.
treatment. Often, especially in dogs, multiple agents are
The authors consider antihypertensive treatment used concurrently.
to be indicated in any dog or cat with a sustained It is usually not possible to restore BP to normal
systolic BP > 200 mm Hg or a diastolic BP > 120 values when treating a hypertensive animal. It
mm Hg, regardless of other clinical findings. should be the veterinarians goal to lower the BP
In both species, an animal with a systolic/diastolic to < 160/100 mm Hg, with emphasis given to the
BP that consistently exceeds 160/100 mm Hg systolic value.
should be considered for treatment if clinical
evaluation has identified abnormalities (e.g.,
Duration of Treatment
retinal lesions or chronic kidney disease) that
could be caused or exacerbated by systemic The diagnosis of hypertension associated with
hypertension. chronic kidney disease necessitates lifelong an-
In animals in which the BP is moderately elevated tihypertensive treatment, with periodic dosage
(systolic/diastolic BP that consistently exceeds adjustments based upon BP measurements.
160/100 mm Hg), but no clinical abnormalities Hypertension associated with hyperthyroidism or
related to systemic hypertension are identified, hyperadrenocorticism can be expected to resolve
the rationale for therapy is less clear. Currently, within 1 to 3 months following effective treat-
some clinicians recommend treatment for ani- ment of the underlying condition, unless chronic
mals in this range, whereas others do not. kidney disease is also present. Occasionally, dogs
Animals with no clinical signs and mildly el- with well-controlled hyperadrenocorticism re-
evated BP (systolic BP 120 to 160 mm Hg and main hypertensive.
diastolic BP 80 to 100 mm Hg) should not be In other patients, the duration of treatment can-
treated. not be predicted, but it may be required lifelong.
Periodic dosage adjustments based upon BP mea-
surements are indicated.
Key Point
Animals with normal BP or in which BP has not Dietary Therapy
been measured should not be treated with an-
tihypertensive agents. Though poorly studied, a low-sodium diet that
provides less than 0.25% sodium on a dry-weight
basis may be introduced. Dietary sodium restric-
tion may be employed as a first step if hyperten-
Antihypertensive Therapy sion is mild (i.e., < 170 mm Hg) and there is no
target organ damage present.
General
In animals with chronic kidney disease and hy-
Systemic arterial BP is the product of the cardiac pertension, it may be more important to maintain
output and the total peripheral resistance, so anti- adequate caloric intake rather than to insist that a
hypertensive therapy is generally aimed at reduc- low-sodium diet be fed. Therefore, drug therapy
ing cardiac output, total peripheral resistance, or is instituted first, and when BP is stabilized, the
both. animal may be switched to a lower sodium diet.
Therapy may be loosely classified as dietary and Obesity can elevate systemic arterial pressure
pharmacologic. in human beings and dogs and, perhaps, in cats.
Treatment is generally conducted by sequential Consequently, weight loss is desirable in obese,
trials. Generally, dosage adjustments or changes hypertensive animals.
in treatment should be instituted no more fre-
quently than every 2 weeks, unless extreme hy-
Pharmacologic Agents: General
pertension necessitating emergency treatment is
present. Medical treatment of hypertension in dogs and
When using pharmacologic agents, a wide range cats has, until recently, been extrapolated from
of dosages should be considered, with initial dos- human protocols. Recommendations for medical
ages at the low end of the range. therapy have included:
Chapter 14 Systemic Hypertension 283
starting drug in the treatment of canine hypertension. Perhaps the best index of hypertensive damage
Enalapril (0.5 mg/kg) is given twice daily, and BP is of the kidney is proteinuria. The presence of
measured after 2 weeks of treatment. microalbuminuria or an elevated urine protein-
If hypertension is still present, then amlodipine (0.1 to-creatinine ratio (>0.5 in dogs, >0.4 in cats) is
mg/kg PO every 24 hours) can be administered with generally an indication for the use of an ACEI (e.g.,
the enalapril. This combination of an ACE inhibitor enalapril or benazepril 0.5 mg/kg once daily in cats
and a calcium channel blocker may be effective; or once to twice daily in dogs).
however, sustained hypertension warrants the
addition of drugs that act by different mechanisms
of action.
Hydralazine, a direct-acting arterial vasodilator,
can be given at a starting dose of 0.5 mg/kg PO
twice a day, and slowly titrated up in 0.5 mg/kg
increments to a maximum dose of 2.0 mg/kg. BP
and serum creatinine should be monitored with
each incremental increase in dose.
Because hydralazine activates the renin-angiotensin- Suggested Readings
aldosterone axis, and aldosterone concentrations
Binns SH, Sisson DD, Buoscio DA, et al.: Doppler ul-
increase in spite of ACEI therapy, the addition of
trasonographic, oscillometric sphygmomanometric,
spironolactone (1 to 2 mg/kg PO twice a day) is
advised to block the effects of aldosterone. and photoplethysmographic techniques for noninva-
If BP remains above 160 mm Hg, then amlodipine sive blood pressure measurement in anesthetized cats,
may be increased to 0.1 mg/kg twice a day (or 0.2 J Vet Intern Med 9:405, 1995.
mg/kg once daily), or a beta blocker may be added Bodey AR, Michell AR, Bovee KC, et al.: Comparison
in order to decrease heart rate and renin release. of direct and indirect (oscillometric) measurements of
arterial blood pressure in conscious dogs, Res Vet Sci
Cats and dogs with chronic kidney disease often 61:17, 1996.
e xhibit systemic hypertension. What is the causative
Brown CAJ, Munday J, Mathur S, et al: Hypertensive en-
factor in this relationship and how should these
cephalopathy in cats with reduced renal function, Vet
animals be managed? How can you tell if hyperten-
Pathol 42:642-649, 2005.
sion is damaging to the kidney?
This has often been referred to as a chicken-and-egg Brown S, Finco D, Navar L: Impaired renal autoregula-
question but it is more properly seen as an example tory ability in dogs with reduced renal mass, J Am
of a complex positive feedback loop that complicates Soc Nephrol 5:1768, 1995.
therapy in animals affected with both problems. High Brown S, Atkins C, Bagley R, et al.: Guidelines for the
systemic arterial BP produces baro trauma within the identification, evaluation, and management of systemic
microvasculature of the kidney, effectively destroying hypertension in dogs and cats: ACVIM Consensus
renal tissue over time (weeks to months). On the other Statement, J Vet Intern Med 21:542-558, 2007.
hand, chronic kidney disease produces abnormalities Brown SA, Brown CA: Single-nephron adaptations to
in body fluid volumes and can alter neurohumoral partial renal ablation in cats, Am J Physiol 269:R1002,
control of BP. These factors combine to make high BP 1996.
relatively common in dogs and cats with chronic kid- Brown SA, Finco DR, Crowell WA, et al.: Single-nephron
ney disease. Furthermore, it is still generally accepted adaptations to partial renal ablation in the dog, Am J
that something has to be wrong with the kidney for Physiol 258:F495, 1990.
sustained systemic hypertension to be present. Brown SA, Walton CL, Crawford P, et al.: Long-term ef-
Interestingly, in the short-term, high BP tends to fects of antihypertensive regimens on renal hemody-
improve glomerular filtration rate. This is why the namics and proteinuria, Kidney Int 43:1210, 1993.
level of azotemia should always be assessed shortly Cowgill LD: Systemic hypertension. In Kirk RW, ed:
(5 to 14 days) after any changes in antihypertensive Current veterinary therapy IX, Philadelphia, 1986,
therapy.
WB Saunders.
Furthermore, vasodilators with intrarenal effects are
Cowgill LD, Kallet AJ: Recognition and management
often preferred for antihypertensive therapy in animals
of hypertension in the dog. In Kirk RW ed: Cur-
with kidney disease, largely because the vasodilatory
effect may help to preserve renal function. rent veterinary therapy VIII, Philadelphia, 1983,
Typical agents to select for initial therapy when both WB Saunders.
hypertension and renal azotemia are present in dogs Finco DR: Association of systemic hypertension with
would be an ACEI such as enalapril or benazepril renal injury in dogs with induced renal failure, J Vet
(0.5 mg/kg once to twice daily) and in cats a calcium Intern Med 18:289, 2004.
channel blocker such as amlodipine (0.1 mg/kg PO Henik R, Snyder P, Volk L: Treatment of systemic hyper-
every 24 hours). tension in cats with amlodipine besylate, J Am Anim
Hosp Assoc 33:226, 1997.
286 Section II Cardiovascular Disease
Jacob F, Polzin DJ, Osborne CA, et al.: Association be- temic hypertension in dogs: five cases (1981-1983),
tween initial systolic blood pressure and risk of devel- J Am Vet Med Assoc 193:486, 1988.
oping a uremic crisis or of dying in dogs with chronic Ortega TM, Feldman EC, Nelson RW, et al.: Systemic
renal failure, J Am Vet Med Assoc 222:322, 2003. arterial blood pressure and urine protein/creatinine
Jensen J, Henik RA, Brownfield M, et al: Plasma renin ratio in dogs with hyperadrenocorticism, J Am Vet
activity, angiotensin I and aldosterone in feline hyper- Med Assoc 209:1724, 1996.
tension associated with chronic renal disease, Am J Remillard RL, Ross JN, Eddy JB: Variance of indirect blood
Vet Res 58:535, 1997. pressure measurements and prevalence of hypertension
Kallet A, Cowgill L, Kass P: Comparison of blood pres- in clinically normal dogs, Am J Vet Res 52:561, 1991.
sure measurements in dogs by use of indirect oscil- Ross LA: Hypertension and chronic renal failure, Semin
lometry in a veterinary clinic versus at home, J Am Vet Med Surg Small Anim 7:221, 1992.
Vet Med Assoc 210:651, 1997. Snyder PS, Henik RA: Feline systemic hypertension.
Labato MA, Ross LA: Diagnosis and management of hy- Proc Twelfth Annual Vet Med Forum. San Francisco,
pertension. In August JR, ed: Consultations in feline 1994, p. 126.
internal medicine, Philadelphia, 1991, WB Saunders. Stiles J, Polzin DJ, Bistner SI: The prevalence of retinop-
Littman MP: Spontaneous systemic hypertension in 24 athy in cats with systemic hypertension and chronic
cats, J Vet Intern Med, 8:79, 1994. renal failure or hyperthyroidism, J Am Anim Hosp
Littman MP, Robertson JL, Bovee KC: Spontaneous sys- Assoc 30:564, 1994.
SECTION III
Treatment of Cardiovascular
Disease
15. Pathophysiology and Therapy 18. Emergency Management and
of Heart Failure Critical Care
Keith N. Strickland Steven G. Cole and Kenneth J. Drobatz
16. Treatment of Cardiac Arrhythmias 19. Anesthesia of the Cardiac Patient
and Conduction Disturbances Thomas K. Day
Marc S. Kraus, Anna R. M. Gelzer, and
20. Cardiac Surgery
Sydney Moise
E. Christopher Orton
17. Cardiopulmonary Resuscitation
21. Pacemaker Therapy
Steven G. Cole and Kenneth J. Drobatz
Janice McIntosh Bright
Chapter 15
macroscopic) abnormality of the heart that may sures are markedly increased, then death can
or may not result in heart failure. occur within hours to weeks (depending on the
Heart failure is the pathophysiologic state that severity of the abnormality). Heart failure can be
occurs when the heart is unable to function at a associated with systolic or diastolic dysfunction.
level commensurate with the requirements of the
metabolizing tissues or can only do so at elevated
filling pressures. Heart Failure
s0040
tion (cardiac preload, venous return) tomatic heart disease to symptomatic heart failure
Afterload is the load against which a muscle ex- has changed from the traditional concept of bio-
erts its contractile force. Cardiac afterload refers mechanical dysfunction to a concept emphasizing
to the blood pressure the ventricle must overcome neuroendocrine dysfunction secondary to chronic
in order to eject blood. biomechanical dysfunction.
The current model embodies the idea that some
u0030
to maintain normal arterial blood pressure and to promote cardiac function and tissue perfu-
flow (cardiac output) while maintaining normal sion. Chronic activation of these compensatory
venous and capillary pressures during rest and mechanisms leads to progressive cardiovascular
exercise. This function is necessary to provide dysfunction culminating in life-threatening con-
adequate blood flow for oxygen and nutrient gestive heart failure (CHF) low-output failure or
delivery to vital tissues (such as the brain, the sudden death.
heart, and the kidneys) as well as for the re- Cardiac dysfunction that leads to the clinical
moval of metabolic waste products from these syndrome of heart failure can be subdivided
tissues. into systolic and diastolic dysfunction. Systolic
288
Chapter 15 Pathophysiology and Therapy of Heart Failure 289
dial contractility, valvular competence, preload, mon causes of systolic dysfunction encoun-
afterload, and heart rate. tered in veterinary medicine. Incompetency
of an atrioventricular valve (endocardiosis,
endocarditis, congenital malformation) allows
Phases of Heart Failure
s0060
Low-output failure occurs when cardiac a positive inotropic effect (Anrep effect). How-
function does not produce adequate car- ever, when the hemodynamic overload is severe
diac output to maintain blood pressure and or chronic, myocardial contractility may be de-
tissue perfusion. pressed. Chronically increased afterload leads to
a reduction in the rate of ejection and the amount
of blood ejected at any given preload, and in-
Myocardial Failure
s0070
Infiltrative cardiomyopathy: neoplastic (e.g., Indeed, most cases of overt heart failure have
lymphosarcoma), amyloidosis some degree of diastolic dysfunction. Adequate
290 Section IiI Treatment of Cardiovascular Disease
tem. Elevation in venous and capillary pressures (RAAS) is a complex neurohormonal compensa-
may result in interstitial and alveolar pulmonary tory system that functions to maintain relatively
edema or ascites through hydrostatic factors. normal blood pressure and tissue perfusion when
cardiac output is reduced. Reduced renal perfu-
sion detected by renal baroreceptors results in
Compensatory Mechanisms release of renin (Figure 15-1). Other factors caus-
s0120
in Chronic Heart Failure ing release of renin include decreased sodium de-
livery to the macula densa, and SNS stimulation
Frank-Starling Mechanism
s0130
Renin
Angiotensinogen Angiotensin I
ACE
Angiotensin II
Aldosterone Vasoconstriction
Figure 15-1. RAA cascade. Reduced renal perfusion is the primary stimulus for renin release, which leads to activation of the
angiotensin-aldosterone system. RAAS activation results in sodium and water retention and peripheral vasoconstriction.
and myocardium. Vascular remodeling (smooth becomes maladaptive when chronically activated
muscle cell growth and hyperplasia, hypertrophy, (Figure 15-2).
and apoptosis; cytokine activation; myocyte and
vascular wall fibrosis) results in decreased vas- Sympathetic Desensitization:
s0170
cular responsiveness to alterations in blood flow, Chronic activation of the SNS is associated with
u0130
decreased vascular compliance, and increased elevated levels of plasma norepinephrine (NE),
afterload. Angiotensin II also causes pathologic cardiac NE depletion, down-regulation and de-
ventricular hypertrophy, exerts cytotoxic effects sensitization of beta-1 adrenergic receptors, and
resulting in myocardial necrosis and loss of myo- abnormal baroreflex function. Plasma NE levels
cardial contractile mass with resultant cardiac appear to be increased because of a combination
dysfunction. of increased release of NE from adrenergic nerve
endings and reduced uptake of NE by adrenergic
Sympathetic Nervous System Activation
s0150
The autonomic nervous system plays a crucial decrease) probably represents the depletion of the
u0120
role in the compensation of heart failure. The neurotransmitter in adrenergic nerve endings.
activity of the SNS is increased in part by baro- The down-regulation of beta-1 adrenergic re-
reflex-mediated parasympathetic withdrawal, as ceptors occurs relatively soon (24 to 72 hours)
well as by activation by the RAAS. Early activa- after the initial SNS activation, making it pro-
tion of the SNS helps to maintain cardiac output, gressively more difficult for the SNS to counter
blood pressure, and tissue perfusion by increas- impaired contractility.
ing venous return to the heart (vasoconstriction Chronic activation of the SNS also overloads
of the splanchnic vessels), vasoconstriction of the heart by increasing venous return (to a heart
other various vascular beds, and positive inotro- that is already volume-overloaded), by increasing
pic and chronotropic cardiac effects. Activation myocardial oxygen consumption (by increasing
of the SNS early in heart failure is beneficial, but heart rate and volume overloading of the heart)
292 Section IiI Treatment of Cardiovascular Disease
Decreased BP
Baroreceptors
Blood returned to
heart and
contractility
Heart rate Strength
of contraction Improved venous
return
f0020
Figure 15-2. Effect of compensatory sympathetic system in response to a reduction in blood pressure. Decreased systemic blood
pressure results in activation of the sympathetic nervous system and a cascade of consequences which are deleterious in the long
term.
mechanism directed toward normalizing cardiac the hypothalamus. Antidiuretic hormone prob-
output, wall tension, and filling pressures. The he- ably plays a limited role in the pathogenesis of
modynamic load imposed on the heart (either vol- CHF. However, chronic volume overload causes
ume or pressure overloading) determines the type an increase in diastolic wall stress, and this leads
of hypertrophy (eccentric vs. concentric). Chronic to replication of sarcomeres in series, elongation
activation of the RAAS and the SNS produces of myocytes, and ventricular dilation.
pathologic changes (remodeling) within the ven- Concentric myocardial hypertrophy (or pres-
tricular myocardium, which contribute to cardiac sure-overload hypertrophy) is characterized by
dysfunction. The result can be myocardial failure thickening of the ventricular walls in response
with low-output signs or elevated filling pressures to increased systolic wall stress, and occurs as
with the risk of CHF. a compensatory mechanism to normalize sys-
Eccentric myocardial hypertrophy (or volume- tolic wall tension. Increased systolic wall stress
u0140
overload hypertrophy) occurs with heart dis- stimulates the replication of sarcomeres in paral-
ease as a compensatory mechanism to allow the lel, increasing myocardium thickness and thereby
ventricle to pump a relatively normal amount normalizing systolic wall stress (via the La Place
of blood in spite of abnormal systolic function. relationship, wall tension=pressureradius/
Eccentric hypertrophy is characterized by cham- wall thickness). The increase in thickness of the
ber dilation, a response to the increase in blood ventricular wall compensates for the increased
volume and venous return associated with acti- systolic wall stress in a pressure-overloaded
vation of the RAAS and SNS. More specifically, ventricle. If the compensatory concentric hy-
the increased venous return is secondary to so- pertrophy is inadequate and the systolic wall
dium (aldosterone effect) and water (antidiuretic stress is increased, then afterload-mismatch
Chapter 15 Pathophysiology and Therapy of Heart Failure 293
and decompensation occur. Interestingly, when and chronic valvular insufficiency in dogs, and
significant eccentric hypertrophy occurs in a cardiomyopathy in cats).
volume-overloaded ventricle, systolic wall ten- Atrial, brain, and C-type natriuretic peptides
sion is increased secondary to the increase in ven- have been identified (ANP, BNP, and CNP,
tricular diameter. Therefore, both eccentric and respectively)
some degree of concentric hypertrophy are pres- BNP is primarily produced in the atria and is re-
ent in severely volume-overloaded ventricles. leased in response to atrial stretch resulting in na-
b0020
are released from endothelial cells, play an im- RAAS activation associated with the reduced re-
portant role in the regulation of vascular tone and nal perfusion, decreased sodium delivery to the
blood pressure. Endothelin-1 is a strong, vaso- macula densa, and SNS activation
constrictive agent with inotropic and mitogenic Renal sodium and water retention to increase
actions; it is a strong stimulus for activation of blood volume and, therefore, venous return to the
the RAAS and SNS. Additionally, Endothelin-1 heart
may play an important role in the pathogenesis of Myocardial hypertrophy (dilation of the affected
pulmonary hypertension. atrium and ventricle) to maintain relatively nor-
Natriuretic peptides are regulators of salt and mal cardiac output and systolic wall tension
water homeostasis and blood pressure control while preventing diastolic filling pressures from
with potential value as diagnostic and prognostic rising
markers in patients with CHF. Natriuretic peptide Stretch-induced release of atrial natriuretic fac-
levels are elevated in many disease conditions re- tor serves to facilitate sodium excretion. The ef-
sulting in expanded fluid volume (such as DCM fects of this factor are quickly negated owing to
294 Section IiI Treatment of Cardiovascular Disease
d egradation by neutral endopeptidases and the ef- Once the compensatory limits are reached,
fects of overstimulation of the RAAS and SNS. further increases in blood volume (associ-
Initially, these mechanisms allow the body to ated with sodium and water retention) and
compensate for the decreased cardiac output by venous return cause an increase in cardiac
increasing blood volume and blood pressure. filling pressures, with threat of CHF develop
However, with chronicity, the compensatory ment.
mechanisms are maladaptive and facilitate pro-
gression of heart failure.
Volume Overload
s0230
contractility. It can be associated with: stroke volume. The difference between vol-
Primary myocardial disease (idiopathic ume overloading secondary to impaired
DCM) contractility (DCM) and valvular insuffi-
Secondary myocardial diseases (chronic con- ciency (MR) is associated with the changes
genital and valvular heart disease, thyrotoxico- in TSV (end-diastolic volume minus end-
sis, taurine deficiency, infectious/inflammatory systolic volume). In MR without myocardial
and infiltrative diseases) failure, TSV is increased to compensate for
Myocardial failure causes systolic dysfunction the amount of blood leaking through the in-
and activation of compensatory mechanisms competent valve. The end-diastolic volume
which increase sodium and water retention to increases, but the end-systolic volume re-
increase venous return to the heart. The ven- mains normal (evidence of normal contrac-
tricles must obtain a larger end-diastolic di- tility), thereby resulting in an increased TSV.
mension to maintain a relatively normal total With impaired contractility, TSV is normal
stroke volume (TSV). As the myocardial func- or decreased (depending on the stage of
tion deteriorates (as noted by a decrease in the disease) because both end-diastolic and
fractional shortening and a decrease in ejection end-systolic volumes have increased. End-
fraction), the ventricles progressively enlarge diastolic volumes increase to compensate for
so that the TSV is maintained, even though the the increased end-systolic volumes, reflect-
percentage of blood being ejected is decreas- ing impaired contractility.
ing. Severe left ventricular dilation causes Shunts such as patent ductus arteriosus, ventricu-
distortion and dilation of the mitral valve an- lar septal defect, and arteriovenous fistula are
nulus, resulting in mitral regurgitation (MR) similar to valvular leaks in that the heart increases
and further volume overloading of the left TSV to compensate for the reduction in forward
ventricle. flow.
Chapter 15 Pathophysiology and Therapy of Heart Failure 295
tolic pressures usually do not cause CHF because tion of ventricular diastolic filling, and reduction
the heart is usually able to compensate for the of stroke volume and cardiac output characterize
increased intraventricular systolic pressures with cardiac tamponade. The clinical course depends
concentric hypertrophy (La Place principle), and on the size and rate of accumulation of the effu-
the ventricular systolic function remains rela- sion, and the compliance of the pericardial sac.
tively normal. Only when the obstruction to flow Acute tamponade is usually associated with
is severe (critical stenosis) or acute does pres- an acute hemorrhage from a neoplastic lesion,
sure overload result in myocardial failure and such as hemangiosarcoma, but may also be
heart failure. More commonly, CHF occurs when associated with rupture of the left atrium sec-
there is a concurrent valvular insufficiency (e.g., ondary to chronic severe MR. As the effusion
pulmonic stenosis with tricuspid regurgitation, accumulates, intrapericardial pressures increase
subvalvular aortic stenosis with MR or aortic re- and eventually exceed the diastolic pressures in
gurgitation, pulmonary hypertension with tricus- the right atrium and ventricle, thereby restrict-
pid regurgitation). ing the venous inflow to the right heart. The
Alternatively, sudden death may occur in dogs restriction of venous return causes a reduction
with severe (noncritical) congenital subvalvu- in right ventricular cardiac output, pulmonary
lar aortic stenosis or possibly valvular pulmonic blood flow, and left-sided venous return that is
stenosis. When the ventricle is severely hyper- associated with a reduction in left ventricular
trophied, coronary perfusion is impaired, and re- stroke volume and cardiac output, and signs of
gions of the myocardium (especially the papillary low-output heart failure.
muscles and subendocardial regions) are at risk Chronic tamponade associated with the slow
of hypoxia. Myocardial hypoxia can result in im- accumulation of pericardial effusion differs
paired contractility as well as ventricular tachyar- from acute tamponade in that the body has time
rhythmias which may degenerate into ventricular to compensate for the impediment of cardiac
fibrillation, leading to sudden cardiac death. inflow, secondary reduction in stroke volume,
and cardiac output. Although compensation
may somewhat normalize cardiac output, signs
Decreased Ventricular Compliance or
s0260
can also increase ventricular stiffness. sociated with increased capillary hydrostatic
Decreased ventricular compliance and abnormal pressures and elevated diastolic intra-atrial and
ventricular relaxation may result in elevated dia- intraventricular pressures. Diseases that cause
stolic intraventricular pressures (filling pressures), diastolic or systolic dysfunction are capable
even though the ventricular diastolic volume is of increasing cardiac filling pressures, leading
not increased. During the course of diastole, for to CHF.
any increase in preload, there is an abnormal in- Low-output failure can be defined as poor car-
crease in intraventricular pressure. Over time, the diac output, resulting in reduced tissue perfusion
corresponding atrium dilates to compensate for and inadequate tissue oxygenation. Generally,
the elevated filling pressure. Once compensatory the term low-output failure is used to describe
dilation of the atrium has reached its limit, further clinical scenarios in which cardiac output is dra-
elevation of the ventricular filling pressure results matically reduced by end-stage, primary, systolic
in the development of edema (or pleural effusion dysfunction.
in cats). Right-sided heart failure may result when the
Pericardial disease with cardiac tamponade is right atrium or right ventricle develops elevated
the clinical syndrome in which there is compres- filling pressures associated with valvular
sion of the heart by fluid within the pericardial insufficiency, pericardial disease, outflow tract
296 Section IiI Treatment of Cardiovascular Disease
establish the clinical course of the present- patient has difficulty breathing when it is lying
ing complaint, as well as the presence of con- down.
current diseases that may complicate heart Nocturnal coughing or dyspnea typically
disease. occurs after the patient has been recumbent
Coughing, tachypnea, dyspnea (respiratory for some time. It is not specific for left-sided
distress), exercise intolerance, lethargy, and CHF.
Chapter 15 Pathophysiology and Therapy of Heart Failure 297
heart failure in animals that are active; however, Arrhythmias are relatively common in animals
u0260
A cardiovascular murmur is a series of auditory the rapid diastolic phase of ventricular filling.
u0250
vibrations associated with turbulent (nonlami- An S3 gallop occurs commonly in dogs with
nar) blood flow and, occasionally, with vibrating heart failure associated with volume overload,
valve leaflets. When blood flow velocities are particularly dogs with DCM. During early dia-
supraphysiologic (i.e., higher than normal physi- stolic filling, blood rushes out of the atrium into
ologic velocities), or when blood viscosity is re- a noncompliant ventricle, which then vibrates,
duced (e.g., with anemia), blood flow tends to be resulting in a low-frequency sound just after S2.
nonlaminar and turbulent. Nonlaminar blood flow A fourth heart sound (S4) gallop occurs just be-
generates acoustic energy that vibrates the struc- fore the first heart sound (S1) and is associated
tures within the heart or the associated vessel(s). with atrial contraction. Ventricular filling in
The intensity (loudness), timing in the cardiac late diastole associated with atrial contraction
cycle, frequency (pitch), configuration (shape), vibrates the noncompliant ventricle, creating
quality, duration, location, and direction of radia- a low-frequency sound just before S1 and the
tion of the sound created by the blood flow are onset of systole. S4 gallop are commonly aus-
important characteristics of cardiac murmurs. cultated in cats with hypertrophic or restrictive
The intensity of the murmur refers to the loud- cardiomyopathy. Summation gallops (S3 and
ness of the murmur and is graded on a scale S4) may occur during periods of tachycardia.
from 1 to 6 (1 being the least audible murmur,
and 6 being the loudest).
Diagnostics
s0330
The configuration of the murmur refers to the Electrocardiography is used to detect cardiac rhythm
u0270
shape of the sound created by the abnormal disturbances, chamber enlargement, or conduction
blood flow, and is described as being either a abnormalities that may be associated with cardiac
plateau (regurgitant murmur) or a crescendo- disease. Electrocardiographic abnormalities are not
decrescendo (ejection murmur) sound. specific for heart failure and therefore should not
A cardiac murmur is present in many dogs be used to determine the presence of heart failure.
with heart failure, but the presence of a Furthermore, a normal electrocardiogram does not
cardiac murmur is not specific for heart rule out the possibility of severe heart disease with
failure. secondary chamber enlargement.
298 Section IiI Treatment of Cardiovascular Disease
Thoracic radiography is important in the evalu- echocardiography allows the clinician to define
u0280
ation of patients with suspected heart disease or structural heart disease and identify CHF in most
CHF. In general, with respect to heart disease and cases. Typically, heart failure is not present with-
heart failure, three questions should be answered out atrial enlargement (with the exception of
when evaluating a thoracic radiograph: pericardial diseases and some other uncommon
Is cardiomegaly present? If so, which side of diseases). The atria are usually compliant and en-
the heart is affected? large as filling pressures increase.
What is the pulmonary vascular pattern (e.g.,
normal, undercirculated, overcirculated, ve-
Differential Diagnoses
s0370
edema, pleural effusion, or ascites)? disease or failure because both may cause cough-
With compensated left-heart failure, the earliest ing, abnormal bronchovesicular sounds, and re-
evidence of pulmonary edema formation is pul- spiratory distress. The presence of pulmonary
monary venous congestion (stage I of pulmo- crackles, a respiratory sinus arrhythmia, and re-
nary edema formation). That is, the pulmonary spiratory distress in a dog without a cardiac mur-
veins are distended and larger than their respec- mur is almost always associated with pulmonary
tive arteries. At this time pulmonary capillary disease rather than with heart failure.
pressures are approximately 15 to 20 mm Hg. Ascites and pleural effusion may occur second-
As pulmonary venous and capillary pressures ary to diseases other than heart failure. Evalua-
progressively increase with left-sided heart fail- tion of the jugular veins may aid in differentiating
ure, decompensation occurs, and fluid leaks into ascites associated with heart failure from ascites
the interstitium (interstitial edema, stage II). associated with hypoproteinemia secondary to
As pulmonary venous and capillary pressures liver or renal disease.
continue to rise (e.g., 30 to 40 mm Hg), the al-
veoli are flooded with edema fluid, and stage III
Therapy of Heart Failure
s0380
lar (centrally located) in distribution, or it may aimed at relieving symptoms and cardiac dys-
be diffuse and generalized. In cats, pulmonary function because, in most cases, heart disease and
edema may appear as a patchy mixed interstitial- heart failure are not curable entities. In addition
alveolar pattern that is not primarily located in to relieving heart failure symptoms, heart failure
the perihilar region. therapy is also directed toward increasing the sur-
Pleural effusion may be evident in cases with bi- vival time of the patient.
ventricular or severe right-sided heart failure in Signs of congestion can be treated with agents
dogs, and may be present with left-sided or bi- that reduce cardiac filling pressures (preload re-
ventricular heart failure in cats. ducers such as diuretics and venodilators) and
agents that facilitate cardiac performance (posi-
Echocardiography tive inotropes and arterial dilators). Modulation
s0360
The three principal modalities of echocardiogra- of the compensatory mechanisms that exacerbate
u0290
phy are two-dimensional, M-mode, and Doppler chronic heart failure has become increasingly im-
evaluation of the heart. Because of the noninva- portant in the therapy of heart failure as under-
sive nature of echocardiography, it has essentially standing of the genesis of heart failure (especially
replaced cardiac catheterization in the diagnosis chronic heart failure) has evolved.
of heart disease in small animals. Echocardiogra- Monotherapy with diuretics and simply restrict-
phy enables the trained specialist to identify dis- ing dietary sodium intake are no longer accepted
eases that may cause or be associated with heart therapies for treating chronic heart failure. In
failure, such as: fact, these therapies may actually promote the
Valvular leaks activation of the compensatory mechanisms
Myocardial failure that are responsible for overloading the failing
Intracardiac or extracardiac shunts heart.
Decreased ventricular compliance It is important to note that the appropriate therapy
Pericardial disease for a given patient is determined by the clinical
Chapter 15 Pathophysiology and Therapy of Heart Failure 299
signs present, the severity of the clinical signs, Severe heart failure is characterized by the
and the underlying disease entity. presence of overt clinical signs associated with
In general, combinations of angiotensin-convert- heart failure at rest. These patients are critically
ing enzyme (ACE) inhibitors, diuretics,a posi- ill and may require intensive monitoring and
tive inotrope represent the conventional therapy aggressive therapy, including combinations of
for chronic heart failure. Adjunctive therapy in ACE inhibitors, furosemide, pimobendan, di-
selected patients may include additional agents goxin, nitrates, and sympathomimetic agents
for heart rate control, nutritional supplementation such as dopamine or dobutamine. The progno-
(e.g., taurine), or additional medications for re- sis for severe heart failure is guarded to poor,
fractory symptomatic heart failure. and these patients generally have short survival
Occult heart disease refers to heart disease times (i.e., days to weeks).
that has resulted in the first detectable chang-
es associated with heart disease (myocardial
dysfunction, chamber dilation, arrhythmias). Therapeutic strategies
s0390
cated in these cases in hopes of slowing the the tendency to conserve sodium and to develop
progression of heart dysfunction and increas- edema. Theoretically, the use of low-sodium di-
ing the time before clinical signs associated ets in combination with vasodilators and ACE in-
with heart failure appear. However, there is hibitors may allow for less reliance on diuretics to
no peer-reviewed evidence supporting their control edema and signs of congestion. Early in
effectiveness in altering the disease course in the course of heart failure, dietary sodium restric-
canine chronic valve disease or DCM. In any tion should be in the form of elimination of high-
case, these patients typically have a good to saltcontaining snacks. We tend to rely on diuretics
guarded prognosis for long-term survival (i.e., in combination with vasodilators and ACE inhibi-
years). tors early in the course of heart failure, and to insti-
Mild heart failure is associated with clinical tute salt restriction when excessively high diuretic
signs such as exercise intolerance. These clini- dosages are required to control signs. Chronic
cal symptoms are usually apparent only when administration of salt-restricted diet may cause
the patient is pushed beyond its hearts capacity sodium conservation through the RAAS, causing
to maintain an appropriate cardiac output during further progression of heart failure. Reduced di-
exercise. These patients show minimal signs of etary sodium intake stimulates the synthesis and
heart failure and, in general, are compensating. secretion of aldosterone. Another disadvantage
Radiographically, cardiomegaly and pulmonary to salt-restricted diets is the unpalatable nature of
venous congestion are present. In cases such as such diets. Salt makes food taste good, so without
these, ACE inhibitors and possibly a positive it, the patient may be reluctant to eat the food, and
intrope/negative chronotrope such as digoxin this may lead to client noncompliance.
and/or a positive inotrope/vasodilator such as
pimobendan are indicated. These patients typi- Key Points
b0040
cally have a guarded prognosis for long-term The general theme regarding sodium restric-
survival (i.e., months to years). tion in patients with heart failure is to avoid
Moderate heart failure is associated with more treats or foods with excessive sodium content.
persistent clinical signs such as coughing, ex-
ercise intolerance, and tachypnea at rest. These
patients have pulmonary edema (or ascites de- l-Carnitine supplementation may be indicated in
u0330
pending on which side of the heart is affected) patients that have myocardial failure associated
and require more aggressive therapy with ACE with definitive myocardial l-carnitine deficiency.
inhibitors, a diuretic such as furosemide, and Some Boxers with cardiomyopathy may respond
possibly digoxin and/or pimobendan. These to l-carnitine supplementation. In most cases,
patients typically have a guarded prognosis for however, it is likely that myocardial l-carnitine
long-term survival (i.e., months). deficiency is a result of the underlying disease
300 Section IiI Treatment of Cardiovascular Disease
DCM secondary to taurine deficiency in cats is un- Figure 15-3. Drawings of the left heart from a dog with
commonly encountered today, it is prudent to evalu- severe mitral regurgitation before and after administration
ate plasma taurine levels or to supplement taurine of an afterload reducing agent. Note that forward flow (out
on a trial basis in all cats with DCM. In patients the aorta) increases with afterload reduction because of the
reduction in systemic vascular resistance. LV, left ventricle; LA,
suffering from taurine deficiencyinduced DCM, left atrium.
supplementation with taurine results in clinical and
echocardiographic improvement typically within 2
to 3 months. Dosage for taurine supplementation:
Dogs: 500 to 1000 mg PO once or twice a day capacitance vessels and the splanchnic veins) and
Cats: 250 to 500 mg PO once or twice a day reducing venous return, which results in lower
n-3 polyunsaturated fatty acids levels are reduced filling pressures (preload).
in dogs with CHF and fish oil supplementation can Classification of vasodilators based on ves-
normalize these plasma fatty acid abnormalities. sels affected:
The author currently recommends a fish oil dosage Arterial (e.g., hydralazine)
to provide 40 mg/kg/day EPA (eicosapentaenoic Venous (e.g., nitroglycerin, isosorbide
acid) and 25 mg/kg/day DHA (docosahexaenoic dinitrate)
acid) for patients with anorexia and/or cardiac Mixed (e.g., nitroprusside, prazosin, ACE
cachexia. inhibitors, pimobendan)
Classification of vasodilators based on mech
anism of action:
Vasodilator Therapy
s0410
duce systemic vascular resistance in patients with Alpha-adrenergic blocking agents (e.g.,
CHF. In doing so, cardiac function is improved. prazosin)
Myocardial systolic wall tension is an important Calcium channel blocking agents (e.g.,
determinant of myocardial oxygen consump- amlodipine, verapamil, diltiazem)
tion. By decreasing systemic vascular resistance ACE inhibitors (e.g., captopril, enalapril,
(and, therefore, afterload and systolic wall tension), lisinopril, benazepril)
arterial vasodilators reduce myocardial oxygen Phosphodiesterase inhibitors (e.g. pimo-
consumption. Additionally, the reduction in after- bendan)
load results in an increase in cardiac output. Arterial
vasodilators decrease the volume of regurgitation
Angiotensin-Converting Enzyme Inhibitors
s0420
gitation (Figure 15-3). Arterial vasodilators may venting the conversion of angiotensin I to angio-
lessen the magnitude of left-to-right shunting in tensin II. Angiotensin II is a potent vasoconstrictor.
patients with ventricular septal defects. However, The decrease in angiotensin II levels results in a re-
arterial vasodilators may exacerbate right-to-left duction in the level of vasoconstriction, as well as
shunting in patients with tetralogy of Fallot or with decreased SNS activity. Furthermore, ACE inhibi-
nonrestrictive ventricular septal defects. tion also results in decreased aldosterone synthesis
Indications: Venous vasodilators are used to re- and secretion, so that there is less sodium and water
duce congestive symptoms by redistributing retention, among many other benefits beyond the
blood volume within the circulatory system (the scope of this discussion.
Chapter 15 Pathophysiology and Therapy of Heart Failure 301
Large, multicenter clinical trials have demon- of ACE inhibitor therapy. Azotemia secondary to
strated the safety and efficacy of ACE inhibitors decreased renal perfusion represents the most im-
in the therapy of CHF secondary to DCM and portant clinical consideration. Azotemia and re-
primary valve disease. ACE inhibitors appear to nal dysfunction secondary to a decrease in renal
significantly decrease the clinical signs of heart perfusion result from loss of protective mecha-
failure when used in combination with conven- nisms to maintain filtration pressures. Angioten-
tional therapy (diuretics with or without digoxin). sin II causes vasoconstriction of the renal efferent
Enalapril has been extensively studied in veteri- arterioles in an effort to maintain glomerular fil-
nary medicine and is approved for the use in dogs tration pressures in the face of decreased renal
in the United States: perfusion. The relative decrease in angiotensin II
The Invasive Multicenter Prospective Veterinary can significantly decrease glomerular perfusion
Enalapril (IMPROVE) study showed a decrease and filtration, resulting in azotemia. Furthermore,
in pulmonary capillary wedge pressure and im- renal dysfunction is more likely to occur in pa-
provement of heart failure status with enalapril. tients with pre-existing renal disease. As a result,
The Cooperative Veterinary Enalapril (COVE) renal function should be evaluated before and 5
study showed that enalapril with digoxin and/or to 7 days after instituting ACE inhibitor therapy,
furosemide significantly decreased clinical signs especially during concurrent diuretic therapy.
of heart failure in DCM or MR. Most complications are likely to occur shortly
The Enalapril Long-term Efficacy Study after beginning therapy, in association with acute
showed increased survival times for dogs treat- cardiac decompensation, or in conjunction with
ed with enalapril. systemic disease that may alter the patients hydra-
Enalapril studies in cats in the late 1990s ap- tion status (e.g., vomiting or diarrhea). Side effects
pear to suggest that ACE inhibitors improve are much more likely to occur with captopril than
control of CHF associated with hypertrophic with the other commonly used ACE inhibitors.
and other forms of cardiomyopathy.
Benazepril therapy has been demonstrated to be
b0050
Key Points
effective in the treatment of systemic hypertension
secondary to chronic renal disease or hypertrophic ACE inhibitors are recommended for patients
cardiomyopathy, as well as in the control of CHF. with asymptomatic myocardial dysfunction;
The earliest time at which ACE inhibition is indi- in patients with symptomatic CHF secondary
to chronic valvular disease, DCM, and other
cated has not been accurately determined, but it
causes of CHF; and in patients with systemic
may be reasonable for ACE inhibitor therapy to be hypertension.
initiated in dogs and cats with signs of advanced,
compensated heart failure (e.g., cardiomegaly
and pulmonary venous congestion), regardless of Agents and dosages
their symptoms. ACE inhibitor therapy in asymp- Captopril (Capoten)
tomatic Doberman Pinschers with occult DCM Dogs: 0.5 to 2.0 mg/kg PO three times a day
may delay the onset of symptomatic CHF. Enalapril (Enacard, Vasotec)
However, there is no indication for therapy with Dogs: 0.5 mg/kg PO once or twice a day
ACE inhibitors in patients with asymptomatic, Cats: 0.25 to 0.5 mg/kg PO twice a day to
chronic valve disease. A large multicenter pla- every other day
cebo controlled double blind study in Europe was Lisinopril (Zestril)
unable to demonstrate a delay in symptomatic Dogs: 0.5 mg/kg PO once daily
heart failure in patients with chronic valve dis- Benazepril (Lotensin)
ease when given enalapril. Dogs: 0.25 to 0.5 mg/kg PO once or twice a
ACE inhibitors should not be used as a primary day
agent (monotherapy) in emergency treatment for Cats: 0.25 to 0.5 mg/kg PO once or twice a
acute CHF. Significant clinical improvement at- day
tributable to ACE inhibition may not be evident
until 2 to 3 weeks after initiation of therapy.
Calcium Channel Blocking Agents
s0430
Anorexia or inappetence, vomiting, hypotension, are calcium channel blocking agents. In general,
and azotemia are the most common side effects they differ with regard to their antiarrhythmic
302 Section IiI Treatment of Cardiovascular Disease
e ffects, their vasodilating effects, and their nega- and cats; and (3) in the treatment of systemic (amlo-
tive inotropic effects. dipine) and pulmonary (diltiazem) hypertension.
Verapamil is used primarily (intravenously) for
Direct-Acting Arterial Vasodilators
s0440
sesses minimal vasodilating properties, but exerts Hydralazine has been evaluated in dogs with
u0370
Dogs: 0.5 to 2.0 mg/kg PO two or three Dogs: Initial dose at 0.5 mg/kg PO; the dose is
times a day gradually increased until a clinical response is elic-
Cats: 7.5 mg PO two or three times a day ited or up to a maximum dose of 3.0 mg/kg BID.
or 45 to 60 mg PO every day of sustained- The endpoints of drug titration can be determined
release formulations by monitoring blood pressure, by the patients
Amlodipine (Norvasc) clinical response, and by obtaining radiographic
Primarily used as therapy for systemic hyper- evidence that pulmonary edema has resolved.
tension in cats and dogs. Cats: 2.5 mg PO once or twice a day
Dogs: 0.05 to 0.2 mg/kg PO once or twice Hydralazine may play a role in emergency therapy for
a day severe MR secondary to ruptured chordae tendineae.
Cats: 0.625 to 1.25 mg PO once or twice a The author rarely uses hydralazine in cats with
day heart failure.
In general, we use calcium channel blockers (1) to Many side effects are associated with administra-
control heart rate and to facilitate ventricular filling tion of hydralazine and limit its usefulness:
and relaxation in cats with hypertrophic cardiomy- Hypotension
opathy; (2) as supplemental therapy for control of Gastrointestinal disturbances
the ventricular response rate in some supraventricu- Reflex tachycardia
lar tachycardias such as atrial fibrillation in dogs Furthermore, there is evidence of enhanced
neurohormonal activity (increased aldosterone
b0050
The indications for nitroprusside therapy are short- ited to the short-term treatment of acute heart
term treatment of refractory, life-threatening CHF failure when other agents are ineffective or con-
in dogs with MR or DCM or critical systemic traindicated. Rarely used in veterinary medicine.
hypertension. Combination therapy with dobuta- Agents and Dosages: Prazosin (Minipress),
mine, digoxin and/or pimobendan, and diuretics titrated to effect
provides the best effect. Small dogs and cats: 0.25 to 1 mg PO three
Agents and dosages times a day
Nitroprusside(Nipride): Medium dogs (<40 lb): 1 to 3 mg PO three
Dogs: intravenous (IV) constant rate infu- times a day
sion at an initial rate of 1.0 g/kg/min (fol- Large dogs (>40 lb): 3 to 10 mg PO three
lowing dilution in 5% dextrose), titrated to times a day
effect, by monitoring blood pressure and
pulmonary capillary wedge pressure, to a
Diuretic Therapy
s0500
Cyanide poisoning may also occur with chronic reversible inhibition of the sodium/potassium/
administration. chloride co-transporter in the thick ascending
Hypotension is easily managed by slowing the limb of the loop of Henle.
rate or by discontinuing the infusion (nitroprus- Furosemide is the most commonly used agent in
side has a very short half-life). this class of diuretics because it is the most po-
tent and has a fast onset of action. The result is
Venous Vasodilators (Nitroglycerin, the obligatory loss of sodium and water into the
s0480
ducers. The development of nitrate tolerance lim- to release of vasodilatory prostaglandins. This
its the continuous use (i.e., more than 36 hours) of vasodilatory effect occurs within the first 20 min-
these agents. Tolerance may be avoided by intermit- utes after IV or intramuscular (IM) administra-
tent use (24 hours on and 24 hours off) and possibly tion, and the peak diuretic effect occurs after 30
concurrent use of ACE inhibitors. to 45 minutes.
Agents and dosages Of interest to the clinician, there is a bioavailability
2% nitroglycerin paste (Nitrol, Nitro-BID) difference between Lasix and generic oral formu-
Dogs: to 2 inches cutaneously three or lations; we therefore do not recommend switching
four times a day; inch per 2.27 kg of back and forth from one formulation to the other.
body weight The peak effect after oral administration of Lasix
Cats: 1 8 to inch three or four times a is 30 minutes to 2 hours.
day Agents and dosages: Furosemide (Lasix, Salix)
Nitroglycerin paste should be applied to hair- Chronic oral administration
less areas such as the pinna or the axillary Dogs: 1 to 2 mg/kg PO two to four times a day
region. If perfusion to the ears is poor (e.g., Cats: 1 to 2 mg/kg PO twice a day
ears are cold), the axilla or groin will provide Parenteral administration (IM or IV)
better absorption. Because nitroglycerin is Dogs: 2 to 8 mg/kg as needed to control edema
absorbed transcutaneously, gloves should be Cats: 1 to 2 mg/kg as needed to control edema
worn during administration. Continuous-rate infusion: 0.66 mg/kg IV bo-
Isosorbide dinitrate (Isordil) lus followed by 0.66 mg/kg/hour
Dogs: 0.2 to 1.0 mg/kg PO three times a day Adverse side effects of furosemide (Lasix) include
electrolyte abnormalities, such as hypokalemia,
Alpha-adrenergic Receptor Antagonists hyponatremia, and hypochloremia (hypochlore-
s0490
CHF, but neither its short-term hemodynamic nor in the dose usually results in resolution of the al-
long-term clinical effects have been documented. kalosis. Severe metabolic alkalosis can be treated
Current indications for its use appear to be lim- with judicious use of half-strength saline with
304 Section IiI Treatment of Cardiovascular Disease
or without 2.5% dextrose. Overzealous diuretic Because of their potassium-sparing effects, they
therapy may cause dehydration, low cardiac out- should be used with caution with concurrent ACE
put, and, possibly, circulatory collapse. Further- inhibitor therapy.
more, diuretics activate systemic compensatory Spironolactone (Aldactone), an aldosterone an-
mechanisms, such as the RAAS and SNS. tagonist, is usually used in conjunction with
In the therapy of heart failure, furosemide should Lasix or Diuril.
always be used in combination with an ACE in- Aldosterone antagonism may serve a cardio-
hibitor; chronic monotherapy with furosemide is protective effect by reversing and inhibiting
not recommended. myocardial and vascular fibrosis. The anti-
aldosterone effect may prove to be an important
b0070
s0530
electrolyte reabsorption. These diuretics are less Digoxin acts by inhibiting sarcolemmal Na+,
u0450
potent natriuretic agents and are usually not suc- K+-ATPase, which causes an accumulation of
cessful in controlling signs of congestion when sodium which is then available for exchange
used as a monotherapy. In general, thiazide di- with extracellular calcium through the Na+-
uretics are administered when heart failure is Ca++ exchanger. The exchange results in
refractory and conventional therapy (digoxin and/ increased intracellular calcium. Calcium is
or pimobendan, ACE inhibitor, and furosemide) then available for interaction with the sarco-
fails to control the clinical signs of congestion. plasmic reticulum (calcium-induced release of
Agents and Dosages sarcoplasmic reticular calcium), and therefore
Chlorothiazide (Diuril): 20 to 40 mg/kg the release of more calcium for interaction with
PO once or twice a day the contractile elements (positive inotropic
Hydrochlorothiazide (Hydrodiuril): 2 to 4 effect). Digitalis glycosides shift the Frank-
mg/kg PO once or twice a day Starling curve upward by increasing the velocity
and force of contraction of the myocardium at
Potassium-Sparing Diuretics any given level of preload. Additionally, digi-
s0540
Generally, the potassium-sparing diuretics are atrioventricular node by both direct and vagal
u0440
weak diuretics that are rarely used as single-agent effects. Digoxin may also partially restore
therapy to control edema in heart failure patients. baroreceptor reflexes that are desensitized
They are most commonly used together with a by the chronically elevated sympathetic tone
more potent diuretic to control refractory edema. associated with CHF.
Chapter 15 Pathophysiology and Therapy of Heart Failure 305
Indications for digoxin therapy: 0.008 mg/kg every day or every other day). Se-
Theoretically, digoxin is indicated in virtually rum digoxin levels should be determined 5 to 7
every patient with CHF and a supraventricu- days after initiation of therapy (therapeutic se-
lar tachycardia (e.g., atrial tachycardia, flutter, rum levels=1.0 to 2.0 ng/ml in most laboratories
or fibrillation). Digoxin is also indicated for [8 to 12 hours post dosing]). The oral dose is
echocardiographically documented myocardial then adjusted based on this trough serum level.
failure and systolic dysfunction (i.e., reduced
Key Point
b0090
requiring a reduction in digoxin dosage. Use 3 ng/ml (still in the toxic range). If the drug
an alternative medication in place of quinidine is discontinued for yet another 1 days, the
whenever possible (e.g., procainamide). serum level should drop from 3 ng/ml to 1.5
Hypothyroid animals often require less digoxin ng/ml. Therefore, in this example, the digoxin
than euthyroid animals. Hyperthyroid animals should be discontinued for approximately 3 to
may also require a decreased dose. Digoxin is 4 days and then continued at approximately
excreted primarily by the kidneys. The pres- one third of the original dose to achieve se-
ence of renal dysfunction often necessitates a rum levels in the therapeutic range. Check
reduction in digoxin dosage or frequency of electrolyte status and correct hypokalemia
administration. if present. Life-threatening arrhythmias may
Dosage should be based on lean body weight. be treated with atropine, lidocaine, or a beta
Obesity, pregnancy, or the presence of ascites blocker (depending on the arrhythmia present).
should be noted, and the dose should be ad- Additionally, a specific antidote (Fab-antibody
justed accordingly. fragments that scavenge the free drug from
Adverse and toxic effects of digitalis glycosides: the body) is available, but its use may be cost
s0580
The main determinants of myocardial oxygen inhibitor that has positive inotropic activity (via
consumption are ventricular wall tension, heart increasing the sensitivity of the contractile ap-
rate, and the state of contractility. Increased con- paratus to calcium) and vasodilatory (via phos-
tractility associated with digoxin therapy results phodiesterase inhibition) effects. Current studies
in increased myocardial oxygen consumption have demonstrated it to increase survival time
that is usually offset by the decrease in heart rate and quality of life in CHF patients with DCM or
and ventricular size (and thus wall tension) and with chronic valve disease.
increased coronary perfusion. There are several clinical trials (some only in ab-
The signs of toxicity are variable, but in general stract form) assessing the use of pimobendan in
fall into one or more of three categories: patients with chronic valve disease, include the
Neurologic (lethargy and depression) PITCH Trial, the Edinburgh Study, the Guelph
Gastrointestinal (inappetence, anorexia, diar- Study, the PERMIT Study, and the VetSCOPE
rhea, nausea, vomiting) Study. The general consensus at this time is that
Cardiac (arrhythmia) pimobendan has beneficial effects, with regards
With oral administration, gastrointestinal signs to survival and quality of life, when administered
almost always occur before arrhythmias. Some to patients with symptomatic chronic valve dis-
of the more common arrhythmias associated ease or DCM.
with digitalis toxicity are first and second-degree Dosage:
atrioventricular block, accelerated junctional Dogs: 0.1 to 0.25 mg/kg PO every 12 hours;
rhythms, ventricular premature complexes, ven- give 1 hour prior to food ingestion
tricular tachycardias, and atrioventricular dis- Cats: no current recommended dosage
sociation. A nonrespiratory sinus arrhythmia in
a patient receiving digoxin may indicate high
Miscellaneous Agents/Adjunctive
s0600
serum levels.
Therapy for Heart Failure
The treatment of digoxin toxicosis is based on
the elimination half-life of the drug and the Bronchodilators, antitussives, sympathomi-
u0480
goal is to return digoxin serum levels to within metics, positive inotropes, and sedatives/tran-
therapeutic range (1 to 2 ng/ml). In healthy quilizers are all agents used as adjunctive
dogs, the serum half-life of digoxin is approxi- therapy in the management of CHF. None of
mately 24 to 36 hours. Therefore, it takes about these agents when used as monotherapy is
1 days to decrease the serum level to half the capable of effectively ameliorating the signs of
original level. CHF. However, these agents may be useful in
CASE EXAMPLE: if the starting serum level decreasing some of the signs associated with
is 6 ng/ml, then if the drug is discontinued for heart failure (coughing, cardiac asthma, and
1 days, the serum level should be around signs of low-output failure).
Chapter 15 Pathophysiology and Therapy of Heart Failure 307
calcium influx. An increase in calcium influx in the Usually not necessary in most patients with CHF
u0520
smooth muscles of the airways results in smooth as long as they are eating and drinking. Dogs and,
muscle relaxation and bronchodilation. Addition- especially, cats may become hypokalemic as a re-
ally, the change in calcium ion movement in other sult of inappetence/anorexia and aggressive con-
tissues, such as nodal and myocardial tissue, results current diuretic therapy. Potassium supplement
in a positive chronotropic and inotropic effect. This dose; cats: 2 to 6 mEq PO per day.
agent may be helpful in dyspneic patients with fa-
tigue of the muscles of respiration. Dogs and cats Oxygen Therapy
s0650
may experience transient gastrointestinal distur- As needed in cases with acute pulmonary edema
u0530
cardia, and hyperexcitability and/or restlessness. The bipyridines, amrinone and milrinone, are
u0540
Occasionally, we use theophylline in patients with agents that are referred to as inotropic vasodilators
complete atrioventricular block that are not candi- because they have mild arteriolar dilating prop-
dates for permanent pacemaker implantation. erties in addition to their inotropic effects. The
Agents and dosages: mechanism of action is an increase in cardiac lev-
Theophylline (Theo-Dur) els of cAMP by inhibition of phosphodiesterase.
Dogs: 9 to 20 mg/kg PO two to four times a day Increased cAMP levels mediate increased calcium
Cats: 4 mg/kg PO three times a day delivery to the contractile elements of the myocyte,
Aminophylline (Aminophyllin) as well as possibly increasing calcium availability
Dogs: 11 mg/kg PO two to four times a day by augmenting the storage and release of calcium
Cats: 5 mg/kg PO three times a day by the sarcoplasmic reticulum. Increases in cAMP
in vascular smooth muscle result in muscular re-
Cough Suppressants laxation and a direct-acting arterial vasodilator
s0620
ing the frequency of coughing in dogs with left The indications for bipyridine therapy are similar
mainstem bronchial compression secondary to to those for digoxin. Amrinone and milrinone are
left atrial enlargement. If chronic airway disease more potent inotropic agents than digoxin, but
is also present, the long-term results of antitus- lack the antiarrhythmic properties. Both agents
sive therapy are often disappointing. tend to increase heart rate and may potentiate ar-
Hydrocodone (Hycodan) rhythmias in some patients.
Dogs: 0.22 mg/kg PO every day to four times Their use at the present time is limited to the
a day treatment of severe refractory myocardial failure.
Cats: Do not use. The route of administration for amrinone and
Butorphanol (Torbutrol) milrinone is intravenous. Amrinone is approved
Dogs: 0.05 to 1 mg/kg PO two to four times a only for short-term IV administration in humans.
day Amrinone (Inocor):
Cats: No established antitussive dose Dogs: 1.0 to 3.0 mg/kg IV bolus or 10 to 80
g/kg/min as a continuous rate infusion
Sedatives and Tranquilizers Adverse and toxic effects associated with amrinone
s0630
May be useful in selected cases. Respiratory distress and milrinone have been described. Thrombocyto-
u0510
may cause anxiety and stress in a patient with CHF. penia, a dose-related increased heart rate, gastroin-
Agents with minimal cardiovascular effects should testinal signs (diarrhea, anorexia), and hypotension
be chosen to prevent exacerbation of the CHF by (at high doses) have been reported. Additionally,
causing hypotension or reduced contractility. these agents appear to be arrhythmogenic (i.e., po-
Morphine sulfate (reduces anxiety, decreases tentiate the development of arrhythmias) in some
sympathetic tone): humans and dogs with heart failure.
308 Section IiI Treatment of Cardiovascular Disease
Dogs: 0.04 to 0.1 g/kg/min IV infusion beta-1 agents such as atenolol and nonselective
following dilution in dextrose agents such as propranolol or carvedilol) are
Dobutaminehydrochloride (Dobutrex): agents that in the past have primarily been used
Dogs: 5 to 20 g/kg/min IV continuous as antiarrhythmic agents in the control of the ven-
infusion diluted in 5% dextrose (monitor tricular response rate to atrial fibrillation. Recent
closely for arrhythmia) evidence has suggested that beta blockade may
Chapter 15 Pathophysiology and Therapy of Heart Failure 309
be effective in the therapy of mild to moderate Dosage: Sildenafil (Viagra): 0.5 to 1.0 mg/kg
CHF. Chronic SNS stimulation results in down- PO two or three times a day
regulation and desensitization of cardiac beta re-
ceptors. Beta blockers have been demonstrated to
Treatment Protocols
s0700
beta blockers may reduce the dynamic outflow veloping heart disease such as those with cer-
tract obstruction seen in some of these patients. tain genetics, a family history of heart disease,
Carvedilol (CoReg), a third-generation, non- a breed predisposition, or concurrent systemic
selective beta blocker with alpha-1 blocking disease with cardiovascular implications. Exam-
activity as well as antioxidative effects, can be ples include the following: cavalier King Charles
administered to stable patients with heart fail- Spaniels are at risk for developing chronic valve
ure for cardioprotective effects at a dosage of disease; Doberman Pinschers are at risk for de-
1.56 mg PO every 24 hours for 1 to 2 weeks, veloping DCM; Boxers are at risk for developing
then 1.56 mg PO every 12 hours, and then up- arrhythmogenic right ventricular cardiomyopa-
ward titration to the maximal tolerated dosage thy, and so on.
(0.4 mg/kg PO every 12 hours). No therapy is indicated for dogs in stage A
Manage predisposing conditions
b0120
Manage systemic hypertension, if present
Key Point No dietary sodium modifications necessary
In general, beta blockers in patients with ad-
vanced cardiac disease should be used only Stage B
s0720
signs of CHF.
Novel Vasodilators (Sildenafil) Same as in stage A
s0690
Sildenafil is a phosphodiesterase V inhibitor that Increase the awareness of signs of CHF (tachy-
has been shown to improve both exercise toler- pnea, dyspnea, coughing)
u0570
ance and quality of life in humans with pulmo- Periodic reevaluation for signs of disease pro-
nary hypertension. gression and complications
Initial clinical observations indicate that sildena- For patients with chronic valve disease, there is
fil may also have a positive effect in dogs with no evidence indicating that there is any benefi-
acquired pulmonary hypertension secondary cial effect of using an ACE inhibitor or pimo-
to chronic valve disease, congenital heart dis- bendan at this stage
ease, chronic pulmonary disease, and heartworm For patients with DCM, there are no drugs
disease. recommended for routine use; however, ACE
Can be used in combination with pimoben- inhibitors, pimobendan, digoxin (if atrial fibril-
dan (Vetmedin) for additional inodilator lation is present), or beta blockers may be initi-
effect. ated in selected patients.
310 Section IiI Treatment of Cardiovascular Disease
Drugs for routine use: furosemide (mandatory), Treat hypoxemia, increase cardiac output, con-
ACE inhibitor, pimobendan tinue previous cardiac drugs (see stage C2),
Drugs for selected patients: spironolactone, and stabilize the patient in hospital with intra-
digoxin, thiazide, amlodipine/hydralazine or venous drugs.
other vasodilator Drugs for routine use: as for stage C2 plus oxy-
Avoid, if possible, excessive sodium intake, gen, IV furosemide, nitroglycerin
beta blockers, corticosteroids, IV fluids (unless Drugs for selected patients: dobutamine, nitro-
required for concurrent disease; requires care- prusside
ful monitoring of the respiratory rate trend)
b0140
Key Point
Key Point Aggressive diuresis (repeated IV boluses or
continuous rate infusion of furosemide) is in-
b0130
s0740
Stage C2
Drugs for routine use: continue current cardiac
mild to moderate CHF is present medications as in stage C plus spironolactone,
u0620
Goals are to attain stage C1 (eliminate pulmonary thiazides, digoxin, subcutaneous furosemide,
edema and/or effusions), improve hemodynam- repeated centesis for effusions, and very low
ics, and to modulate neurohormonal activation. sodium intake.
In patients with chronic valve disease, the use Drugs for selected patients: As per stage C3
of furosemide is mandatory and the addition of For chronic valve disease, consider additional
ACE inhibitor with or without pimobendan is vasodilation with amlodipine or hydralazine.
recommended. There is currently no consensus For DCM, dobutamine (continuous rate in-
on which to use first in combination with fu- fusion for 48 hours every 3 weeks) may be
rosemide, although initiation of both agents is helpful.
reasonable (at this time there are no studies that
have evaluated the efficacy of the combination
Specific Disease Treatment
s0770
is recommended to control the ventricular re- without Congestive Heart Failure (Stage B)
sponse rate if atrial fibrillation is present. Beta ACE inhibitor therapy is initiated when there is
u0650
blockers should not be used. clinical evidence that the heart disease present
In patients with symptomatic DCM, furose- has led to heart failure and activation of com-
mide, ACE inhibitor, and pimobendan are rec- pensatory mechanisms (RAAS). Compensated
ommended. Digoxin (with or without diltia- heart failure can usually be identified with tho-
zem) is recommended to control the ventricular racic radiography. For example, the presence of
Chapter 15 Pathophysiology and Therapy of Heart Failure 311
pulmonary venous congestion with left atrial and respiratory rate indicates adequate preload reduc-
ventricular enlargement in a 10-year-old minia- tion. Once the respiratory rate has stabilized in the
ture poodle with a loud left apical holosystolic normal range (usually less than 30 breaths per min-
Murmur secondary to MR Probably represents ute), the diuretic dose is tapered down to the lowest
compensated heart failure. dose capable of controlling the signs of CHF.
In this scenario, enalapril (0.5 mg/kg) or some A trend of increasing resting respiratory rate sug-
other ACE inhibitor may be initiated (with pre- gests worsening of the pulmonary edema and the
treatment and 1-week post-treatment renal evalu- need for higher dosages of diuretics or the ad-
ations) once daily, although there is no evidence dition of other medications such as intermittent
that this therapy will delay the onset of clinical nitrate therapy (nitroglycerin to 1 inch cutane-
signs. Some dogs with primary valve disease ously every 8 to 12 hours). Beware of nitroglyc-
develop significant left atrial enlargement sec- erine tolerance as described previously.
ondary to MR. These dogs become symptom-
atic (coughing) because there is compression of Chronic Valve Disease with Symptomatic
s0800
the left mainstem bronchus by the enlarged left Congestive Heart Failure (Stage C3)
atrium. Dogs with severe CHF secondary to primary valve
u0670
These cases require the therapeutic efforts to be disease are symptomatic at rest and may require
aimed at reducing the MR (vasodilation with ACE aggressive therapy to control pulmonary edema.
inhibitors, preload reduction with diuretics, and These patients typically require relatively high
heart rate control with digoxin) and suppressing doses of furosemide as well as optimized doses
the cough reflex (butorphanol or hydrocodone). of ACE inhibitor and pimobendan.
Coughing in these patients often becomes refrac- If the patient is dyspneic, hospitalization is in-
tory to medical therapy. dicated to provide oxygen therapy in addition to
close monitoring and parenteral administration of
Chronic Valve Disease with Symptomatic furosemide. Adjunctive therapy with nitroglyc-
s0790
clinical signs of moderate CHF. The earliest signs fusion is present. Furosemide (2 to 4 mg/kg IV)
of decompensation are usually not noticed by the is administered, and the respiratory rate is moni-
pets owner. Elevated respiratory rates during rest tored for a trend of decreasing respiratory rate. If
(tachypnea) may be mistaken for panting, and are no decline in respiratory rate is observed within
often overlooked. Tachypnea is associated with the 1 to 2 hours, furosemide is again administered at
onset of interstitial (stage II) pulmonary edema. the same or a slightly higher dose. The respira-
In addition to tachypnea, dogs with moderate tory rate is again monitored, and the preceding is
CHF may also exhibit exercise intolerance or repeated if there is no improvement. As the respi-
coughing. Again, thoracic radiography can reveal ratory rate decreases, the dosage and frequency
the presence of interstitial pulmonary edema (in- of administration are reduced to the lowest dose
creased interstitial pattern, enlarged pulmonary effective in controlling the pulmonary edema.
veins with fuzzy, indistinct borders, and concur- Pretreatment evaluation of renal function and
rent left atrial and ventricular enlargement) as hydration status aids in selecting the appropriate
well as bronchial compression, if present. furosemide dose.
The appropriate therapy for this patient includes In the presence of refractory, severe, chronic CHF,
ACE inhibitor therapy (enalapril 0.5 mg/kg PO the addition of spironolactone with or without a
twice a day), furosemide (2 to 4 mg/kg PO two or thiazide to conventional therapy may help control
three times a day), with or without pimobendan edema formation. Furthermore, intermittent ther-
(0.25 mg/kg PO every 12 hours on an empty stom- apy with nitrates, such as nitroglycerin or isosor-
ach). Digoxin is usually initiated if: bide dinitrate, may also aid in reducing ventricular
Myocardial failure is present filling pressures and the formation of edema.
Atrial fibrillation or other supraventricular
tachycardia is present Mild Heart Failure Secondary to Dilated
s0810
The resting respiratory rate can be used to monitor tion, or evidence of myocardial failure (reduced
the response to therapy. A trend of decreasing resting fractional shortening percentage and increased
312 Section IiI Treatment of Cardiovascular Disease
mitral valve E-point septal separation), particu- Furosemide (up to 6 to 8 mg/kg IV) may be given
larly in dogs that are predisposed to idiopathic every 1 to 2 hours until the resting respiratory rate
DCM (e.g., Doberman Pinschers and others), is decreasing. Then administer furosemide (2 to 4
suggests a diagnosis of occult DCM. mg/kg IV) every 4 to 8 hours, depending on the
Although these dogs are usually asymptomatic, status of the patient. The goal is to taper the dose
they often have progressive heart failure. ACE in- to the lowest effective dose and the frequency
hibitor therapy (enalapril 0.5 mg PO once or twice of administration to two to three times a day as
a day or benazepril 0.25 mg PO once a day) can quickly as possible.
be initiated in these dogs in an attempt to prolong If intravenous dobutamine/nitroprusside therapy is
the asymptomatic phase of the disease course. necessary to control the symptoms of heart failure,
Beta-adrenergic blocking agents may also be in- the nitroprusside dose should be adjusted to de-
dicated in these patients. crease mean or systolic arterial blood pressure by
Digoxin and/or pimobendan therapy is also in- 15 to 30 mm Hg. The long-term survival of dogs
dicated in patients with myocardial failure, with severe, life-threatening heart failure is poor.
however therapy is usually not initiated unless
CHF is present. Some Spaniel breeds (American Feline Cardiomyopathy (Dilated
s0840
mentation instituted (500 mg PO twice a day) if myopathy is based on the type of cardiomyopa-
indicated. thy present and the presence of symptoms (i.e.,
symptomatic CHF). Evaluation of the patient
Moderate Heart Failure Secondary to Dilated with electrocardiography, thoracic radiography,
s0820
Cardiomyopathy with Symptomatic Congestive and echocardiography usually enables the clini-
Heart Failure (Stage C) cian to characterize the cardiomyopathy as be-
As heart failure progresses, filling pressures even- ing associated with myocardial systolic failure
u0690
tually become elevated and pulmonary edema (DCM and, sometimes, restrictive cardiomyopa-
may develop. thy [RCM]) or diastolic dysfunction (hypertro-
The therapeutic protocol in this patient is essen- phic cardiomypathy [HCM] and RCM).
tially the same as that for a patient with moderate In general, cats with primary systolic dysfunction
heart failure secondary to MR. The only differ- are symptomatic at diagnosis. These cats receive
ence is that pimobendan and/or digoxin is initiated combinations of digoxin (a fourth of a 0.125 mg
earlier in the disease course of cardiomyopathy. tablet PO once a day or every other day, with dose
Conventional therapy for this patient with symp- adjustment based on trough serum levels about 2
tomatic heart failure consists of an ACE inhibi- weeks after initiation of therapy), enalapril (1 to
tor, furosemide, and pimobendan. These patients 2 mg PO every other day to twice a day for cats
frequently have cardiac rhythm disturbances that depending on renal status), and furosemide (6.25
may be associated with symptoms or may be ag to 12.5 mg PO once or twice a day).
gravating the CHF. In this scenario, antiarrhythmic There seems to be an increased risk of intracar-
therapy is indicated (e. g., digoxin with or with diac thrombus formation if marked left atrial
out diltiazem to control the ventricular response enlargement is present. In this scenario, aspirin
to atrial fibrillation). Antiarrhythmic therapy is (25 mg/kg PO every 3 days) or warfarin sodium
typically not indicated in patients with arrhyth (Coumadin) can be initiated. The initial dose for
mias that are not associated with clinical signs of warfarin is 0.5 mg every 24 hours for a 3- to 5-kg
reduced cardiac output and poor tissue perfusion. cat, monitored with either prothrombin time (PT),
activated partial thromboplastin time, or proteins
Severe Heart Failure Secondary to Dilated induced by vitamin K antagonists. Anticoagulants
s0830
severe symptomatic heart failure. Oxygen ther- compared with antiplatelet agents such as aspirin.
apy, ACE inhibitors, pimobendan, furosemide, However, serious side effects (hemorrhage) and
and, possibly, dobutamine and nitroprusside may the need for close monitoring of bleeding times
be necessary to control pulmonary edema in life- may limit their use. Furthermore, the recurrence
threatening heart failure. rate for thromboembolism in cardiomyopathic
Chapter 15 Pathophysiology and Therapy of Heart Failure 313
cats is high, regardless of the agent used. There IV every 3 to 4 hours) and topical 2 % nitroglycerin
is some evidence that Plavix (clopidogrel; 18.75 ( to inch every 8 hours) are usually effective
mg PO every 24 hours) may prevent thrombus in reducing filling pressures, therefore facilitating
formation in cats at risk of intracardiac thrombus the resolution of the pulmonary edema. The dosing
formation. Low-molecular-weight heparins such frequency and dosage of furosemide are reduced
as dalteparin (Fragmin; 100 U/kg subcutaneously once clinical improvement is noted, as evidenced
every 24 hours) or enoxaparin (Lovonox; 1 to 1.5 by a reduction in resing respiratory rate.
mg/kg subcutaneously every 12 to 24 hours) may In addition to preload reducers, an agent to im-
also have beneficial effects in cats at risk. How- prove diastolic function (beta blocker or cal
ever, these dosages have largely been borrowed cium channel blocker) may be used. Caution
from the human literature and specific dosages should be exercised when administering beta
have not been established in cats. blockers to patients with severe CHF and pos-
Cats with HCM may be completely asymptomatic sible myocardial failure. Oxygen therapy is also
or may present with tachypnea and dyspnea asso- indicated.
ciated with decompensated diastolic heart failure. The medical management of feline RCM is simi-
There is some controversy as to which agent is the lar to the therapy for DCM because systolic dys-
drug of choice in cats with diastolic dysfunction. function is usually present in both. Combinations
Calcium channel blockers (diltiazem) and beta of enalapril, digoxin, and furosemide are cur-
blockers (atenolol) facilitate diastolic function, rently recommended.
but in different ways. Beta blockers probably fa-
cilitate diastolic function only by decreasing the Pericardial Disease
s0850
heart rate and myocardial oxygen consumption. The management of chronic pericardial effusion
u0720
Calcium channel blockers facilitate diastolic and cardiac tamponade is quite straightforward.
function by improving myocardial relaxation An echocardiogram is performed to confirm the
through normalization of abnormal myocardial diagnosis of pericardial effusion and to attempt
calcium currents as well as by coronary vasodila- to ascertain if the underlying cause is neoplasia.
tion to improve myocardial perfusion. If the prognosis is favorable, pericardiocentesis is
In asymptomatic cats with HCM, the therapy is performed to relieve the compression on the heart
based on the presence of tachycardia, dynamic left by the elevated intrapericardial pressure. If the ef-
ventricular outflow obstruction, and the severity of fusion returns more than once, a pericardectomy
concentric hypertrophy and left atrial enlargement. is recommended (see chapter 11).
If tachycardia (heart rate more than 200 beats per
minute), dynamic left ventricular outflow obstruc- Congestive Heart Failure Associated with
s0860
tion, and marked hypertrophy are present, therapy Chronic Heartworm Disease:
with a beta blocker is initiated (atenolol 6.25 to 12.5 The approach to dogs with CHF associated
u0730
mg PO once or twice a day). Beta blockers appear with chronic heartworm disease involves cage
to be more effective than calcium channel blockers rest, diuretic therapy, and heartworm adulticide
in controlling the heart rate in tachycardic cats. Ad- therapy. These patients are cage rested a mini-
ditionally, beta blockers are probably more effective mum of 1 week before adulticide therapy (staged
in reducing the dynamic outflow tract obstruction melarsomine adulticide protocol). Heart failure
seen in some cats with HCM. Beta blockers should medications (ACE inhibitors, furosemide, spi-
be avoided if decompensated CHF is present. ronolactone, pimobendan, sildenafil) may be
Tachycardia, CHF, and thromboembolism are discontinued in some patients 4 to 8 weeks after
considered to be negative prognostic indicators adulticide therapy (see Chapter 10).
in cardiomyopathic cats.
Frequently Asked Questions
b0150
Suggested Readings
Bulmer BJ and Sisson DD: Therapy of heart failure. In
Ettinger SJ ed: Textbook of veterinary internal medi-
cine, ed 6, Philadelphia, 2005, WB Saunders.
Colucci WS, Braunwald E: Pathophysiology of heart
failure. In Braunwald E, ed: Heart disease: a textbook
of cardiovascular medicine, ed 5, Philadelphia, 1997,
WB Saunders.
Chapter 16
Table 16-1 Agents for Rate Control/Abolishing Arrhythmias in Canine Patients with
Supraventricular Arrhythmias
The benefits of a 24-hour Holter recording If treatment is instituted, it is critical to obtain a re-
include in-depth assessment of quantity and peat Holter recording after 1 or 2 weeks to determine
quality of the arrhythmia(s). The following if the drugs are efficacious at suppressing the ab-
parameters should be examined: Number of normal rhythms, or possibly harmful by being pro-
abnormal beats (supraventricular and or ven- arrhythmic, that is causing ventricular arrhythmias or
tricular) relative to overall number of beats, du- excessive pauses. This can only be established if a
ration and rate of runs of abnormal beats; the comparison to the pre-drug baseline is performed.
average hourly and daily heart rate, the amount If a Holter shows that a drug is effective, we rec-
of time when the heart rate is greater than 120 ommend monitoring the progression of the ar-
or lesser than 50 bpm as well as the presence rhythmia by repeat Holter recordings every 6 to 12
and length of pauses. A diary kept by the cli- months. If an animal experiences recurrent syn-
ent or hospital staff with the sleep/wakefulness cope during that time, an immediate repeat Holter
activity or observed events such as syncope is recommended.
or excessive anxiety or panting help correlate In animals that need to be stabilized immediately
ECG changes on the Holter with clinical signs. (no time for a baseline 24-hour Holter record-
These parameters are vital for a baseline evalu- ing prior to intravenous antiarrhythmics), it is
ation of a patients arrhythmias and needs for still advised to acquire a post-treatment Holter
antiarrhythmic therapy. recording to evaluate drug efficacy and possible
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 317
Table 16-2 Agents for Rate Control/Abolishing Arrhythmias in Canine Patients with Ventricular
Arrhythmias
Drug Oral administration Intravenous administration Indication
toxicity once the dog is stabilized and receiving An SVA is AV node independent, if the ECG
chronic oral antiarrhythmic therapy. contains P waves not conducted to the ventricle
without termination of the SVA. Interventions
t Supraventricular such as vagal maneuvers or drugs that slow AV
node conduction can help identify the underlying
Arrhythmias mechanism:
If the atrial activation rate is unchanged (PP
SVAs include rhythms that originate in the sinus interval the same) following the intervention,
node, atrial tissue and AV junction. Importantly, but the ventricular rate slows due to AV block,
SVA must be differentiated from accelerated normal the SVA is likely AV node independent.
sinus rhythm. Physiologic sinus tachycardia can be If the intervention results in abolishment of the
caused by many conditions including febrile states, SVA and restoration of a normal sinus rhythm
anemia, heart failure, adrenergic medications and (even if it is only transient), the arrhythmia is
anxiety. In these cases, management should fore- likely AV node dependent.
most be focused on correcting the underlying cause Examples of AV nodeindependent rhythms in-
or disease resulting in increased sympathetic tone. clude sinus node reentrant tachycardia, AF, AFL,
Because of the mechanism of action of antiarrhyth- and ectopic atrial tachycardia. These arrhythmias
mic drugs, it is useful to assess SVA as either AV can be challenging to manage, since the antiarrhyth-
node independent (does not need the AV node to mic drugs (NCB, KCB or combinations thereof)
sustain the rhythm) or AV node dependent (path- are often not very efficacious for suppression of
way requires the AV node to sustain the rhythm). these arrhythmias. If the abnormal rhythm cannot
318 Section III Treatment of Cardiovascular Disease
be abolished with drugs, the secondary mode of clinical signs of heart failure. AF can also occur in
treatment aims at controlling the ventricular re- the absence of overt structural heart disease (lone
sponse rate by slowing the AV node conduction or primary AF). In these cases, the ventricular re-
with CCBs, BBs or digoxin. sponse rate can be normal or only mildly elevated.
AV nodedependent SVAs include AV reentrant
tachycardia (accessory pathway [AP] mediated)
and AV nodal reentrant tachycardia. AV node Key Point
dependent arrhythmias can usually be treated with The management of AF largely depends on
drugs that target the AV node (CCBs and BBs). the average heart rate. A baseline 24-hour
Holter recording, acquired in the home en-
vironment is ideal to determine the average
heart rate of a patient.
Key Point
To help guide treatment of SVAs, they should
be characterized as AV node dependent or in-
dependent. The following flow chart (Figure 16-1) should
serve to identify patients in need of treatment
for AF and to decide which therapeutic ap-
proach might be best in each individual case.
Atrial Fibrillation
AF is one of the most commonly seen SVAs in
Therapy
veterinary practice. In dogs and cats, AF is usually a
chronic arrhythmia associated with advanced stages AF is anAV nodeindependent arrhythmia, caused
of chronic AV valve insufficiency or cardiomyopa- by multiple simultaneous intra-atrial reentrant cir-
thy. In those patients, the ventricular response rate cuits. Medical conversion of AF to sinus rhythm
is often markedly elevated, which contributes to the with drugs is very difficult and rarely achieved in
AF on ECG
Obtain average HR
by 24h Holter recording
Figure 16-1. Flow chart describing the approach to treatment of atrial fibrillation (AF) based on the average heart rate (HR) of a patient
as determined by a 24-hour Holter recording. AF, Atrial fibrillation; HR, heart rate; bpm, beats per minute; DCM, dilated cardiomyopathy.
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 319
Figure 16-2. Management of dogs with AF with a fast heart rate (average heart rate > 180 bpm). HR, Heart rate; bpm; beats
per minute; CRI, constant-rate infusion.
canine patients. In most cases, ventricular rate con- average heart rate. The authors prioritize treat-
trol via slowing of AV node conduction with diltia- ment according to three general categories of
zem and or digoxin is the goal (drug dosages are ventricular response rate: (1) fast (Figure 16-2:
listed in Table 16-1). The veterinary literature also average heart rate faster than 180 bpm), (2) mod-
cites atenolol as effective for rate control of AF. erate (Figure 16-3: average heart rate 130 to 160
The authors do not have much personal experience bpm) and (3) slow (Figure 16-4: heart rate around
with atenolol for this purpose. The reluctance to 100 bpm). The dosages for the drug listed in
use atenolol for rate control stems in part from the Figures 16-2, 16-3 and 16-4 are provided in
concomitant degree of advanced myocardial fail- Table 16-1.
ure in many patients with AF. In our experience Treatment of AF in cats is challenging. There is
diltiazem XR is very well tolerated even in dogs usually significant underlying heart disease pres-
with severe systolic myocardial dysfunction. ent, resulting in markedly enlarged atria and very
Dogs with normal cardiac function or only mild rapid AF. Medical management for rate control
dysfunction and normal to moderately elevated with a target heart rate of 130 to 150 bpm may
ventricular response rates may be candidates for be achieved using either CCB or BB (for drug
electric cardioversion of AF to sinus rhythm. dosages for antiarrhythmic drugs in cats see
Medical management varies with the initial aver- Table 16-3).
age heart rate and overall condition of the dog Occasionally, the administration of narcotics has
(Figures 16-2 through 16-4). Treatment can be been associated with the induction of AF in large
tailored to the patient based on the approximate dogs. This is likely caused by the increased vagal
320 Section III Treatment of Cardiovascular Disease
Diltiazem XR PO Electric
+/ digoxin PO cardioversion
Figure 16-3. Management of dogs with AF with a moderately elevated average heart rate of 130 to 160 bpm. HR, Heart rate;
bpm, beats per minute; AF, atrial fibrillation.
tone that occurs with narcotics. Treatment with and the goal of cardioversion is to avoid structural
2 mg/kg lidocaine IV within 4 hours of onset has or functional remodeling from chronic AF, even if
been demonstrated to restore sinus rhythm. Va- the heart rate is slow. The rate of recurrence of AF
golytic drugs (atropine) should prevent onset or after successful cardioversion is high and morbidity
recurrence of AF in such cases. associated with repeat transthoracic cardioversions
under general anesthesia make this management
Key Point less practical. Pretreatment with sotalol, amiodarone
or angiotensin-converting enzyme inhibitors may
Digoxin monotherapy does not control the
ventricular response rate adequately during improve the chances of cardioversion and lessen
times of excitement, stress or exercise. Thus, the rate of recurrence of AF; however, no studies in
dogs with AF and moderate to fast heart rates veterinary medicine have proven these concepts.
will require combination therapy of digoxin
with diltiazem or atenolol. Transthoracic Electrical Cardioversion
Procedure
Procedure requires a brief general anesthesia
Electric Cardioversion (Rhythm Control) Fast Patch electrodes are recommended instead
In a subgroup of canine patients with mild struc- of hand-held paddles to optimize electrode posi-
tural heart disease or lone AF, electric cardioversion tion for cardioversion.
of AF to sinus rhythm can be achieved. The patients Dog is shaved before application of the patch
selected for this treatment are well compensated over the heart on both lateral sides of the thorax.
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 321
Figure 16-4. Management of dogs with AF with a low average heart rate ( 100 bpm). HR, Heart rate; bpm, beats per minute;
AF, atrial fibrillation.
Table 16-3 Agents for Rate Control/Abolishing Arrhythmias in Feline Patients with Arrhythmias
Drug Oral administration Intravenous administration Indication
Dog is positioned in lateral recumbency to optimally with CCBs or BBs is used effectively in dogs (for
position heart between the two patch electrodes. drug dosages see Table 16-1). Digoxin monother-
Defibrillator ECG cables need to record patients apy is ineffective for management of AFL.
ECG and synchronize to the R waves. With false A post-drug 24-hour Holter should be obtained to
synchronization to T waves (occurs if T wave is determine if drugs are effective at suppressing the
taller than the R wave) the cardioversion shock AFL or producing the desired AV block, thereby
can induce VF! slowing the ventricular response adequately. It
Using a monophasic defibrillator: also allows survey for drug toxicity, manifest as
Start with 4 J/kg; If no cardioversion occurs, bradycardia or pauses secondary to excessive AV
increase dose by 50 J and repeat until a maxi- block. Pauses, if they occur only during sleep or
mum of 360 J. rest, are usually of no concern.
Using a biphasic defibrillator:
Start with 1 to 2 J/kg; If no cardioversion
Ectopic Atrial
occurs, increase dose by 50 J and repeat until
Tachycardia
a max of 360 J.
Short, transient runs of ventricular tachycardia Atrial tachycardia (AT) occurs when ectopic foci in
(VT) or sinus pauses or AV block are common the atria develop the ability to fire rapidly on their
following electric cardioversion. own. It is an AV nodeindependent arrhythmia.
Ectopic AT is often paroxysmal and may display a
gradual onset and offset (warm-up and cool-down
Atrial Flutter period) if the underlying mechanism involves ab-
Atrial flutter (AFL) is relatively uncommon in normal automaticity. The heart rate can vary from
veterinary patients. Theoretically, AFL could 150 to 300 bpm and can cause anxiety or panting
set the stage for development of AF due to the in affected dogs. In cats ectopic AT is rare.
remodeling that occurs with continuous rapid A baseline 24-hour Holter should be obtained to
activation of the atrial myocardium. In some determine what percentage of time a dog is in AT,
patients AFL co-exists with AF on a 24-hour and how fast the heart rate is during the AT.
Holter, which might represent a transition phase
to chronic AF. AFL is an AV nodeindependent
Therapy
intra-atrial macro-reentry rhythm. The atrial acti-
vation rate (PP interval) is 300 to 600 bpm. AFL Ideally, suppression of the rapidly firing atrial fo-
is paroxysmal or chronic and can be associated cus is attempted by using sotalol, amiodarone or
with excessively high ventricular response rates. procainamide. In people, propafenone is used for
AV conduction usually changes between 1:1 and treatment of AT, but we have not found these agents
3:1 or 2:1 due to variable degrees of AV block. efficacious in our patients. In fact, targeting the ab-
A baseline 24-hour Holter is recommended to de- normal rhythm directly with these drugs is often
termine of the arrhythmia is chronic or paroxys- unsuccessful. Thus, as a second choice, therapy for
mal. If it is chronic, drug therapy is indicated. AT should be aimed at slowing AV node conduction
If it is paroxysmal and infrequent, treatment with CCBs or BBs to reduce the ventricular response.
may be postponed, but a reevaluation by Holter Digoxin is ineffective for management of AT.
6 months later should be performed to check for A post-drug 24-hour Holter should be obtained to
progression from paroxysmal to chronic AFL or determine if drugs are effective at suppressing the
presence of concurrent AF. AT or producing the desired AV block, thus slowing
the ventricular response adequately. The Holter also
allows survey for excessive AV block; this may be
Drug Therapy
undesired if it occurs other than during rest or sleep.
Ideally, therapy is aimed at suppressing the atrial
reentry circuit using sotalol, amiodarone or pro- Key Point
cainamide; however, abolishing the AFL with
Although amiodarone is a potent antiarrhythmic
drugs is often unsuccessful; propafenone and
drug, its benefits must be balanced against its
flecainide are used in humans with AFL, but the slow onset to action and adverse effects which
authors have had little success in dogs with these include hepatic toxicity, gastrointestinal distur-
drugs. The adequate dose for dogs has not been bances and blood dyscrasias in canine patients.
identified. Rate-control via slowing of the AV node
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 323
the form of a pronounced sinus arrhythmia or and a sympathomimetic (e.g., albuterol: Proventil
regular sinus bradycardia. This pathologic brady- 0.02 to 0.05 mg/kg PO two to three times a day) or
cardia often persists during excitement or exer- a phosphodiesterase inhibitor (e.g.,theophylline;
cise. The bradycardia is either primary, which is Theo-Dur 20 mg/kg PO twice a day).
a form of sick sinus syndrome (see next section) In the authors experience, erratic and poor efficacy
or secondary to an underlying systemic disease or as well as adverse effects such as anxiety, excessive
drug toxicity (e.g., narcotics or overdosing of panting, anorexia or gastrointestinal signs are signif-
BBs, CCBs, or digoxin). icant disadvantages to these therapies; therefore, we
Secondary sinus bradycardia is usually caused by usually do not prescribe these drugs in our clinic.
excessive vagal tone elicited by a systemic disease.
Central nervous system disease (increased intra-
Sick Sinus Syndrome
cranial or intraocular pressure or head trauma),
severe pain, or respiratory or gastrointestinal dis- The spontaneous sinus node discharge is either
ease can all cause increased vagal tone and sinus slower than normal (primary sinus bradycardia)
bradycardia. A vagal maneuver (e.g., carotid sinus or intermittently absent (sinus arrest or exit block
massage) can cause transient sinus bradycardia by from the sinus node). In the latter, there are pauses
the same mechanism of action. Correction of the of various durations without P waves or an escape
underlying condition or discontinuation of drugs rhythm. The subsidiary pacemaker tissue (AV node
will usually resolve secondary sinus bradycardia. and Purkinje fibers) is often also abnormal, resulting
Clinical signs may be absent (incidental finding) or in inadequate escape rhythms, such that complete
dogs may display weakness, exercise intolerance asystole (pauses) can last up to 10 seconds. Minia-
or syncope. A 24-hour Holter may be required to ture Schnauzers, Cocker Spaniels, West Highland
determine the severity of bradycardia and possible White Terriers and Dachshunds are over-repre-
association of clinical signs with the slow heart rate. sented. Doberman Pinschers are also reported to
Mild exercise intolerance is often underrecognized have syncope associated with long sinus pauses,
by owners and mistakenly attributed to old age. suggestive of sick sinus syndrome (SSS).
In cats, sinus rhythm at less than 120 bpm can Clinical signs range from exercise intolerance
be considered bradycardia, and heart rates below and lethargy to syncope. Dogs with SSS manifest
100 bpm are often associated with lethargy or as primary sinus bradycardia typically show only
syncope in cats. mild exercise intolerance, which is often under-
recognized by owners and mistakenly attributed
to old age. SSS may be incidentally diagnosed
Treatment
during a routine pre-anesthesia workup in a ge-
The decision to treat sinus bradycardia should be riatric dog. If these dogs are treated with a pace-
based on clinical signs and the degree of brady- maker, owners often are delighted by the return
cardia. In patients experiencing syncope or epi- of youth and energy in their old dogs.
sodic weakness, pacemaker therapy is indicated. Due to the intermittent nature of the sinus pauses in
In an animal with no clinical signs, sinus bradycar- some cases, a 24-hour Holter is often necessary to
dia may be waited out with close monitoring. definitively determine the cause of clinical signs.
If the animal appears unstable and pacemaker
therapy is not an option, medical therapy aimed
Treatment
at abolishing high vagal tone can be attempted for
temporary support. An atropine response test may Pacemaker therapy is indicated for syncopal or le-
help identify patients that would benefit from such thargic dogs with SSS. In dogs with intact AV node
medical management. Following injection of atro- function, transvenous placement of a pacing lead
pine 0.02 mg/kg (0.01 to 0.04) IM or IV, the baseline in the right atrium or auricle can successfully abol-
heart rate should increase by 50% to 100% within ish the sinus pauses. In dogs with concomitant AV
5 to 10 minutes (initial worsening of AV block is a node dysfunction, the lead should be placed in the
normal transient response). Patients experiencing right ventricle or dual chamber pacing performed.
at least a partial response to atropine may be candi- Some cases have brady-tachy syndrome, where
dates for medical management of sinus bradycar- in addition to the sinus pauses, supraventricular
dia. Treatment options include either a combination tachyarrhythmias (e.g., atrial tachycardia, flut-
of a vagolytic drug (e.g., probantheline bromide: ter or fibrillation) are present. In such cases a
Pro-Banthine 0.25 to 0.5 mg/kg PO twice a day) 24-hour Holter should be obtained to determine
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 325
the clinical relevance of the SVA and require- therapy will lead to insulin secretion that will drive
ment for antiarrhythmic therapy. Antiarrhythmic potassium back into the cells. More aggressive
therapy may be necessary if the SVA persists therapy involves intravenous sodium bicarbonate
post pacemaker implantation. In many cases, (1 to 2 mEq/kg IV slowly over 20 minutes) to drive
SVA spontaneously resolves once the long sinus K back into the cell. Alternatively, slow intravenous
pauses are prevented by the pacemaker. administration of 0.5 U/kg of regular insulin cou-
If the animal does not have syncope and shows pled with 2 g of dextrose per unit of insulin can be
either no or only mild clinical signs, medical administered. Monitoring for hypoglycemia post
management can be attempted (see medical treat- treatment is required. Calcium gluconate (0.5 to
ment of sinus bradycardia). 1 ml/kg of a 10% solution) may be given by very
However, many of the mild forms of SSS tend slow intravenous administration for refractory
to progress over weeks or months to the point of cases of hyperkalemia. This is cardioprotective
syncope, and pacemaker implantation will even- because the increased extracellular Ca2+ makes
tually be required. more sodium channels available for activation.
It is the authors experience that medical man-
agement is ineffective in dogs with syncope and
pacemaker therapy is always recommended. Atrioventricular (AV)
Conduction Abnormalities
Atrial Standstill AV Block, First Degree
Atrial standstill occurs when the atrial myocar- Prolonged conduction time through the AV node,
dium is not able to depolarize, and P waves cannot results in an increased PR interval of 0.13 second
be identified on the surface ECG. The two main in dogs and 0.09 second in cats. There are normal
causes are (1) persistent atrial standstill or silent P waves and QRS complexes, conducting at a
atrium due to primary atrial muscle disease and 1:1 ratio. No treatment is required
(2) secondary atrial standstill caused by hyper-
kalemia (i.e., renal failure, ruptured bladder, Ad-
AV Block, Second Degree
disons disease, or other electrolyte imbalances).
Hyperkalemia alters atrial transmembrane resting There are normalP wave and QRS complexes with
potential and the atria become inexcitable at very a constant PR interval, but intermittently P waves
high plasma K+ levels. Atrial standstill is uncom- are not followed by QRS complexes. In Mobitz type
mon in dogs and exceedingly rare in cats. I (Wenckebach) AV block, the PR interval gradu-
ally prolongs before a P wave is blocked. This form
of second-degree AV block is less frequent in dogs.
Therapy
Mobitz type II AV block demonstrates a consistent
If atrial muscle disease is causing atrial standstill, PR interval prior to a blocked P wave. Mobitz type
pacemaker therapy is required. Because the atria II AV block may represent a more advanced degree
are structurally abnormal, the pacing lead has to of conduction abnormality that occurs in the AV
be placed in the right ventricle. Unfortunately, the junction, His bundle, or below. Occasional single
primary cardiac muscle disease progressively af- blocked P waves are of no clinical significance.
fects the ventricles. Within 1 to 2 years, ventricular In high grade second-degree AV block, there
myocardial dysfunction and significant AV valve are several consecutive blocked P waves. Clinical
regurgitation may develop and pacemaker failure signs depend on the length of ventricular asys-
may ensue due to lack of capture. tole. In cases with intermittent high grade sec-
For atrial standstill secondary to hyperkalemia, ond-degree AV block, a 24-hour Holter may be
emergency therapy according to the severity of the required to make a definitive diagnosis. If clinical
hyperkalemia and bradycardia is required. Intra- signs such as lethargy or syncope are observed,
venous fluids are the primary treatment. This will pacemaker therapy is indicated.
lower potassium values by dilution and increased
excretion. Acceptable fluids include normal sa-
AV Block, Complete or Third Degree
line, half-strength saline with 2.5% dextrose, or
5% dextrose in water. Alternatively, potassium None of the P waves conduct through the AV
can be lowered by promoting entry of K ions back node, thus the atrial and ventricular activities
into the intracellular space. The dextrose in fluid are independent. The atrial rate (PP interval)
326 Section III Treatment of Cardiovascular Disease
is faster than the ventricular (escape) rate dif- and Great Danes with dilated cardiomyopathy
ferentiating complete AV block from AV dis- (DCM), and German shepherds with inherited
sociation due to accelerated idioventricular ventricular arrhythmias. Dogs with congenital
rhythms. The ventricular escape rhythm is usu- heart disease, such as severe subaortic or pulmonic
ally regular and below 40 bpm, whereas a low stenosis are predisposed to development of
AV junctional escape rhythm has a rate of 40 ventricular arrhythmias, likely due to abnormal
to 60 bpm in dogs. In cats with complete AV myocardial perfusion secondary to myocardial
block the ventricular escape rhythm varies from hypertrophy. These arrhythmias can be worse
60 to 100 bpm. during exercise and may be exacerbated during
Complete AV block is a primary abnormality of cardiac catheterization for angiography or in-
the AV conducting system (AV node). However, terventional therapy. Catheter contact with the
it is important to evaluate the animals elec- endocardium can elicit ventricular arrhythmias
trolyte and acid-base status. Systemic diseases and even cause VF.
causing hyperkalemia such as Addisons disease Furthermore, significant ventricular arrhythmias
or urethral obstruction can cause AV block that can be seen in any dog hit by a car (traumatic myo-
is reversible with normalization of K levels. carditis), large breed dogs with gastric torsion or
In cats hyperthyroidism can cause significant AV dogs with neoplasia involving the myocardium.
node disease, which may or may not be reversible However, in many patients with ventricular arrhyth-
with normalization of thyroid levels. Third-degree mias a cause can not be identified.
AV block is often not as life threatening in cats as
in dogs, and cats with collapse episodes may live
Treatment of Ventricular
for longer than 1 year without pacemaker im-
Tachycardia
plantation. They often succumb to other systemic
diseases or structural heart disease rather than the VT is recognized by abnormally wide and bizarre
actual bradyarrhythmia QRS complex morphology. P waves are present
but may be hiding in the QRS-T complexes. AV
dissociation occurs due to the accelerated ventric-
Treatment of Complete AV Block
ular rate as compared to the sinus rate. VT can be
If no underlying abnormalities are discovered, a monomorphic (where each QRS complex is iden-
permanent cardiac pacemaker is the only effec- tical) or polymorphic (where the QRS complexes
tive treatment. Ideally, pacing systems that allow are constantly variable). Rapid, polymorphic VT
sensing of P waves in the atria and subsequent is considered the most unstable arrhythmia, be-
pacing of the ventricles are used (i.e., dual-cham- cause it is most likely to degenerate into VF.
ber or single lead atrial sensing-ventricular pac- From a treatment perspective it is also important
ing systems). to differentiate between fast VT (170 to 350
bpm) and slow VT (rate 80 to 160 bpm).
t Ventricular Arrhythmias Fast VT causes significantly reduced cardiac
output and clinical signs depend on the duration
of the episode of abnormal rhythm. Affected an-
General Remarks
imals may experience syncope or weakness or
Ventricular arrhythmias may occur in structurally sudden death, or no signs at all. It warrants anti-
normal hearts (hereditary arrhythmias) or may be arrhythmic therapy either to convert the arrhyth-
a consequence of myocardial abnormalities associ- mia to sinus rhythm or at least to slow down the
ated with cardiomyopathy, significant valvular dis- rate of the VT or reduce the length of the runs.
ease or myocarditis. To date, there is no medical Slow VT may be unrelated to structural cardiac
therapy available that is known to prevent sudden disease but associated with underlying systemic
death in animals afflicted with ventricular tachyar- disease or can occur transiently after a gastric
rhythmias. However, clinical signs such as syncope dilatation-volvulus or hit-by-car (traumatic myo-
or episodic weakness can be alleviated in some carditis). It often does not require antiarrhythmic
animals with appropriate medical therapy. Clini- treatment. Instead supportive care and monitor-
cally important ventricular arrhythmias are most ing of the underlying condition is imperative;
commonly identified in certain breeds such as however, if affected animals show signs of hy-
Boxers with arrhythmogenic right ventricular potension or lethargy, then they may benefit from
cardiomyopathy (ARVC), Doberman Pinschers treatment of slow VT.
Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances 327
Meurs KM, Spier AW, Wright NA, et al: Comparison of Moise NS: Diagnosis and management of canine
the effects of four antiarrhythmic treatments for famil- arrhythmias. In Fox PR, Sisson D, Moise NS, eds:
ial ventricular arrhythmias in Boxers, J Am Vet Med Textbook of canine and feline cardiology, ed 2, Phila-
Assoc 221(4):522-527, 2002. delphia, 1999, WB Saunders.
Moise NS, Gilmour RF Jr, Riccio ML, Flahive WF Jr: Di-
agnosis of inherited ventricular tachycardia in German
shepherd dogs, J Am Vet Med Assoc 210(3):
403-410, 1997.
Chapter 17
Cardiopulmonary Resuscitation
Steven G. Cole and Kenneth J. Drobatz
Introduction
The prognosis for patients requiring CPR is
Cardiopulmonary resuscitation (CPR) describes guarded, and long-term survival is generally
a set of techniques to provide circulatory and less than 10%. The likelihood of a successful
ventilatory support following cardiopulmonary outcome is improved when an arrest is rapidly
arrest (CPA). CPR encompasses both basic life recognized and a reversible cause is identified
support and advanced life support. Basic life and addressed.
support includes the ABCs of resuscitation and CPR is most likely to be successful when the team
involves establishing an airway, providing man- is prepared, the techniques are practiced, commu-
ual ventilation, and performing external chest nication is clear, and the resuscitation takes place
compressions or internal cardiac compressions in a well-equipped area within the hospital.
to generate blood flow. Advanced life support in-
cludes the Ds and Es of resuscitation, including Key Point
drug therapy, defibrillation, and electrocardio-
gram (ECG) analysis during resuscitation. The CPR is a potentially lifesaving procedure that
requires preparation, coordination, and com-
goal of CPR is to maximize blood flow and oxy-
munication to achieve optimal results.
gen delivery to the heart and brain until return
of spontaneous circulation (ROSC) is achieved
and the underlying cause of the arrest may be
addressed.
CPA is defined as the cessation of spontane- Basic Life Support
ous circulation and ventilation. Causes of CPA
Airway
include primary myocardial disease (although
this is rare in veterinary patients), hypotension Establishing an airway is the first step in perform-
(secondary to hypovolemia, sepsis, or drug ing basic life support. Orotracheal intubation is
administration), hypoxemia (secondary to hy- generally performed in a routine fashion, and this
poventilation or lung disease), metabolic de- may be facilitated by the use of a laryngoscope
rangements (e.g., severe metabolic acidosis) or and/or a stylet for the endotracheal tube. It is also
electrolyte abnormalities (e.g., hyperkalemia). helpful to have suction available if secretions or
It is important to recognize that these predis- blood obscure visualization of the glottis. In situ-
posing causes of arrest may be associated with ations where the glottis cannot be visualized, the
either reversible or irreversible underlying dis- larynx may be directly palpated and the endotra-
ease processes. cheal tube may be guided by feel.
333
334 Section III Treatment of Cardiovascular Disease
In rare situations, an emergency tracheostomy (e.g., pneumothorax, pleural effusion, diaphrag-
is required. This technique may be performed in matic hernia, mass lesions).
less than 30 seconds after rapidly clipping and
prepping the ventral cervical region. A midline
Circulation
incision is performed and sharp dissection is
used to expose the trachea. Care is taken dur- Artificial circulation during CPR may be pro-
ing dissection to remain on midline (between the vided by performing external chest compressions
sternohyothyroideus muscles) in order to avoid or internal cardiac massage. The goal of either
vascular structures. Once the trachea has been technique is to maximize blood flow to the coro-
isolated, a transverse incision is made between nary and cerebral vasculature.
cervical rings (approximately 50% of the diam- Myocardial perfusion pressure is the best predictor
eter) and a cuffed tracheostomy tube is inserted. of ROSC in human patients and animal models of
A standard endotracheal tube may also be used in CPR, and it is represented by the following equa-
this situation. tion: MPP=aortic diastolic pressurecentral
Once an airway is in place, it is important to con- venous pressure.
firm correct tube placement. This may be done by Cerebral perfusion pressure drives cerebral blood
direct visualization, cervical palpation, auscul- flow and is represented by the following equa-
tation of lung sounds, and observing chest wall tion: CPP=Mean arterial pressureIntracranial
movement. The use of end-tidal carbon dioxide pressure.
(CO2) monitoring in this situation is also use- There are two theories describing the mechanism
ful, as tracheal gas is always higher in CO2 than of blood flow during external chest compres-
esophageal gas. Once placement is confirmed, it sions. The cardiac pump theory describes actual
is vital to secure the endotracheal tube, as inad- compression of the heart through the chest wall
vertent tube dislodgement is very common in an and is likely to occur in small patients (< 15 kg).
arrest situation. The thoracic pump theory describes blood flow as
Problems during an arrest (i.e., unable to auscult a result of phasic increases in intrathoracic pres-
lung sounds, chest wall not moving with venti- sure and has been documented in larger animals
lation) should prompt rapid reevaluation of en- (> 15 kg).
dotracheal tube placement. It is also important External chest compressions should be per-
to ensure that the cuff has been inflated, as this formed with the patient in lateral recumbency.
is often the source of problems. If airway prob- The chest may be compressed circumferen-
lems have been ruled out, difficulty ventilating a tially or directly over the heart in small patients
patient during an arrest suggests severe pleural (< 15 kg) and at the widest point of the chest
space, airway, or parenchymal disease. in larger patients (> 15 kg). The rate of chest
compressions should be 100 to 120 per min-
ute with a ratio of compression to relaxation
Breathing
of 50:50. While higher compression rates have
Patients should be manually ventilated with 100% been shown to generate greater cardiac output,
oxygen. Methods for providing positive pressure it is difficult to sustain higher rates for extended
ventilation in an arrest situation include the use of periods of time during CPR. Compressions
an Ambu-bag or an anesthesia machine. should be given with enough force to decrease
Respiratory rate should be between 10 to 24 the diameter of the chest wall by approximately
breaths/minute. It should be noted that excessive 25% to 33%.
ventilation often occurs during CPR. It has been Interposed abdominal compression (IAC) may
shown in animal models that increasing respira- be used to improve the efficacy of external chest
tory rates results in higher mean intrathoracic compressions. With this technique, the abdo-
pressures, decreased myocardial perfusion pres- men is compressed during diastole (relaxation
sure, and decreased survival. phase of chest compression) in order to increase
Normal chest wall motion should be observed the pressure gradient favoring blood return to the
and peak pressure of less than 20 cm H2O should chest, thereby improving cardiac output, blood
be maintained if possible. Problems with de- pressure, and myocardial and cerebral perfusion
creased compliance or diminished chest wall pressure.
motion may include airway obstruction, severe Even optimal external chest compression produces
parenchymal disease, or pleural space disease approximately 20% of normal cardiac output.
Chapter 17 Cardiopulmonary Resuscitation 335
of an arrest often dictate changes in therapy (dogs and cats, 0.01 to 0.02 mg/kg) is favored
(Figure 17-1). in people, due, in part, to worse neurologic out-
A retrospective study of veterinary patients comes with initial high dose therapy. Conversely,
undergoing CPR has shown that common ini- high-dose epinephrine (dogs and cats, 0.1 to 0.2
tial arrest rhythms include pulseless electrical mg/kg) has been shown to improve results in dog
activity, asystole, ventricular fibrillation, and models of CPR. Epinephrine may be given IV, IT
sinus bradycardia. or IO, and a shortcut for high-dose epinephrine
Although ventricular fibrillation is most respon- is 1 ml/10 kg, and the dose may be repeated at
sive to treatment (defibrillation), a recent study 5-minute intervals.
of veterinary patients surviving CPR found that Vasopressin is a noncatecholamine vasopressor
asystole was the most common initial rhythm drug that has recently been included in human
identified. CPR guidelines. Potential advantages of vasopres-
sin (compared to epinephrine) include efficacy
in the presence of acidosis, lack of potentially
Drug Therapy
harmful beta effects, and a longer half-life. The
See Table 17-1 for drug therapy guidelines role of vasopressin in CPR is still being inves-
Intravenous fluids may be administered in shock tigated, however there is evidence that this drug
doses (90 ml/kg in dogs and 60 ml/kg in cats) to may be equivalent to or even superior to epineph-
patients that are hypovolemic. Intravenous fluids rine is some situations. The dose of vasopressin is
may also be useful to help flush drugs from pe- 0.8 /kg (dogs and cats), and the dose may be re-
ripheral sites into the central circulation. It should peated at 5 minute intervals.
be noted, however, that myocardial perfusion Lidocaine is indicated in ventricular fibrilla-
pressure may be reduced by significant increases tion or pulseless ventricular tachycardia that is
in central venous pressure, and that bolus fluid not responsive to initial defibrillation attempts.
therapy may be counterproductive in patients that Like other antiarrhythmic drugs, lidocaine may
are euvolemic or volume overloaded at the time increase the defibrillation threshold. Addition-
of arrest. ally, lidocaine must be used with care in the post-
Atropineis a vagolytic drug that abolishes para- arrest period, as its use may suppress a functional
sympathetic tone. It is indicated in patients with ventricular escape rhythm. The dose of lidocaine
bradycardias (as may occur in vagal events), as is 2 mg/kg (dogs, IV, IO, IT), and a shortcut dose
well as in pulseless electrical activity and asys- for the 2% (20 mg/ml) solution is 1 ml/10 kg.
tole. It should be noted that high doses of atro- Amiodarone has been incorporated into human
pine may cause a profound tachycardia in patients CPR guidelines, and has been favorably com-
with perfusing rhythms, and that the dose is often pared to lidocaine in ventricular fibrillation that
reduced by 50% to 75% in these situations. The is refractory to defibrillation. There is limited ex-
dose of atropine is 0.04 mg/kg (dogs and cats, can perience with amiodarone in the context of CPR
be given IV, IT, IO). Atropine is available in a con- in veterinary patients. The dose of amiodarone
centration of 0.54 mg/ml, and a shortcut dose is is 5 to 10 mg/kg (dogs, IV), and it is diluted in
1 ml/10 kg. The dose may be repeated at 5 minute 5% dextrose prior to administration. Hypoten-
intervals. sion is a common occurrence during amiodarone
Epinephrine is a potent alpha and beta cate- administration.
cholamine receptor agonist. Experimental studies Sodium bicarbonate is not routinely recom-
have shown that it is the alpha (vasoconstrictor) mended for use in all arrest situations. It is in-
effects rather than the beta (chronotropic/inotro- dicated, however, in patients with a preexisting
pic) effects that are most important in achieving acidosis, patients with hyperkalemia, and in pro-
ROSC. This is due to the increased peripheral longed (> 10 minute) arrests. The dose for sodium
resistance created by adrenergic stimulation and bicarbonate is 1 to 2 mEq/kg (dogs and cats, IV,
the resultant increase in aortic pressure. This IO). A shortcut dose is 1 ml/kg of a standard 1
increase in aortic pressure leads to an increase mEq/ml solution. Sodium bicarbonate should not
in myocardial perfusion pressure and increased be given intratracheally, as this will inactivate
likelihood of successful resuscitation. Epineph- surfactant and have deleterious effects on pulmo-
rine is indicated in all cardiac arrest situations. nary function.
There are both high- and low-dose recommen- Calcium gluconate is also not routinely recom-
dations for epinephrine in CPR. The low dose mended in all arrest situations, as its use may
Cardiopulmonary Arrest
VF/Pulseless VT Asystole/Bradycardia/PEA
Defibrillate 2-10 joules/kg (external) Drug therapy Atropine (0.04 mg/kg IV)
0.2-1 joule/kg (internal) Use lower dose if palpable pulse
Provide up to 3 consecutive shocks or suspected vagal arrest
before resuming CPR for 1-2 min.
Epinephrine (0.01-0.1 mg/kg IV)
Drug therapy Epinephrine (0.01-0.1 mg/kg IV) May be repeated at 3-5 min.
or intervals
Vasopressin (0.8 units/kg IV) or
Vasopressin (0.8 units/kg IV)
Lidocaine (2 mg/kg IV) Give one time only
or
Amiodarone (5 mg/kg IV)
Anesthesia-related arrest
Turn off vaporizer, flush circuit
Administer specific drug reversal agent
Low-dose epinephrine (0.01 mg/kg) where indicated
During CPR
Consider sodium bicarbonate (1-2 mEq/kg IV) Indicated in patients with significant pre-exsting metabolic
acidosis, hyperkalemia, or with prolonged (>10 min) CPA
Consider calcium gluconate (50-100 mg/kg IV) Indicated in patients with hyperkalemia or ionized hypocalcemia
Consider magnesium sulfate (30 mg/kg IV) Indicated in patients with hypomagnesemia
Search for underlying causes of arrest Run stat bloodwork (PCV/TS/BG/Blood Gas/Electrolytes)
Figure 17-1. Algorithm for performing CPR in veterinary patients. (Adapted from Cole SG, Otto CM, Hughes D: Cardiopulmo-
nary cerebral resuscitation in small animals: a clinical practice review. Part II. J Vet Emerg Crit Care 13[1]:13-23, 2003.)
338 Section III Treatment of Cardiovascular Disease
Table 17-1 Guidelines for Drug Therapy and Initial Defibrillator Settings (Monophasic Waveform
Defibrillators) During CPR
Adapted from Cole SG, Otto CM, Hughes D: Cardiopulmonary cerebral resuscitation in small animals: a clinical practice review. Part
II. J Vet Emerg Crit Care 13(1):13-23, 2003.
e xacerbate ischemia-reperfusion injury. It is indi- attachments for an accessory flat paddle (often
cated in patients with hyperkalemia and in patients called a posterior paddle) that may be placed un-
with known hypocalcemia. The dose of calcium glu- der the patient, with the handheld paddle placed
conate is 50 to 100 mg/kg (dogs and cats, IV, IO) over the heart on opposite sides of the chest wall.
Magnesium sulfate is indicated in patients with It is important to use large amounts of contact gel
known hypomagnesemia, and in rare ventricular ar- in order to prevent the current from arcing across
rhythmias (e.g. torsades de pointes). The dose of mag- the surface of the skin rather than being delivered
nesium sulfate is 30 mg/kg (dogs and cats, IV, IO) through the chest. Arcing of current is inefficient,
and may be potentially dangerous, especially if al-
cohol has been placed on the patient. Because of the
Defibrillation
risk of combustion during defibrillation, alcohol (to
See Table 17-1 for defibrillation guidelines increase ECG contact) should not be used during
Electrical defibrillation is the only effective CPR. ECG contact gel is a much safer alternative.
method to convert ventricular fibrillation to a per- Clear communication during defibrillation is
fusing rhythm. Defibrillation is also indicated in also important to ensure safety. The operator
patients with pulseless ventricular tachycardia. must both inform the other resuscitation team
The defibrillator must be used properly to mini- members of an impending defibrillation attempt
mize risks to members of the resuscitation team. It and confirm that no member of the team is in
is strongly recommended that the patient be placed contact with the patient or table prior to deliver-
in lateral recumbency for both CPR and defibril- ing a shock. Because of this, a standard protocol
lation. Attempting to defibrillate a patient in dor- is followed for each defibrillation. This protocol
sal recumbency may allow the limbs to contact a is as follows: (1) confirm ventricular fibrillation
team member. This may lead to the unintentional or pulseless ventricular tachycardia, (2) apply
delivery of current to a staff member and a poten- contact gel, (3) confirm current to be delivered
tially harmful situation. Most defibrillators have and charge defibrillator, (4) halt ongoing CPR,
Chapter 17 Cardiopulmonary Resuscitation 339
(5) call Clear, (6) confirm that all personnel tilation that typically occurs during CPR). On
are clear of the patient (especially limbs) and the other hand, venous blood gas results reflect
table, (7) deliver current, (8) monitor success of the metabolic and respiratory acidosis that char-
defibrillation. acterizes the local tissue environment in the face
The dose of energy for initial defibrillation is 3 to of hypoperfusion and decreased clearance of
5 J/kg. This corresponds to 10 to 15 J for a cat, metabolic byproducts. Because of this, venous
30 to 100 J for a small dog, 100 to 200 J for a blood gas results are more useful in the monitor-
medium dog, and 200 to 300 J for a large dog. ing of CPR.
If an initial shock is not successful, up to 2 ad-
ditional shocks are given, increasing the energy
delivered by 50%. If there is no conversion of the Key Point
rhythm after a total of three shocks, CPR is re-
Advanced life support techniques include the
sumed for 1 to 2 minutes before defibrillation is
implementation of drug therapy and defibril-
attempted again. lation. These interventions are based upon
the circumstances unique to each arrest and
Monitoring CPR Efforts provide options to augment the effectiveness
of basic life support.
Patient monitoring during CPR can be difficult,
and some standard techniques may be potentially
misleading in an arrest situation. Special Situations
Palpation of femoral pulses during chest com-
Anesthetic Arrests
pression is an encouraging finding; however, the
presence of pulses (and a discernible pulse pres- In general, anesthetic related arrests are rare;
sure) does necessarily correspond to adequate however, arrests that occur in conjunction with
arterial blood pressure or perfusion pressures. anesthesia are usually rapidly recognized, and
Direct arterial pressure measurement is ideal, al- some retrospective veterinary studies demon-
though this is generally only feasible in patients strate that these patients are the most likely to
with a previously placed arterial line. be successfully resuscitated.
As mentioned above, ECG monitoring is vital Steps to take in an anesthetic related arrest in-
during CPR, as this often dictates the type and clude turning off gas anesthesia and flushing
timing of intervention. ECG findings must always the anesthetic circuit, reversing injectable an-
be interpreted in the light of physical examination esthetic agents with naloxone (for opioids) at
parameters. This is especially important when an 0.02 to 0.04 mg/kg (dogs and cats, IV), flumaze-
apparent escape rhythm is present. The presence nil (for benzodiazepines) at 0.02 to 0.04 mg/kg
of auscultable heart sounds and, often, palpable (dogs and cats, IV), or yohimbine/atipamenzole
pulses, indicates ROSC. Without these findings, (for alpha-2 agonists) at 0.1 to 0.2 mg/kg (dogs
the rhythm represents pulseless electrical activity and cats, IV) and instituting standard CPR.
and CPR should be continued. Immediate open-chest CPR should be performed
End-tidal CO2 monitoring is an easily applied in patients undergoing thoracotomy and should
and extremely useful monitoring tool in CPR. If be considered in patients undergoing celiotomy
ventilation is constant, end-tidal CO2 is linearly (via a transdiaphragmatic approach).
related to pulmonary blood flow and, by exten- Possible underlying causes such as hypoven-
sion, cardiac output. As with myocardial perfu- tilation, hypoxemia, hypotension, or arrhyth-
sion pressure, higher end-tidal CO2 during CPR mias should be investigated and corrected
has been shown to correlate with increased like- immediately.
lihood of successful resuscitation. Additionally,
because end-tidal CO2 is a surrogate marker for
Vagal Events
blood flow, marked increases in this parameter
serves as a useful indicator of ROSC. Vagal events, characterized by bradycardia, hy-
Blood gas analysis may be misleading during potension and collapse, may occur in critically ill
CPR. Despite the low-flow state and global tissue patients, especially in conjunction with cough-
ischemia that occurs, arterial blood gas results ing, retching, vomiting, or straining to defecate.
may appear relatively normal after equilibration In extreme cases, bradycardia may be profound
with alveolar gas (especially with the hyperven- and lead to asystole.
340 Section III Treatment of Cardiovascular Disease
Atropine is the treatment of choice in patients and normocapnia should be maintained. This
with symptomatic bradycardia, and it should be limits increases in intracranial pressure created
noted that significant (although transient) tachy- by hypercapnia-induced cerebral vasodilation,
cardia is often seen in patients with perfusing as well as prevents hypocapnia-related cerebral
rhythms given a full arrest dose (dogs and cats, vasoconstriction and diminished cerebral blood
0.04 mg/kg IV, IM, IT). Because of this, the at- flow. Many patients that suffer protracted periods
ropine dose may be reduced to a fourth to half of of CPA do not ventilate effectively in the imme-
the arrest dose (dogs and cats, 0.01 to 0.02 mg/kg diate (< 24 hour) post-arrest period and require
IV, IM, IT) in patients with palpable pulses. mechanical ventilation to maintain normocapnia.
Respiratory arrest may accompany these events, Induced hypothermia has been shown to be bene-
and prompt intubation and manual ventilation is ficial in improving neurologic outcome following
indicated. CPR in human patients. Although this is difficult
Most patients suffering a witnessed vagal arrest to translate to clinical veterinary patients, over-
respond remarkably well to prompt intubation, zealous rewarming of mildly hypothermic pa-
ventilation, and atropine administration. Full tients is not recommended.
CPR should be instituted if no response to initial
therapy occurs.
Intensive Care
Patients resuscitated from CPA may suffer a range
Post-Resuscitation Care of post-resuscitation syndromes affecting multiple
organ systems. The severity of these abnormalities
Preventing Rearrest
is dependent on the duration of the arrest as well as
Many patients that are initially resuscitated suffer the condition of the patient prior to the episode.
an additional episode of CPA within the first few In addition to neurologic dysfunction, post-ar-
hours, and often few minutes, following ROSC. rest patients often have significant cardiovas-
A rapid search for underlying causes of the arrest cular (arrhythmia, myocardial dysfunction,
must be undertaken, and these must be addressed hypotension), renal (acute renal failure), and
immediately. Special emphasis should be placed gastrointestinal (shock gut) sequelae. The low-
on finding reversible disease processes, such as flow state during CPA and CPR creates global
drug-induced hypotension, hypovolemia, hy- ischemia followed by subsequent reperfusion
poventilation, anemia, or electrolyte abnormali- and leads to systemic inflammation (systemic
ties, as these situations are most likely to result in inflammatory response syndrome) and activa-
successful outcomes when appropriately treated. tion of the coagulation cascade and disseminated
intravascular coagulation. There is also the pos-
sibility that CPR has created iatrogenic injury
Cerebral Protection
(rib fractures, pulmonary contusion) or has re-
Cerebral ischemia (and subsequent reperfusion) sulted in additional management concerns (post-
may lead to long-term neurologic dysfunction in pa- thoracotomy or post-tracheostomy patients).
tients suffering CPA and subsequent resuscitation. Intensive monitoring and supportive care is re-
This has led to the creation of the acronym CPCR, quired to address these conditions, as well as con-
which stands for cardiopulmonary cerebral resusci- ditions underlying the arrest. It is not common for
tation and reflects the importance of neurologic out- post-CPA patients to require pressor therapy, me-
come when assessing the success of resuscitation. chanical ventilation, or other advanced therapy to
Measures to limit progressive neurologic injury in survive the post-arrest period and be discharged
post-CPA patients include head elevation to 30 de- from the hospital.
grees. This should be accomplished by elevating the
entire chest, neck, and head to avoid acute kinking Key Point
of the neck and possible jugular vein compression.
Post-resuscitation care is essential to the
Mannitol may be given at a dose of 0.25 to 1.0
ultimate success of CPR. Intensive monitoring
gram/kg IV (dogs and cats) over 20 minutes to treat and supportive care is necessary to identify
cerebral edema, improve cerebral microvascular and address the underlying cause of CPA
flow, and to provide free radical scavenging effects. as well as to manage post-resuscitation
Ventilatory status should be evaluated (either by syndromes.
end-tidal CO2, or ideally by blood gas analysis,
Chapter 17 Cardiopulmonary Resuscitation 341
Emergency Management
and Critical Care
Steven G. Cole and Kenneth J. Drobatz
not uncommon, as primary cardiovascular prob- vasculature, pulmonary parenchyma and pleural
lems may have wide-ranging effects on all major space. It represents the gold standard in docu-
organ systems. menting CHF in the form of pulmonary edema
Physical examination findings consistent with and/or pleural effusion.
primary cardiac emergencies are variable de- Echocardiography provides information about
pending upon the specific condition. cardiac structure and function. It is typically used
Mucous membranes may be pale secondary to confirm a suspected diagnosis, determine se-
to vasoconstriction or cyanotic secondary to verity of disease, assess myocardial contractility,
hypoxemia. Capillary refill time is commonly and detect intracardiac or proximal pulmonary
prolonged due to diminished cardiac output artery thrombi. Echocardiography is particularly
and hypoperfusion. Decreased tissue perfusion useful in assessing patients with pericardial effu-
is more commonly seen in instances of low sion for cardiac neoplasia.
output failure vs. congestive failure.
The majority of cases of canine and feline heart Key Point
failure are accompanied by an audible murmur
or gallop. Diminished heart sounds occur in Animals presenting with emergency prob-
lems related to heart disease are often not
cases of pericardial or pleural effusion or se-
stable enough for prolonged diagnostic tests.
vere myocardial failure. Empiric therapy for the most likely cardiac
Bradyarrhythmias or tachyarrhythmias are problem based on signalment, history, physi-
common, and are often associated with irreg- cal examination, and chest radiographs is
ular rhythms and diminished pulse quality or often performed. In many cases, appropriate
pulse deficits. therapy can be instituted without the need
Pulsus paradoxus, where pulse strength gets for an immediate echocardiographic exam.
weaker on inspiration is detected in approxi-
mately 50% of cases of pericardial effusion.
Tachypnea and respiratory distress is often
Emergency Treatment
present. In cases of pulmonary edema, auscul-
ofHeart Failure
tation will commonly reveal harsh lung sounds
or crackles. In cases of pleural effusion, lung Treatment of heart failure involves thefollowing:
sounds are commonly diminished ventrally. Identification and remediation of underlying
Animals suffering from low output failure of- causes
ten have a low body temperature and depressed Elimination of aggravating conditions (i.e., car-
mentation. diac depressants, hypertension, arrhythmias)
Jugular pulses or distension is commonly de- Control of congestion
tected in animals with right-sided heart failure. Improvement of myocardial contractility
Improvement of myocardial relaxation
Reduction of cardiac work
Diagnostic Tests
Reduction of pathologic remodeling and neu-
Diagnostic tests include electrocardiography rohormonal activation
(ECG), pulse oximetry, blood pressure measure-
ment, chest radiographs and echocardiography.
Congestive Heart Failure
A lead II ECG is usually sufficient for the rapid
diagnosis of most cardiac rhythm disturbances. CHF results from elevated cardiac filling pres-
Pulse oximetry provides a useful estimate of he- sures that cause pulmonary or systemic venous
moglobin saturation and arterial oxygen content, hypertension and extravasation of fluid into the
findings that may be further evaluated by arterial interstitial space or a body cavity.
blood gas analysis. The location of this fluid is dependent upon the
Noninvasive blood pressure measurement may be failing ventricle (left-sided, right-sided, or bi-
accomplished via Doppler or oscillometric tech- ventricular failure) and the subsequent signs
niques, and reflects cardiac output and vasomotor of CHF relates to the magnitude of the fluid
tone. It is useful in the recognition of shock states accumulation.
and in monitoring therapeutic interventions. CHF is the result of many cardiac diseases in-
Chest radiography is the ideal method to assess cluding chronic valvular disease, cardiomy-
size and shape of the cardiac silhouette, pulmonary opathies, infectious endocarditis, myocarditis,
344 Section III Treatment of Cardiovascular Disease
rapidly when the cage is opened. Thus, an oxy- The needle should be introduced just cranial
gen cage is less effective when patients require to a rib to avoid the intercostal vessels and
frequent treatments or physical examination. advanced into the pleural space. The needle
Patients should receive oxygen supplementa- should be redirected or the procedure termi-
tion until their respiratory rate and effort have nated once lung tissue is felt at the tip of the
improved and/or objective measurements of needle or fluid is no longer able to be aspirated.
pulmonary function (i.e., pulse oximetry or Both sides of the chest should be aspirated as
arterial blood gas) have returned to normal. If bilateral fluid accumulation is found in the ma-
possible, the fraction of inspired oxygen should jority of cats with pleural effusion secondary
be tapered over 6 to 12 hours to allow the pa- to CHF. It is not uncommon to remove 200 to
tient to adjust to breathing room air. 300 ml of fluid from the thorax of cats with
For patients with fulminant LCHF and massive severe pleural effusion.
pulmonary edema, standard oxygen supple-
mentation may not be sufficient to prevent ei-
Right-Sided Congestive Heart Failure
ther respiratory or ventilatory failure. In these
cases, only early intubation and mechanical Right-sided congestive heart failure (RCHF) is
ventilation will provide the respiratory support much less common in patients presenting to the
necessary to sustain life. Mechanical ventila- emergency room. An exception is pericardial
tion is a significant commitment for both the effusion and cardiac tamponade (see Pericar-
owner and clinician; however, in many cases, dial Effusion below). RCHF results from ele-
mechanical ventilation may be weaned after vated right atrial and central venous pressures.
only a short period (1 to 2 days) following ag- Conditions that may result in elevated central
gressive medical management of CHF. vencus pressure (CVP) include tricuspid valve
The use of anxiolytic agents in the treatment insufficiency or stenosis, pulmonic valve in-
of CHF is common in human medicine and sufficiency or stenosis, pulmonary hyperten-
may also be useful in veterinary patients. Low- sion, and right ventricular systolic or diastolic
dose morphine (dogs, 0.1 mg/kg IV every 4 dysfunction.
to 6 hours as needed), butorphanol (dogs and Clinical signs of RCHF are related to the presence
cats, 0.1 to 0.2 mg/kg IV every 4hours), diaz- of pleural effusion, ascites, or peripheral edema
epam or midazolam (dogs and cats, 0.1 to 0.3 that results from increased right atrial pressure.
mg/kg IV every 4 hours), or low doses of Patients with large volume pleural effusion may
acepromazine (dogs and cats, 0.005 to 0.02 mg/ present in respiratory distress and with dull lung
kg IV every 6 to 8 hours) can be administered. sounds. Patients with ascites will present with a
Therapeutic Thoracocentesis distended abdomen and may have respiratory
Cats with significant pleural effusions associated compromise. Additional indications of RCHF
with LCHF experience significant benefit from are the presence of distended jugular veins and
therapeutic thoracocentesis. Some cats will tol- prominent jugular pulses, as well as the presence
erate the thoracocentesis with minimal restraint, of a heart murmur (particularly with a maximal
although many cats require some degree of se- intensity at the left heart base or the right side of
dation (butorphanol [0.1 to 0.2 mg/kg] in com- the chest). Other changes such as a split S2 sound
bination with diazepam or midazolam [0.1 to or gallop rhythm are variable dependent upon the
0.3 mg/kg]). underlying disease.
Thoracocentesis is generally performed be- Emergency therapy for RCHF consists of tho-
tween the seventh and ninth intercostal spaces racocentesis for large volume pleural effusions
at the level of the costochondral junction. The (see previous section).
area is clipped and aseptically prepared prior In animals with tense ascites, abdominocentesis
to initiating the procedure. Thoracocentesis in may be performed to reduce pressure on the dia-
cats is generally performed with a 21-gauge phragm and improve ventilation. Abdominocen-
butterfly catheter attached to a three-way stop- tesis can be performed with equipment similar to
cock and a 10-ml or 20-ml syringe. In extreme- thoracocentesis.
ly obese cats, a 22-gauge needle and extension The procedure may be performed standing
set is used in place of the butterfly catheter. In or with the patient in left lateral recumbency,
larger dogs, a 16- or 18-gauge catheter with a which reduces the likelihood of lacerating
60-ml syringe may be used. the spleen. An area caudal to the umbilicus
Chapter 18 Emergency Management and Critical Care 347
is clipped and prepared aseptically, and the of metastatic lung disease may be present. The
needle or catheter is induced on or just lateral cardiac silhouette often has a classic globoid
to the midline. An alternative technique uses appearance; however, this may not be true in
two or more short 16- to 18-gauge catheters cases of acute pericardial effusion. A brief echo-
placed just caudal and to either side of the cardiographic exam can generally confirm the
umbilicus. The animal remains standing dur- presence of pericardial effusion.
ing the procedure and fluid is allowed to drain
passively. Debate exists about the volume of
fluid that can be removed safely from an ani- Key Point
mal with ascites. Most dogs will tolerate the The differentiation of pericardial effusion
removal of 50 to 100 ml/kg of ascites without from pleural effusion on echocardiographic
untoward effects. exam can be challenging. Pericardial effusion
is recognized by the circular appearance of
hypoechoic fluid surrounding the heart. This
Pericardial Effusion fluid is bordered by the hyperechoic pericar-
dium. Cardiac tamponade may be recog-
Pericardial effusion typically results from an un-
nized as collapse of the right atrium, and in
derlying neoplasia, such as hemangiosarcoma, some cases, an underlying cause for the ef-
heart base tumors, lymphoma, or mesothelioma. fusion is seen, such as a mass involving the
Other causes of pericardial effusion include in- right atrium or atrioventricular (AV) groove.
flammatory or infectious pericarditis, restrictive In patients with pleural but not pericardial ef-
pericarditis, coagulopathy, atrial rupture second- fusion, the fluid does not encircle the heart,
ary to chronic dilation, and blunt or penetrating and lung tissue as well as mediastinal tissue
thoracic trauma. Small volume pericardial effu- may be seen within the effusion.
sions associated with CHF may also occur, and
this phenomenon is relatively common in cats.
Clinical signs result from cardiac tamponade and Although blood tests are not often a primary di-
RCHF and may include abdominal distension agnostic tool in the diagnosis of pericardial effu-
from ascites, tachypnea from pleural effusion, sion, documenting the presence of a coagulopathy
weakness, lethargy, or collapse. is vital in the management of those patients in
Physical examination findings include tachy- which this is a primary cause of the pericardial
cardia and dull heart sounds on auscultation. effusion. Additionally, it should be recognized
In some cases, pulsus paradoxus (decrement of that patients with more chronic pericardial ef-
pulse pressure pulse quality that occurs during fusions may develop hyponatremia and hyper-
the inspiratory phase of the respiratory cycle) kalemia. These pseudo-Addisonian electrolyte
may be recognized. Additional physical exam changes result from the enhanced antidiuretic
findings may include jugular distension and hormone secretion and decreased renal perfu-
prominent jugular pulses, abdominal distension sion that occurs secondary to decreased effec-
with a palpable fluid wave, and dull ventral lung tive circulating volume in these patients. These
sounds if pleural effusion is present. A depressed abnormalities rapidly resolve with the resolution
mentation and delayed capillary refill is sugges- of cardiac tamponade.
tive of cardiovascular collapse and hypoperfusion The emergency treatment of symptomatic peri-
in severe cases. cardial effusion and cardiac tamponade involves
Diagnostic test results consistent with pericar- volume expansion and pericardiocentesis.
dial effusion and cardiac tamponade include Volume expansion using partial shock doses
sinus tachycardia with diminished complex (30 to 45 ml/kg) of an isotonic crystalloid tran-
size on the ECG, with or without the pres- siently increases right atrial pressure. This may
ence of electrical alternans. Electrical alternans improve stroke volume and cardiac output and
describes an alternation in the height of the often results in clinical improvement while
R wave of the QRS complex, and results from steps are taken to perform pericardiocentesis.
beat to beat changes in the mean electrical axis Pericardiocentesis is the treatment of choice for
as the heart moves within the fluid filled pericar- the initial management of cardiac tamponade
dium. Chest radiographs often demonstrate an en- and is a life-saving procedure in many cases.
larged cardiac silhouette, as well as distension of To perform pericardiocentesis, the patient is
the caudal vena cava. Pleural effusion or evidence placed in left lateral recumbency. Sedation may
348 Section III Treatment of Cardiovascular Disease
be required in some patients, and conservative ollowing the procedure, the patient should
F
doses of an opioid in combination with a ben- be monitored for recurrent effusion. Fur-
zodiazepine are generally well tolerated. Other ther management of pericardial effusion
patients require only local anesthesia. involves a complete echocardiogram and
An area from the third to the seventh inter- the consideration of more definitive therapy
costal spaces is clipped and prepared asep- such as a subtotal pericardectomy or a tho-
tically, and a local anesthetic is infiltrated racoscopic pericardial window.
at the fifth intercostal space at the level of
the costochondral junction. A small stab in- Key Point
cision is made in the skin, and a catheter In patients that are clinically stable, a com-
is advanced through the chest wall, just plete echocardiographic examination is often
cranial to the sixth rib. In large dogs, a 14- performed prior to pericardiocentesis as the
gauge, 12-cm over-the-needle catheter is presence of effusion supplies useful echocar-
used, whereas a 16-gauge, 8-cm over-the- diographic contrast in the attempt to identify
needle catheter is used in smaller dogs. In cardiac neoplasms.
very small dogs, or in cats, an 18-gauge, 2-
inch over-the-needle catheter may be used.
The catheter is slowly advanced toward the
Forward (Low-Output) Heart Failure
pericardium. Generally, the catheter may
be felt as first the chest wall and then the Forward heart failure is the result of impaired
pericardium is punctured. Entrance into the myocardial function and results in diminished
pericardium is accompanied by the presence cardiac output and cardiogenic shock. Common
of fluid flashing back into the catheter hub. causes of forward heart failure include dilated
This may be recognized sooner if a syringe cardiomyopathy and myocardial failure second-
is attached to the needle and a slight nega- ary to end-stage chronic valvular disease, or
tive pressure is applied as it is advanced, doxorubicin toxicity. Significant tachyarrhyth-
or if the needle has been filled with sterile mias and bradyarrhythmias may also result in a
saline prior to the procedure. form of forward heart failure.
Once the pericardium has been punctured, Clinical signs of cardiogenic shock include weak-
the catheter is advanced off the stylet, and ness, lethargy, and collapse. Respiratory signs may
attached to an extension set with a three-way be seen if CHF is also present. Physical examina-
stopcock and syringe. The pericardial fluid tion findings associated with forward heart failure
is aspirated, and fluid should be immediately include hypothermia, pallor, delayed capillary re-
placed into an activated clotting time tube. fill time, tachycardia, and poor pulse quality. Heart
This allows pericardial fluid, which should sounds may be diminished or a heart murmur and/
not clot, to be differentiated from peripheral or gallop rhythm may be heard. The presence of
blood, which should clot. As the pericardi- pulmonary edema or pleural effusion will produce
um is drained, additional samples should be characteristic changes on auscultation.
obtained for fluid analysis and cytology. The clinical diagnosis of forward heart failure is
The ECG should be monitored during the made by finding evidence of decreased myocar-
procedure for the presence of ventricular dial function in combination with hypotension
arrhythmias that occur when the catheter and clinical signs of hypoperfusion. Decreased
contacts the epicardium. If present, these ar- systolic function is documented using echo-
rhythmias may be treated by slightly with- cardiography and is evidenced by diminished
drawing the catheter or with an intravenous fractional shortening, increased left ventricular
bolus of lidocaine (dogs, 2 mg/kg). The ECG end-systolic dimension, increased E-point to sep-
is also useful to confirm the effectiveness of tal separation, and decreased aortic and pulmonic
the procedure, as the heart rate often returns flows. Chest radiographs may document the
to the normal range and electrical alternans presence and severity of concurrent CHF, and a
disappears as the heart is decompressed. lead II ECG will help identify significant rhythm
Once fluid can no longer be aspirated, disturbances.
the catheter is withdrawn. Confirmation Treatment of forward heart failure involves efforts
of a successful pericardiocentesis may be to improve myocardial performance and cardiac
obtained with a brief recheck ultrasound. output. This may be accomplished by ensuring
Chapter 18 Emergency Management and Critical Care 349
that adequate preload is present and by providing Cardiac arrhythmias are common in emergency
inotropic support. patients and may be associated with alterations
Clinical estimates of preload may be obtained in autonomic tone or responsiveness, drug expo-
by measuring left and right ventricular filling sure, electrolyte abnormalities, impaired myo-
pressures. cardial oxygen delivery, myocardial trauma or
Right ventricular filling pressures may be inflammation, and primary myocardial disease.
assessed by placing a central venous cath- In many situations, these cardiac rhythm distur-
eter and measuring the CVP. Normal CVP bances represent the cardiac effects of a systemic
ranges between 0 and 8 cm H2O, although disease and do not require specific treatment. In
wide variability exists between patients. other cases, aggressive intervention is required to
Left ventricular filling pressures may be address unstable rhythms or life-threatening per-
assessed by placing a pulmonary artery fusion deficits.
catheter and measuring pulmonary capil- Physical examination findings consistent with a
lary wedge (occlusion) pressures (PCWP). cardiac rhythm disturbance include bradycardia
Normal PCWP ranges between 5 and 14 cm or tachycardia, an irregular rhythm on auscul-
H2O. In animals with low CVP or PCWP, tation, and the identification of pulse deficits.
judicious fluid therapy may be used to in- Depressed mentation or collapse may also be en-
crease preload and cardiac output. If the countered, and syncope may be observed in cases
CVP or PCWP is normal or high, fluid ther- of acute, arrhythmia-induced decreases in cere-
apy is not likely to be of benefit and may bral perfusion.
precipitate CHF. Confirmation of cardiac rhythm disturbances is
Inotropic support is indicated in cases of cardio- achieved by ECG. Obtaining a lead II rhythm
genic shock secondary to myocardial systolic strip is often sufficient to diagnose most rhythm
dysfunction. disturbances. However, a 6- or 10-lead ECG may
Dobutamine (dogs, 2 to 15 mcg/kg/min; cats, be helpful to accurately identify and characterize
1 to 5 mcg/kg/min) is generally the first line complex arrhythmias.
agent in dogs due to its ability to increase con-
tractility without significant increases in heart Key Point
rate. Dobutamine may also be used in cats, al-
Cardiac rhythm disorders may be intermit-
though gastrointestinal and neurologic side ef- tent and may not be noted on a single lead
fects usually limit utility. II ECG. Detection of rhythm disorders some-
Dopamine(dogs and cats, 2 to 8 mcg/kg/min) times requires 24-hour telemetric, Holter, or
may also be used. Dopamine should be used event monitoring.
with caution; however, as it has alpha-adren-
ergic effects at higher doses and may increase
afterload and cause reductions in cardiac out-
Bradyarrhythmias
put. In patients with a pulmonary artery cath-
eter, cardiac output may be obtained by the Bradycardia is a relatively uncommon finding in
thermodilution method. Combined with mea- patients presenting to the emergency room.
surements of direct arterial blood pressure and Clinical signs associated with bradyarrhythmias in-
calculation of systemic vascular resistance, clude weakness, lethargy, depression, and syncope.
this allows for the most effective clinical as- Causes of symptomatic bradyarrhythmias in
sessment of hemodynamics and the response emergency patients include increased vagal tone,
to therapy. electrolyte abnormalities, hypothermia, drug tox-
Oral pimobendan therapy (0.25mg PO every icities, and significant disturbances of the cardiac
12 hours) should be considered if intravenous conduction system.
therapy is not possible. ECG rhythms seen in bradycardic patients in-
clude sinus bradycardia, atrial standstill, sinus
arrest, and high-grade second- or third-degree AV
Cardiac Rhythm block.
Disturbances
See Chapter 16, Treatment of Cardiac Arrhyth- Sinus Bradycardia
mias and Conduction Disturbances, for further In emergency patients, sinus bradycardia is most
discussion. often seen associated with increased vagal tone.
350 Section III Treatment of Cardiovascular Disease
Increased vagal tone may result from intra- agents such as glycopyrrolate. Although the car-
abdominal or intrathoracic diseases, or from diac arrest dose of atropine is 0.04 mg/kg, lower
coughing, vomiting, retching, or straining to doses (0.005 to 0.01 mg/kg) are often effective
urinate or defecate. The Cushing reflex, which in patients with bradycardia, and these doses are
occurs secondary to head trauma or other less likely to be associated with rebound sinus
causes of elevated intracranial pressure, also tachycardia. Intravenous administration is ideal
produces sinus bradycardia. In this situation, (rarely, a brief centrally induced exacerbation of
bradycardia is associated with hypertension bradycardia may occur with this route), although
that is produced by a massive discharge from atropine may also be administered via intra-
the medullary vasomotor center. tracheal, intraosseous, or intramuscular routes.
Other causes of sinus bradycardia include abso- Along with atropine administration, efforts to
lute or relative drug overdoses, especially of an- identify and correct the underlying cause of the
esthetic agents such as opioids, benzodiazepines, increased vagal tone are necessary.
or alpha-2 adrenergic agonists. Cardiac or vaso- Atropine is also indicated in treating sinus bra-
active medications, including calcium channel dycardia associated with anesthetic agents, as
blockers, beta-adrenergic blockers, digoxin, and are measures to decrease the depth of anesthesia
cholinergic agents, may also produce sinus bra- and to administer specific drug reversal agents.
dycardia either by increases in vagal tone or by Opioids may be reversed with Naloxone (0.03
reducing sympathetic tone. mg/kg IV, IM, or SQ) and benzodiazepines may
Sinus bradycardia may also be associated with be reversed with Flumazenil (0.03 mg/kg IV,
hypothermia or severe hypoglycemia (blood glu- IM, or SQ). Sinus bradycardia associated with
cose less than 50 mg/dl). the administration of parasympathomimetics is
Management of symptomatic sinus bradycardia also atropine responsive. There are specific rec-
generally centers on the identification and treat- ommendations for the management of patients
ment of underlying factors. In cases of hypother- receiving overdoses of cardiac medications
mia or hypoglycemia, the heart rate and clinical such as digoxin, calcium channel blockers or
signs often improve markedly once these factors beta-adrenergic blockers. These guidelines are
are identified and addressed. Hypothermia is best discussed later.
managed by the use of an indirect heating method
such as a warm air blanket. This may help mini- Second- and Third-Degree Atrioventricular Block
mize overheating or detrimental vasodilation that High-grade second-degree AV block and third-
may occur with direct heat sources such as heat- degree AV block represent severe disruptions
ing pads or hot water bottles. Intravenous fluids of the normal cardiac conduction system. Al-
that have been warmed to body temperature are though structural heart diseases, such as myo-
also appropriate in patients without contraindica- cardial fibrosis, inflammation, or infiltration,
tions to fluid therapy. are thought to be responsible for most cases
Although neurologic signs usually predominate of severe AV block, these rhythms may also
over bradycardia, symptomatic hypoglycemia be seen in patients with systemic disease or
may be treated with a bolus of 0.25 to 1 gram/ drug toxicities. Drugs associated with second
kg of 50% dextrose that has been diluted 50:50 or third-degree AV block include digoxin, cal-
with 0.9% saline. Additional dextrose bolus cium channel blockers and beta-adrenergic
therapy or a dextrose infusion may be necessary blockers
while causes of hypoglycemia (such as insulin Most emergency patients with high-grade second
overdose, hypoadrenocorticism, paraneoplastic and third-degree AV block will have clinical signs
syndrome, systemic inflammatory response syn- relating to decreased cardiac output such as leth-
drome, or sepsis) are investigated. argy, depressed mentation, and, commonly, syn-
Increased vagal tone secondary to intrathoracic cope. Rarely, these rhythms will be documented
disease, intra-abdominal disease, coughing, gag- in an otherwise asymptomatic patient. These
ging, retching, or straining may cause severe asymptomatic patients (generally cats) often
sinus bradycardia that results in cardiovascular have third-degree AV block with a relatively high
collapse or syncope. In these situations, immedi- ventricular rate supporting an adequate cardiac
ate administration of a parasympatholytic agent output.
is necessary. Due to its rapid onset of action and Medical management of high-grade second-
short half-life, atropine is preferred over other and third-degree AV block consists of initial
Chapter 18 Emergency Management and Critical Care 351
parasympatholytic therapy followed by sympa- This is most common in cats with urethral ob-
thomimetic drugs. struction, but also occurs in cases of acute renal
Initially, atropine may be given at the full va- failure, uroperitoneum, hypoadrenocorticism,
golytic dose of 0.4 mg/kg IV. This is often ef- and reperfusion injury.
fective in elevating the rate of discharge of the Hyperkalemia produces a characteristic set of
sinus node, but is only rarely effective in im- changes on the ECG, however, the concentra-
proving the AV block in these patients. tion at which these changes are noted is vari-
Alternate therapy consists of beta-1 agonist able. Changes rarely occur if K+ is < 6 mmol/L.
drugs given in an effort to accelerate the ven- The sequence of changes involves tented/
tricular escape rate. Isoproterenol (dogs, 0.04 spiked T waves, flattening of the P waves, pro-
to 0.08 mcg/kg/min) is commonly used in this longation of the P-R interval, bradycardia, loss
manner, although this drug can cause hypoten- of P waves (atrial standstill), prolongation of
sion secondary to vasodilation. An alternative the QRS complex, and finally merging of the
drug is dopamine (dogs and cats, 2 to 8 mcg/ QRS and T wave complexes to form a sine
kg/min) at the beta agonist dose. Dobutamine wave pattern.
is another beta-1 agonist; however, it has less Ventricular arrhythmias, ventricular fibrillation,
of a positive chronotropic effect than dopamine. and asystole may also occur secondary to severe
Beta-1 agonists are also indicated in the treat- hyperkalemia.
ment of beta-adrenergic blocker overdose. The management of life-threatening hyperkale-
Whereas these drugs may be effective in some mia involves three phases: immediate cardiopro-
cases, an alternative therapy involves the use tection, redistribution of serum potassium, and
of glucagon (dogs, 200 mcg/kg). A bolus removal of potassium from the body.
of may increase cardiac rate and contractil- Immediate cardioprotection is achieved via the
ity. If a response is noted then glucagon may use of intravenous calcium gluconate (dogs
be continued (dogs, 150 mcg/kg/min CRI). and cats, 50 to 100 mg/kg as a slow [3 to 5
Glucagon may be used in dogs with calcium minute] IV bolus). Overly rapid administra-
channel blocker overdose at a similar dosage. tion results in worsening bradycardia and po-
When medical management is ineffective, artifi- tentially severe ventricular arrhythmias. The
cial pacemaker therapy is indicated in the treat- onset of action of calcium gluconate is usually
ment of symptomatic AV block (see Chapter 21, rapid (within 5 minutes). The duration of effect
Pacemaker Implantation). is limited, however, and hyperkalemic ECG
Temporary transthoracic or transvenous pacing changes will recur unless steps are taken to re-
are considered emergency treatment to stabi- duce the serum potassium level.
lize a patient until diagnostic tests may be per- Serum potassium may be transiently lowered
formed or definitive therapy may be planned. If by redistribution into the intracellular space us-
no underlying cause, such as a drug overdose or ing regular insulin (dogs and cats, 0.25 /kg;
toxicity, is identified, patients with symptomatic accompanied by dextrose bolus of 0.5 g/kg to
AV block require the placement of a permanent help prevent iatrogenic hypoglycemia). Dex-
pacemaker. trose supplementation is also added to ongoing
intravenous fluid therapy for 6 to 12 hours to
Sinus Arrest prevent a decrease in blood glucose later in the
The most common cause of symptomatic sinus course of treatment.
arrest is sick sinus syndrome, a condition charac- An alternative or adjunct to regular insulin
terized by periods of supraventricular tachycardia therapy is the use of sodium bicarbonate
interspersed with periods of sinus arrest. Although (dogs and cats, 1 to 2 mEq/kg given over
this condition may occur in a number of breeds, it 10 to 15 minutes).
is seen most often in Miniature Schnauzers. Man- Definitive management involves removing
agement is similar to patients with symptomatic potassium from the body. This is generally
AV block. accomplished by establishing urine flow (re-
lieving urethral obstruction, placing a perito-
Hyperkalemic Cardiotoxicity neal drainage catheter) and fluid diuresis. If
Although not a primary cardiac abnormality, hy- adequate urine flow is unable to be achieved,
perkalemic cardiotoxicity is a frequent cause of patients are considered candidates for either
symptomatic bradycardia in emergency patients. peritoneal dialysis or hemodialysis.
352 Section III Treatment of Cardiovascular Disease
Esmolol(see dose listed under Sinus Tachycar- disease, such as dilated cardiomyopathy,
dia) is generally preferred to other beta-block- arrhythmogenic cardiomyopathy, hypertrophic
ing agents, such as propanolol, due to its short cardiomyopathy, chronic valvular diasease, aor-
half-life that allows rapid titration of effect. tic or pulmonic stenosis, myocarditis, or cardiac
The use of a calcium channel blocker is an al- neoplasia. Ventricular arrhythmias may also be
ternative to beta-blocking agents. Diltiazem seen in a variety of noncardiac conditions, es-
(dogs and cats, 0.1 to 0.25 mg/kg and followed pecially in patients with elevated sympathetic
by 2 to 5 mcg/kg/min CRI) has a less pro- tone or inflammatory mediators, and with elec-
nounced negative inotropic effect than equiva- trolyte disturbances such as hypocalcemia and
lent doses of esmolol. hypokalemia.
Other choices for anti-arrhythmic therapy of As with supraventricular tachycardia, long-stand-
supraventricular tachycardia include procain- ing ventricular tachycardia may produce myo-
amide and amiodarone. cardial failure in patients with otherwise normal
Procainamide (dogs, 6 to 8 mg/kg, followed hearts. This tachycardia-induced cardiomyopathy
by 25 to 50 mcg/kg/min CRI) is a fast sodium results in chamber dilation and diminished sys-
channel blocker, and can be used for both tolic function, and can result in CHF.
supraventricular and ventricular arrhythmias. Patients with symptomatic ventricular tachy-
Amiodarone (dogs, slow (20 to 30 minute) cardia usually present with symptoms such as
bolus of 5 to 10 mg/kg diluted in 5% dextrose weakness, lethargy, or collapse. Paroxsysmal
in water) acts to prolong the action potential. ventricular tachycardia may result in syncope or
Amiodarone may cause significant hypo- episodes of near-syncope.
tension, vasodilation and pruritis during IV Treatment of ventricular tachycardia involves at-
administration, and long-term use may be as- tempts to identify and specifically treat any un-
sociated with hepatic dysfunction in dogs. derlying cause of the tachycardia.
In many patients, ventricular arrhythmias respond
Ventricular Tachycardia to interventions such as fluid resuscitation in hy-
Ventricular arrhythmias are very common in povolemic patients, the administration of blood
emergency patients, and ventricular complexes products in anemic animals, the implementation
are recognized by a wide and bizarre QRS mor- of oxygen therapy in hypoxemic patients, and
phology. In many cases, such as isolated ven- the use of analgesics in painful patients.
tricular premature complexes, these rhythm Pharmacologic therapy of ventricular tachycar-
disturbances do not require treatment. However, dia in an emergency situation involves the use of
treatment is recommended if there are frequent injectable anti-arrhythmic agents. Initial choices
or multifocal ventricular premature complexes, for anti-arrhythmic therapy include class I agents
if the coupling interval is very rapid creating such as lidocaine or procainamide. Alternatives
an R-on-T morphology, if there is sustained include beta-adrenergic blockers, or class III
ventricular tachycardia (rates greater than 160 agents such as amiodarone.
bpm), or if there are clinical or hemodynamic Lidocaine (dogs, 2 mg/kg IV bolus up to 8
sequelae. mg/kg and followed by 25 to 80 mcg/kg/min
An accelerated idioventricular rhythm is very CRI) is generally a first line choice in dogs.
common in patients with noncardiac disease. Cats are much more likely to develop adverse
This rhythm is recognized as a regular, mono- effects (gastrointestinal signs, neurologic signs
morphic ventricular rhythm that is very simi- including seizures) and the dose is significantly
lar in rate to the underlying sinus rhythm, and decreased to prevent these signs (cats, 0.25 to
fusion complexes may be recognized during 0.5 mg/kg IV bolus followed by 10 to 20 mcg/
transitions between the ventricular and sinus kg/min CRI).
rhythm. In general, this rhythm does not pro- Procainamide (dogs, 8 to 15 mg/kg slow IV
duce significant hemodynamic abnormalities bolus followed by 25 to 50 mcg/kg/min) may
and does not require therapy. also be used to treat ventricular tachycardia.
Ventricular tachycardias result from abnor- Rapid administration may cause significant hy-
malities within the ventricular myocardium and potension.
occur due to abnormal automaticity, triggered Esmolol (see dose listed under sinus tachycar-
activity, or re-entrant circuits. Ventricular ar- dia) is generally preferred to other beta blockers
rhythmias may occur due to primary cardiac due to its short half-life. As with procainamide,
354 Section III Treatment of Cardiovascular Disease
esmolol may cause hypotension, which is sec- acute limb paresis secondary to obstruction of ar-
ondary to potent negative inotropic effects. terial blood flow and subsequent tissue ischemia.
Amiodarone (see dose under supraventricular Cats most commonly present with paraparesis,
tachycardia) may also be used for the treatment but may also present with unilateral hindlimb
symptomatic ventricular tachycardia, however paresis or forelimb paresis. Cats may also em-
vasodilation and systemic hypotension are bolize other organs, such as the brain, kidneys,
common during administration in dogs. or gastrointestinal tract. CHF may be present,
As mentioned previously, in rare cases, a wide- although arterial embolization may occur alone.
complex tachycardia may result from a su- All cats benefit from analgesia and from treat-
praventricular focus due to the presence of a ment of any concurrent heart failure while in the
bundle branch block in the specialized conduc- emergency room. Thrombolytic agents such as
tion system. Lidocaine is unlikely to be effec- streptokinase or tissue plasminogen activator
tive, whereas procainamide, beta blockers, or may accelerate clot dissolution, however their
calcium channel blockers are more likely to be use has not provided definitive evidence of bene-
useful in the diagnosis and management of these fit in clinical trials. In addition, these agents may
patients. cause significant complications including severe
hemorrhage and fatal reperfusion syndromes.
Key Point Conservative therapy involves the provision of
supportive care and analgesia and some cats will
The morphology of ventricular premature
complexes and ventricular escape beats is re-establish arterial blood flow and regain func-
identical. The use of anti-arrhythmics in a pa- tion in ischemic limbs within 2 to 3 days.
tient with ventricular escapes may cause sup- Analgesia in the form of fentanyl (cats, 2 to 5
pression of the escape rhythm with disastrous g/kg/hr CRI for 12 to 18 hours as a fentanyl
consequences. patch takes effect), butorphanol (cats, 0.1 to
0.2 mg/kg IV every 4 to 6 hours), or buprenor-
phine (cats, 0.005 to 0.015 mg/kg IV every 6
to 8 hours) is used. Other opioids such as hy-
Thromboembolic Disease dromorphone, oxymorphone, or morphine may
See Chapter 8 for additional discussion. also be used.
Cardiac emergencies associated with thrombo- Anticoagulation with unfractionated or low-
embolic disease may either be the cause or the molecular-weight heparin may be useful to help
result of severe cardiac disease. Massive pul- reduce clot propagation, and is generally well
monary thromboembolism may cause heart tolerated by cats. Unfractionated heparin (cats,
disease by significantly increasing right ven- 150 to 250 g/kg SQ every 6 to 8 hours or as a
tricular afterload. This results in severe pulmo- CRI of 20 to 50 g/kg/hr at a low fluid rate) or
nary hypertension, and may precipitate acute low-molecular-weight heparin (e.g., dalteparin,
right-sided heart failure and cardiogenic shock. cats, 100 to 150 g/kg SQ every 12 to 24 hours)
This occurs more commonly in dogs than cats is used. Unfractionated heparin will cause pro-
and is generally associated with an underlying longation of the PTT, and a clinical target is to
hypercoagulable state that results in pathologic achieve a PTT 1.5 to 2.5 times the normal value.
clot formation. Conditions associated with pul- Low-molecular-weight heparin activity is typi-
monary thromboembolism include hyperadreno- cally monitored via a factor Xa assay that is not
corticism, immune-mediated hemolytic anemia, readily available to veterinarians. However, the
sepsis, disseminated intravascular coagulation, PTT will be prolonged in patients at risk for
protein losing nephropathy and enteropathy, and hemorrhage secondary to low-molecular-weight
neoplasia. heparin administration. All heparinized patients
More commonly, emergency patients present should be monitored for signs of clinical bleed-
with thromboembolic disease resulting from car- ing and should not have jugular venipuncture or
diac disease. This is especially common in cats cystocentesis performed. In addition, all cats that
with cardiomyopathy and associated left atrial en- present to the emergency room with feline aor-
largement. These patients are prone to the devel- tic thromboembolism should be monitored for
opment of blood clots that subsequently embolize hyperkalemia, azotemia, hypotension, cardiac
the systemic arterial tree. This condition, known arrhythmias and signs of cardiovascular collapse
as feline aortic thromboembolism, often causes that may accompany reperfusion injury.
Chapter 18 Emergency Management and Critical Care 355
Introduction
a nesthetic drugs, the presence of arrhythmias,
Anesthesia of the patient with heart disease can be and the potential for anesthetic drugs to predis-
a challenge. Most veterinary patients with heart dis- pose to the production of arrhythmias.
ease that are presented for sedation or anesthesia do Knowledge of the length of sedation or anesthe-
not have clinical signs of heart failure. Anesthetic sia that is desired and recognition of the need for
protocols that are routinely used for normal patients analgesia are also important.
without heart disease can result in acute decompen- Virtually all anesthetic drugs directly depress
sation in patients with heart disease. Differences be- cardiac function, alter vascular tone, or modify
tween dogs and cats in the response to anesthetic and normal cardiovascular regulatory mechanisms.
analgesic drugs can compound the complex nature One magic bullet anesthetic protocol that will
of cardiac anesthesia. In addition, most patients with safely anesthetize any dog or cat with heart dis-
heart disease may be treated with a variety of cardiac ease does not exist.
drugs that may interact with anesthetic drugs. This Each patient and each etiology of cardiac disease
chapter provides a general view of anesthetic drugs should be considered on an individual basis to provide
that are indicated and contraindicated in dogs and the safest sedation, analgesic or anesthetic protocol.
cats with heart disease. Anesthetic considerations for
specific cardiac diseases are also presented.
Key Point
Key Point The general rule of thumb is to devise an an-
esthetic plan that provides minimal cardiopul-
Suggested anesthetic protocols for dogs and monary depression and returns the patient to
cats are presented based on the functional preanesthetic status as soon and as safely as
classes of heart failure. possible.
Additional Tests
Digitalis Glycosides
Thoracic radiography and an electrocardiogram
(ECG) should be performed as well. If a complete A common side effect of digoxin administra-
cardiac diagnostic evaluation has been performed tion is ventricular arrhythmias. There is the pos-
less than 1 to 2 weeks previous to anesthesia, and sibility of an increase in arrhythmogenesis with
the patients physical status has not changed, a concurrent use of sympathomimetics (dopamine,
physical examination and electrocardiogram are dobutamine, norepinephrine, epinephrine) during
the only diagnostic tests that require repetition. anesthesia. Isoflurane, sevoflurane and opioids
Complete blood count and serum chemistries have not been associated with increased inci-
should be performed at the discretion of the vet- dence of arrhythmias secondary to digitalis.
erinarian, with particular attention to renal val- Hypokalemia, most commonly caused by chronic
ues and electrolytes. use of loop diuretics, can exacerbate digitalis toxic-
ity. Acute onset of hypokalemia can occur during an-
esthesia as a result of hyperventilation (hypocarbia
Cardiac Drugs and and concurrent respiratory alkalosis) and can exac-
Potential Anesthetic erbate preexisting hypokalemia caused by diuretics.
Drug Interactions
Diuretics Key Point
The loop diuretic, furosemide, is the most com- Always obtain a blood digitalis level prior to
monly used diuretic in patients with heart disease. anesthesia.
The most common electrolyte disturbance pro-
duced by furosemide is hypokalemia. Hypokale-
Vasodilators
mia can result in tachyarrhythmias or predispose
to digoxin toxicity. Furosemide may promote de- Hydralazine is an arteriodilator that can cause
hydration and predispose the patient to hypoten- reflex tachycardia and fluid and water retention.
sion during sedation or anesthesia. Tachycardia secondary to use of sympathomi-
The potassium sparing diuretic, spironolactone, metics (dopamine, dobutamine, norepinephrine,
can result in hyperkalemia if used alone for ex- epinephrine) during anesthesia can be exacer-
tended periods of time. Hyperkalemia may result bated with the use of hydralazine. Fluid adminis-
in arrhythmias, with equal likelihood of tachyar- tration must be minimized and monitored closely.
rhythmias or bradyarrhythmias. Acepromazine, isoflurane and sevoflurane may
The thiazide diuretic, chlorothiazide, has similar exacerbate arteriodilation and predispose to arte-
side effects as the loop diuretics with chronic use. rial hypotension.
Chapter 19 Anesthesia of the Cardiac Patient 359
and hypercarbia can result in the production or production of arrhythmias, especially ventricular
worsening of arrhythmias. All intubated patients arrhythmias. Halothane should not be used in a
should also have ventilation supported. The gen- dog or cat with cardiac disease.
eral rule is that four to six breaths should be de- Methoxyflurane is of more historical significance
livered each minute. Expired carbon dioxide can than is used in practice. The effects on inotropy
be monitored with a capnometer (see Monitoring) and the possibility for arrhythmias fall between
to ensure adequate ventilation. those of isoflurane, sevoflurane (discussed later)
and halothane. Methoxyflurane is more likely to
produce a prolonged recovery.
Anesthetic Drugs that are Contraindicated
Mask induction with isoflurane or sevoflurane
in Patients with Cardiac Disease
is not recommended in cardiac patients. Most
The following sedatives and anesthetic drugs animals become very excited during mask in-
are contraindicated in patients with heart dis- duction, even with adequate preanesthetic medi-
ease, regardless of the etiology. The benefits of cation, which could predispose to arrhythmias
convenience, effectiveness, or ease of admin- and increased myocardial work secondary to the
istration and lower cost do not justify the use stress response. Isoflurane has a very pungent
of these drugs because of the profound cardio- odor and may result in laryngospasm, especially
pulmonary depression, the increased possibil- in cats, though sevoflurane is less pungent. En-
ity of arrhythmia production, or the length of vironmental contamination with isoflurane and
recovery time. sevoflurane administered by mask is a very
important consideration for the safety of all
Alpha-2 Adrenergic Drugs personnel.
Xylazine and medetomidine are potent respiratory
and cardiac depressants. Decreased heart rate is
usually responsive to anticholinergics. Xylazine Anesthetic Drugs that
can also decrease heart rate by a central mecha- should be Used with Caution
nism of decreased sympathetic outflow that will
Preanesthetic Medication
not be responsive to anticholinergics. Xylazine
decreases myocardial contractility, resulting in Tranquilizers
decreased cardiac output and hypotension. Me- The phenothiazine, acepromazine, is considered
detomidine results in intense vasoconstriction a major tranquilizer owing to the high reliability
and decreased cardiac output. Decreased heart of producing mental calming. It is also the most
rate is usually a result of intense vasoconstriction. commonly used tranquilizer in small animals.
Administration of an anticholinergic will greatly The primary cardiovascular effect is peripheral
increase cardiac work. vasodilation, with minimal effects on contractil-
ity and respiration. Hypotension can occur, and is
Barbiturates primarily treated with intravenous fluids and, in
Pentobarbital has a duration of action of approxi- severe cases, peripheral vasoconstriction agents
mately 45 to 60 minutes and results in prolonged (phenylephrine, norepinephrine). The sedative and
recoveries. Pentobarbital is also a potent respi- cardiovascular effects are of long duration (4 to
ratory and cardiovascular depressant at dosages 6 hours), though the effects are not reversible.
used for general anesthesia. Acepromazine can be used effectively and safely
Amobarbital (intermediate duration) and phe- at very low dosages in otherwise healthy cardiac
nobarbital (long duration of action) are barbitu- patients
rates with an extremely long duration of action
and have cardiopulmonary effects inappropri- Anticholinergics
ate for use as anesthetics or sedatives in cardiac Atropine and glycopyrrolate are primary used
patients. to maintain heart rate during anesthesia or seda-
tion and are generally not recommended unless
Inhalation Anesthetics used with anesthetic drugs that are likely to lower
Halothane is not used commonly, but is still heart rate (opioids) through increased parasym-
available to some extent. Halothane is the most pathetic tone. The potential side effects include
potent negative inotrope of the inhalation anes- the production of tachyarrhythmias (ventricular
thetics and it predisposes the myocardium to the or supraventricular). The increase in myocardial
Chapter 19 Anesthesia of the Cardiac Patient 361
e ffects are vomiting and bradycardia. Bradycardia and an opioid. The neuroleptanalgesia com-
is usually anticholinergic responsive. Depression binations that are recommended for patients
of respiration is dose dependent. with heart disease include any combination of
Hydromorphone and Oxymorphone a benzodiazepine and an opioid. Intravenous or
Opioid agonists have similar clinical effects and intramuscular administration may be used to
are 10 times more potent analgesia compared produce an effect.
with morphine. Usually more effective than mor- Opioid-Diazepam Combinations
phine in producing sedation when used alone, The preferred neuroleptanalgesia for patients
though even more effective in a neuroleptanal- with heart disease is the combination of an opi-
gesic combination. Potential for decreased heart oid with a benzodiazepine. The most reliable se-
rate (parasympathomimetic). Less respiratory dation occurs with an opioid agonist (morphine,
depression than with morphine. Vomiting likely, hydromorphone/oxymorphone, fentanyl) com-
though less likely compared with morphine. Can pared to opioid agonist/antagonist (butorpha-
also be used as an induction agent in compro- nol) and partial opioid agonist (buprenorphine)
mised patients. combinations. Intramuscular administration
Butorphanol produces effects within 15 minutes. Panting is
Opioid agonist/antagonist that is usually less a prominent feature when opioid agonists are
effective than oxymorphone or hydromorphone in used in dogs (not cats), and respiratory depres-
producing sedation alone or in a neuroleptanalgesic sion can be pronounced. Bradycardia is more
combination. There is minimal cardiopulmonary likely with opioid agonist combinations, and is
depression, and it is unlikely to produce bradycar- responsive to anticholinergics.
dia. Aceiling effect occurs regarding sedation
and analgesia. This means that higher doses be-
yond the recommended maximum dose (approxi-
mately 0.8 mg/kg) do not produce more sedation Key Point
or analgesia. Vomiting is a rare side effect. Very A neuroleptanalgesia combination using
poor analgesic for moderate to severe pain. acepromazine will produce the most pro-
Buprenorphine found sedative effect; however, aceproma-
Buprenorphine is a partial opioid agonist that zine has a long duration of effect, including
is 20 times more potent in producing analgesia the effect of vasodilation, and has no reversal
when compared with morphine. It is generally agent. The clinician must weigh the risks and
a poor sedative when used alone, though benefits of using acepromazine.
slightly more effective in a neuroleptanalgesia
combination. There is minimal cardiopulmonary
depression and a ceiling effect occurs similar
to butorphanol. The onset of action is 20 to 30
Intravenous Induction
minutes and there is a long duration of effect.
Agents
Repeat injections of naloxone are required to
maintain antagonism of effects, if required.
Fentanyl Barbiturates
Fentanyl is an opioid agonist that is 100 times more Thiopental can be used safely and reliably in
potent in producing analgesia when compared patients with cardiac disease. Rapid induction
with morphine. The onset of action is very rapid and recovery follow a single intravenous
and it can be used as an intravenous induction dose as a result of rapid redistribution to lean
agent in dogs. The duration of action is extremely tissue. Cumulative effects occur if more than
short, making fentanyl an ideal agent for a con- one intravenous dose is administered, which
tinuous-rate infusion (CRI) to maintain general will result in prolonged recovery. Transient
anesthesia. Bradycardia is more likely to occur decreases in blood pressure occur as a re-
and responds to anticholinergic administration sult of decreased contractility. Apnea can be
(preferred) or a decrease in the rate of infusion. prominent, and may be partly related to speed
of induction. Thiopental can be used effectively
Neuroleptanalgesia and safely in otherwise healthy patients at very
Neuroleptanalgesia is defined as the effect low dosages following adequate preanesthetic
produced by the combination of a tranquilizer medication.
Chapter 19 Anesthesia of the Cardiac Patient 363
Dissociatives Etomidate
Ketamine is used commonly as an induction Etomidate is an imidazole derivative unrelated to
agent in patients with heart disease but should barbiturates and opioids. Etomidate induction is
not be used alone. Always combine ketamine characterized as a very rapid induction with a very
with diazepam or midazolam to minimize ad- rapid and smooth recovery. Induction with etomi-
verse effects of rigidity and possible seizures. date results in a much less desirable induction and
Induction with ketamine and diazepam results recovery if administered alone without preanes-
in a rapid induction of anesthesia. The combi- thetic medication. Severe myoclonus activity can
nation will increase heart rate, maintain arte- occur when used alone. Minimal cardiopulmonary
rial blood pressure, and have minimal effects depression and minimal effect on cardiac electrical
on respiration, though apnea has been reported activity makes etomidate an ideal intravenous in-
with ketamine-diazepam combination. Poten- duction agent for the less stable patient with heart
tial side effects include myoclonus activity and disease after appropriate preanesthetic medication.
rough recovery. Cats with HCM should not be Etomidate is prepared in a propylene glycol base
administered ketamine or ketamine-diazepam and has a high osmolality. Intermittent bolus or
as sole agents. Administration of ketamine or constant rate infusion is not recommended owing
ketamine-diazepam after neuroleptanalgesia to possibility of acute red blood cell lysis.
may decrease untoward cardiovascular effects
related to dissociatives.
Tiletamine and Zolazepam Maintenance of Anesthesia
The effects are similar to ketamine-diazepam
Inhalation Anesthetics
when administered as an intravenous bolus for
induction. There is less myoclonus activity Isoflurane and Sevoflurane
and a generally smoother induction. There are Each inhalation anesthetic has a very similar clini-
longer and potentially rougher recoveries than cal effect of rapid induction and recovery. Minimal
ketamine-diazepam when used as a sole agent effects on cardiac rhythm and contractility result
without preanesthetic medication. Preanes- in minimal decreases in cardiac output. The main
thetic medication is highly recommended prior cardiovascular effect is dose-dependent peripheral
to use of tiletamine-zolazepam. Higher doses vasodilation, which is the primary mechanism of
will be required if no preanesthetic medication hypotension induced by isoflurane and sevoflu-
is administered, and there is a potential for lon- rane. A general rule is to administer the lowest ef-
ger recoveries. There are likely the same con- fective concentration of isoflurane or sevoflurane
siderations in cats with HCM as with ketamine that will maintain a surgical depth of anesthesia.
combinations. The use of preanesthetic medications and intrave-
nous induction agents is highly recommended, and
will lower the amount of isoflurane necessary to
maintain a surgical depth of anesthesia. Each are
Nonbarbiturates
potent respiratory depressants that can be additive
Propofol with opioids, and manual ventilation is mandatory
Propofol is classified as a phenolic compound to prevent hypoxemia and hypercarbia.
unrelated to opioids, barbiturates, or steroid
anesthetics. Propofol induction is character- Nitrous Oxide
ized as a very rapid and smooth induction with Nitrous oxide used in combination with oxygen
a very rapid and smooth recovery. Noncumu- cannot alone produce anesthesia. Therefore, it is
lative effects make propofol an ideal drug for used as an adjunct to inhalation anesthesia only.
constant rate infusions. Transient decreases in Use of nitrous oxide can lower the inhalation
arterial blood pressure occur and are produced anesthetic requirement. Safety considerations
by a decrease in myocardial contractility. A re- (life threatening hypoxemia) prevent widespread
flex increase in heart rate is likely. Apnea can use of nitrous oxide.
be profound, and is closely associated with
speed of injection. Use of preanesthetic medi- Key Point
cation greatly reduces the dose of propofol re- Only experienced anesthetists should use ni-
quired for induction of anesthesia, and reduces trous oxide.
the possibility of decreases in blood pressure.
364 Section III Treatment of Cardiovascular Disease
Opioids
Injectable General
Cats are more likely to become excited from the
Anesthesia
effects of opioids and, at times, to neuroleptanal-
Injectable anesthetics can be used to maintain a gesic combinations of diazepam and an opioid.
surgical plane of general anesthesia. The defi- Cats do not have as profound sedative effects
nition of general anesthesia is the production from neuroleptanalgesic combinations. Some
of sleep, muscle relaxation, and analgesia. All dogs become laterally recumbent after certain
three criteria can be met effectively and safely neuroleptanalgesic combinations, whereas cats
with injectable anesthetics. Specific examples rarely respond in the same manner. The general
will be offered at the end of the chapter, though rule is that an effective neuroleptanalgesia in
general concepts of using all injectable agents cats occurs when the cat assumes sternal recum-
are offered below. bency, is very amenable to mild restraint and has
mydriasis.
Preanesthetic Medication and Propofol Vomiting occurs less frequently in cats.
The neuroleptanalgesic combination of an Dogs develop miosis when an opioid is adminis-
opioid and a benzodiazepine is administered tered and cats develop mydriasis.
intramuscularly.
Induction and CRI of propofol with an initial Dissociatives
induction dose of 1 to 5 mg/kg, IV followed The dissociatives are the primary class of anes-
by a CRI administered by syringe pump or drip thetic drugs recommended for chemical restraint
at a rate of 0.14 to 0.4 mg/kg/min, IV, depend- in cats. The dissociatives are used primarily as
ing on other anesthetic drugs used as preanes- intravenous induction agents in dogs. Ketamine
thetic medication and the achieved effect. Higher should never be used as a sole anesthetic in the
infusion rates are required to maintain surgical dog. Ketamine can be used alone in the cat, though
plane of anesthesia and to maintain an endotra- muscle rigidity and salivation can be profound.
cheal tube. Tiletamine and zolazepam are metabolized dif-
Intermittent boluses of propofol can be used ferently in cats and dogs, which can explain the
instead of a CRI. Administer propofol by slow general recovery characteristics. Tiletamine is
bolus at a dosage of 0.5 to 1.0 mg/kg, IV fol- metabolized at a more rapid rate than zolazepam
lowing initial induction dose, depending on in cats, and recoveries tend to be smooth. The
other anesthetic drugs used as preanesthetic reverse occurs in dogs, where zolazepam is me-
medication. tabolized at a more rapid rate, and recoveries tend
to be rough. Use alone with extreme caution in
Preanesthetic Medication cats with HCM. Anecdotal reports of pulmonary
and Ketamine-Diazepam edema have been reported in cats.
The neuroleptanalgesic combination of an
opioid and a benzodiazepine is administered Propofol
intramuscularly. There is evidence that multiple exposures (con-
The induction dose of ketamine and diazepam is secutive days) of cats to propofol can result in
1 ml/10 kg of a 50:50 mixture. Generally, one oxidative injury to feline red blood cells. One an-
fourth to one third of the initial induction dose esthetic episode of propofol (induction, CRI, or
can be administered as an intermittent bolus, de- intermittent boluses) will not produce oxidative
pending on other anesthetic drugs used as pre- injury to feline red blood cells. Propofol should
anesthetic medication. not be used as an anesthetic technique for consec-
utive, multiple use therapy as in radiation therapy
or bandage care in cats.
Species Differences
(Dog vs. Cat) in Anesthetic
Drug Effects Adjunct Techniques
Local and Regional Anesthesia/Analgesia
Tranquilizers
Compared with dogs, cats are less responsive to Local and regional anesthesia/analgesia tech-
the mental calming effects of an equivalent dose niques are highly effective at reducing the amount
of acepromazine when used alone. of inhalation anesthetic required to maintain
Chapter 19 Anesthesia of the Cardiac Patient 365
a nesthesia. Many techniques are available and the residual analgesia occurs following surgery due
specific technique is dependent upon the location to the short duration of action.
of the surgical procedure. Please refer to specific Bupivicaine (0.25%) used as a sole agent is not
anesthesia and analgesia texts for description of recommended for surgery, unless 15 to 20 minutes
the available techniques. of time is allotted prior to surgery to permit maxi-
mum effect of bupivacaine. A dose of 1 ml/4.5 kg
is administered.
Local Anesthetic Drugs
A combination of morphine, lidocaine (2%),
Lidocaine (2%) and bupivacaine (0.25%) are the and bupivacaine (0.5%) can be used to provide
most commonly used local anesthetics. Lidocaine immediate and postoperative analgesia. Morphine
has a rapid onset (5 minutes) and short duration (0.1 mg/kg) is diluted with a 50:50 mixture of li-
(60 minutes) of action. Bupivacaine has a lon- docaine (2%) and bupivacaine (0.5%) at a dose of
ger onset (15 to 20 minutes) and duration (2 to 4 1 ml/4.5 kg. The end concentration of bupivacaine
hours) of action. All nerve types are blocked with is 0.25% as 0.5% bupivacaine is contraindicated
local anesthetics. Therefore, regional analgesia in the epidural space.
techniques such as lumbosacral anesthesia will Occasionally, an epidural technique in dogs
result in temporary rear limb paralysis. results in appearance of cerebrospinal fluid in
the spinal needle. There is no cerebrospinal fluid
within the epidural space; therefore, the spinal
Opioids
needle has entered the subarachnoid space. The
Morphine can be used in lumbosacral epidural anesthetist can either remove the spinal needle
techniques for prolonged analgesia. However, and attempt the procedure again, or half of the
morphine should not be used alone to provide sur- agents can be administered in the subarachnoid
gical anesthesia, as morphine blocks nerves that space. Administration of local anesthesia in the
conduct pain pathways only and is meant for post- subarachnoid space is called spinal anesthesia.
operative analgesia. The onset of action is up to A common complication of epidural anesthesia
one hour and analgesia has been reported to be up to is inadvertent needle puncture of a blood ves-
12 to 24 hours. Movement of limbs is maintained, sel. The local anesthetic combination should
as motor nerves are not affected by morphine. not be administered if blood enters the spinal
needle.
Infiltration Techniques
Lumbosacral EpiduralCats
Lidocaine (2%) can be infiltrated subcutaneously A major anatomical difference in cats com-
to a maximum dose of 10 mg/kg in dogs and cats. pared to dogs is that the spinal cord terminates
Lidocaine can be diluted to 1% to obtain more to- in the sacral vertebral segments in cats com-
tal volume to block a larger area. Bupivacaine is pared to the caudal lumbar (L4-5) in dogs. Epi-
not recommended as a sole agent for infiltration dural techniques are more difficult in cats and
due to a long onset of action. the chance of entering the subarachnoid space
is more likely in cats. Administer half of the
volume of local anesthetic if cerebrospinal fluid
Regional Techniques is obtained in the spinal needle. Administration
of local anesthesia in the subarachnoid space is
Lumbosacral EpiduralDogs called spinal anesthesia. There is also the pos-
Anesthesia and/or analgesia is produced caudal sibility of spinal cord injury in cats.
to the umbilicus. The combinations of local anesthetics and opi-
Morphine used as a sole agent0.1 ml/kg di- oids used in dogs are the same for cats.
luted with 1 ml/4.5 kg sterile saline. A mor-
phine epidural must be administered prior Intercostal Nerve Blocks
to the surgical procedure. Analgesia effects Regional anesthesia for a lateral thoracotomy can
should be expected primarily during the post- be obtained by placing the local anesthetic at the
operative period and should not be relied upon dorsal most aspect of the intercostal nerves at
during surgery. the site of incision and two intercostals spaces
Lidocaine (2%) used as a sole agent is admin- cranial and caudal. The maximum dose of lido-
istered at 1 ml/4.5 kg prior to surgery. Minimal caine (10 mg/kg) should not be exceeded.
366 Section III Treatment of Cardiovascular Disease
Advanced Cardiovascular
Oxygen Therapy
MonitoringCardiac Output
Cardiac output monitoring requires pulmonary Some patients may require oxygen by facemask,
artery catheterization to obtain cardiovascu- nasal cannula, oxygen cage, or incubator until
lar values that can provide information regard- completely recovered from anesthesia or sedation
ing ventricular function. (Box 19-1). Cardiac to maximize oxygen delivery parameters.
output computers remain extremely high-cost
expenditures.
Electrocardiographic Monitoring
Key PointS Monitor cardiac rate and rhythm continuously
until the patient is completely recovered from
Cardiac output is not synonymous with anesthesia or sedation. Some anesthetic drugs
arterial blood pressure. Please note in Box
(ketamine and inhalation anesthetics) can predis-
19-1 that cardiac output is a determinant of
the calculation for blood pressure. pose to cardiac arrhythmias.
An advance in cardiac output monitoring
that may become clinically available for dogs Cardiovascular Monitoring
and cats is lithium dilution cardiac output.
The decision to monitor blood pressure and
CVP should be determined by the severity
of heart disease, stability of the patient, the
Fluid Therapy reason for surgical intervention and the car-
Most patients with heart disease that are anes- diovascular status during anesthesia and sur-
thetized with inhalation anesthetics will re- gery. Some patients will not require further
quire intravenous fluid support. The fluid of monitoring while some patients, such as a
choice for the patient with heart disease is usu- dog with dilated cardiomyopathy undergoing
ally a sodium-restricted crystalloid fluid (0.45% surgery to correct gastric dilatation-volvulus,
NaCl/2.5% dextrose or 0.45% NaCl). The rate may require all available monitoring. Invasive
of fluid therapy administration, however, is far postoperative monitoring may be required in
more important than the type of fluid adminis- some patients.
tered. The rate should be less than the recom-
mended fluid rate during anesthesia of normal,
healthy patients (10 ml/kg/hr). A general rule
Analgesia
would be to decrease the fluid rate to approxi- Always provide analgesia if an invasive procedure
mately one fourth to one third of the rate for a or surgery was performed. Preemptive analgesia
normal patient, yielding a rate of 2 to 3 ml/kg/h. should be practiced at all times. Preemptive anal-
Less stable patients with heart disease and those gesia is defined as analgesic techniques that are
patients anesthetized for emergency surgery that applied prior to surgical stimulation. Incorporat-
present with signs of heart failure should have ing analgesic agents (opioids) in the preanesthetic
CVP measured to aid in monitoring fluid ther- medication is the easiest method of preemptive
apy. Colloid fluids should be used with caution analgesia. Analgesia should be performed on a
Chapter 19 Anesthesia of the Cardiac Patient 369
Key Point
Potent opioid agonists are usually not re- ASA III or IV Patients: Medical Procedure
quired for these types of minor procedures. or Minor, Minimally Invasive Surgical
Procedures
Injectable Anesthesia Technique
A neuroleptanalgesic combination of diazepam
ASA II Patients: Major Surgery
(0.4 mg/kg, IM) and butorphanol (0.4 mg/kg,
An injectable anesthesia technique to maintain an- IM) is administered as the preanesthetic medica-
esthesia is usually not required as these patients are tion. Atropine is not recommended to minimize
considered very stable prior to anesthesia and surgery production of tachyarrhythmias.
and should be able to tolerate inhalation anesthetics Induction can be achieved using ketamine-
as the primary technique to maintain anesthesia. diazepam (1 ml/10 kg of a 50:50 mixture, IV)
and anesthesia can be maintained using intermit-
Inhalation Anesthesia Technique tent boluses of a third to a fourth the initial dose of
A neuroleptanalgesic combination of aceproma- ketamine-diazepam if additional anesthesia time is
zine (0.025 mg/kg, IM) and hydromorphone required. Alternatively, induction and maintenance
(0.2 mg/kg, IM) can be used for preanesthetic of anesthesia can be achieved using propofol (2 to
medication. Atropine (0.22 mg/kg, IM) is rec- 6 mg/kg, IV) for induction followed by either CRI
ommended for smaller dogs (< 5 kg) only. (0.14 to 0.4 mg/kg/min) of intermittent bolus (0.5
to 1.0 mg/kg, IV). Etomidate (1 to 2 mg/kg, IV)
should be used as the induction agent if cardiac ar-
Key PointS
rhythmias are present. Endotracheal intubation may
Potent opioid agonists are preferred over be necessary, but is not required. Supplemental oxy-
opioid agonist/antagonists to provide ad- gen should be administered with this technique.
equate preemptive analgesia. Physical parameters, ECG, and Doppler blood
Ketamine-diazepam (1 ml/10 kg of a
pressure can be used for monitoring during the
50:50 mixture, IV) is preferred to induce
anesthesia over propofol (2 to 6 mg/kg,
procedure.
IV) due to a longer duration of action that
will initially reduce the dose of inhalation Key Point
anesthetic. An inhalation anesthetic technique for a med-
Adjuncts to general anesthesia can be used ical or minor surgical procedure is not indi-
to minimize use of inhalation anesthetics. cated for ASA III-IV cardiac patients.
372 Section III Treatment of Cardiovascular Disease
Key Points
ASA IV DogsEmergency
Pericardiocentesis
Anesthesia of ASA III or IV patients for major
surgery will require intensive monitoring of Dogs that require an emergency pericardiocen-
anesthesia, cardiovascular parameters, and tesis typically present with signs of collapse,
the patient. right heart failure and/or ventricular arrhythmias
Neuroleptanalgesic combination of diaze- all related to pericardial tamponade. Most dogs
pam (0.2 mg/kg, IV) and fentanyl (1 mg/kg, will require only an infiltration of local anesthetic
IV) should be administered as preanesthetic (lidocaine) in the skin and intercostals muscula-
medication. Atropine (0.22 mg/kg, IV) may ture at the site of needle puncture for pericardio-
be necessary if bradycardia occurs. centesis. Occasionally, dogs will require sedation
Fentanyl (5 to 10 mg/kg) is recommended in addition to local anesthesia. The neuroleptan-
for induction of anesthesia. Induction with
algesia combination of diazepam (0.2 mg/kg,
fentanyl is not considered a rapid induction
IV) and butorphanol (0.2 mg/kg, IV) is recom-
and may take 30 to 60 seconds or more.
Alternative induction with etomidate (1 mended. Cardiac output is highly dependent on
to 2 mg/kg, IV) should be administered for heart rate during pericardial tamponade and bu-
induction if arrhythmias are present. torphanol is least likely to decrease heart rate. At-
A CRI of fentanyl (5 to 10 mg/kg/hr) ad- ropine is not recommended. An induction agent
ministered by a dedicated syringe pump is may be necessary in addition to sedation in some
recommended to maintain a surgical plane of instances. Etomidate (1 to 2 mg/kg, IV) is the
anesthesia. drug of choice as there are minimal to no cardio-
Ventilation should be provided at all times pulmonary effects.
during anesthesia and surgery. Lidocaine and
ketamine can be administered for analgesia
in a separate bag of fluids. Epidural analgesia
Common Cardiac Diseases
for abdominal procedures is recommended.
Other local anesthetic techniques are dictat-
and Anesthesia Techniques
ed by the location of surgery. NMRDs can be for Cats
used if blood pressure is low and the patient Hypertrophic Cardiomyopathy
is not adequately anesthetized. Pancuronium
(0.02 to 0.04 mg/kg, IV) has a longer duration The most common cardiac disease in cats is hyper-
of action than atracurium (0.25 mg/kg, IV). trophic cardiomyopathy (HCM). Hypertrophic car-
Blood pressure (direct is preferred over in- diomyopathy is characterized primarily as diastolic
direct methods), ECG, capnometry, pulse dysfunction with normal ventricular contraction.
oximetry, and physical parameters are con- Increases in heart rate and ventricular tachyarrhyth-
tinuously monitored. mias caused by anesthetic drugs are best avoided.
Paddleford RR, Harvey RC: Anesthesia for selected dis- Preanesthetics and anesthetic adjuncts. In Thurmon JC,
eases: cardiovascular dysfunction. In Thurmon JC, Tranquilli WJ, Benson GJ, eds: Lumb and Jones
Tranquilli WJ, Benson GJ, eds: Lumb and Jones veterinary anesthesia, ed 3, Baltimore, 1996,
veterinary anesthesia, ed 3, Baltimore, 1996, Wil- Williams & Wilkins.
liams & Wilkins.
Chapter 20
Cardiac Surgery
E. Christopher Orton
Introduction
Cardiac surgery is increasingly an option for man- little or no operative mortality when performed by
agement of congenital and acquired cardiac condi- experienced surgeons.
tions in small animals. Some cardiac surgeries are PDA ligation is undertaken through a left fourth
widely available, whereas open cardiac repairs that thoracotomy in the dog and a left fifth thoracotomy
require cardiopulmonary bypass (CPB) are currently in a cat (Figure 20-1). The most frequent surgical
only performed at a few regional centers. Some car- complication is hemorrhage during ductus dissec-
diac surgeries are performed with curative intent, tion. If significant hemorrhage occurs during dis-
whereas others are considered palliative only. Car- section, the ductus should be closed with
diac surgeries include closed cardiac surgeries, car- pledget-buttressed mattress sutures with or without
diac surgeries performed during inflow occlusion, division of the ductus.
and cardiac surgeries performed under CPB.
Pulmonic and Aortic Valve Dilation
Closed Cardiac Surgery Pulmonic stenosis (PS) and subvalvular aortic ste-
nosis (SAS) are relatively common congenital heart
Patent Ductus Arteriosus Ligation
defects in dogs. Despite the relative importance of
With few exceptions, closure of patent ductus arteri- PS, the natural history of untreated PS in dogs is
osus (PDA) is indicated in all small animals with this not well documented. Dogs with moderate PS may
defect. Closure can be accomplished by catheter- tolerate the defect relatively well for many years.
based occlusion methods or surgical ligation. Al- Transpulmonic pressure gradients > 100 mm Hg
though each has theoretical advantages, both are considered an indication for intervention, espe-
approaches are successful in the hands of an experi- cially if animals are exhibiting activity intolerance,
enced operator and neither approach should be re- syncope, or have concurrent tricuspid regurgitation.
garded as always superior or preferred. Choosing an The natural history of untreated SAS in dogs is bet-
approach depends on several factors, including cli- ter understood. Dogs with transaortic pressure gra-
ent preference, availability of equipment and exper- dients >80mmHg are known to be at risk for
tise, and urgency of the procedure. PDA closure is sudden cardiac death early in life. Gradient reduc-
curative when performed early in life before the on- tion by valve dilation is assumed, but not proven, to
set of severe ventricular remodeling, systolic dys- be palliative for dogs with PS. Valve dilation for
function, or functional mitral regurgitation (MR). SAS does not result in sustained decreases in trans-
Surgical ligation of PDA can be accomplished with aortic pressure gradients. Current evidence suggests
376
Chapter 20 Cardiac Surgery 377
B C
Figure 20-1. PDA ligation. The vagus nerve courses over the ductus arteriosus and serves as an anatomic landmark for
identification of the ductus arteriosus (A). The vagus nerve is isolated at the level of the ductus and gently retracted with one or two
sutures (B). Occasionally a persistent left cranial vena cava may overlie the ductus arteriosus. In this case, the vein should be
carefully isolated and retracted with the vagus nerve. The ductus arteriosus is isolated by blunt dissection without opening the
pericardium. Dissection of the caudal aspect of the ductus is accomplished by passing right-angled forceps behind the ductus
parallel to the transverse plane. Dissection of the cranial aspect of the ductus is accomplished by angling the forceps caudally at
approximately a 45-degree angle. Dissection is completed by passing the forceps medial to ductus from a caudal to cranial direction
(C). Two heavy silk ligatures are passed around the ductus by grasping the ligature with right-angled forceps. The ductus
arteriosus is closed by slowly tightening and tying the ligature.
little or no palliative benefit from valve dilation or for animals that fail balloon-catheter placement
surgical treatment of SAS. across the PS, or when equipment for cardiac cath-
Catheter-based balloon valvuloplasty is preferred eterization is not available. Surgical valve dilation
to surgical valve dilation of PS because it as a less of PS is performed through a left fourth thoracot-
invasive. Surgical valve dilation of PS is indicated omy (Figure 20-2).
378 Section III Treatment of Cardiovascular Disease
B
A
Figure 20-2. Pulmonary valve dilation. The pericardium over the right outflow tract is opened and sutured to the thoracotomy
incision. A buttressed mattress suture is placed in the right ventricular outflow tract and passed through a tourniquet (A). A stab
incision is made in the ventricle within the confines of the mattress suture. A dilating instrument is passed into the right ventricular
outflow tract and across the pulmonic valve (B). The pulmonic valve is dilated several times. The ventricular incision is closed by
tying the mattress suture.
Pericardiectomy
Pericardial disease can result from neoplasia, bac-
terial or mycotic infection, foreign body, or idio-
pathic causes. Pericardial disease can take the form
of acute or chronic pericardial effusion, constrictive
pericarditis, or constrictive-effusive pericarditis.
These conditions can result in pathophysiologic
syndromes of acute cardiac tamponade, chronic
cardiac tamponade, or pericardial constriction.
Pericardiectomy is indicated for the management
of chronic pericardial effusions, particularly when
the effusion recurs after pericardiocentesis. Pericar-
diectomy is either palliative or curative depending
Figure 20-3. Pulmonary artery banding. The pericardium on the underlying cause of pericardial effusion.
is opened and sutured to the thoracotomy incision. The pul- Pericardiectomy is the only viable treatment for an-
monary artery is separated from the aorta by sharp and blunt imals with constrictive or constrictive-effusive
dissection. A large cotton or Teflon tape is passed around the
pulmonary artery just distal to the pulmonic valve. The tape is
pericarditis.
tightened to reduce circumference of the pulmonary artery. Pericardiectomy can be performed via either a
right or left thoracotomy, or a median sternotomy.
Median sternotomy has the advantages of provid-
ing access to both ventricles and requiring less car-
diac manipulation, and thus is preferred by many
is to increase pulmonary blood flow without creating surgeons (Figure 20-5). Excision of the pericardium
an overwhelming left-to-right shunt. The desired re- ventral to the phrenic nerves (i.e., subphrenic peri-
sult is a measured increase in pulmonary blood flow cardiectomy) is adequate in most cases. In animals
that lessens hypoxemia by lessening the shunt-to- with constrictive pericarditis, the pericardium may
pulmonary flow ratio. Systemictopulmonary shunt have to be separated from the epicardium by blunt
is indicated for animals that have resting cyanosis, and sharp dissection. Additionally, epicardial de-
debilitating activity intolerance or persistent polycy- cortication may be necessary to relieve constrictive
themia (polycythemia vera > 70%) that requires fre- physiology in animals with pericarditis. Epicardial
quent phlebotomy. Most veterinary experience is decortication entails careful separation of a fibrous
based on various modifications of the classic Blalock- layer from the myocardium by sharp dissection.
Taussig shunt. The original Blalock-Taussig shunt Decortication should not be attempted over the atria
consisted of dividing the left subclavian artery and or portions of the ventricles containing major coro-
performing an end-to-side anastomosis of the distal nary vessels.
end of the divided artery to the pulmonary artery.
In animals, the left subclavian artery generally does
Atrial Appendectomy
not have sufficient length to reach the pulmonary ar-
tery without kinking. Several modifications of Atrial appendectomy is occasionally indicated for
the classic procedure have been devised including palliative removal of a right atrial hemangiosar-
a synthetic vascular graft matched in size to the coma or for thrombosis of the right or left atrial ap-
subclavian artery, harvesting the left subclavian ar- pendage associated with atrial fibrillation. In the
tery as a free autogenous graft, or using autogenous case of hemangiosarcoma, atrial appendectomy is
jugular vein. Animals can receive significant pallia- often combined with pericardiectomy and is per-
tion from any of the previous methods so long as formed via a median sternotomy. Atrial appendec-
pulmonary blood flow is increased to an appropriate tomy for atrial thrombosis is performed via fifth
degree. thoracotomy on the right or left side (Figure 20-6).
380 Section III Treatment of Cardiovascular Disease
A B
Figure 20-4. Systemictopulmonary artery shunt. The pericardium is opened and sutured to the thoracotomy incision.
Tangential vascular clamps are placed on the pulmonary artery and ascending aorta, and incisions are made in each vessel
(A). The autogenous or synthetic graft is interposed between the aorta and pulmonary artery by two end-to-side anastomosis
using simple continuous suture patterns with polypropylene or polytetrafluoroethylene suture. The vascular clamps on the pul-
monary artery and aorta are released (B).
A B
Figure 20-6. Atrial appendectomy. Excision of the atrial appendage is accomplished by placing a continuous mattress suture
pattern across the base of the atrial appendage with the aid of a vascular clamp (A). The atrial appendage is excised and the
atriotomy incision is over sewn with a continuous suture pattern (B).
upon release of inflow occlusion. Drugs and invasive balloon-dilation valvuloplasty. Dogs with
equipment for full cardiac resuscitation must be severe PS characterized by valve dysplasia or dy-
immediately available after inflow occlusion. namic outflow obstruction, or both, are more likely
Gentle cardiac massage may be necessary after to require a patch-graft. Several surgical tech-
inflow occlusion to reestablish cardiac function. niques for applying a patch-graft to the right ven-
Digital occlusion of the descending aorta during tricular outflow tract during brief inflow occlusion
this period helps direct cardiac output to the heart have been described. All techniques are plagued
and brain. by relatively high operative risk and inconsistent
Inflow occlusion can be accomplished from a results, even in the hands of experienced surgeons.
left or right fifth thoracotomy, or a median ster- (Alternatively, pulmonic patch-graft can be ac-
notomy depending on the cardiac surgery being complished with the aid of CPB, which reduces
performed. Direct access to the cranial and cau- operative risk and allows for more deliberate
dal vena cava and azygous vein for inflow occlu- placement of the graft, thereby enhancing the ef-
sion is obtained readily from a right thoracotomy fectiveness of the procedure.) A well-executed
or median sternotomy. The vena cavae and azy- patch-graft generally results in more effective and
gous vein are accessed by dissecting through the more sustained pressure gradient reduction com-
mediastinum from a left thoracotomy. Tape tour- pared to valve dilation techniques. Occasionally
niquets are passed around the vena cavae and dogs will develop right-sided congestive heart
azygous vein for inflow occlusion. The right failure as a late sequela to pulmonary patch-graft
phrenic nerve should be excluded from the tour- despite good pressure gradient reduction. The
niquets to avoid nerve injury. cause of this late failure is not entirely clear and
may be multifactorial. Contributing causes could
Pulmonary Patch-Graft
include tricuspid regurgitation, right ventricular
Pulmonary patch-graft can be considered for dogs systolic dysfunction, and pulmonic insufficiency.
with severe PS who are exhibiting activity intoler- Pulmonic insufficiency is an expected conse-
ance or are considered at risk for developing heart quence of the patch-graft procedure and may be
failure or sudden cardiac death. Because of the less tolerated than previously thought. English
risk associated with this surgery, the threshold for bulldogs and boxers with PS must be evaluated for
performing this surgery should be fairly high. Pul- the presence of an anomalous left coronary artery.
monic patch-graft generally is undertaken in dogs If present, this anomaly precludes pulmonic
who have failed to be adequately palliated by less patch-graft.
382 Section III Treatment of Cardiovascular Disease
Figure 20-7. Pulmonary patch graft. Tape tourniquets are passed around the vena cavae and azygous vein for inflow occlusion
(A). Access to the azygous vein is obtained by dissecting dorsal to the descending aorta. A partial-thickness incision is made in
the right ventricular outflow tract (B). An oval expanded polytetrafluoroethylene (ePTFE) patch-graft is sutured to the ventricu-
lotomy incision and the cranial aspect of the pulmonary artery (C). After initiation of venous inflow occlusion, an incision is made
in the pulmonary artery beneath the patch and extended full thickness across the pulmonic valve annulus and previously made
partial-thickness incision in the right ventricular outflow tract. The unsutured portion of the patch graft is closed with a tangential
vascular clamp to minimize circulatory arrest time. Inflow occlusion is discontinued and the heart is resuscitated as necessary. The
unsutured portion of the patch graft is then closed and the vascular clamp removed.
Patch-graft correction of the PS by inflow occlu- brief inflow occlusion. The surgery is performed via a
sion is performed through a left fifth thoracotomy right fifth thoracotomy. Tapes are placed around the
(Figure 20-7). cranial and caudal vena cavae and azygous vein for
inflow occlusion. The pericardium is opened ventral
to the phrenic nerve. The location of the membrane is
Cor Triatriatum Repair
often apparent by an indentation in the atrial wall.
Cor triatriatum is an uncommon congenital defect Stay sutures are placed in the lateral atrial wall to con-
in companion animals that results from persistence trol the atriotomy incision during inflow occlusion.
of an embryonic membrane that divides the atrium The atrium is opened transversely across the defect
into two chambers. The separation can occur in ei- during inflow occlusion. The abnormal membrane is
ther the right (cor triatriatum dexter) or left atrium excised. A tangential vascular clamp is used to close
(cor triatriatum sinister). the atriotomy as inflow occlusion is discontinued. Ve-
Surgical correction of cor triatriatum dexter is by nous blood should flow from the atriotomy as the
membranectomy through a right atriotomy during clamp is placed to remove air from the heart.
Chapter 20 Cardiac Surgery 383
The atriotomy is closed with a continuous horizontal by one of two strategies depending on the cardiac ap-
mattress pattern over sewn with a simple continuous proach. Bicaval venous cannulation utilizes two angled
pattern. cannulae, one in each vena cava, and is required when-
Successful surgical correction of cor triatriatum ever the cardiac approach is through the right atrium.
sinister with resolution of pulmonary edema by closed Atriocaval cannulation utilizes a single two-stage can-
dilation of the atrial septum is reported in a cat. nula introduced into the right atrium and caudal vena
cava via the right atrial appendage. Lastly, a cannula is
placed in the ascending aorta for administration of car-
Intracardiac Masses and Foreign Bodies
dioplegia solution and to vent the left heart during dis-
Intracardiac masses can include benign and malig- continuation of CBP. During the open cardiac repair,
nant neoplasias, atrial or ventricular thrombus, and the aorta is cross-clamped and cardioplegia solution is
penetrating foreign bodies. These intracardiac masses administered to arrest and cool the myocardium.
and foreign bodies can, under certain circumstances,
be removed from the heart with the aid of inflow oc-
Ventricular Septal Defect Repair
clusion. Most cardiac neoplasia in dogs is malignant
and attempts at surgical excision of these tumors is Definitive repair of VSD in dogs can be undertaken
rarely rewarding. Myxomas are an exception to this with the aid of CPB. Indications are the same as de-
general rule. These benign pediculated cardiac tu- scribed for pulmonary artery banding. Definitive
mors can become large enough to obstruct cardiac VSD repair, like PDA closure, is curative so long as
flow and are amendable to excision during inflow oc- it is undertaken before severe myocardial dysfunc-
clusion. Intracardiac thrombus should be considered tion or pulmonary hypertension develop.
for surgical removal when it is not associated with Open repair of perimembranous VSD is accom-
severe underlying cardiomyopathy. Penetrating for- plished through a right fifth thoracotomy. Venous can-
eign bodies such as pellets or bullets should be re- nulation is bicaval to allow complete isolation of the
moved if they lodge within a cardiac chamber. right atrium. The defect is approached through a right
Frequently these foreign bodies are surrounded by atriotomy. The septal leaflet of the tricuspid valve is
large amounts of hair that cause complications if not retracted to expose the defect. The defect is closed
removed. Whenever possible intracardiac masses with a Dacron or polytetrafluoroethylene (PTFE)
should be approached via an atriotomy rather than a patch secured with pledget-buttressed mattress su-
ventriculotomy. An exception would be a large myx- tures. Mattress sutures should be placed with partial
oma in the right ventricular outflow tract. thickness bites from the right side to avoid injury to
atrioventricular conduction.
Cardiac Surgery with
Cardiopulmonary Bypass Atrial and Atrioventricular
Septal Defect Repair
CPB is a procedure that provides flow of oxygenated
blood to the patient by diverting flow away from the Various forms of atrial septal defect and atrioventricu-
heart and lungs through an extracorporeal circuit. lar septal defect have been described in small animals.
CPB provides a motionless and bloodless operative As with VSD, surgical closure of atrial septal defect
field, and time to perform complex cardiac repairs. can be undertaken with the aid of CPB with curative
The disadvantages of CPB are its cost and consider- intent. Indications for surgery include cardiomegaly,
able associated cardiopulmonary, metabolic, hemato- the size defect on echocardiography, pulmonary over-
logic, and systemic inflammatory derangements. circulation on radiographs, hepatic venous congestion
CPB is performed by a team consisting of the sur- on ultrasound, and a Doppler-measured transatrial
geon, perfusionist, anesthesiologist, and their assis- septal flow velocity > 0.45 m/sec. Surgical correction
tants. A principal role of the surgical team is to perform of atrial septal defect under CBP is similar to that of
a series of cannulations to connect the animal to the VSD and has been described.
CPB circuit. Prior to cannulation the patient is com-
pletely anticoagulated with sodium heparin (300 units/
Tetralogy of Fallot Repair
kg IV). Arterial cannulation for the return of oxygen-
ated blood to the patient is accomplished via a single Definitive repair of tetralogy of Fallot under CPB
cannula placed in a femoral artery. Blood is diverted can be undertaken in dogs with curative intent. In-
from the right heart to the CBP circuit by means of dications for surgery are the same as described pre-
venous cannulae. Venous cannulation is accomplished viously for systemictopulmonary artery shunt.
384 Section III Treatment of Cardiovascular Disease
The repair is accomplished via a median sternotomy chance of surviving mitral valve replacement is
and involves closure of the VSD and correction of 60% to 90% depending on the patient. Options for
PS via a right ventriculotomy. mitral valve replacement are mechanical valves or
glutaraldehyde-fixed tissue valves. Glutaralde-
hyde-fixed tissue valves include porcine aortic
Double-Chambered Right Ventricle Repair
valves and bovine pericardial valves. Mechanical
Double-chambered right ventricle (DCRV) is an valves have infinite durability, but require life-
uncommon congenital heart defect of dogs charac- long anticoagulation therapy to prevent valve
terized by a fibromuscular diaphragm at the junc- thrombosis. Despite low operative mortality and
tion of the inflow and outflow portions of the right excellent short-term results, valve replacement
ventricle. The defect obstructs flow through the with mechanical prostheses is not recommended
mid-portion of the ventricle and causes hypertro- in dogs because of a high incidence of late-term
phy of the proximal portion of the right ventricle thrombosis despite anticoagulation therapy. Tis-
giving it a double-chambered appearance. The sue valves have a finite lifespan (about 7 to 15
pathophysiology and natural history of DCRV are years in human patients), but are less susceptible
presumed to be similar to PS. Indications for sur- to thrombosis, and thrombosis is less catastrophic
gery are essentially the same as for PS although when it occurs. Other mechanisms of tissue valve
dogs with DCRV may tolerate less of a pressure prosthetic failure are structural tearing of leaflets,
gradient compared to dogs with PS. leaflet calcification, or an exuberant inflammatory
Surgical correction for DCRV is undertaken with response known as pannus. Anticoagulation ther-
CPB and has been described. The pulmonic valve apy with warfarin is required for 3 months after
is preserved. Surgical correction can be expected to valve replacement with a tissue valve. Atrial fi-
improve exercise capacity and reduce the risk of brillation occurs in about 20% of human patients
developing heart failure. undergoing mitral valve surgery and this sequela
has been observed in dogs undergoing valve re-
placement as well. Adminstration of amiodarone
Mitral Valve Replacement
10 days before and after surgery decreases the risk
MR is the most common cause of cardiac disabil- of developing atrial fibrillation after mitral valve
ity and death in dogs. Causes of MR include degen- surgery and is currently recommended for dogs.
erative mitral valve disease, congenital mitral valve Dogs that develop atrial fibrillation or flutter after
dysplasia, and functional MR secondary to dilated valve replacement should undergo pharmacologic
cardiomyopathy. Mitral valve replacement can be or electrical cardioversion if the arrhythmia per-
performed in dogs to correct severe MR second- sists for more than 6 weeks after surgery. Dogs
ary to acquired mitral valve disease or congenital with chronic atrial fibrillation at the time of mitral
mitral dysplasia. Indications for considering mitral valve replacement should undergo prophylactic
valve replacement are diuretic-dependent conges- left atrial appendectomy to decrease the risk of
tive heart failure or severe left ventricular or atrial atrial thrombosis after surgery. While the long-
dilation (left ventricular diastolic volume index term durability of glutaraldehyde-fixed tissue
> 180 ml/m2), or both. Relative contraindications for valves in dogs has not been established, the short-
mitral valve surgery are very severe left ventricular term results have been encouraging. The proce-
dilation (>300 ml/m2), or severe secondary systolic dure is limited to dogs with a lean body weight of
dysfunction (>90 ml/m2). Atrial fibrillation is not a about 10 kg by the size of the smallest available
contraindication for surgery, but it does complicate valve prosthesis (19 mm). Mitral valve replace-
the management after surgery. Serious systemic or ment is considered a palliative therapy in that the
noncardiac diseases are strong contraindications for consequences of a diseased native valve are sub-
the surgery. stituted by the inherent management and potential
Mitral valve replacement is currently the pre- complications of a valve prosthesis. That said,
ferred surgical option for most dogs with severe successful mitral valve replacement generally re-
MR and heart failure. The advantages of mitral verses congestive heart failure so long as second-
valve replacement are perfect correction of MR ary changes in the myocardium are not too
and a lower operative death. Disadvantages of mi- advanced at the time of surgery. Mitral valve re-
tral valve replacement are the need for a prosthe- placement can be expected to remain curative for
sis (expense, limitations on patient size) and for heart failure so long as the prosthesis remains
anticoagulation therapy after surgery. The estimated functional.
Chapter 20 Cardiac Surgery 385
Surgical procedure for mitral valve replacement on the case. As with mitral valve replacement,
under CPB in the dog has been described. g lutaraldehyde-fixed tissue valves are currently rec-
ommended over mechanical valves. Three months
of anticoagulation therapy is required after tricuspid
Mitral Valve Repair
valve replacement with a tissue valve. Expected out-
Mitral valve repair can be undertaken for dogs with come is similar to dogs undergoing mitral valve
moderate to severe MR caused by acquired degen- replacement. Dramatic reductions in heart size and
erative mitral valve disease. Dogs with congenital resolution of heart failure can be expected so long as
mitral valve dysplasia are sometimes amendable to the valve prosthesis remains functional.
valve repair. The principle advantages of mitral Tricuspid valve replacement is performed via a
valve repair are the avoidance of anticoagulation right fifth thoracotomy. Bicaval venous cannulation
after surgery and the lack of a need for an expensive is utilized to isolate the right atrium. Approach to
prosthesis. The disadvantages of mitral valve repair the tricuspid valve is through the right atrium. Sur-
are a less predictable outcome compared to valve gical technique for tricuspid valve replacement is
replacement and a higher operative death rate. The similar to mitral valve replacement.
later is directly related to the difficulty in achieving
perfect correction of MR when the valve is repaired.
Suggested ReadingS
Mitral valve repair is best undertaken in dogs that
have structural defects isolated to one valve leaflet Bureau S, Monnet E, Orton EC: Evaluation of survival
before the onset of congestive heart failure. Most rate and prognostic indicators for surgical treatment
dogs are beyond mitral valve repair by the time they of left-to-right patent ductus arteriosus in dogs: 52
are in severe heart failure. Because of the inherent cases (1995-2003), J Am Vet Med Assoc 227:1794,
difficulty of mitral repair, the estimated chance of 2005.
success is 60% to 75% depending on patient size, Griffiths LG, Boon J, Orton EC: Evaluation of techniques
age, duration of heart failure, severity of left ven- and outcomes of mitral valve repair in dogs, J Am Vet
tricular dilation, and degree of secondary systolic Med Assoc 224:1941-1945, 2004.
Kienle RD, Thomas WP, Pion DP: The natural history of
dysfunction.
canine congenital subaortic stenosis, J Vet Intern Med
Mitral valve repair employs a variety of surgical 8:423,1994.
techniques to address the fundamental causes of Linn KA, Orton EC: Closed transventricular valve dila-
MR. Surgical techniques for mitral valve repair in tion of subvalvular aortic stenosis in dogs, Vet Surg
the dog have been described. 21:441, 1992.
Martin J, Orton EC, Boon J, et al: Surgical correction of
double-chambered right ventricle in dogs, J Am Vet
Tricuspid Valve Replacement Med Assoc 220:770-774, 2002.
Congenital tricuspid dysplasia is a malformation of Meurs KM, Lehmkuhl LB, Bonagura JD: Survival times
the tricuspid valve that occurs in several large in dogs with severe subvalvular aortic stenosis treated
breeds of dog including Labrador retrievers, with balloon valvuloplasty or atenolol, J Am Vet Med
Assoc 227:420, 2005.
Golden retrievers, and German shepherds. Tricus-
Monnet E, Orton EC, Gaynor J, et al: Partial atrioven-
pid regurgitation is the most common hemody- tricular septal defect: diagnosis and surgical repair in
namic manifestation, although tricuspid stenosis is two dogs, J Am Vet Med Assoc 211:569-572, 1997.
possible. Tricuspid valve replacement can be con- Orton EC, Hackett TA, Mama K, Boon JA: Technique
sidered for dogs with severe tricuspid regurgitation and outcome of mitral valve replacement in dogs,
due to congenital tricuspid dysplasia. Tricuspid J Am Vet Med Assoc 226:1508-1511, 2005.
valve replacement must be undertaken sooner dur- Orton EC, Mama K, Hellyer P, Hackett TB: Open surgi-
ing the course of disease than mitral valve replace- cal repair of tetralogy of Fallot in two dogs, J Am Vet
ment. General indications for tricuspid valve Med Assoc 219:1089-1093, 2001.
replacement are severe tricuspid regurgitation re- Orton EC, Herndon GD, Boon J, et al: Intermediate-
sulting in severe or progressive cardiomegaly or term outcome in dogs with subvalvular aortic steno-
sis: influence of open surgical correction, J Am Vet
hepatic venous enlargement, or both. Dogs with
Med Assoc 216:364, 2000.
medically refractory congestive heart failure should Wander KW, Monnet E, Orton EC: Surgical correction
not undergo tricuspid valve replacement. Atrial of cor triatriatum sinister in a kitten, J Am Anim Hosp
fibrillation is a complicating factor, but not an con- Assoc 34:383, 1998.
traindication for surgery. The estimated chance
of surviving surgery is 70% to 90% depending
Chapter 21
Pacemaker Therapy
Janice McIntosh Bright
Figure 21-2. Shown are distal tips of two epicardial pac- Single- vs. Dual-Chamber Pacing
ing leads. The lead at the bottom of the photo is a unipolar
lead with a single electrode (cathode) which has an epicardial
The original goal of permanent cardiac pacing
stab-in fixation mechanism. The lead at the top of the photo was to alleviate hemodynamic instability resulting
is a bipolar lead with two suture-on electrodes (cathode and from an abnormally low ventricular rate, and this
anode). remains the primary goal of pacemaker therapy
in most veterinary patients. However, it is now
recognized that cardiac output is dependent, not
(usually the distal electrode on a transvenous solely on ventricular rate, but also on physiologic
bipolar lead) is the cathode, and the other is the heart rate variation, synchrony between atrial
anode. Electrical impulses travel to the cathode and ventricular contraction, and the ventricular
from the pulse generator and return to the anode activation sequence. Modern cardiac pacing has
to complete the circuit. In the majority of cases a evolved in people from single-chamber ventricu-
bipolar pacing system is preferred because there lar pacing to dual-chamber (atrial and ventricular
is less potential for electromagnetic interference sensing and pacing) primarily to provide pacing
(EMI) with bipolar pacing and because of absence with AV synchrony.
of skeletal muscle stimulation. AV synchrony is attained either by pacing the
Although lead length should be given consider- atrium or by sensing intrinsic atrial activity and
ation prior to pacemaker implantation, length is tracking this activity. Either a paced atrial depo-
often determined by availability. Most leads are larization or an endogenous atrial depolarization
longer than necessary, and excess length can be triggers an AV delay, programmable in length,
accommodated within the generator pocket; how- after which the ventricle is paced (if intrinsic
ever, in large or giant breed dogs, adequate lead ventricular activity is not sensed). Atrial synchro-
length may become an important factor. nous pacing provides not only AV synchrony but
also physiologic heart rate variation (see Pacing
Modes).
Although AV synchrony may not be clinically
important for many dogs and cats needing
Key Point
chronotropic support, pacing that provides
When selecting a permanent pacing lead, AV synchrony will provide higher systemic
it is imperative that the lead be compatible pressure and lower ventricular filling pres-
with the pacing site selected (epicardial vs.
sures than single-chamber ventricular pacing.
endocardial, atrial vs. ventricular), that the
Therefore, dual-chamber pacing to provide
lead and generator be of compatible size
(typically IS-1), that the polarity of the lead AV synchrony is likely to be important in ani-
matches polarity of the generator, and that mals with underlying structural heart disease
the lead is of sufficient length. or in working animals such as military dogs and
agility dogs.
Chapter 21 Pacemaker Therapy 389
Position I II III IV V
Chamber(s) Chamber(s) Response to Rate modulation Multisite
paced sensed sensing pacing
O=None O=None O=None O=None O=None
A=Atrium A=Atrium T=Triggered R=Rate A=Atrium
responsive
V=Ventricle V=Ventricle I=Inhibited V=Ventricle
D=Dual (A+V) D=Dual (A+V) D=Dual (T+I) D=Dual (A+V)
Dual-chamber pacing is becoming increasingly position the letter I indicates that a sensed ele
used in veterinary medicine as a means of provid- ctrical event inhibits the output pulse and causes
ing both heart rate response and AV synchrony. the generator to recycle for one or more tim-
Disadvantages of dual-chamber pacing include its ing cycles. The letter T indicates that an output
more complex programming, increased expense pulse is triggered in response to a sensed elec-
(when two leads are used), and the technical chal- trical event. A letter D in this position indicates
lenge of placing atrial sensing/pacing leads in that both I and T responses can occur, and
small patients. this designation is limited to dual-chamber
Normalization of the left ventricular activation systems.
sequence may be achieved by means of site- The fourth letter (position IV) of the pacemaker
specific pacing within the right atrium and right nomenclature code refers to presence or absence
ventricle. of rate modulation. A letter R in this position
designates that the generator has one or more
sensors (such as a motion sensor or a minute
Pacemaker Nomenclature
ventilation sensor) to adjust the paced heart rate
Pacing nomenclature was established in 1974 and independently of intrinsic cardiac activity.
updated in 2002 for use in human medicine. This The fifth letter (position V) of the code is used
nomenclature also applies to veterinary pacemaker to indicate whether multisite pacing is present in:
therapy, and awareness of the nomenclature is A=one or both atria, V=one or both ventricles,
important for understanding cardiac pacing. Pac- D=any combination of the atria and ventricles, or
ing nomenclature classifies pacing based on the O=none of the cardiac chambers. For example,
site and mode of both pacing and sensing using a a patient with a dual-chamber rate-responsive
series of three to five letters (Table 21-1). pacemaker with biventricular stimulation would
The first letter (position I) indicates the cardiac be designated having a DDDRV pacing system.
chamber or chambers in which pacing occurs: Currently, the fifth letter is often omitted when
A=atrium, V=ventricle, D=dual chamber describing pacing of veterinary patients because
(both A and V), and O=none. multisite pacing within the atria and ventricles is
The second letter (position II) indicates the rarely done.
chamber or chambers in which sensing of elec-
trical activity occurs. The letters are the same
Pacing Modes
as those for the first position. (Some pacemaker
manufacturers use the letter S in both the first and At the present time, the most commonly used
the second positions to indicate that a generator is pacing mode in veterinary patients and in human
capable of pacing or sensing only a single cardiac patients worldwide is single-chamber, ventricular
chamber.) inhibited synchronous pacing either with (VVIR)
The third letter (position III) refers to the mode or without (VVI) rate response. In this mode
of response to sensed electrical activity. In this the artificial pacing stimulus is delivered to the
390 Section III Treatment of Cardiovascular Disease
Figure 21-3. This figure shows a lead II ECG rhythm strip (top) and a simultaneous intracardiac electrogram (bottom) recorded
from the pacing lead of a canine patient with complete AV block and a bipolar VVIR pacemaker. Small arrows labeled P indicate
pacing stimuli, and each small pacing stimulus artifact results in a paced QRS complex. The tenth QRS complex is an endogenous
ventricular depolarization that is sensed by the generator resulting in brief interruption of the paced rhythm. The sensed intrinsic
activity resets the timing of the next paced beat (25 mm/s).
Figure 21-5. This six-lead II ECG was recorded from a dog with a transvenous VDD pacing system implanted because of
high-grade second-degree AV block. The dog has normal sinus node function resulting in normal-appearing P waves with sinus-
arrhythmia. The P waves are sensed by the generator and after a delay of 120 ms, there are pacing stimulus artifacts (arrow)
followed immediately by paced QRS complexes, which have left bundle branch block morphology (arrowhead). The ninth and
twelfth complexes are endogenous QRS complexes resulting from conduction of the P waves through the AV node. These QRS
complexes have right bundle branch block morphology (25 mm/s).
Figure 21-6. Lateral (A) and ventrodorsal (B) thoracic radiographs showing typical placement of a transvenous pacing lead in
a dog. The lead tip is at the right ventricular apex.
Radiographs should be obtained immediately after Right jugular venipuncture should not be at-
implantation to document final lead position(s). tempted after implantation, and a halter or gentle
Permanent transvenous pacing leads are typi- leader should be used instead of a neck lead to
cally inserted into the right external jugular vein avoid damaging transvenous pacing wires.
and advanced fluoroscopically into the ventricle When a transvenous pacing system is used, the
leaving the lead tip in the most apical portion of generator is usually placed into a subcutaneous
the right ventricle angled toward the diaphragm pocket made on the dorsolateral region of the
(Figure 21-6). The rare exception would be site neck. If a unipolar system has been used, skeletal
specific placement of a transvenous ventricular muscle twitching may occur with each paced beat
lead in the right ventricular outflow tract done in in the area of the generator pocket.
attempt to reduce mitral regurgitation and remod- Perioperative antibiotics are generally adminis-
eling in patients with valvular disease or dilated tered intravenously at the time of implantation
cardiomyopathy. and 8 hours following implantation.
Chapter 21 Pacemaker Therapy 393
Figure 21-7. Lateral thoracic radiograph obtained from the same dog as in Figure 21-6 after dislodgement of the lead. Note
that the distal tip of the lead is now located at the level of the tricuspid valve rather than at the apex. This radiograph was taken
after reoccurrence of bradycardia caused by lack of contact between the cathode and the myocardium.
A B
Figure 21-8. A, This radiograph was obtained from a dog with intermittent failure to pace caused by a loose connection at the
interface of the unipolar lead and the connector block. The loose connection occurred because the lead pin was not adequately
secured at the time of pacemaker implantation. Note that the connector pin (arrow) has withdrawn from the block (arrowhead)
and is not passing all of the way through the block screw. B, For comparison, this radiograph shows an appropriately engaged
connector pin from a patient with a bipolar pacing lead. The connector pin (arrow) is visible beyond the connection block
screw (arrowhead).
Figure 21-10. A simultaneous lead I, II, and III ECG recorded from a dog with a malfunctioning unipolar pacemaker. The ECG
shows numerous pacing stimuli that do not depolarize the myocardium (intermittent failure to capture) (arrows).
surface ECG to show timing of pacing and sensing QRS complexes may cause multiple restarting
on the monitor, and a hard copy tracing may also of the refractory period causing the generator
be obtained (see Figure 21-3). to switch to asynchronous pacing. The recom-
Output programming, referring to programming mended method for programming of the refrac-
of the pulse width and voltage amplitude of the tory period is that the refractory period should
pacing signals, is the most important aspect of include the T wave and be slightly longer than the
programming that should be done routinely. Out- QT interval; however, dogs and cats with concur-
put should be high enough to provide an adequate rent tachyarrhthmias may require programming
pacing margin of safety while also maintaining with a slightly shorter refractory period to pre-
output as low as possible to maximize battery vent noise reversion.
longevity. Although there is no consensus regard- Although a pacemaker programmer is often
ing the best way to program output parameters, necessary for trouble shooting and thoroughly
acceptable methods include doubling the thresh- evaluating pacemaker function, standard ECG
old voltage amplitude, tripling the pulse width at recording may also be helpful. The ECG ap-
threshold, and plotting strength duration curves. pearance of paced beats differs from that of en-
Because capture threshold usually increases im- dogenous beats. A paced beat includes a pacing
mediately after pacemaker implantation as heal- stimulus artifact, a depolarization wave, and a re-
ing occurs, energy output should be set relatively polarization wave. The pacing stimulus artifact is
high at implant and then reprogrammed after typically small with bipolar pacing and relatively
healing (approximately 8 weeks after implant). large with unipolar pacing (see Figures 21-5 and
Sensing parameters also need to be programmed 21-10). The QRS morphology of a paced beat
and checked. Appropriate sensing of intrinsic will depend on location of the ventricular pacing
cardiac activity is extremely important for proper lead; transvenous pacing from the right ventricu-
pacemaker function whether the patient has a lar apex usually produces QRS complexes with
single- or dual-chamber pacing system. A common a left bundle branch block configuration in the
programming error is over sensing of T waves in frontal plane leads (see Figure 21-5). If the pacing
canine patients. This problem can usually be cor- mode is VVI or VVIR the paced beats are inhib-
rected by increasing the sensing threshold. ited by sensed spontaneous beats, and the basic
Appropriate programming of the refractory pe- pacing cycle is reset.
riod is also essential for correct pacemaker func- ECG abnormalities in patients with pacemakers
tion. If the refractory period is too long, intrinsic may be broadly classified as failure to capture,
396 Section III Treatment of Cardiovascular Disease
failure to output, and abnormal sensing. Failure to mode is that it is appropriate only for treatment of
capture is recognized as a pacing stimulus artifact patients with bradycardia caused by AV block. There-
without ventricular depolarization (see Figure fore, this method of pacing cannot be used in patients
21-10). Causes of failure to capture include lead with atrial fibrillation, atrial standstill, or sinus node
dislodgement, high thresholds with inadequately dysfunction. Furthermore, VDD pacing is limited to
programmed output, partial lead fracture, insula- patients large enough to accommodate two leads or a
special VDD lead.
tion defect, impending battery depletion, poor or
incompatible connection of the lead to the gen- What is an appropriate diagnostic approach for a pa-
erator, and functional noncapture (pacing stimu- tient with an implanted pacemaker that has reoccur-
lus during the refractory period of a spontaneous rence of clinical signs suggestive of bradyarrhythmia?
A physical examination and standard ECG should be
beat). done. The physical examination will confirm brady-
Failure to pace is recognized as failure of the gen- cardia if the pacemaker dysfunction is continuous.
erator to deliver an appropriately timed stimulus. Occasionally, event recording or Holter monitoring is
This problem is often caused by oversensing, but needed to confirm bradycardia that is episodic as a re-
it may be due to true failure of the generator or sult of intermittent pacemaker dysfunction. Physical
to circuit interruption (the electrical signal does exam may occasionally reveal a cause of pacemaker
not reach the heart). Reasons for true failure to dysfunction such as significant generator migration
causing traction on a pacing lead. Standard ECG is
output include circuit failure, complete or inter- used to identify underlying rhythm which, in turn,
mittent lead wire fracture, intermittent or perma- may confirm sustained pacemaker malfunction. In
nent loose screw set, incompatible lead, battery addition, standard ECG may help identify a specific
depletion, internal insulation fracture (bipolar cause of pacemaker malfunction. For example, regu-
lead), and lack of anodal contact (unipolar lead). lar pacing stimuli that occur at a rate below the lower
When a pacemaker battery reaches the end state programmed rate suggest battery depletion. Pacing
of depletion, either failure to capture because of stimuli with appropriate timing but without capture
may indicate lead dislodgement, lead fracture, lead
reduced voltage output or failure to pace because insulation defect, or inadequate capture threshold.
of total battery depletion may occur. Survey radiographs may confirm fractures or macro-
Sensing abnormalities, both under sensing and dislodgements of pacing leads. Use of a pacemaker
oversensing, may also be recognized on a surface programmer to evaluate output and sensing, to test
ECG in many patients. Causes of sensing abnor- lead impedance, and to determine capture thresholds
malities include lead dislodgement or poor lead is often necessary for definitive diagnosis of the cause
positioning, lead insulation failure, circuit failure, of pacemaker dysfunction.
magnet application, malfunction of the generator
(reed switch), EMI, and battery depletion.
Frequently Asked
Questions Suggested Readings
When and why should dual-chamber pacing be done? Bernstein AD, Daubert JC, Fletcher RD, et al: North
Dual-chamber pacing provides AV synchrony where- American Society of Pacing and Electrophysiology/
as single-chamber ventricular pacing does not. Pac- British Pacing and Electrophysiology Group: The re-
ing with AV synchrony reduces ventricular filling vised NASPE/BPEG generic code for antibradycar-
pressures and mitral regurgitation compared to VVI dia, adaptive-rate, and multisite pacing, Pacing Clin
(or VVIR) pacing. Therefore, dual-chamber pacing Electrophysiol 25:260-264, 2002.
is preferable in patients with chronic valvular disease Bonagura JD, Helphrey ML, Muir WW: Complications
or myocardial disease. AV synchrony is also essential associated with permanent pacemaker implantation in
for high level athletic activity, and, therefore, dual- the dog. J Am Vet Med Assoc 182:149-155, 1983.
chamber pacing should be considered in athletic dogs Bulmer BJ, Oyama MA, Lamont LA, et al: Implantation of
and working dogs. Placement of a VDD lead or two a single-lead atrioventricular synchronous (VDD) pace-
conventional transvenous leads is technically difficult, maker in a dog with naturally occurring 3rd-degree atrio-
however, in animals weighing less than 10 kg. ventricular block, J Vet Intern Med 16:197-200, 2002.
What are the major advantages of atrial synchronous Bulmer BJ, Oyama MA, Sisson DD: Acute hemodynamic
pacing (VDD pacing) compared to ventricular inhib- consequences of physiologic VDD pacing in dogs
ited synchronous pacing (VVI)? with naturally occurring third degree atrioventricular
Advantages of VDD pacing include chronotropic block, J Vet Intern Med 16(abstract):341, 2002.
competence based on intrinsic sinus rate and restora- Gammage M, Lieberman RA: Selective site pacing.
tion of AV synchrony. A disadvantage of this pacing Medtonic Technical Concept Paper, Minneapolis,
2004, Medtronic Inc.
Chapter 21 Pacemaker Therapy 397
Moise NS, Estrada A: Noise reversion in paced dogs, Prosek R, Sisson DD, Oyama MA: Runaway pacemaker
J Vet Card 4:13-21, 2002. in a dog, J Vet Inter Med 18:242-244, 2004.
Oyama MA, Sisson DD, Lehmkuhl LB: Practices and Sisson D, Thomas WP, Woodfield J, et al: Permanent
outcome of artificial cardiac pacing in 154 dogs, J Vet transvenous pacemaker implantation in forty dogs,
Intern Med 15:229-239, 2001. JVet Intern Med 5:322-331, 1991.
Petrie J-P: Permanent transvenous cardiac pacing, Clin
Tech Small Anim Pract 20:164-172, 2005.
Phibbs B, Marriott HJL: Complications of permanent trans-
venous pacing, N Engl J Med 312:1428-1432, 1985.
Appendix 1
Canine Breed Predilections for
Heart Disease
Kathleen E. Cavanagh and francis W. K. Smith, jr.
Advancing technology has provided clinicians with Drugs are listed in alphabetical order by generic
ever more powerful and effective drugs for treating name. The order of presentation in no way reflects the
diseases. As more drugs become available, it be- preference for use. General recommendations for ther-
comes progressively more difficult for practitioners apy may be found in the main body of this document.
to make rational choices between similar drugs. It is
also difficult to be aware of the numerous side effects,
contraindications, and drug interactions of the many Key to Formulary
cardiopulmonary drugs available. The following Abbreviations
tables and charts have been designed and provided
in the hope of facilitating rational drug selections for ACE angiotensin-converting enzyme
the treatment of cardiopulmonary disease. ACT activated clotting time
An attempt has been made to make these tables as ADP adenosine diphosphate
complete as possible, while focusing on the more com- APTT activated partial thromboplastin time
mon or serious side effects and drug interactions. For a BP blood pressure
more exhaustive review of individual drugs, the reader Cap capsule
should refer to the package insert and drug chapters in CHF congestive heart failure
this book. The reader should also follow the current COPD chronic obstructive pulmonary disease
veterinary literature, as new dosing recommendations CRI constant-rate infusion
may become available as a result of clinical use and CV cardiovascular
scientific research. This advice is especially appropri- D5W 5% dextrose in water
ate for new or infrequently used drugs. ECG electrocardiogram
g gram
GFR glomerular filtration rate
DISCLOSURE GI gastrointestinal
Medicine is a science that is constantly changing. IM intramuscular
Changes in treatment and drug therapy are re- Inj injectable
quired with new research and clinical experiences. INR international normalization ratio
The author, editor, and publisher of this book have IO intraosseous
made every effort to ensure that the drug dosage IT intratracheal
schedules are accurate. The drug dosages are based IV intravenous
on the standards accepted at the time of publica- LRS lacated Ringers solution
tion. The product information sheet included in the mcg microgram
package of each drug should be checked before the mg milligram
drug is administered to be certain that changes have mL milliliter
not been made in the recommended dose of or in P0 per os (oral)
the contraindications for administration. Primary PT prothrombin time
responsibility for decisions regarding treatment of q every, as in q 8 h = every 8 hours
patients remains with the attending clinician. All SC subcutaneous
patients should be carefully monitored for desired Tab tablet
efficacious and undesired toxic effects while insti- U units
tuting, titrating, and maintaining therapy. WPW Wolff-Parkinson-White syndrome
402
Cardiopulmonary DrugsFormulations, Indications, Dosages
Acetylsalicylic Tab: 81, 325 mg Prevention of thromboembolism D: 5-10 mg/kg PO q 24-48 h Platelet inhibitor
acid C: 25 mg/kg PO q 3 days Nonsteroidal antiinflammatory drug
(Aspirin) (81 mg/cat q 72 h PO) Not 100% effective in preventing emboli
May decrease efficacy of ACE inhibitors
Albuterol Tab: 2, 4 mg Bronchodilation in D: 0.02-0.05 mg/kg PO q 8 h Beta-2 agonist bronchodilator
(Proventil, Syrup: 0.4 mg/mL patients with reversible C: Same Reduce dose by 50% first 4 days to prevent
Ventolin) obstructive lung disease and anxiety side effect
asthma Decrease dose with renal disease
Symptomatic bradycardia
Aminophylline Tab: 100, 200 mg Asthma, COPD D: 11 mg/kg q 6-8 h, PO, IV, IM Methylxanthine bronchodilator
(Aminophyllin) Ampules: 25 mg/mL Symptomatic bradycardia (slowly IV) Reduce dose with CHF, liver disease
Oral solution: 21 mg/mL C: 5 mg/kg q 8-12 h; PO)
Amiloride Tab: 5 mg See Triamterene D: 1.25 mg/10 kg PO q 12-24 h with See Triamterene
(Midamor) food
Amiodarone Tab: 200 mg severe refractory atrial D: Loading dose of 10 mg/kg PO Class III antiarrhythmic
(Cordarone) and ventricular arrhythmias q 12 h for 1 week, thereafter 5 mg/kg Use as last resort for recurrent unstable ven-
PO q 12-24 h tricular tachycardia; takes weeks to achieve
C: None therapeutic levels
Amlodipine Tab: 2.5, 5, 10 mg Systemic hypertension D: 0.05-0.20 mg/kg PO q 12-24 h Dihydropyridine calcium channel blocker
besylate C: 0.18 mg/kg PO q 24 h (0.625-1.25 Monitor for hypotension
(Norvasc) mg/cat q 24 h)
Amrinone Ampule: 5 mg/mL Short-term management D: 1-3 mg/kg bolus, then 30-100 mcg/ Phosphodiesterase inhibitor
lactate of severe myocardial failure kg/min CRI (titrate up to effect) Can use with digoxin and catecholamines
(Inocor) C: Same Positive inotrope with arterial vasodilating
properties
Do not administer in solutions with dextrose
Pretreat with digitalis in patients with atrial
fibrillation
Appendix 2
Atenolol Tab: 25, 50, 100 mg Atrial and ventricular arrhyth- D: 0.25-1.5 mg/kg PO q 12-24 h Beta-1 selective beta-blocker
(Tenormin) Oral suspension: 25 mg/mL mias, hypertrophic cardio- C: 6.25-12.5 mg PO q 12-24 h Less bronchoconstriction and vasoconstriction
myopathy, hypertension, aortic than nonselective beta-blockers
stenosis Taper dose when discontinue therapy
403
Continued
Cardiopulmonary DrugsFormulations, Indications, Dosagescontd
404
Atropine sulfate Inj: 0.05, 0.1, 0.3, 0.4, 0.5, Sinus bradycardia, atrio- D: 0.01-0.04 mg/kg IV, IM, IO Anticholinergic
0.8, 1.0 mg/mL ventricular block, sick sinus 0.02-0.04mg/kg SC q 6-8h May transiently worsen bradyarrhythmia
Appendix
syndrome, cardiac arrest (IT: double dose) More potent chronotropic effects than glyco-
C: Same pyrrolate
Benazepril Tab: 5, 20 mg Balanced vasodilation in CHF, D: 0.25-0.50 mg/kg PO q24h ACE inhibitor
(Fortekor-Canada), hypertension C: 0.25-0.5 mg/kg q24h Monitor electrolytes and renal function
Lotensin Renal disease in cats (2.5 mg/cat/day) Excreted in bile and urine
Butorphanol tartrate Inj: 0.5, 1, 2 mg/mL Nonproductive cough D: 0.055-0.11 mg/kg Narcotic cough suppressant
(Torbutrol, Stadol) Tab: 1, 5, 10 mg (COPD, tracheal collapse) SC q 6-12 h; 0.55 mg/kg More potent than dextromethorphan
(Torbutrol) q 6-12 h PO
C: None
Carnitine Tab: 330 mg Canine dilated cardiomyopathy D: 50-100 mg/kg PO q 8 h Amino acid
(Carnitor) Can be purchased accompanied by taurine or C: None L isomer is active form
in bulk as powder carnitine deficiency Not effective in all cases
Carvedilol Tab: 3.125, 6.25, Myocardial failure D: 0.1-0.5 mg/kg q Alpha and nonselective beta blocker
(Coreg) 12.5 mg 12 h (based on Do not use with atrioventricular block
pharmacokinetic studies, may be Monitor closely for worsening of heart failure
able to titrate to 1.5 mg/kg Absorption highly variable in dogs
PO q 12 h if tolerated)
Start slowly at 0.05-0.1 mg/kg
PO q 12 h for 2 weeks; up-titrate
the dose every 2-4 weeks
C: Not established
Chlorothiazide Tab: 250, 500 mg Diseases associated D: 20-40 mg/kg PO q 12 h Thiazide diuretic
(Diuril) Oral suspension: with fluid retention C: Same Less potent than loop diuretics
50 mg/mL (CHF, hepatic disease, Not effective with low GFR (renal failure)
nephrotic syndrome), Can use with loop diuretics for increased diure-
hypertension sis, but reduce initial thiazide dose by 50%
May precipitate hepatic encephalopathy in
patients with severe liver disease
Drug Dog Dose (D)
Trade Name Formulation Indications Cat Dose (C) Comments
Clopidogrel Tab: 75 mg Prevention of thromboembolism D: 10 mg/kg loading dose followed Platelet inhibitor (ADP receptor blocker)
(Plavix) in cats that have already had a by 2-4 mg/kgPO q 24 h Can be used in combination with aspirin or
thrombembolic event or are at C: 18.75 mg PO q 24 h heparin
high risk for thromboembolism Be aware of possibility of hemorrhage when
using combinations of platelet inhibitors and
anticoagulants
Dalteparin Inj: 16 mg Antithrombotic D: 100-150 U/kg SC q 8 h Low-molecular-weight heparin
(Fragmin) (2500 U)/0.2 mL; 32 mg C: 180 U/kg SC q 6 h Dose extrapolated from humans and pharma-
(5000 U/0.02 mL) cokinetic studies in animals; optimal dose in
prefilled syringes; dogs and cats unknown
64 mg (10,000 U)/mL Less likely to cause bleeding complications
multidose vials than warfarin
Expensive
Dextromethorphan In many OTC Nonproductive cough (COPD, D: 2 mg/kg PO q 6-8 h Nonnarcotic cough suppressant
cough formulas tracheal collapse) C: Same Only cough suppressant safe for use in cats
Digoxin Tab: 0.125, 0.25, Supraventricular arrhythmias, D: Maintenance dose: 0.22 mg/m2 PO Digitalis glycoside
(Lanoxin) 0.5 mg myocardial failure q12 h, 0.0055-0.01 mg/kg PO q12 h Toxicity potentiated by hypokalemia, hypo-
Inj: 0.25 mg/mL Oral loading dose: Twice the natremia, hypercalcemia, hypothyroidism,
Elixir: 0.05 mg/mL maintenance dose for the first hypoxia
Cap: 0.05, 0.1, 0.2 mg 24-48 h Dose on lean body weight, reduce dose
C: 0.01 mg/kg PO q 48 h (Tab 10%-15% with elixirs
preferred), 0.007 mg/kg PO q 48 h Therapeutic range 0.5-2 ng/mL; 8 hours after
(w/Lasix and aspirin) a dose.
Studies in humans show longer survival with
range of 0.5-1 ng/ml than with 1-2 ng/ml.
Continued
Appendix 2
405
Cardiopulmonary DrugsFormulations, Indications, Dosagescontd
406
Diltiazem Tab: 30, 60, 90, 120 mg Supraventricular arrhythmias, D: 0.5-2 mg/kg PO q 8 h Calcium channel blocker
(Cardizem, Dilacor) Inj: 5 mg/mL hypertrophic cardiomyopathy, (consider higher dose of Less myocardial depression than verapamil
Cardizem CD: 120, 180, hypertension 5 mg/kg based on recent studies), Dilacor XR capsules contain 60-mg tablets that
Appendix
300 mg 0.1-0.2 mg/kg IV bolus, then are used for dosing cats
Dilacor XR: 120, 180, 2-6 mcg/kg/min IV CRI
240 mg Dilacor XR: 1.5-6 mg/kg PO q 24 h
C: 1.0-2.5 mg/kg PO q 8 h, 0.1-0.2 mg/
kg IV bolus, then 2-6 mcg/kg/min IV
CRI, Dilacor XR: 30-60 mg PO q 24 h
Dobutamine HCl Inj: 12.5 mg/mL Short-term management D: 2.5-20 mcg/kg/min (titrate up to Beta-adrenergic agonist
(Dobutrex) of severe myocardial failure effect). Administer in D5W Monitor ECG, BP, and pulse quality
C: 2-10 mcg/kg/min (titrate up to Preferable to dopamine in CHF but more
effect). Administer in D5W expensive
Inotropic effect is dose dependent
Less arrhythmogenic than most other
catecholamines
Use with caution in cats
Dopamine HCl Inj: 40, 80, or Shock, short-term D: 2-10 mcg/kg/min (titrate up to Dopaminergic agonist
(Intropin, Dopastat) 160 mg/mL management of severe effect). Administer in D5W, Monitor ECG, BP, and pulse quality
myocardial failure saline, or LRS May cause tissue necrosis if extravasation
Anuric or oliguric renal failure C: Same occurs
Can administer intraosseously
Enalapril maleate Tab: 1, 2.5, 5, 10, 20 mg Balanced vasodilation in CHF, D: 0.5 mg/kg PO q 12-24 h (titrate ACE inhibitor
(Enacard) hypertension up to effect) Monitor renal function and electrolytes
C: 0.25-0.5 mg/kg PO q 24-48 h Increased survival in heart failure patients
(titrate up to effect) Decrease dose with renal disease
Drug Dog Dose (D)
Trade Name Formulation Indications Cat Dose (C) Comments
Enoxaparin Inj: 30mg/0.3 mL Antithrombotic D: 0.8 mg/kg SC q 12 h Low-molecular-weight heparin
(Lovenox) C: 1.25 mg/kg SC q 12 h Dose-extrapolated from humans and pharma-
cokinetic studies in animals. Optimal dose in
dogs and cats
unknown
Less likely to cause bleeding complications
than warfarin
Expensive
Epinephrine Inj: 1:1000 conc Cardiac arrest D: 0.2 mg/kg IV, IO q 3-5 min. Double Beta-adrenergic agonist
(Adrenalin) (1 mg/mL) dose for IT administration Monitor with ECG
1:10000 conc C: Same Previously recommended dose of 0.02 mg/kg
(0.1 mg/mL) may be a safer starting dose if a defibrillator
is not available
Esmolol Inj: 100, Short-term management D: 50-500 (usually 50-100) mcg/kg IV Ultra-short-acting beta-selective beta adrener-
(Brevibloc) 250 mg/mL of supraventricular bolus every 5 min (up to 500 mcg/kg gic blocker
tachyarrhythmias, ventricular max), 50-200 mcg/kg/min CRI
tachycardia, and systemic C: Same
hypertension
Furosemide Tab: 12.5, 20, Diseases associated with fluid D: 2-6 mg/kg PO, IM, IV q 8-48 h, Loop diuretic
(Lasix) 40, 50, 80 mg retention (CHF, hepatic 2-8 mg/kg IV q 1-2 h for severe Decreased oral absorption in decompensated
Inj: 10 and disease, nephrotic syndrome), pulmonary edema CHF
50 mg/mL hypertension CRI: 0.66 mg/kg IV bolus followed by Monitor hydration and electrolytes
Oral solution: 0.66 mg/kg/h IV Hypokalemia uncommon in dogs unless
10 mg/mL C: 1-4 mg/kg PO, IM, IV q 12-48 h. anorexic or high dose
Titrate to lowest effective dose for May precipitate hepatic encephalopathy in
maintenance patients with severe liver disease
Bioavailability reduced with food
Glycopyrrolate Inj: 0.2 mg/mL Sinus bradycardia, atrio D: 0.005-0.01 mg/kg IV, IM, Anticholinergic
(Robinul) ventricularblock, sick sinus 0.01-0.02 mg/kg SC Longer duration of action with less of a
syndrome C: Same chronotropic effect than atropine
Heparin Inj: 1000, 5000, Short-term prevention D: Loading dose: Anticoagulant
(Calciparine, 10,000 U/mL of thromboembolism 100-500 U/kg SC q 8 h Antidote: Protamine sulfate
Liquaemin) Chronic dose: 10-50 /kg q 6-8 h Maintain APTT or ACT at 2-2.5 times the
C: Loading dose: pretreatment values
Appendix 2
100-300 U/kg SC q 8 h
Continued
407
408
Hydralazine HCl Tab: 10, 25, 50, 100 mg Arterial dilation in CHF, D: 1-3 mg/kg PO q12h (titrate up to Direct-acting arterial vasodilator
(Apresoline) Inj: 20 mg/mL hypertension effect) Causes sodium retention, requiring increased
Appendix
Europe)
C: None
Continued
409
410
Nitroprusside sodium Inj: 50 mg/vial Short-term balanced vasodilation D: 1-10 mcg/kg/min in D5W Nitrate vasodilator
(Nipride, Nitropress) in severe CHF C: Unknown Protect solution from light
Adjust drip rate to maintain mean arterial
pressure of ~70 mm Hg
Discontinue if metabolic acidosis develops
Large dose or prolonged use may cause
cyanide toxicity
Omega-3 fatty acids Heart failure (to counter cachex- D: C: 50-250 mg/kg/24 h PO Fatty acid
(ALA, EPA and/or ia); renal hypertension; ventricu- Side effects rare
DHA) lar arrhythmias
Pimobendan Chewable tablets: 1.25 mg, Licensed for treating dogs with D: 0.25 mg/kg q 12 h PO Phosphodiesterase III inhibitor and a calcium
(Vetmedin) 5 mg (USA) signs of mild, moderate, or C:1.25 mg/cat q 12 h PO (anecdotal) sensitizer that acts as an inotropic vasodilator
Capsules: 1.25 mg, 2.5 mg, severe CHF (modified NYHA Do not use in aortic stenosis, hypertrophic
5 mg (Canada, Europe, Class II, III, or IV) due to cardiomyopathy, or other conditions in which
and Australia) dilated cardiomyopathy or an augmentation of cardiac output is
valvular insufficiency. inappropriate
Prazosin HCl Cap: 1, 2, 5 mg Balanced vasodilation in CHF, D: 1 mg/15 kg PO q 8 h. Titrate to Direct acting vasodilator
(Minipress) hypertension effect Tolerance develops
C: None
Drug Dog Dose (D)
Trade Name Formulation Indications Cat Dose (C) Comments
Procainamide Cap: 250, 375, 500 mg Ventricular and supraventricular D: 10-30 mg/kg IM, PO q 6 h; 2 mg/kg Class 1 antiarrhythmic agent
(Pronestyl, generic) Tab: 250, 375, 500 mg arrhythmias, WPW IV over 3-5 min up to total dose of Beware hypotension with IV administration
Tab: CR, SR: 250, 500, 20 mg/kg; 20-50 mcg/kg/min CRI Effects increased by high potassium and
750, 1000 mg C: 3-8 mg/kg PO, IM, q 6-8 h decreased by low potassium
Inj: 100, 500 mg/mL Monitor ECG: 25% prolongation of QRS is
sign of toxicity
Fewer gastrointestinal and cardiovascular side
effects than quinidine
Use with caution in cats
Reduce dose with severe renal and liver disease
Use largely replaced by mexiletine and sotalol
Propranolol Tab: 10, 20, 40, 60, Atrial and ventricular arrhyth- D: 0.2-1.0 mg/kg PO q 8 h; Nonselective beta blocker
(Inderal) 80, 90 mg mias, hypertrophic cardio- 0.02-0.06 mg/kg IV over 5-10 minutes Start with low dose and titrate to effect
Inj: 1 mg/mL myopathy, hypertension, C: < 4.5 kg: 2.5-5 mg PO q 8-12 h; Taper dose when discontinue therapy
Solution: 4, 8, 80 mg/mL thyrotoxicosis > 4.5 kg: 5 mg PO 8-12 h; Reduce dose with liver disease
0.02-0.06 mg/kg IV over 5-10 minutes Beware of possible bronchoconstriction
Quinidine gluconate Tab: 324 mg Ventricular and supraventricular D: 6-20 mg/kg PO, IM q 6 h; Class 1 antiarrhythmic
(Quinaglute Dura- Inj: 80 mg/mL arrhythmias, WPW, conversion 6-20 mg/kg PO q 8 h with sustained Decrease digoxin dose 50% when using
Tabs) Tab: 275 mg of atrial fibrillation release products; 5-10 mg/kg quinidine
Quinidine poly Tab: 100, 200, 300 mg IV (very slowly) Effects increased by high potassium and
galacturonate C: None decreased by low potassium
(Cardioquin) Note: Dose calculated for quinidine Monitor ECG: 25% prolongation of QRS is
Quinidine sulfate Tab SR: 300 mg base equivalent, which varies with sign of toxicity
(Quinidex) Cap: 200, 300 mg each quinidine salt. Has vagolytic, negative inotropic, and
Inj: 200 mg/mL See Comments. vasodilating properties
Reduce dose in CHF, hepatic disease, and
hypoalbuminemia
Quinidine base (%) in each quinidine salt:
quinidine gluconate (62%): 324 mg
tab = 200 mg quinidine
Quinidine polygalacturonate (60%);
275 mg tab = 166 mg quinidine
Quinidine sulfate (83%); 200 mg tab = 166 mg
quinidine
Use largely replaced by mexiletine and sotalol
Appendix 2
Sildenafil Tab: 25, 50, 100 mg Pulmonary hypertension D: 0.5-1 mg/kg q 12 h (higher dose Phosphodiesterase 5 inhibiting vasodilator
(Viagra) of 2-3 mg/kg q 8 h may be tolerated Expensive
and needed May be effective for pulmonary hypertension*
C: Same
411
Continued
Cardiopulmonary DrugsFormulations, Indications, Dosagescontd
412
Spironolactone Tab: 25, 50, 100 mg Diseases associated with fluid D: 1-2 mg/kg PO q 12 h Potassium-sparing diuretic
(Aldactone) retention (CHF, hepatic disease, C: Same 2-3 days to achieve peak effect
nephrotic syndrome), hyperten- D,C: 0.5-1.0 mg/kg/day (possible Weak diuretic
sion, hypokalemia cardiac anti-remodeling) Usually combines with a loop diuretic
Ulcerative facial dermatitis in third of cats
Taurine Tab: 250 mg Dilated cardiomyopathy (cats) D: 500 mg PO q 12 h Amino acid
(Taurine V) Cap: 500 mg as a generic and selective cases in dogs C: 250 mg PO q12 h Clinical improvements noted in 4-10 days
(especially the American Echo improvement usually by 6 weeks
Cocker Spaniel) Continue supplement for 12-16 weeks while
correcting diet
Terbutaline Tablet: 2.5, 5 mg Asthma, COPD D: 1.25-5 mg/dog PO q 8-12 h Beta-2 agonist bronchodilator
(Brethine, Bricanyl) Inj: 1 mg/mL C: 0.1 mg/kg PO q 12 h; Reduce dose by 50% first 4 days to prevent
0.05 mg/kg SC, IM, IV restless behavior.
Decrease dose with renal disease
Theophylline Tab: 100, 200, 300, Asthma, COPD, sick sinus D: 9 mg/kg PO q 8-12 h; Extended Methylxanthine bronchodilator
(Extended Release) 450 mg syndrome release: 10 mg/kg PO q 12 h Extended release dose based on Inwood
Cap: 50, 75, 125, 200 mg C: 4 mg/kg PO q 12 h; Extended release Laboratories formulation
tab: 15 mg/kg PO q 24 h at night; Reduce dose with CHF, liver disease,
Extended release cap: 19 mg/kg PO cimetidine, orbifloxacin, enrofloxacin
q 24 h at night Reduce dose by 50% first 4 days to prevent
anxiety side effect
Therapeutic range: 10-20 mcg/mL
Dose on lean body weight
Tocainide Tab: 400, 600 mg Ventricular arrhythmias D: 10-20 mg/kg PO q 8-12 h Class I Antiarrhythmic
(Tonocard) C: None Oral analog of lidocaine
Giving with food may decrease gastrointestinal
upset
Drug Dog Dose (D)
Trade Name Formulation Indications Cat Dose (C) Comments
Triamterene Cap: 50, 100 mg Diseases associated with fluid D: 1-2 mg/kg PO q 12 h Potassium-sparing diuretic
(Dyrenium) retention (CHF, hepatic disease, C: Same Weak diuretic
nephrotic syndrome), hyperten- Usually combined with loop diuretic
sion, hypokalemia Does not block aldosterone
Verapamil Tab: 80, 120, 240 mg Supraventricular arrhythmias, D: 0.05-0.2 mg/kg slow IV (1-2 min) in Calcium channel blocker
(Calan, Isoptin) Inj: 2.5 mg/mL hypertrophic cardiomyopathy boluses of 0.05 mg/kg given at 10-30 Diltiazem is a safer alternative in heart failure
minute intervals (to effect) to a maxi- Potent vasodilator and negative inotrope
mum cumulative dose of 0.2 mg/kg
C: None
Warfarin Tab: 2, 2.5, 5, 7.5, 10 mg Prevention of thromboembolism D: 0.1-0.2 mg/kg PO q 24 h Anticoagulant
(Coumadin) C: Same Initiate therapy with 4 days of heparin to pre-
vent initial hypercoagulable state
Control animals lifestyle and environment to
minimize risk of trauma
Adjust dose to maintain PT at 1.5-2 times
baseline value or INR of 2-3
BW (kg) ml/hr
5 10
10 20
20 40
30 60
40 80
50 100
60 120
70 140
A pp e ndi x 3
Echocardiographic Normals
Weight (kg)
Parameter 3 5 7 10 15 20 25 30 35 40 50
LVIDd 24.6 27.4 30.0 32.7 37.1 41.4 44.8 48.3 51.7 54.8 60.7
(mm) (6.2) (5.2) (4.5) (3.5) (2.4) (2.2) (2.9) (3.9) (5.0) (6.1) (8.3)
LVIDs 13.6 16.0 17.9 20.6 24.3 28.0 31.0 33.9 36.9 39.6 44.6
(mm) (5.5) (4.7) (4.0) (3.1) (2.1) (2.0) (2.5) (3.4) (4.5) (5.4) (7.4)
LVPWd 5.0 5.4 5.7 6.2 6.8 7.4 7.9 8.4 8.9 9.3 10.2
(mm) (2.1) (1.7) (1.5) (1.2) (0.8) (0.7) (1.0) (1.3) (1.7) (2.0) (2.8)
LVPWs 7.2 7.9 8.4 9.2 10.2 11.3 12.1 13.0 13.8 14.5 16.0
(mm) (1.7) (1.6) (1.4) (1.3) (1.1) (1.1) (1.2) (1.3) (1.5) (1.7) (2.2)
IVSd 5.8 6.2 6.5 7.0 7.6 8.2 8.7 9.2 9.7 10.2 11.0
(mm) (2.1) (1.7) (1.5) (1.2) (0.8) (0.7) (0.9) (1.3) (1.7) (2.0) (2.7)
IVSs 9.8 10.2 10.4 10.9 11.5 12.3 13.0 13.9 14.6 15.4
(mm) (2.6) (2.2) (2.0) (1.7) (1.2) (1.1) (1.5) (2.3) (2.6) (3.5)
LA 12.7 14.0 15.0 16.3 18.3 20.2 21.8 23.3 24.8 26.2 28.8
(mm) (5.3) (4.5) (3.8) (3.0) (2.0) (1.9) (2.4) (3.3) (4.3) (5.2) (7.1)
Ao 13.8 15.3 16.4 18.1 20.4 22.8 24.6 26.4 28.3 30.0 33.1
(mm) (3.6) (3.0) (2.6) (2.0) (1.4) (1.3) (1.6) (2.2) (2.9) (3.5) (4.8)
From Ware WA: Diagnostic tests for the cardiovascular system. In Nelson RW, Couto CG (eds): essentials of small animal internal
medicine. St. Louis, 1992, Mosby. Data from Bonagura JD, OGrady MR, Herring DS: Echocardiography: principles of interpretation.
Vet Clin North Am Small Anim Pract 15:1177, 1985.
LVIDd, left ventricular internal dimension at end diastole; LVIDs, left ventricular internal dimension at end systole; LVPWd, left
ventricular posterior wall at end diastole; LVPWs, left ventricular posterior wall at end systole; IVSd, interventricular septum at end
diastole; IVSs, interventricular septum at end systole; LA, left atrium (systole); Ao, aortic root (diastole).
*Fractional shortening: 28% to 40%; mitral valve E point to septal separation: <5 to 6 mm. Mean value given,SD in parentheses
below.
415
416 Appendix
RVIDd, right ventricular internal dimension at end diastole; LVIDd, left ventricular internal dimension at end diastole; LVIDs, left ven-
tricular internal dimension at end systole; SF, shortening fraction; LVPWd, left ventricular posterior wall at end diastole; LVPWs, left
ventricular posterior wall at end systole; IVSd, interventricular septum at end diastole; IVSs, interventricular septum at end systole; LA,
left atrium (systole); Ao, aortic root (end diastole); EPSS, E point to septal separation; PEP (s), pre-ejection period (seconds); LVET (s),
left ventricular ejection time (seconds); Vcf (circumf/s), velocity of circumferential fiber shortening.
*Data from Jacobs G, Knight DH: M-Mode echocardiographic measurements in nonanesthetized healthy cats: effects of body weight,
Median and Range of Observed Heart Rate and Echocardiographic Measurements of Dogs of Four
Different Breeds (Differing Somatotypes)
From Morrison, S.A., et al: Effect of breed and body weight on echocardiographic values in four breeds of dogs of differing somato-
types, J Vet Intern Med, 6:223, 1992.
LVWD, left ventricular wall thickness at end-diastole; LVWS, left ventricular wall thickness at systole; LVCD, left ventricular cham-
ber dimension at end-diastole; LVCS, left ventricular chamber dimension at systole; FS, percent fractional shortening; EPSS, E-point
septal separation; RVCD, right ventricular chamber dimension at end-diastole; IVSD, interventricular septal thickness at end-diastole;
IVSS, interventricular septal thickness at systole; AO, aortic root; LA, left atrium.
*Median.
Range.
Index
418
Index 419
Anesthesia of cardiac patient, 356-375 Anesthetic drug interactions, cardiac drugs and (Continued)
adjunct techniques, 364-365 combination drug therapy, 359
infiltration techniques, 365 digitalis glycosides, 358
local and regional anesthesia/analgesia, 364-365 diuretics, 358
local anesthetic drugs, 365 nonsteroidal anti-inflammatory drugs, 359
opioids, 365 vasodilators, 358-359
aftercare, 368 Anesthetic drugs contraindicated in patients with cardiac disease
analgesia, 368-370 alpha-2 adrenergic drugs, 360
continuous rate infusion of opioids, 369-370 barbiturates, 360
opioid analgesia techniques, 369 inhalation anesthetics, 360
anesthetic drug selection and supportive care, 359-360 Anesthetics
anesthetic drugs contraindicated in patients with cardiac inhalation, 360
disease, 360 protocols in dogs and cats, 370-372
oxygenation and ventilatory support, 359-360 Anesthetized patients, classification of physical status for, 357t
sedation or general anesthesia, 359 Angiography, nonselective, 102-103
anesthetic drugs that should be used with caution, 360-361 Angiotensin-converting enzyme inhibitors (ACEIs), cardiac
intravenous induction agents, 361 drugs and anesthetic drug interactions, 358
preanesthetic medications, 360-361 Anterior fascicular block, left, 72
anesthetics protocols in dogs and cats, 370-372 Anterior mitral valve leaflet, 129f
canine pericardial disease, 372 Antiarrhythmic agents, 145
cardiac diseases and anesthesia techniques for cats, 372-373 cardiac drugs and anesthetic drug interactions, 359
cardiac drugs and anesthetic drug interactions, 358-359 Antibradycardia pacing, pacemaker nomenclature for, 389t
angiotensin-converting enzyme inhibitors (ACEIs), 358 Anticholinergics, 360-361
antiarrhythmic agents, 359 Aorta
calcium channel blockers, 359 enlargement of aortic arch and, 39
class I antiarrhythmic agents, 359 M-mode measurements of left heart and, 92f
combination drug therapy, 359 Aortic arch and aorta, enlargement of, 39
digitalis glycosides, 358 causes of aortic arch enlargement, 39
diuretics, 358 differential diagnosis, 39
nonsteroidal anti-inflammatory drugs, 359 radiographic signs, 39
vasodilators, 358-359 Aortic diameters, measurement of, left atrial and, 93f
care during sedation and anesthesia, 366-368 Aortic stenosis, 223-227, 226f. See also Subaortic stenosis,
invasive monitoring, 367-368 congenital
noninvasive monitoring, 366-367 anatomy, 223
injectable general anesthesia, 364 diagnosis, 223
intravenous induction agents, 362-363 diagnostic testing, 224-227
maintenance of anesthesia, 363 natural history, 227
pericardiocentesis, 372 pathophysiology, 223
preanesthetic considerations, 356-358 physical examination, 224
additional tests, 358 prognosis, 227
anesthetic risk classification, 357 therapy, 227
diagnosis of etiology of heart disease, 356-357 Aortic valve
functional classification of heart failure, 357 dilation, 376-378
laboratory tests, 358 endocarditis, 134f, 135f
physical examination, 358 incompetence, 136f
preanesthetic diagnostic evaluation, 358 APCs. See Atrial premature complexes (APCs)
regional techniques, 365-366 Appendectomy, atrial, 379, 381f
intercostal nerve blocks, 365 Apresoline (hydralazine), 283, 284, 302
intrapleural analgesia, 366 Arrhythmias
lumbosacral epidural - cats, 365 breed-specific, 328-329
lumbosacral epidural - dogs, 365 cardiac, 49, 315-332
nondepolarizing muscle relaxants drugs (NMRDs), 366 classification of cardiac, 62b
species differences in anesthetic drug effects, 364 and conduction disturbances, 63-65
specific cardiac diseases and recommended aesthetic feline patients with, 321t
protocols, 370 heard on auscultation, 20
useful anesthetic drugs normal, sinus, 65
preanesthetic medication, 361 supraventricular, 316t, 317
tranquilizers, 361-362 ventricular, 317t, 326
Anesthetic drug interactions, cardiac drugs and, 358-359 Arterial vasodilators, 144-145
angiotensin-converting enzyme inhibitors (ACEIs), 358 Arterial vasodilators, direct-acting, 302-303
antiarrhythmic agents, 359 alpha-adrenergic receptor antagonists, 303
calcium channel blockers, 359 prazosin (Minipress), 303
class I antiarrhythmic agents, 359
420 Index
Arterial vasodilators, direct-acting (Continued) Auscultatory method, 279
hydralazine, 302 AV. See Arterioventricular (AV)
sodium nitroprusside, 302-303 AVNRT. See Atrioventricular nodal reentrant tachycardia (AVNRT)
nitroprusside (Nipride), 302-303 AVRT. See Atrioventricular reentrant tachycardia (AVRT)
venous vasodilators, 303 Azotemia, development of, 129
isosorbide dinitrate, 303
nitroglycerin, 303 B
Artery banding, pulmonary, 378, 379f Balloon-tipped cardiac catheter, 104f
Artery shunt, systemic-to-pulmonary, 378-379, 380f Banding, pulmonary artery, 378, 379f
Artificial pacemaker, 76 Barbiturates, 360, 362-363. See also Thiobarbiturates
Artioventricular valve dysplasia, 236-238 Basal serum thyroid hormone, altering, 245b
anatomy, 237 Beat
diagnosis, 237 junctional escape, 74
diagnostic testing, 238 ventricular escape, 74-76
pathophysiology, 237 Benazepril, 283
physical elimination, 237 Benzodiazepines, 361
prognosis, 238 Beta blockers, adrenergic, 160
therapy, 238 Beta-adrenergic blocking agents, 145
Ascites, 7-8 Beta-adrenergic receptor blockers, 308-309
Ascites in dogs, 8f Biomarkers, cardiac neurohormones and, 105
Ascites in dogs, cause of, 8b Bipolar standard leads, three, 53f
Ashmans phenomenon, 76 Bipolar VVIR pacemaker, 390f
Asthma-like syndrome, feline, 194, 197 Blindness, cat with acute, 278f
Asymptomatic MVD, 124-125 Block. See also Left bundle branch block (LBBB); Right
Asymptomatic occult disease, treatment of, 145-146 bundle branch block (RBBB)
Asystole, ventricular, 74, 329-330 complete heart, 72
AT. See Atrial tachycardia (AT) first-degree AV, 71
Atenolol, 160, 283 left anterior fascicular, 72
Atrial and aortic diameters, measurement of, left, 93f second-degree AV, 71
Atrial and atrioventricular septal defect repair, 383 sinus, 67
Atrial appendectomy, 379, 381f third-degree AV, 72
Atrial enlargement, dog with severe left, 34f Blocking agents
Atrial fibrillation (AF), 66, 142f, 318-322, 318f beta-adrenergic, 145
dogs with, 319f, 320f, 321f calcium channel, 301-302
therapy, 318-322 Blood pressure
Atrial flutter (AFL), 66, 322 compensatory sympathetic system and reduction in, 292f
drug therapy for, 322 consequences and clinical signs of high, 278-279
Atrial premature complexes (APCs), 66 measurement of, 279-281
Atrial premature complexes (APCs) with aberrant Borreliosis (Lyme disease), 271
conduction, 74 Boxer with large heart base mass, 265f
Atrial standstill, 67 Bradyarrhythmias, 349-351
Atrial tachycardia (AT), 66 hyperkalemic cardiotoxicity, 351
ectopic, 322 second and third-degree AV block, 350-351
Atrial thrombus, left, 10f sinus arrest, 351
Atrioventricular (AV) block sinus bradycardia, 349-350
canine patient with complete, 390f Bradyarrhythmias and conduction disturbances, 323
dog with high-grade second-degree, 391f Bradycardia pacing. See Antibradycardia pacing
first-degree, 71 Bradycardias
second-degree, 71 recurrence of, 393f
third-degree, 72 sinus, 65, 323-324
Atrioventricular (AV) conduction abnormalities, 325-326 Breed, 2
AV block Breed-specific arrhythmias, 328-329
complete or third degree, 325-326 Buprenorphine, 362
first degree, 325 Butorphanol (Torbutrol), 307, 362
second degree, 325
treatment of complete AV block, 326
C
Atrioventricular (AV) junctional tachycardia, 67 Cachexia, cardiac, 9b
Atrioventricular nodal reentrant tachycardia (AVNRT), 323 Calcium channel blockers, 160-161
Atrioventricular reentrant tachycardia (AVRT), 323 cardiac drugs and anesthetic drug interactions, 359
Atropine, 336 Calcium channel blocking agents, 301-302
Auscultation, 16-17 amlodipine (Norvasc), 302
arrhythmias heard on, 20 diltiazem (Cardizem, Dilacor), 302
in dog, 16f nifedipine, 302
in dog and cat, 17t verapamil, 302
Calcium gluconate, 336-338
Index 421
Calcium-sensitizing agents, 148 Cardiac disease, diagnostic techniques for
Canine. See also Dogs evaluation of (Continued)
degenerative valvular disease, 126t technique, 101-102
pericardial disease, 372 cardiac catheterization, 103-104
with transvenous VDD pacing system, 390f clinical utility, 104
Canine and feline ECG valves, normal, 57t indications, 103
Canine and feline electrocardiography, lead systems limitations, risks, and costs, 104
used in, 52b technique, 103-104
Canine cardiomyopathy, 139-150 cardiac neurohormones and biomarkers, 105
dilated cardiomyopathy, 139-149 cardiac troponins, 105
hypertrophic cardiomyopathy (HCM), 149 continuous in-hospital electrocardiographic
Canine patients monitoring, 99-100
with complete AV block, 390f limitations, 100
supraventricular arrhythmias in, 316t technique, 99-100
ventricular arrhythmias in, 317t Holter monitoring and cardiac event recording, 101-102
Carbon monoxide (CO), 267-268 cardiac event recorders (CERs), 102
Cardiac arrhythmias indications, 101
classification of, 62b technique, 101-102
documentation of, 49 natriuretic peptides (atrial and B-type), 105-106
Cardiac arrhythmias and conduction disturbances, clinical utility, 106
treatment of, 315-332 indications, 105
atrial fibrillation (AF), 318-322 limitations, risk, and costs, 106
therapy, 318-322 technique, 106
atrial flutter (AFL), 322 newer cardiac imaging techniques, 106-107
atrioventricular (AV) conduction abnormalities, 325-326 computed tomography (CT), 106
AV block, complete or third degree, 325-326 limitations, 107
AV block, first degree, 325 magnetic resonance imaging (MRI), 107
AV block, second degree, 325 nuclear cardiology, 107
treatment of complete AV block, 326 nonselective angiography, 102-103
atrioventricular nodal reentrant tachycardia (AVNRT), 323 clinical utility, 103
atrioventricular reentrant tachycardia (AVRT), 323 indications, 102
breed-specific arrhythmias, 328-329 limitations, risk, and costs, 103
ectopic atrial tachycardia (AT), 322 technique, 102-103
sick sinus syndrome (SSS), 324-325 provocative electrocardiographic techniques, 100-101
treatment, 324-325 clinical utility, 100-101
sinus bradycardia, 323-324 inhibition of vagal tone, 100
treatment, 324 vagal maneuver, 100
treatment of cardiac arrhythmias, 315-318 serologic testing, 104-105
treatment of ventricular tachycardia (VT), 326-328 clinical utility, 105
acute intravenous antiarrythymic therapy, 327 indications, 104-105
chronic oral antiarrythymic therapy, 327-328 limitations, risk, and costs, 105
ventricular asystole, 329-330 technique, 105
ventricular fibrillation, 330 Cardiac diseases
Cardiac cachexia in dog, problems contributing to, 9b and anesthesia techniques for cats, 372-373
Cardiac catheter, balloon-tipped, 104f radiographic signs of congenital and acquired, 43t
Cardiac catheterization, 103-104 Cardiac diseases, anesthetic drugs contraindicated
indications, 103 in patients with
technique, 103-104 alpha-2 adrenergic drugs, 360
angiocardiography, 103-104 barbiturates, 360
oximetry, 103 inhalation anesthetics, 360
Cardiac chamber activation, 56f Cardiac drugs and anesthetic drug interactions, 358-359
Cardiac conditions, common acquired, 93-97 angiotensin-converting enzyme
2 D changes, 93-94 inhibitors (ACEIs), 358
degenerative mitral valve disease, 93 antiarrhythmic agents, 359
dilated cardiomyopathy (DCM), 94-95 calcium channel blockers, 359
hypertrophic cardiomyopathy (HCM), 95 class I antiarrhythmic agents, 359
pericardial disease, 95-97 combination drug therapy, 359
Cardiac conduction and genesis of waveforms, 51-52 digitalis glycosides, 358
Cardiac conduction system, 55f diuretics, 358
Cardiac disease, diagnostic techniques for nonsteroidal anti-inflammatory drugs, 359
evaluation of, 99-107 vasodilators, 358-359
ambulatory electrocardiography, 101-102 Cardiac event recorders (CERs), 102
cardiac event recorders (CERs), 102 Cardiac hemangiosarcoma, 205-209
indications, 101 Cardiac hemangiosarcoma, dog with, 206f
422 Index
Cardiac imaging techniques, newer, 106-107 Cardiac patient, anesthesia of (Continued)
computed tomography (CT), 106 regional techniques, 365-366
limitations, 107 intercostal nerve blocks, 365
magnetic resonance imaging (MRI), 107 intrapleural analgesia, 366
nuclear cardiology, 107 lumbosacral epidural - cats, 365
Cardiac lymphoma lumbosacral epidural - dogs, 365
cat with, 264f nondepolarizing muscle relaxants drugs (NMRDs), 366
dog diagnosed with, 263f species differences in anesthetic drug effects, 364
Cardiac masses and foreign bodies. See intracardiac masses specific cardiac diseases and recommended aesthetic
and foreign bodies protocols, 370
Cardiac murmur, cough and, 115t useful anesthetic drugs
Cardiac neurohormones and biomarkers, 105 preanesthetic medication, 361
cardiac troponins, 105 tranquilizers, 361-362
clinical utility, 105 Cardiac rhythm disturbances, 297, 342, 349-354
indications, 105 bradyarrhythmias, 349-351
limitations, 105 hyperkalemic cardiotoxicity, 351
technique, 105 second and third-degree AV block, 350-351
Cardiac patient, anesthesia of, 356-375 sinus arrest, 351
adjunct techniques, 364-365 sinus bradycardia, 349-350
infiltration techniques, 365 tachyarrhythmias
local and regional anesthesia/analgesia, 364-365 sinus tachycardia, 352
local anesthetic drugs, 365 supraventricular tachycardia, 352-353
opioids, 365 ventricular tachycardia, 353-354
aftercare, 368 Cardiac silhouette, generalized enlargement of, 179f
analgesia, 368-370 Cardiac size, vertebral scale system of, 31f
continuous rate infusion of opioids, 369-370 Cardiac surgery, 376-385
opioid analgesia techniques, 369 with cardiopulmonary bypass (CPB), 383-385
anesthetic drug selection and supportive care, 359-360 atrial and atrioventricular septal defect repair, 383
anesthetic drugs contraindicated in patients with cardiac double-chambered right ventricle (DCRV) repair, 384
disease, 360 mitral valve repair, 385
oxygenation and ventilatory support, 359-360 mitral valve replacement (MR), 384-385
sedation or general anesthesia, 359 tetralogy of Fallot repair, 383-384
anesthetic drugs that should be used with tricuspid valve replacement, 385
caution, 360-361 ventricular septal defect (VSD) repair, 383
intravenous induction agents, 361 closed, 376-380
preanesthetic medications, 360-361 atrial appendectomy, 379
anesthetics protocols in dogs and cats, 370-372 patent ductus arteriosus (PDA) ligation, 376
canine pericardial disease, 372 pericardiectomy, 379
cardiac drugs and anesthetic drug interactions, 358-359 pulmonary artery banding, 378
angiotensin-converting enzyme inhibitors pulmonic and aortic valve dilation, 376-378
(ACEIs), 358 systemic-to-pulmonary artery shunt, 378-379
antiarrhythmic agents, 359 with inflow occlusion, 380-383
calcium channel blockers, 359 cor triatriatum repair, 382-383
class I antiarrhythmic agents, 359 intracardiac masses and foreign bodies, 383
combination drug therapy, 359 pulmonary patch graft, 381-382
digitalis glycosides, 358 Cardiac tumors, 210
diuretics, 358 Cardiac tumors, pericardial disorders and, 200-214
nonsteroidal anti-inflammatory drugs, 359 causes of pericardial effusion, 205-212
vasodilators, 358-359 cardiac hemangiosarcoma, 205-209
care during sedation and anesthesia, 366-368 neoplastic, 205-210
invasive monitoring, 367-368 pericardial effusions, 200-205
noninvasive monitoring, 366-367 chief complaints and history, 200
injectable general anesthesia, 364 diagnostic procedures, 201-204
intravenous induction agents, 362-363 incidence, 200
maintenance of anesthesia, 363 physical examination findings, 200-201
pericardiocentesis, 372 signalment, 200
preanesthetic considerations, 356-358 Cardiac-related pathology, projection selection in, 27-28
additional tests, 358 pleural effusion, 28
anesthetic risk classification, 357 pulmonary edema, 27-28
diagnosis of etiology of heart disease, 356-357 Cardiogenic pulmonary edema, 27f
functional classification of heart failure, 357 Cardiology, nuclear, 107
laboratory tests, 358 Cardiomyopathies
physical examination, 358 canine, 139-150
preanesthetic diagnostic evaluation, 358 dilated cardiomyopathy, 139-149
Index 423
Cardiomyopathies (Continued) Cardiomyopathies, feline (Continued)
hypertrophic cardiomyopathy (HCM), 149 prognosis, 169-170
in cat, 165f signalment, 168
cat with unclassified form of, 167f therapy, 168-169
dilated, 154f therapy, 154-156
neurogenic, 273 thyrotoxic heart disease, 170-172
right ventricular, 140f ancillary tests, 171-172
Cardiomyopathies, feline, 151-175 pathophysiology, 171
acromegalic heart disease, 172-173 physical examination, 171
ancillary tests, 173 present complaints, 171
historical perspective, 172-173 prognosis, 172
pathology, 173 signalment, 171
pathophysiology, 173 therapy, 172
physical examination, 173 unclassified feline cardiomyopathies, 165-166
presenting complaints, 173 ancillary tests, 166
prognosis, 173 pathophysiology, 165
signalment, 173 physical examination, 166
therapy, 173 presenting complaints, 166
ancillary tests, 153-154 prognosis, 166
classification, 151-152 signalment, 166
clinical classification and pathophysiology, 152 therapy, 166
feline dilated cardiomyopathy (DCM), 161-163 Cardiomyopathies, unclassified feline, 165-166
ancillary tests, 162 ancillary tests, 166
pathology, 163 pathophysiology, 165
pathophysiology, 162 physical examination, 166
physical examination, 162 presenting complaints, 166
presenting complaints, 162 prognosis, 166
prognosis, 162-163 signalment, 166
signalment, 162 therapy, 166
therapy, 162 Cardiopulmonary bypass (CPB), cardiac
feline restrictive cardiomyopathy (RCM), 164-165 surgery with, 383-385
ancillary tests, 164 atrial and atrioventricular septal defect repair, 383
pathology, 164-165 double-chambered right ventricle (DCRV) repair, 384
pathophysiology, 164 mitral valve repair, 385
physical examination, 164 mitral valve replacement (MR), 384-385
presenting complaints, 164 tetralogy of Fallot repair, 383-384
prognosis, 164 ventricular septal defect (VSD) repair, 383
signalment, 164 Cardiopulmonary resuscitation (CPR), 333-341
therapy, 164 advanced life support, 335-339
hypertrophic cardiomyopathy defibrillator, 338-339
clinical classification, 157-158 drug therapy, 336-338
echocardiography, 158-160 electrocardiography, 335-336
pathology, 161 establishing access for drug and fluid therapy, 335
pathophysiology, 157-158 monitoring CPR efforts, 339
presenting complaints, 158 basic life support, 333-335
prognosis, 161 airway, 333-334
signalment, 158 breathing, 334
therapy, 160-161 circulation, 334-335
hypertrophic cardiomyopathy (HCM), 157-161 performing in veterinary patients, 337f
infectious myocarditis, 174 post-resuscitation care, 340
neoplastic infiltration of heart, 173-174 cerebral protection, 340
drugs, toxins, and physical injury, 174 intensive care, 340
historical perspective, 173-174 preventing rearrest, 340
pathology, 156 special situations, 339-340
physical examination, 153 anesthetic arrest, 339
presenting complaints, 152-153 vagal events, 339-340
prognosis, 156 Cardiotoxicity
signalment, 152-153 doxorubicin, 269-271
taurine deficiency induced myocardial failure, 166-170 hyperkalemic, 351
ancillary tests, 168 Cardiovascular collapse, hyperkalemia in, dog with, 247f
pathology, 170 Cardiovascular effects of systemic diseases, 240-276
pathophysiology, 168 anemia, 261-262
physical examination, 168 cardiac pathophysiology, 261
presenting complaints, 168 diagnosis, 261-262
424 Index
Cardiovascular effects of systemic diseases (Continued) Cardiovascular effects of systemic diseases (Continued)
prognosis, 262 diagnosis, 246-248
therapy, 262 therapy, 248
borreliosis (Lyme disease), 271 hypoglycemia, 259-260
carbon monoxide (CO), 267-268 cardiac pathophysiology, 259
Chagas disease, 271-272 diagnosis, 259
chemodectoma, 262-266 prognosis, 259-260
cardiac pathophysiology, 263 therapy, 259
diagnosis, 263-264 hypothermia, 267
prognosis, 264-265 hypothyroidism, 243-246
therapy, 264 cardiac pathophysiology, 244
chocolate toxicity, 269 diagnosis, 244-245
diabetes mellitus, 252-253 therapy, 245-246
cardiac pathophysiology, 252-253 infectious/inflammatory diseases, 270-271
diagnosis, 253 Lyme disease, 271
prognosis, 253 metabolic disturbances, 253
therapy, 253 neurogenic cardiomyopathy, 273
disorders associated with hypercalcemia, 256-257 oleander toxicity, 269
cardiac pathophysiology, 256 pancreatitis, 274
diagnosis, 256-257 parvovirus, 272
prognosis, 257 pheochromocytoma, 251-252
therapy, 257 cardiac pathophysiology, 251-252
disorders associated with hyperkalemia, 253-254 diagnosis, 252
disorders associated with hypocalcemia, 257-259 prognosis, 252
cardiac pathophysiology, 258 therapy, 252
diagnosis, 258 systemic lupus erythematosus (SLE), 272-273
prognosis, 259 toad poisoning, 268
therapy, 258-259 traumatic myocarditis, 274-275
disorders associated with hypokalemia, 254-256 trypanosomiasis (Chagas disease), 271-272
cardiac pathophysiology, 254 uremia, 260-261
diagnosis, 254 cardiac pathophysiology, 260
prognosis, 256 diagnosis, 260
therapy, 254-256 prognosis, 261
disorders associated with hypomagnesemia and therapy, 260-261
hypermagnesemia, 259 Cardiovascular function, assessing in emergency
doxorubicin cardiotoxicity, 269-271 patient, 342-343
cardiac pathophysiology, 269-270 diagnostic tests, 343
diagnosis, 270 physical examination, 342-343
therapy, 270 Cardiovascular system, physical and chemical agents
endocrine diseases, 240 that affect, 266
gastric dilation-volvulus complex (GDV), 273-274 Cardizem (diltiazem), 160-161, 302
hemangiosarcoma, 262 Cardizem CD, 161
hyperadrenocorticism, 248-250 Care, critical, 342-355
diagnosis, 249-250 Carvedilol (CoReg), 148, 309
pathophysiology, 249 Catheter, balloon-tipped cardiac, 104f
prognosis, 250 Catheterization, cardiac, 103-104
therapy, 250 Cats
hyperpyrexia, 266-267 acromegaly in, 250-251
cardiac pathophysiology, 266 with acute blindness, 278f
diagnosis, 266 anesthetics protocols in dogs and, 370-372
prognosis, 267 atypical cardiomyopathy in, 165f
therapy, 266-267 auscultation in dog and, 17t
hypersomatotropism in cats, 250-251 cardiac diseases and anesthesia techniques for, 372-373
cardiovascular pathophysiology, 250-251 with cardiac lymphoma, 264f
diagnosis, 251 characteristics of coughs in, 4t
prognosis, 251 with dilated cardiomyopathy, 154f
therapy, 251 dilated cardiomyopathy (DCM) in, 163f
hyperthyroidism, 240-243 hypersomatotropism in, 250-251
cardiac pathophysiology, 240-241 with hypertrophic cardiomyopathy, 155f, 159f, 160f
diagnosis, 241-242 life-threatening dyspnea in, 155f
prognosis, 243 with myocardial failure associated with taurine
therapy, 243 deficiency, 169f, 170f
hypoadrenocorticism, 246-248 with myxoma, 264f
cardiac pathophysiology, 246 with saddle thrombus in, 10f
Index 425
Cats (Continued) Conduction disturbances, treatment of cardiac
screening for heartworm infection, 188-189f arrhythmias and (Continued)
syncope causes in dogs and, 7b sick sinus syndrome (SSS), 324-325
with unclassified form of cardiomyopathy, 167f treatment, 324-325
with urinary obstruction, hyperkalemia in, 255f sinus bradycardia, 323-324
CERs. See Cardiac event recorders (CERs) treatment, 324
Chagas disease, 271-272 treatment of cardiac arrhythmias, 315-318
Chamber enlargement, vessel and, 36f, 37f treatment of ventricular tachycardia (VT), 326-328
Chambers and outflow tract of right side of heart, 34f acute intravenous antiarrythymic therapy, 327
Channel blockers, calcium, 160-161 chronic oral antiarrythymic therapy, 327-328
Chemical agents that affect cardiovascular system, ventricular asystole, 329-330
physical and, 266 ventricular fibrillation, 330
Chemodectoma, 262-266 Conduction system, cardiac, 55f
cardiac pathophysiology, 263 Congenital and acquired cardiac disease, radiographic signs of, 43t
diagnosis, 263-264 Congenital defects according to pathophysiology, 216b
prognosis, 264-265 Congenital heart disease, 215-239
therapy, 264 aortic stenosis, 223-227
CHF. See Congestive heart failure (CHF) anatomy, 223
Chlorothiazide (Diuril), 304 diagnosis, 223
Chocolate toxicity, 269 diagnostic testing, 224-227
Chronic heart failure, compensatory mechanisms in, 290-294 natural history, 227
additional compensatory mechanisms, 293 pathophysiology, 223
compensatory mechanisms, 293-294 physical examination, 224
Frank-Starling mechanism, 290 prognosis, 227
myocardial hypertrophy, 292-293 therapy, 227
neuroendocrine mechanisms, 293 artioventricular valve dysplasia, 236-238
renin-angiotension-aldosterone system (RAAS), 290-291 anatomy, 237
sympathetic nervous system activation, 291-292 diagnosis, 237
Chronic tamponade, 295 diagnostic testing, 238
Class I antiarrhythmic agents, cardiac drugs and anesthetic pathophysiology, 237
drug interactions, 359 physical elimination, 237
Closed cardiac surgery, 376-380 prognosis, 238
Coenzyme Q10, 149 therapy, 238
Collapsed trachea, 58f auscultatory findings in, 217t
Color flow Doppler, 83 diagnosis, 215-217
Color flow echocardiographic studies of mitral functional murmur, 218
regurgitation, 86f hereditary aspects, 215
Compensatory sympathetic system and reduction in blood incidence, 215
pressure, 292f innocent murmur, 218
Complexes pulmonic stenosis (PS), 227-231
atrial premature, 66 diagnosis, 228
junctional premature, 66 diagnostic testing, 229
Computed tomography (CT), 106 differential diagnosis, 229-230
Conduction natural history, 230
atrial premature complexes (APCs) with aberrant, 74 pathophysiology, 228
electrical impulse, 56f physical education, 228-229
Conduction abnormalities, atrioventricular (AV), 325-326 prognosis, 231
Conduction disturbances therapy, 231
arrhythmias and, 63-65 specific defects, 218-223
bradyarrhythmias and, 323 diagnosis, 218-219
Conduction disturbances, treatment of cardiac diagnostic testing, 220-222
arrhythmias and, 315-332 differential diagnosis, 222
atrial fibrillation (AF), 318-322 patent ductus arteriosus (PDA), 218
therapy, 318-322 pathophysiology, 218
atrial flutter (AFL), 322 physical examination, 219-220
atrioventricular (AV) conduction abnormalities, 325-326 prognosis, 222-223
AV block, complete or third degree, 325-326 therapy, 222-223
AV block, first degree, 325 Tetralogy of Fallot, 235-236
AV block, second degree, 325 diagnosis, 236
treatment of complete AV block, 326 diagnostic testing, 236
atrioventricular nodal reentrant tachycardia (AVNRT), 323 pathophysiology, 235
atrioventricular reentrant tachycardia (AVRT), 323 physical examination, 236
breed-specific arrhythmias, 328-329 prognosis, 236
ectopic atrial tachycardia (AT), 322 therapy, 236
426 Index
Congenital heart disease (Continued) Degenerative mitral valve disease (MVD), 116f, 117f
therapy, 217-218 Degenerative valvular disease, canine, 126t
ventricular septal defect (VSD), 231-235 Detector, flat-panel, 44f
anatomy, 231 Diabetes mellitus, 252-253
diagnosis, 232 cardiac pathophysiology, 252-253
diagnostic testing, 233-234 diagnosis, 253
pathophysiology, 231-232 prognosis, 253
physical examination, 232 therapy, 253
prognosis, 234-235 Diastolic dysfunction, 289-290
therapy, 234-235 Diazepam. See also Ketamine-diazepam; Opioid-diazepam
Congenital subaortic stenosis, 225f combinations
Congestive heart failure (CHF), 110, 153f, 288, 343-344 Diethylcarbamazine, 198
caused by advanced MR, 128-129 Diffusion, pericardial, 42f
treatment of severe life-threatening, 146 Digital radiography, introduction to, 42-46
Continuous-wave (CW) Doppler, 81 Digitalis glycosides, cardiac drugs and anesthetic drug
Cor pulmonale and pulmonary thromboembolism, 176-182 interactions, 358
clinical presentation, 177 Digoxin, 304-306
history and clinical signs, 177 Dilacor (diltiazem), 160-161, 302
diagnostic testing, 178-181 Dilacor XR, 161
catheterization, 180-181 Dilated cardiomyopathy (DCM), 94-95, 139-149, 142f, 143f
echocardiography, 179-180 in cat, 163f
electrocardiography, 178 cat with, 154f
laboratory testing, 178 concomitant abnormalities in moderate or severe, 142-144
radiographs, 178 diagnostic tests, 140-142
etiology, 177 chest radiography, 141
physical examination, 178 echocardiography, 141-142
physiology, 176-177 dog with, 97f
therapy, 181 history and physical examination findings, 140
Cor pulmonale, causes of, 177b asymptomatic occult phase, 140
Cor triatriatum repair, 382-383 overt clinical phase, 140
CoReg (carvedilol), 148, 309 natural history, 139-140
Coughing, 4-5 asymptomatic occult phase, 139-140
Coughs overt clinical phase, 140
and cardiac murmurs, 115t nutritional deficiencies, 144
caused by airway compression, 125-126 prevalence, 139
characteristics in dogs and cats, 4t prognosis, 149
CPB. See cardiopulmonary bypass (CPB) signalman, 139
CPR. See Cardiopulmonary resuscitation (CPR) treatment, 144-145
Critical care, emergency management and, 342-355 of asymptomatic occult disease, 145-146
assessing cardiovascular function, 342-343 drug classes used for, 144-145
diagnostic tests, 343 treatment of overt clinical disease
physical examination, 342-343 additional oral medications, 147-149
cardiac rhythm disturbances, 342, 349-354 chronic oral treatment, 146-147
bradyarrhythmias, 349-351 treatment of DCM accompanied by atrial fibrillation, 147
tachyarrhythmias, 352-354 treatment of refractory heart disease, 147
emergency treatment of heart failure, 343-349 treatment of severe life-threatening CHF, 146
congestive heart failure (CHF), 343-344 Dilated cardiomyopathy (DCM), feline, 161-163
forward (low-output) heart failure, 348-349 ancillary tests, 162
left-sided congestive heart failure (LCHF), 344-346 pathology, 163
pericardial effusion, 347-348 pathophysiology, 162
right-sided congestive heart failure (RCHF), 346-347 physical examination, 162
heart failure, 342 presenting complaints, 162
thromboembolic disease, 354 prognosis, 162-163
thromboembolism, 342 signalment, 162
CT. See Computed tomography (CT) therapy, 162
Cuff placement over cranial tibial artery in dog, 280f Dilation
Cushings disease, 248-250 pulmonary valve, 378f
CW. See Continuous-wave (CW) Doppler pulmonic and aortic valve, 376-378
Cyanosis, 8 Diltiazem (Cardizem, Dilacor), 160-161, 302
Dirofilaria immitis, lifecycle of, 184f
D Diseases
DCM. See Dilated cardiomyopathy (DCM) Addisons, 246-248
DCRV. See Double-chambered right ventricle (DCRV) canine degenerative valvular, 126t
Defibrillator settings, drug therapy and initial, 338t Chagas, 271-272
Index 427
Diseases (Continued) Diuretic therapy, 144, 303-306
Cushings, 248-250 digitalis glycoside therapy, 304-306
dog with myxomatous mitral valve, 96f digoxin, 304-306
infectious/inflammatory, 270-271 long diuretic, 303-304
Lyme, 271 furosemide (Lasix), 303-304
parenchymal lung, 191-193 pimobendan, 306
pericardial, 95-97 potassium-sparing diuretics, 304
thromboembolic, 354 spironolactone (Aldactone), 304
Diseases, acquired valvular, 110-138 thiazide diuretics, 304
degenerative mitral valve disease (MVD), 110-131 chlorothiazide (Diuril), 304
clinical presentation, 112-115 hydrochlorothiazide (Hydrodiuril), 304
diagnostic findings, 115-124 Diuretics, 358
etiopathogenesis, 111 Diuril (chlorothiazide), 304
incidence, 110 Dobutamine hydrochloride (Dobutrex), 308
pathology, 111 Dobutrex (dobutamine hydrochloride), 308
pathophysiology, 111-112 Dog and cat, auscultation in, 17t
prevalence, 110 Dog with cardiovascular collapse, hyperkalemia in, 247f
infective endocarditis, 131-137 Dogs
clinical presentation, 132-133 with atrial fibrillation (AF), 319f, 320f, 321f
diagnostic findings, 133-135 auscultation in, 16f
etiopathogenesis, 131-132 cardiac cachexia in, 9b
incidence, 131 with cardiac hemangiosarcoma, 206f
pathophysiology, 132 characteristics of coughs in, 4t
prevalence, 131 with collapsed trachea, 58f
prognosis, 137 cuff placement over cranial tibial artery in, 280f
therapy, 135-137 diagnosed with cardiac lymphoma, 263f
Diseases, heartworm, 183-199 diagnosis of heartworm infection (HWI) in, 188f
classification of severity, 194-197 with dilated cardiomyopathy (DCM), 97f
adjuncts to adulticide therapy, 197 with heart base tumor, 207f
confirmation of adulticide efficacy, 196-197 with heartworm disease, 191f
initiating macrolide prophylaxis in infected heartworms in right heart of, 192f
dogs, 196 with high-grade second-degree AV block, 391f
rapid microfilaricide therapy, 196 with hypokalemia, 255f
treatment, 194-196 with intermittent failure to pace, 394f
clinical pathology, 187-191 left bundle branch block (LBBB) in, 72f
clinical signs, 185-186 with malfunctioning unipolar pacemaker, 395f
diagnosis, 186-187 with mitral regurgitation, 300f
etiology, 183 with MVD, 115
history, 185 with myxomatous mitral valve disease, 96f
lifecycle, 183 with pericardial effusion (PE), 202f, 203f, 204f
macrolide efficacy against adult heartworms, 199 pericardiocentesis in, 208f
missed doses of oral macrolide prophylactic with pulmonary hypertension, 180f
drugs, 199 with pulmonary stenosis, 58f
pathogenesis, 185 receiving macrolide prophylaxis, 199
prevalence, 184 with severe hypocalcemia, 258f
prevention, 197-198 with severe left atrial enlargement, 34f
diethylcarbamazine, 198 with severe pulmonic stenosis, 96f
ivermectin (Heartgard), 198 severe right ventricular enlargement in, 58f
milbemycin (Interceptor), 198 with systolic murmur (SM), 113f
moxidectin (Advantage Multi), 198 transvenous pacing lead in, 392f
retesting dogs receiving macrolide prophylaxis, 199 ventricular pre-excitation in, 71f
sequelae of heartworm infection, 191-194 Dogs and cats
allergic pneumonitis, 193 anesthetics protocols in, 370-372
feline asthma-like syndrome, 194 syncope causes in, 7b
parenchymal lung disease, 191-193 Dopamine hydrochloride (Intropin), 308
pulmonary eosinophilic granulomatosis, 193 Doppler
treatment of sequelae, 197 color flow, 83
allergic pneumonitis, 197 continuous-wave (CW), 81
feline asthma-like syndrome, 197 echocardiographic studies, 84-85f
pulmonary eosinophilic granulomatosis, 197 echocardiography, 78-81, 226
pulmonary thromboembolism, 197 flow meter, 279
Dissociative, 364 high-pulse repetition frequency, 81-83
Dissociatives, 361, 363 pulsed wave, 81
Distended jugular veins, causes of, 12b Doppler imaging. See Tissue Doppler imaging (TDI)
428 Index
Doppler ultrasound, echocardiography and, 78-98 Echocardiographic evaluation
common acquired cardiac conditions, 93-97 of ventricular diastolic function, 87f
2 D changes, 93-94 of ventricular systolic function, 94-95f
degenerative mitral valve disease, 93 Echocardiographic measurements, 89-93
dilated cardiomyopathy (DCM), 94-95 Echocardiographic studies
hypertrophic cardiomyopathy (HCM), 95 Doppler, 84-85f
pericardial disease, 95-97 of mitral regurgitation, 86f
echocardiographic measurements, 89-93 Echocardiographic technique, 87-88
aortic and pulmonic stenosis, 91-93 Echocardiographic views, 88-89
aortic insufficiency, 91 Echocardiographic views, right parasternal, 79-81f
chamber dimensions, 89 Echocardiography
diastolic function, 91 Doppler, 78-81, 226
E point to septal separation (EPSS), 90 M-mode, 78
ejection fraction (EF%), 90 spectral Doppler, 81
end-systolic volume index (ESVI), 90 two-dimensional, 78
index of sphericity, 89 Echocardiography and Doppler ultrasound, 78-98
LA diameter, 90 common acquired cardiac conditions, 93-97
LV diameter, 89 2 D changes, 93-94
LV fractional shortening (FS%), 90 degenerative mitral valve disease, 93
LV wall thickness, 90 dilated cardiomyopathy (DCM), 94-95
mitral insufficiency, 91 hypertrophic cardiomyopathy (HCM), 95
systolic function, 90 echocardiographic measurements, 89-93
systolic time intervals, 91 aortic and pulmonic stenosis, 91-93
transmitral flow, 91 aortic insufficiency, 91
valve function, 91 chamber dimensions, 89
echocardiographic technique, 87-88 diastolic function, 91
echocardiographic views, 88-89 E point to septal separation (EPSS), 90
types of imaging, 78-87 ejection fraction (EF%), 90
applications, 83-87 end-systolic volume index (ESVI), 90
color flow Doppler, 83 index of sphericity, 89
continuous-wave (CW) Doppler, 81 LA diameter, 90
Doppler echocardiography, 78-81 LV diameter, 89
high-pulse repetition frequency Doppler, 81-83 LV fractional shortening (FS%), 90
M-mode echocardiography, 78 LV wall thickness, 90
pulsed wave Doppler, 81 mitral insufficiency, 91
spectral Doppler echocardiography, 81 systolic function, 90
tissue Doppler imaging (TDI), 83 systolic time intervals, 91
two-dimensional echocardiography, 78 transmitral flow, 91
Dorsoventral and ventrodorsal projections, 32-35 valve function, 91
cardiac parameters, 32-35 echocardiographic technique, 87-88
vessel parameters, 35 echocardiographic views, 88-89
Dorsoventral projection, pulmonary vasculature in, 33f types of imaging, 78-87
Dorsoventral/ventrodorsal projection, 26-27 applications, 83-87
Dorsoventral/ventrodorsal thoracic radiographic projection, 26f color flow Doppler, 83
Double-chambered right ventricle (DCRV) repair, 384 continuous-wave (CW) Doppler, 81
Doxorubicin cardiotoxicity, 269-271 Doppler echocardiography, 78-81
cardiac pathophysiology, 269-270 high-pulse repetition frequency Doppler, 81-83
diagnosis, 270 M-mode echocardiography, 78
therapy, 270 pulsed wave Doppler, 81
Drug therapy spectral Doppler echocardiography, 81
combination, 359 tissue Doppler imaging (TDI), 83
and initial defibrillator settings, 338t two-dimensional echocardiography, 78
Drugs. See also specifically named drugs Echogenic worms, 192f
alpha-2 adrenergic, 360 Ectopic atrial tachycardia (AT), 322
macrolide prophylactic, 199 Edema
Dysplasia cardiogenic pulmonary, 27f
artioventricular valve, 236-238 pulmonary, 27-28
tricuspid valve, 237f Effusions
Dyspnea, 5-6 pericardial, 42, 200-212, 347-348
in cat, 155f pleural, 28, 28f, 29f
causes of, 5b Electrical impulse conduction, 56f
Electrocardiograms (ECGs), 386
E atrial fibrillation, 61f
ECGs. See Electrocardiograms (ECGs) atrial premature complexes, 60f
Echocardiograms (ECGs) of left heart, 82-83f
Index 429
Electrocardiograms (ECGs) (Continued) Electrocardiography (Continued)
atrial standstill, 68f sinus tachycardia, 65-66
atrial tachycardia, 61f disturbances of supraventricular impulse
electrical alternans, 59f formation, 66-67
electrode positioned for surgical monitoring, 54f atrial fibrillation, 66
evaluation of, 52-54 atrial flutter, 66
first-degree AV block, 68f atrial premature complexes, 66
hand-held wireless, 54f atrial tachycardia, 66
heart sounds and relationship to, 18f atrioventricular junctional tachycardia, 67
multiform ventricular premature complexes, 70f junctional premature complexes, 66
normal canine and feline valves, 57t supraventricular tachycardia, 67
normal sinus arrhythmia, 60f disturbances of ventricular impulse formation, 73-74
recording, 50-51 ventricular asystole, 74
right bundle branch block, 69f ventricular fibrillation, 74
run of ventricular premature complexes, 70f ventricular premature complexes (VPCs), 73
second-degree AV block, 68f ventricular tachycardia, 73-74
sinus arrest, 60f electrocardiograms in clinical practice, 49-50
ST segment depression ion, 59f chamber enlargement patterns, 49
ST segment elevation, 59f documentation of cardiac arrhythmias, 49
third-degree AV block, 69f miscellaneous indications for
unifocal ventricular premature complexes, 69f electrocardiography, 49-50
wireless printout report, 55f escape rhythms, 74-76
Electrocardiograms (ECGs) in clinical practice junctional escape beat, 74
chamber enlargement patterns, 49 junctional rhythm, 74
documentation of cardiac arrhythmias, 49 ventricular escape beat, 74-76
miscellaneous indications for electrocardiography, 49-50 ventricular escape rhythm, 76
Electrocardiographic monitoring, continuous in-hospital, 99- evaluation of electrocardiograms, 52-54
100 evaluation of waveforms, 54-63
limitations, 100 P wave, 54-55
technique, 99-100 PR interval, 55
Electrocardiographic techniques, provocative, 100-101 QRS complex, 55-62
clinical utility, 100-101 QT interval, 62-63
atropine response test, 101 ST segment, 62
post exercise ECG, 101 T wave, 63
vagal maneuver, 100-101 lead systems used in canine and feline, 52b
inhibition of vagal tone, 100 miscellaneous
atropine response test, 100 artificial pacemaker, 76
postexercise ECG, 100 Ashmans phenomenon, 76
vagal maneuver, 100 parasystole, 76
cardioid body massage, 100 normal rhythms, 65
ocular pressure, 100 normal sinus arrhythmia, 65
Electrocardiography, 49-77 normal sinus rhythm, 65
ambulatory, 101-102 wandering sinus pacemaker, 65
arrhythmias and conduction disturbances, 63-65 recording electrocardiograms, 50-51
cardiac conduction and waveforms, 51-52 sick sinus syndrome (SSS), 75f
disturbances of both impulse formation and impulse ventricular fibrillation, 75f
conduction, 74 ventricular tachycardia, 75f
atrial premature complexes (APCs) with aberrant Electrocardiography, principles of, 50
conduction, 74 obtaining electrocardiographic leads, 50
sick sinus syndrome (SSS), 74 standard lead systems, 50
disturbances of impulse conduction, 67-73 Electronic stethoscope, 3M Littman, 16f
atrial standstill, 67 Emergency management and critical care, 342-355
complete heart block, 72 assessing cardiovascular function, 342-343
first-degree AV block, 71 diagnostic tests, 343
left anterior fascicular block, 72 physical examination, 342-343
left bundle branch block (LBBB), 72 cardiac rhythm disturbances, 342, 349-354
right bundle branch block (RBBB), 72-73 bradyarrhythmias, 349-351
second-degree AV block, 71 tachyarrhythmias, 352-354
sinus block, 67 emergency treatment of heart failure, 343-349
third-degree AV block, 72 congestive heart failure (CHF), 343-344
ventricular pre-expectation syndrome, 67-71 forward (low-output) heart failure, 348-349
disturbances of sinus impulse formation, 65-66 left-sided congestive heart failure (LCHF), 344-346
sinus arrest, 65 pericardial effusion, 347-348
sinus bradycardia, 65 right-sided congestive heart failure (RCHF), 346-347
430 Index
Emergency management and critical care (Continued) Feline cardiomyopathies (Continued)
heart failure, 342 prognosis, 173
thromboembolic disease, 354 signalment, 173
thromboembolism, 342 therapy, 173
Enalapril, 283 ancillary tests, 153-154
Endocarditis, aortic valve, 135f classification, 151-152
Endocarditis, infective, 131-137 clinical classification and pathophysiology, 152
clinical presentation, 132-133 feline dilated cardiomyopathy (DCM), 161-163
history, 132 ancillary tests, 162
physical findings, 132-133 pathology, 163
diagnostic findings, 133-135 pathophysiology, 162
electrocardiographic findings, 133 physical examination, 162
electrocardiography, 133 presenting complaints, 162
thoracic radiography, 133 prognosis, 162-163
etiopathogenesis, 131-132 signalment, 162
incidence, 131 therapy, 162
pathophysiology, 132 feline restrictive cardiomyopathy (RCM), 164-165
prevalence, 131 ancillary tests, 164
prognosis, 137 pathology, 164-165
therapy, 135-137 pathophysiology, 164
Endocarditis, mitral valve, 135f physical examination, 164
Endocarditis, severer, 130f presenting complaints, 164
Endocrine diseases, 240 prognosis, 164
Epicardial pacing leads, 388f signalment, 164
Epinephrine, 336 therapy, 164
Escape beat hypertrophic cardiomyopathy (HCM), 157-161
junctional, 74 clinical classification, 157-158
ventricular, 74-76 echocardiography, 158-160
Escape rhythms, 74-76 pathology, 161
junctional escape beat, 74 pathophysiology, 157-158
junctional rhythm, 74 presenting complaints, 158
ventricular, 76 prognosis, 161
ventricular escape beat, 74-76 signalment, 158
ventricular escape rhythm, 76 therapy, 160-161
Etomidate, 363 infectious myocarditis, 174
Examination, physical, 10-23 neoplastic infiltration of heart, 173-174
abdominal palpitation, 13-14 drugs, toxins, and physical injury, 174
abnormal heart sounds, 18-20 historical perspective, 173-174
arrhythmias heard on auscultation, 20 pathology, 156
auscultation, 16-17 physical examination, 153
femoral pulses, 14-15 presenting complaints, 152-153
head, 11-12 prognosis, 156
miscellaneous sounds auscultated in thorax, 21-23 signalment, 152-153
murmurs, 20-21 taurine deficiency - induced myocardial failure, 166-170
neck, 12-13 ancillary tests, 168
normal heart sounds, 17-18 pathology, 170
observation, 10-11 pathophysiology, 168
percussion, 15 physical examination, 168
skin, 14 presenting complaints, 168
stethoscope, 15-16 prognosis, 169-170
tracheal palpitation, 13 signalment, 168
Exercise intolerance, weakness and, 7, 7b therapy, 168-169
therapy, 154-156
F thyrotoxic heart disease, 170-172
Fascicular block, left anterior, 72 ancillary tests, 171-172
Feline. See also Cats pathophysiology, 171
Feline asthma-like syndrome, 194, 197 physical examination, 171
Feline cardiomyopathies, 151-175 present complaints, 171
acromegalic heart disease, 172-173 prognosis, 172
ancillary tests, 173 signalment, 171
historical perspective, 172-173 therapy, 172
pathology, 173 Feline cardiomyopathies, unclassified, 165-166
pathophysiology, 173 ancillary tests, 166
physical examination, 173 pathophysiology, 165
presenting complaints, 173
Index 431
Feline cardiomyopathies, unclassified (Continued) Heart, radiology of, 24-48
physical examination, 166 evaluation of heart chamber enlargement, 36-39
presenting complaints, 166 right atrial enlargement, 36-38
prognosis, 166 evaluation of pulmonary circulation, 40
signalment, 166 under circulation, 40
therapy, 166 introduction to digital radiography, 42-46
Feline dilated cardiomyopathy (DCM), 161-163 introduction to teleradiology, 47
ancillary tests, 162 noncardiac-related variables and cardiac disease, 35-36
pathology, 163 cardiac position, 35-36
pathophysiology, 162 cardiac size and lateral projection, 36
physical examination, 162 projection selection in cardiac-related pathology, 27-28
presenting complaints, 162 pleural effusion, 28
prognosis, 162-163 pulmonary edema, 27-28
signalment, 162 radiographic anatomy, 28-35
therapy, 162 dorsoventral and ventrodorsal projections, 32-35
Feline ECG valves, normal canine and, 57t lateral thoracic radiographic projection, 28-32
Feline electrocardiography, lead systems used in canine and, 52b radiographic diagnosis of heart failure, 40-42
Feline lead, close-up normal, 56f left-heart failure, 41-42
Feline patients with arrhythmias, 321t right-heart failure, 40-41
Feline restrictive cardiomyopathy (RCM), 164-165 radiographic diagnosis of pericardial effusion, 42
ancillary tests, 164 radiographic interpretation, 35
pathology, 164-165 radiographic technique, 24-27
pathophysiology, 164 exposure technique, 24
physical examination, 164 film quality, 24
presenting complaints, 164 radiographic projections, 24-27
prognosis, 164 summary of radiographic signs, 42
signalment, 164 Heart and aorta, M-mode measurements of left, 92f
therapy, 164 Heart base mass, Boxer with large, 265f
Femoral pulses, 14-15 Heart base tumors, 209
Fentanyl, 362 dog with, 207f
Fibrillation. See also Atrial fibrillation (AF) Heart block, complete, 72
atrial, 66, 142f Heart chamber enlargement, evaluation of, 36-39
ventricular, 74, 330 enlargement of aortic arch and aorta, 39
Film scanner, x-ray, 46f causes of aortic arch enlargement, 39
First (S1) heart sound, changes in, 19b differential diagnosis, 39
First-degree AV block, 71 radiographic signs, 39
Fish oil supplements, 149 enlargement of pulmonary artery, 39
Flat-panel detector, 44f causes of pulmonary artery segment enlargement, 39
Flow meter, Doppler, 279 differential diagnosis, 39
Flutter, atrial, 66 radiographic signs, 39
Forward (low-output) heart failure, 348-349 left atrial enlargement, 38-39
Frank-Starling mechanism, 290 causes of left atrial enlargement, 39
Functional murmur, 218 differential diagnosis, 39
Furosemide (Lasix), 284, 303-304 radiographic signs, 38-39
left ventricle enlargement, 39
G causes of ventricular enlargement, 39
Gastric dilation-volvulus complex (GDV), 273-274 radiographic signs, 39
GDV. See Gastric dilation-volvulus complex (GDV) right atrial enlargement, 36-38
Graft, pulmonary patch, 381-382, 382f causes of right atrial enlargement, 37
Granulomatosis, pulmonary eosinophilic, 193, 197 differential diagnosis, 37-38
radiographic signs, 36-37
H right ventricular enlargement, 38
Hand-held wireless ECG, 54f causes of right ventricular enlargements, 38
HCM. See Hypertrophic cardiomyopathy (HCM) radiographic signs, 38
Head, 11-12 Heart chamber, lateral thoracic radiographic
Heart projection of, 30f
chambers and outflow tract of right side of, 34f Heart disease, acromegalic, 172-173
important systemic disorders that affect, 241b ancillary tests, 173
lateral thoracic radiographic projection of, 29f, 30f historical perspective, 172-173
left ventricular outflow tract of, 33f pathology, 173
limb leads surround, 51f pathophysiology, 173
M-mode echocardiograms of left, 82-83f physical examination, 173
Heart, neoplastic infiltration of, 173-174 presenting complaints, 173
drugs, toxins, and physical injury, 174 prognosis, 173
historical perspective, 173-174
432 Index
Heart disease, acromegalic (Continued) Heart disease, thyrotoxic (Continued)
signalment, 173 physical examination, 171
therapy, 173 present complaints, 171
Heart disease, auscultatory findings in congenital, 217t prognosis, 172
Heart disease, congenital, 215-239 signalment, 171
aortic stenosis, 223-227 therapy, 172
anatomy, 223 Heart diseases, neoplastic and infiltrative, 262
diagnosis, 223 Heart enlargement
diagnostic testing, 224-227 left, 38f
natural history, 227 right, 37f
pathophysiology, 223 Heart failure. See also Congestive heart failure (CHF)
physical examination, 224 diastolic dysfunction, 289-290
prognosis, 227 excessive afterload, 289
therapy, 227 inadequate preload, 289
artioventricular valve dysplasia, 236-238 myocardial failure, 289
anatomy, 237 pathophysiology, 288-289
diagnosis, 237 phases of, 289
diagnostic testing, 238 valvular insufficiency, 289
pathophysiology, 237 Heart failure, clinical descriptions of, 295-296
physical elimination, 237 congestive heart failure (CHF), 295
prognosis, 238 left-sided failure, 296
therapy, 238 low-output failure, 295
diagnosis, 215-217 right-sided heart failure, 295-296
functional murmur, 218 Heart failure, compensatory mechanisms in chronic
hereditary aspects, 215 additional compensatory mechanisms, 293
incidence, 215 compensatory mechanisms, 293-294
innocent murmur, 218 Frank-Starling mechanism, 290
pulmonic stenosis (PS), 227-231 myocardial hypertrophy, 292-293
diagnosis, 228 neuroendocrine mechanisms, 293
diagnostic testing, 229 renin-angiotension-aldosterone system
differential diagnosis, 229-230 (RAAS), 290-291
natural history, 230 sympathetic nervous system activation, 291-292
pathophysiology, 228 Heart failure, diagnosis of, 296-299
physical education, 228-229 cardiovascular physical examination findings, 297
prognosis, 231 cardiac rhythm disturbances, 297
therapy, 231 murmur, 297
specific defects, 218-223 diagnostics, 297-298
diagnosis, 218-219 differential diagnoses, 298
diagnostic testing, 220-222 history, 296-297
differential diagnosis, 222 therapy of heart failure, 298-299
patent ductus arteriosus (PDA), 218 Heart failure, emergency treatment of, 343-349
pathophysiology, 218 congestive heart failure (CHF), 343-344
physical examination, 219-220 forward (low-output) heart failure, 348-349
prognosis, 222-223 left-sided congestive heart failure (LCHF), 344-346
therapy, 222-223 diagnostics, 344
Tetralogy of Fallot, 235-236 diuretic therapy, 344
diagnosis, 236 oxygen therapy, 345-346
diagnostic testing, 236 positive inotropic agents, 345
pathophysiology, 235 therapeutic thoracentesis, 346
physical examination, 236 treatment, 344
prognosis, 236 vasodilator therapy, 345
therapy, 236 pericardial effusion, 347-348
therapy, 217-218 right-sided congestive heart failure
ventricular septal defect (VSD), 231-235 (RCHF), 346-347
anatomy, 231 Heart failure, management of, 299-309
diagnosis, 232 ACE inhibitors, 300-301
diagnostic testing, 233-234 calcium channel blocking agents, 301-302
pathophysiology, 231-232 dietary modification, 299-300
physical examination, 232 L-Carnitine, 299-300
prognosis, 234-235 n-3 polyunsaturated fatty acids, 300
therapy, 234-235 taurine supplementation, 300
Heart disease, thyrotoxic, 170-172 direct-acting arterial vasodilators, 302-303
ancillary tests, 171-172 hydralazine (Apresoline), 302
pathophysiology, 171 nitroprusside (Nipride), 303
Index 433
Heart failure, management of (Continued) Heart failure, types of, 294-295
diuretic therapy, 303-306 abnormal ventricular relaxation, 295
miscellaneous agents/adjunctive therapy for atrioventricular valvular insufficiency, 294
heart failure, 306-309 decreased ventricular compliance, 295
vasodilator therapy, 300 myocardial failure, 294
Heart failure, miscellaneous agents/adjunctive pressure overload, 295
therapy for, 306-309 volume overload, 294
beta-adrenergic receptor blockers, 308-309 Heart murmurs, types and their causes, 21t
carvedilol (CoReg), 309 Heart sound, changes in first (S1), 19b
bronchodilators, 307 Heart sound, changes in second (S2), 19b
aminophylline (Aminophyllin), 307 Heart sounds
theophylline (Theo-Dur), 307 abnormal, 18-20, 20t
cough suppressants, 307 causes of changes in, 13b
butorphanol (Torbutrol), 307 normal, 17-18
hydrocodone (Hycodan), 307 and relationship to ECG, 18f
novel vasodilators, 309 Heartgard, (ivermectin), 198
sildenafil (Viagra), 309 Heartworm disease, 183-199
oxygen therapy, 307 classification of severity, 194-197
positive inotropic therapy, 307-308 adjuncts to adulticide therapy, 197
amrinone (Inocor), 307 confirmation of adulticide efficacy, 196-197
potassium supplements, 307 initiating macrolide prophylaxis in infected dogs, 196
sedatives and tranquilizers, 307 rapid microfilaricide therapy, 196
acepromazine, 307 treatment, 194-196
butorphanol (Torbutrol), 307 clinical pathology, 187-191
morphine sulfate, 307 clinical signs, 185-186
sympathomimetics, 308 clinical signs associated with feline, 186b
dobutamine hydrochloride (Dobutrex), 308 diagnosis, 186-187
dopamine hydrochloride (Intropin), 308 dog with, 191f
isoproterenol hydrochloride (Isuprel), 308 etiology, 183
Heart failure, pathophysiology and therapy of, 288-314 history, 185
clinical descriptions of heart failure, 295-296 lifecycle, 183
compensatory mechanisms in chronic heart failure, 290-294 macrolide efficacy against adult heartworms, 199
definitions, 288 missed doses of oral macrolide prophylactic drugs, 199
diagnosis of heart failure, 296-299 pathogenesis, 185
management of heart failure, 299-309 prevalence, 184
specific disease treatment prevention, 197-198
CHF associated with chronic heartworm disease, 313 diethylcarbamazine, 198
chronic valve disease, 310-311 ivermectin (Heartgard), 198
chronic valve disease with symptomatic CHF, 311 milbemycin (Interceptor), 198
feline cardiomyopathy, 312-313 moxidectin (Advantage Multi), 198
mild heart failure secondary to DCM, 311-312 retesting dogs receiving macrolide prophylaxis, 199
mitral regurgitation without CHF, 310-311 sequelae of heartworm infection, 191-194
moderate heart failure secondary to DCM with symptom- allergic pneumonitis, 193
atic CHF, 312 feline asthma-like syndrome, 194
pericardial disease, 313 parenchymal lung disease, 191-193
severe heart failure secondary to DCM, 312 pulmonary eosinophilic granulomatosis, 193
treatment protocols, 309-313 treatment of sequelae, 197
specific disease treatment, 310-313 allergic pneumonitis, 197
Stage A, 309 feline asthma-like syndrome, 197
Stage B, 309 pulmonary eosinophilic granulomatosis, 197
Stage C1, 310 pulmonary thromboembolism, 197
Stage C2, 310 Heartworm disease, classification of, 194t
Stage C3, 310 Heartworm infection (HWI)
Stage D, 310 diagnosis in cats, 189f
types of heart failure, 294-295 in dogs, 188f
Heart failure, radiographic diagnosis of, 40-42 screening cats for, 188-189f
left-heart failure, 41-42 sequelae of, 191-194
physiologic phenomenon, 41 allergic pneumonitis, 193
radiographic signs, 41-42 parenchymal lung disease, 191-193
right-heart failure Heartworms, macrolide efficacy against adult, 199
causes of pleural effusion secondary to right-heart Heartworms in right heart of dog, 192f
failure, 40-41 Heat stroke, 266-267
physiologic phenomenon, 40 Hemangiosarcoma, 262
radiographic signs, 40-41 Hemangiosarcoma, cardiac, 205-209
434 Index
Hemoptysis, 6 Hypersomatotropism in cats, 250-251
causes of, 6b cardiovascular pathophysiology, 250-251
High blood pressure, consequences and clinical diagnosis, 251
signs of, 278-279 prognosis, 251
High-grade second-degree AV block, dog with, 391f therapy, 251
High-pulse repetition frequency Doppler, 81-83 Hypertension, systemic, 277-286, 278f
History, medical, 2-4 antihypertensive therapy, 282-284
history, 3-4 beta blockers, 283
signalment, 2-3 dietary therapy, 282
age, 2 diuretics, 284
breed, 2 duration of treatment, 282
sex, 2-3 pharmacologic agents, 282-283
utilization of animal, 3 vasodilators, 283
weight, 3 choice of animals to treat, 281-282
specific symptoms, 4-10 treatment guidelines, 281-282
ascites, 7-8 consequences and clinical signs of high blood pressure,
coughing, 4-5 278-279
cyanosis, 8 cardiac, 278-279
dyspnea, 5-6 neurologic, 278
hemoptysis, 6 ocular, 278
paresis, 10 renal, 278
syncope, 6-7 emergency management of hypertension, 284
weakness and exercise intolerance, 7 patient selection, 284
weight loss, 8-9 follow-up care and additional medications, 284
History and physical examination, 2-23 measurement of blood pressure, 279-281
Holter monitoring and cardiac event recording anxiety-induced artifact, 281
cardiac event recorders (CERs), 102 cuff size and placement, 279-280
application, 102 environment, 280
implantable CERs, 102 methods, 279
use of CERs, 102 patient selection, 279
indications, 101 personnel, 280
technique, 101-102 record keeping, 280
Holter of CER monitor electrodes, vest secures, 101f techniques, 281
Hormones, altering basal serum thyroid, 245b white coat effect, 281
HWI. See Heartworm infection (HWI) population at risk, 277-278
Hycodan (hydrocodone), 307 cats, 277
Hydralazine (Apresoline), 283, 284, 302 dogs, 277-278
Hydrochlorothiazide (Hydrodiuril), 304 Hyperthyroidism, 240-243
Hydrocodone (Hycodan), 307 cardiac pathophysiology, 240-241
Hydrodiuril (hydrochlorothiazide), 304 diagnosis, 241-242
Hydromorphone, 362 prognosis, 243
Hyperadrenocorticism, 248-250 therapy, 243
diagnosis, 249-250 Hypertrophic cardiomyopathy (HCM), 95, 149, 155f, 157-161
pathophysiology, 249 cat with, 159f, 160f
prognosis, 250 clinical classification, 157-158
therapy, 250 echocardiography, 158-160
Hypercalcemia, disorders associated with, 256-257 pathology, 161
cardiac pathophysiology, 256 pathophysiology, 157-158
diagnosis, 256-257 presenting complaints, 158
prognosis, 257 prognosis, 161
therapy, 257 signalment, 158
Hyperemic mucous membranes in dog, 11f therapy, 160-161
Hyperkalemia adrenergic beta blockers, 160
in cat with urinary obstruction, 255f calcium channel blockers, 160-161
disorders associated with, 253-254 Hypertrophy, myocardial, 292-293
in dog with cardiovascular collapse, 247f Hypoadrenocorticism, 246-248
Hyperkalemic cardiotoxicity, 351 cardiac pathophysiology, 246
Hypermagnesemia, disorders associated with hypomagnesemia diagnosis, 246-248
and, 259 therapy, 248
Hyperpyrexia, 266-267 Hypocalcemia, disorders associated with, 257-259
cardiac pathophysiology, 266 cardiac pathophysiology, 258
diagnosis, 266 diagnosis, 258
prognosis, 267 prognosis, 259
therapy, 266-267 therapy, 258-259
Index 435
Hypocalcemia, dog with severe, 258f Innocent murmur, 218
Hypoglycemia, 259-260 Inocor (amrinone), 307
cardiac pathophysiology, 259 Inodilators, 145
diagnosis, 259 Interceptor, (milbemycin), 198
prognosis, 259-260 Intracardiac masses and foreign bodies, 383
therapy, 259 Intravenous induction agents, 361, 362-363
Hypokalemia, disorders associated with, 254-256 barbiturates, 362-363
cardiac pathophysiology, 254 dissociatives, 361, 363
diagnosis, 254 inhalation anesthetics, 361
prognosis, 256 propofol, 361
therapy, 254-256 thiobarbiturates, 361
Hypokalemia, dog with, 255f tiletamine, 363
Hypomagnesemia and hypermagnesemia, disorders associated zolazepam, 363
with, 259 Intropin (dopamine hydrochloride), 308
Hypothermia, 267 Isoflurane, 363
Hypothyroidism, 243-246 Isoproterenol hydrochloride (Isuprel), 308
cardiac pathophysiology, 244 Isordil (isosorbide dinitrate), 303
diagnosis, 244-245 Isosorbide dinitrate (Isordil), 303
therapy, 245-246 Isuprel (isoproterenol hydrochloride), 308
Ivermectin (Heartgard), 198
I
Idiopathic pericardial effusion, 211-212 J
Idioventricular rhythm, accelerated, 274f Jugular pulses, abnormal, 12b
Imaging, cardiac, 106-107 Jugular veins, distended, 12b
Impulse conduction, disturbances of, 67-73 Junctional escape beat, 74
atrial standstill, 67 Junctional premature complexes, 66
complete heart block, 72 Junctional rhythm, 74
first-degree AV block, 71
left anterior fascicular block, 72 K
left bundle branch block (LBBB), 72 Ketamine-diazepam, 364
right bundle branch block (RBBB), 72-73
second-degree AV block, 71
L
sinus block, 67 Large-breed dogs with mitral valve disease, 115
third-degree AV block, 72 Lasix (furosemide), 284, 303-304
ventricular pre-expectation syndrome, 67-71 Lateral thoracic projection, pulmonary vascular
Impulse formation and impulse conduction, disturbances of anatomy in, 32f
both, 74 Lateral thoracic radiographic projection, 25f
atrial premature complexes (APCs) with aberrant conduc- of heart, 29f, 30f
tion, 74 of heart chamber, 30f
sick sinus syndrome (SSS), 74 of pleural effusion, 28f
Independence, technique, 45f LBBB. See Left bundle branch block (LBBB)
Infectious myocarditis, 174 l-Carnitine, 148, 299-300
Infectious/inflammatory diseases, 270-271 LCHF. See Left-sided congestive heart failure (LCHF)
pathophysiology, 270-271 Leads
therapy, 271 close-up normal feline, 56f
Infective endocarditis, 131-137 epicardial pacing, 388f
clinical presentation, 132-133 systems used in canine and feline electrocardiography, 52b
history, 132 three bipolar standard, 53f
physical findings, 132-133 Left anterior fascicular block, 72
diagnostic findings, 133-135 Left atrial and aortic diameters, measurement of, 93f
electrocardiographic findings, 133 Left atrial enlargement
electrocardiography, 133 causes of left atrial enlargement, 39
thoracic radiography, 133 differential diagnosis, 39
etiopathogenesis, 131-132 dog with severe, 34f
incidence, 131 radiographic signs, 38-39
pathophysiology, 132 Left atrial thrombus, 10f
prevalence, 131 Left bundle branch block (LBBB) in dog, 72f
prognosis, 137 Left heart and aorta, M-mode measurements of, 92f
therapy, 135-137 Left heart, M-mode echocardiograms of, 82-83f
Infiltrative heart diseases, neoplastic and, 262 Left ventricle enlargement, 39
Inflammatory diseases. See Infectious/inflammatory diseases causes of ventricular enlargement, 39
Inhalation anesthetics, 360, 361, 363 radiographic signs, 39
Inhibitors, ACE, 300-301 Left ventricular outflow tract of heart, 33f
In-hospital electrocardiographic monitoring, Left ventricular papillary muscles, 119f, 120f
continuous, 99-100 Left-heart enlargement, 38f
436 Index
Left-sided congestive heart failure (LCHF), 344-346 Mitral regurgitation, 121f
diagnostics, 344 color-flow echocardiographic studies of, 86f
diuretic therapy, 344 compensated, 58f
oxygen therapy, 345-346 dog with, 300f
positive inotropic agents, 345 due to degenerative disease, 121f, 122f
therapeutic thoracentesis, 346 Mitral valve degeneration, severe, 111f
treatment, 344 Mitral valve disease (MVD)
vasodilator therapy, 345 asymptomatic, 124-125
Lidocaine, 336 dog with myxomatous, 96f
Life support, advanced, 335-339 large-breed dogs with, 115
defibrillator, 338-339 mitral valve incompetence due to degenerative, 123f
drug therapy, 336-338 subclinical, 124-125
amiodarone, 336 treatment of CHF caused by, 126-128
atropine, 336 Mitral valve disease (MVD), degenerative, 110-131, 116f, 117f
calcium gluconate, 336-338 clinical presentation, 112-115
epinephrine, 336 history, 112-113
intravenous fluids, 336 large-breed dogs with MVD, 115
lidocaine, 336 patients with MR and concurrent respiratory tract disease,
magnesium sulfate, 338 114-115
sodium bicarbonate, 336 physical findings, 113-114
vasopressin, 336 complications of MVD and its treatment, 129-131
electrocardiography, 335-336 development of azotemia, 129
establishing access for drug and fluid therapy, 335 diuretic and ACE inhibitor administration, 129
monitoring CPR efforts, 339 prognosis, 131
Lifecycle of Dirofilaria immitis, 184f pulmonary hypertension, 130-131
Ligation, PDA, 377f rupture of chordae tendineae, 129-130
Limb leads surround heart, 51f diagnostic findings
Littman electronic stethoscope, 3M, 16f echocardiography, 118-122
Lung disease, parenchymal, 191-193 electrocardiography, 124
Lyme disease, 271 merits of radiography and echocardiography in MR, 122
Lymphoma, cardiac, 263f, 264f radiographic appearance of left arterial enlargement, 115
radiographic findings of pulmonary congestion and
M edema, 115-118
Macrolide efficacy against adult heartworms, 199 thoracic radiography, 115
Macrolide prophylactic drugs, missed doses of oral, 199 etiopathogenesis, 111
Macrolide prophylaxis, retesting dogs receiving, 199 incidence, 110
Magnetic resonance imaging (MRI), 107 pathology, 111
Management, emergency, 342-355 pathophysiology, 111-112
Mannitol, 340 prevalence, 110
Medical history, 2-4 therapy, 124-129
history, 3-4 asymptomatic MVD, 124-125
signalment, 2-3 cough caused by airway compression, 125-126
age, 2 neuroendocrine modulation, 128
breed, 2 subclinical MVD, 124-125
sex, 2-3 therapy of severe CHF caused by advanced MR, 128-129
utilization of animal, 3 treatment of CHF caused by MVD, 126-128
weight, 3 Mitral valve endocarditis, 135f
specific symptoms, 4-10 Mitral valve incompetence
ascites, 7-8 due to degenerative mitral valve disease (MVD), 123f
coughing, 4-5 severe, 116f
cyanosis, 8 Mitral valve leaflet, anterior, 129f
dyspnea, 5-6 Mitral valve regurgitation (MR), 112, 118f, 124f
hemoptysis, 6 therapy of severe CHF caused by advanced, 128-129
paresis, 10 Mitral valve repair, 385
syncope, 6-7 Mitral valve replacement (MR), 384-385
weakness and exercise intolerance, 7 M-mode echocardiograms of left heart, 82-83f
weight loss, 8-9 M-mode echocardiography, 78
Medications. See Specifically named medications M-mode measurements of left heart and aorta, 92f
Membranes in dog, hyperemic mucous, 11f Morphine, 361-362
Mesothelioma, 209-210 Morphine sulfate, 307
Metabolic disturbances, 253 Moxidectin (Advantage Multi), 198
Metoprolol, 148 MR. See Mitral valve reguritation (MR)Mitral valve
Mid-systolic click, 114f replacement (MR)
Milbemycin (Interceptor), 198 MRI. See Magnetic resonance imaging (MRI)
Minipress (prazosin), 303
Index 437
Mucous membranes in dog, hyperemic, 11f Nonselective angiography (Continued)
Murmur. See also Systolic murmur (SM) limitations, risk, and costs, 103
Murmurs, 20-21 technique, 102-103
cardiac, 115t Nonsteroidal anti-inflammatory drugs, cardiac drugs and
functional, 218 anesthetic drug interactions, 359
heart, 21t Normal feline lead, close-up, 56f
innocent, 218 Normal heart sounds, 17-18
timing and duration of, 22f Norvasc (amlodipine), 302
timing and quality of, 22f Nuclear cardiology, 107
Muscles, left ventricular papillary, 119f, 120f
Myocardial failure, 289 O
Myocardial failure associated with taurine deficiency, cat with, Observation, 10-11
169f, 170f Occult disease, treatment of asymptomatic, 145-146
Myocardial failure, induced, 166-170 Oleander toxicity, 269
ancillary tests, 168 Opioid-diazepam combinations, 362
pathology, 170 Opioids, 361, 364, 365
pathophysiology, 168 Oscillometric technique, 279
physical examination, 168 Outflow tract of right side of heart, chambers and, 34f
presenting complaints, 168 Oxymorphone, 362
prognosis, 169-170
signalment, 168 P
therapy, 168-169 P wave, 54-55
Myocardial hypertrophy, 292-293 Pace, dog with intermittent failure to, 394f
Myocarditis Pacemaker nomenclature for antibradycardia pacing, 389t
infectious, 174 Pacemaker system, failure of, 394f
traumatic, 274-275 Pacemaker therapy, 386-397
Myxoma, cat with, 264f components and types of pacing systems, 387-391
Myxomatous mitral valve disease, dog with, 96f pacemaker nomenclature, 389
pacing modes, 389-391
N pacing with chronotropic competence, 388
N-3 polyunsaturated fatty acids, 300 rate responsiveness, 388
Natriuretic peptides (atrial and B-type), 105-106 single- vs. dual-chamber pacing, 388-389
clinical utility, 106 indications for pacing, 386
limitations, risk, and costs, 106 pacemaker complications, 393-394
technique, 106 pacemaker implementation, 391-393
Neck, 12-13 pacemaker programming and follow-up, 394-396
Neoplastic and infiltrative heart diseases, 262 pre-implantation evaluation, 386-387
Neoplastic infiltration of heart, 173-174 Pacemakers
drugs, toxins, and physical injury, 174 artificial, 76
historical perspective, 173-174 bipolar VVIR, 390f
Neuroendocrine modulation, 128 dog with malfunctioning unipolar, 395f
Neurogenic cardiomyopathy, 273 wandering sinus, 65
Neurohormones, cardiac, 105 Pacing leads
Neuroleptanalgesia, 362 in dog, 392f
Newer cardiac imaging techniques, 106-107 epicardial, 388f
computed tomography (CT), 106 transvenous, 387f, 392f
limitations, 107 Pacing system, canine with transvenous VDD, 390f
magnetic resonance imaging (MRI), 107 Palpable apex beat, causes of shifting of, 13b
nuclear cardiology, 107 Palpitation
Nifedipine, 302 abdominal, 13-14
calcium channel blocking agents, 302 tracheal, 13
Nipride (nitroprusside), 302-303 Pancreatitis, 274
Nitroglycerin paste (Nitrol, Nitro-BID), 303 Papillary muscles, left ventricular, 119f, 120f
Nitrol, Nitro-BID (nitroglycerin paste), 303 Parasternal echocardiographic views, right, 79-81f
Nitroprusside (Nipride), 302-303 Parasystole, 76
Nitrous oxide, 363 Parenchymal lung disease, 191-193
Nonbarbiturates Paresis, 10
etomidate, 363 Parvovirus, 272
propofol, 363 Patch graft, pulmonary, 381-382, 382f
Noncardiac-related variables and cardiac disease, 35-36 Patent ductus arteriosus, 105f
cardiac position, 35-36 Patent ductus arteriosus (PDA), 218
cardiac size and lateral projection, 36 in 3-month old poodle, 221f
Nonselective angiography, 102-103 coil embolization procedure, 224f
clinical utility, 103 ligation, 376, 377f
indications, 102 pathophysiology and genesis of clinical findings in, 219f
438 Index
Pathophysiology, congenital defects according to, 216b Pimobendan, 148, 306
PDA. See Patent ductus arteriosus (PDA) Pleural effusion, 28
PE. See Pericardial effusion (PE) lateral thoracic radiographic projection of, 28f
Peptides, natriuretic, 105-106 ventrodorsal thoracic radiographic projection of, 29f
Percussion, 15 PMI. See Point of maximum intensity (PMI)
Pericardial disease, 95-97 Pneumonitis, allergic, 193, 197
Pericardial disorders and cardiac tumors, 200-214 Point of maximum intensity (PMI), 13, 13b
causes of pericardial effusion, 205-212 Poisoning, toad, 268
cardiac hemangiosarcoma, 205-209 Poodle, patent ductus arteriosus (PDA) in
neoplastic, 205-210 3-month old, 221f
pericardial effusions, 200-205 Positive inotropic therapy, 144
chief complaints and history, 200 Potassium supplementation, guidelines for, 256t
diagnostic procedures, 201-204 PR interval, 55
incidence, 200 Prazosin (Minipress), 303
physical examination findings, 200-201 Preanesthetic considerations, 356-358
signalment, 200 additional tests, 358
Pericardial effusions (PEs), 42f, 200-205, 262f, 347-348 anesthetic risk classification, 357
causes of, 205-212 diagnosis of etiology of heart disease, 356-357
cardiac hemangiosarcoma, 205-209 functional classification of heart failure disease, 357
heart base tumors, 209 laboratory tests, 358
hemorrhage, 211 physical examination, 358
idiopathic pericardial effusion, 211-212 preanesthetic diagnostic evaluation, 358
infectious, 210 Preanesthetic medications
mesothelioma, 209-210 anticholinergics, 360-361
miscellaneous, 211 tranquilizers, 360
miscellaneous cardiac tumors, 210 Pre-excitation syndrome, summary of, 71t
neoplastic, 205-210 Printout report, wireless ECG, 55f
chief complaints and history, 200 Propofol, 361, 363, 364
diagnostic procedures, 201-204 PS. See Pulmonic stenosis (PS)
dogs with, 202f, 203f, 204f Pulmonary artery (PA)
incidence, 200 banding, 378, 379f
initial patient stabilization, 204-205 enlargement of, 39
pericardiocentesis, 204-205 causes of pulmonary artery segment enlargement, 39
physical examination findings, 200-201 differential diagnosis, 39
radiographic diagnosis of, 42 radiographic signs, 39
signalment, 200 severely diluted, 192f
Pericardiectomy, 379, 380f shunt. See Systemic-to-pulmonary artery shunt
Pericardiocentesis, 204-205 Pulmonary circulation, evaluation of
in dog, 208f under circulation, 40
Phenoxybenzamine, 283 causes of pulmonary under circulation, 40
Pheochromocytoma, 251-252 differential diagnosis, 40
cardiac pathophysiology, 251-252 radiographic signs, 40
diagnosis, 252 overcirculation, 40
prognosis, 252 causes of pulmonary overcirculation, 40
therapy, 252 differential diagnosis, 40
Photoplethysmograph, 279 radiographic signs, 40
Physical and chemical agents that affect cardiovascular system, 266 Pulmonary edema, 27-28
Physical examination, 10-23 Pulmonary edema, cardiogenic, 27f
abdominal palpitation, 13-14 Pulmonary eosinophilic granulomatosis, 193, 197
abnormal heart sounds, 18-20 Pulmonary hypertension, dog with, 180f
arrhythmias heard on auscultation, 20 Pulmonary patch graft, 381-382, 382f
auscultation, 16-17 Pulmonary thromboembolism, 197
femoral pulses, 14-15 predisposing conditions for, 177b
head, 11-12 Pulmonary thromboembolism, cor pulmonale and, 176-182
history and, 2-23 clinical presentation, 177
miscellaneous sounds auscultated in thorax, 21-23 history and clinical signs, 177
murmurs, 20-21 diagnostic testing, 178-181
neck, 12-13 catheterization, 180-181
normal heart sounds, 17-18 echocardiography, 179-180
observation, 10-11 electrocardiography, 178
percussion, 15 laboratory testing, 178
skin, 14 radiographs, 178
stethoscope, 15-16 etiology, 177
tracheal palpitation, 13 physical examination, 178
Index 439
Pulmonary thromboembolism, cor pulmonale and (Continued) Restrictive cardiomyopathy (RCM), feline (Continued)
physiology, 176-177 pathophysiology, 164
therapy, 181 physical examination, 164
Pulmonary valve presenting complaints, 164
dilation, 378f prognosis, 164
regurgitation, 193f signalment, 164
Pulmonary vascular anatomy in lateral thoracic projection, 32f therapy, 164
Pulmonary vasculature in dorsoventral projection, 33f Rhythm disturbances, cardiac, 297, 342, 349-354
Pulmonary venous vasculature, 27f Rhythms
Pulmonic and aortic valve dilation, 376-378 accelerated idioventricular, 274f
Pulmonic stenosis (PS), 227-231, 228f, 229f, 230f escape, 74-76
diagnosis, 228 junctional, 74
diagnostic testing, 229 normal sinus, 65
differential diagnosis, 229-230 ventricular escape, 76
dog with, 58f Right bundle branch block (RBBB), 72-73
dog with severe, 96f Right parasternal echocardiographic views, 79-81f
natural history, 230 Right sided systolic murmur, 235f
pathophysiology, 228 Right ventricular cardiomyopathy, 140f
physical education, 228-229 Right-heart enlargement, 37f
prognosis, 231 Right-sided congestive heart failure (RCHF), 346-347
therapy, 231
Pulsed wave Doppler, 81 S
Pulses Saddle thrombus in cat, 10f
abnormal jugular, 12b Scanner, x-ray film, 46f
femoral, 14-15 Second (S2) heart sound, changes in, 19b
types and causes of, 14t Second-degree AV block, 71
Second-degree AV block, dog with high-grade, 391f
Q Septal defect. See Ventricular septal defect (VSD)
QRS complex, 55-62 Serologic testing, 104-105
QT interval, 62-63 clinical utility, 105
indications, 104-105
R limitations, risk, and costs, 105
RAA cascade, 291f technique, 105
RAAS. See Renin-angiotension-aldosterone system (RAAS) Serum thyroid hormone, altering basal, 245b
Radiographic anatomy, 28-35 Sevoflurane, 363
dorsoventral and ventrodorsal projections, 32-35 Shunt, systemic-to-pulmonary artery, 378-379, 380f
cardiac parameters, 32-35 Sick sinus syndrome (SSS), 74, 324-325
vessel parameters, 35 treatment, 324-325
lateral thoracic radiographic projection, 28-32 Signs, radiographic, 42, 43t
cardiac parameters, 28-32 Sildenafil (Viagra), 309
vessel parameters, 32 Sinus arrest, 65, 351
Radiographic interpretation, 35 Sinus arrhythmia, normal, 65
Radiographic projections Sinus block, 67
dorsoventral/ventrodorsal projection, 26-27 Sinus bradycardia, 65, 323-324, 349-350
dorsoventral/ventrodorsal thoracic, 26f treatment, 324
Radiographic signs Sinus pacemaker, wandering, 65
of congenital and acquired cardiac disease, 43t Sinus rhythm, normal, 65
summary of, 42 Sinus tachycardia, 65-66, 352
Radiographic technique Skin, 14
exposure technique, 24 SLE. See Systemic lupus erythematosus (SLE)
film quality, 24 SM. See Systolic murmur (SM)
radiographic projections Small animal thoracic radiographic
dorsoventral/ventrodorsal projection, 26-27 technique chart, 25t
lateral projection, 24-26 Sodium bicarbonate, 336
Radiography, digital, 42-46 Sodium nitroprusside, 284, 302-303
Radiology of heart, 24-48 Sounds
RBBB. See Right bundle branch block (RBBB) abnormal heart, 18-20, 20t
RCHF. See Right-sided congestive heart failure (RCHF) auscultated in thorax, 21-23
RCM. See Restrictive cardiomyopathy (RCM), feline heart, 13b, 18f, 19b
Renin-angiotension-aldosterone system (RAAS), 290-291 normal heart, 17-18
Repair, cor triatriatum, 382-383 Spectral Doppler echocardiography, 81
Report, wireless ECG printout, 55f Spironolactone (Aldactone), 148, 284, 304
Restrictive cardiomyopathy (RCM), feline, 164-165 SSS. See Sick sinus syndrome (SSS)
ancillary tests, 164 ST segment, 62
pathology, 164-165
440 Index
Stenosis Systemic diseases, cardiovascular effects of (Continued)
aortic, 223-227, 226f Chagas disease, 271-272
congenital subaortic, 225f chemodectoma, 262-266
pulmonic. See Pulmonic stenosis (PS) cardiac pathophysiology, 263
Stethoscope, 15-16 diagnosis, 263-264
3M Littman electronic, 16f prognosis, 264-265
Subaortic stenosis, congenital, 225f therapy, 264
Subclinical MVD, 124-125 chocolate toxicity, 269
Supraventricular arrhythmias, 317 diabetes mellitus, 252-253
Supraventricular arrhythmias in canine patients, 316t cardiac pathophysiology, 252-253
Supraventricular impulse formation, disturbances of, 66-67 diagnosis, 253
atrial fibrillation, 66 prognosis, 253
atrial flutter, 66 therapy, 253
atrial premature complexes, 66 disorders associated with hypercalcemia, 256-257
atrial tachycardia, 66 cardiac pathophysiology, 256
atrioventricular junctional tachycardia, 67 diagnosis, 256-257
junctional premature complexes, 66 prognosis, 257
supraventricular tachycardia, 67 therapy, 257
Supraventricular tachycardia, 67, 106f, 352-353 disorders associated with hyperkalemia, 253-254
Surgery, cardiac, 376-385 diagnosis, therapy, and prognosis, 254
with cardiopulmonary bypass (CPB), 383-385 disorders associated with hypocalcemia, 257-259
atrial and atrioventricular septal defect repair, 383 cardiac pathophysiology, 258
double-chambered right ventricle (DCRV) repair, 384 diagnosis, 258
mitral valve repair, 385 prognosis, 259
mitral valve replacement (MR), 384-385 therapy, 258-259
tetralogy of Fallot repair, 383-384 disorders associated with hypokalemia, 254-256
tricuspid valve replacement, 385 cardiac pathophysiology, 254
ventricular septal defect (VSD) repair, 383 diagnosis, 254
closed, 376-380 prognosis, 256
atrial appendectomy, 379 therapy, 254-256
patent ductus arteriosus (PDA) ligation, 376 disorders associated with hypomagnesemia and hypermag-
pericardiectomy, 379 nesemia, 259
pulmonary artery banding, 378 doxorubicin cardiotoxicity, 269-271
pulmonic and aortic valve dilation, 376-378 cardiac pathophysiology, 269-270
systemic-to-pulmonary artery shunt, 378-379 diagnosis, 270
with inflow occlusion, 380-383 therapy, 270
cor triatriatum repair, 382-383 endocrine diseases, 240
intracardiac masses and foreign bodies, 383 gastric dilation-volvulus complex (GDV), 273-274
pulmonary patch graft, 381-382 hemangiosarcoma, 262
Surgical monitoring, probes positioned for, 54f hyperadrenocorticism, 248-250
Symptoms, specific, 4-10 diagnosis, 249-250
ascites, 7-8 pathophysiology, 249
coughing, 4-5 prognosis, 250
cyanosis, 8 therapy, 250
dyspnea, 5-6 hyperpyrexia, 266-267
hemoptysis, 6 cardiac pathophysiology, 266
paresis, 10 diagnosis, 266
syncope, 6-7 prognosis, 267
weakness and exercise intolerance, 7 therapy, 266-267
weight loss, 8-9 hypersomatotropism in cats, 250-251
Syncope, 6-7 cardiovascular pathophysiology, 250-251
causes in dogs and cats, 7b diagnosis, 251
Syndromes prognosis, 251
summary of pre-excitation, 71t therapy, 251
ventricular pre-expectation, 67-71 hyperthyroidism, 240-243
Systemic blood pressure, obtaining, 280f cardiac pathophysiology, 240-241
Systemic diseases, cardiovascular effects of, 240-276 diagnosis, 241-242
anemia, 261-262 prognosis, 243
cardiac pathophysiology, 261 therapy, 243
diagnosis, 261-262 hypoadrenocorticism, 246-248
prognosis, 262 cardiac pathophysiology, 246
therapy, 262 diagnosis, 246-248
borreliosis (Lyme disease), 271 therapy, 248
carbon monoxide (CO), 267-268 hypoglycemia, 259-260
Index 441
Systemic diseases, cardiovascular Systemic lupus erythematosus (SLE), 272-273
effects of (Continued) Systemic-to-pulmonary artery shunt, 378-379, 380f
cardiac pathophysiology, 259 Systolic click. See Mid-systolic click
diagnosis, 259 Systolic murmur (SM)
prognosis, 259-260 dog with, 113f
therapy, 259 right-sided, 235f
hypothermia, 267
hypothyroidism, 243-246 T
cardiac pathophysiology, 244 T wave, 63
diagnosis, 244-245 Tachyarrhythmias
therapy, 245-246 sinus tachycardia, 352
infectious/inflammatory diseases, 270-271 supraventricular tachycardia, 352-353
Lyme disease, 271 ventricular tachycardia, 353-354
metabolic disturbances, 253 Tachycardias
neurogenic cardiomyopathy, 273 atrial, 66
oleander toxicity, 269 atrioventricular junctional, 67
pancreatitis, 274 sinus, 65-66
parvovirus, 272 supraventricular, 67, 106f, 352-353
pheochromocytoma, 251-252 ventricular, 73-74
cardiac pathophysiology, 251-252 Tamponades
diagnosis, 252 acute, 295
prognosis, 252 chronic, 295
therapy, 252 Taurine deficiency, cat with myocardial failure associated with,
systemic lupus erythematosus (SLE), 272-273 169f, 170f
toad poisoning, 268 Taurine deficiency - induced myocardial failure, 166-170
traumatic myocarditis, 274-275 ancillary tests, 168
trypanosomiasis (Chagas disease), 271-272 pathology, 170
uremia, 260-261 pathophysiology, 168
cardiac pathophysiology, 260 physical examination, 168
diagnosis, 260 presenting complaints, 168
prognosis, 261 prognosis, 169-170
therapy, 260-261 signalment, 168
Systemic hypertension, 277-286, 278f therapy, 168-169
antihypertensive therapy, 282-284 Taurine supplementation, 148, 300
beta blockers, 283 TDI. See Tissue Doppler imaging (TDI)
dietary therapy, 282 Technique independence, 45f
diuretics, 284 Teleradiology, introduction to, 47
duration of treatment, 282 Temperature probe positioned for surgical monitoring, 54f
pharmacologic agents, 282-283 Tetralogy of Fallot, 11f, 235-236
vasodilators, 283 diagnosis, 236
choice of animals to treat, 281-282 diagnostic testing, 236
treatment guidelines, 281-282 pathophysiology, 235
consequences and clinical signs of high blood physical examination, 236
pressure, 278-279 prognosis, 236
cardiac, 278-279 repair, 383-384
neurologic, 278 therapy, 236
ocular, 278 Theo-Dur (theophylline), 307
renal, 278 Theophylline (Theo-Dur), 307
emergency management of hypertension, 284 Therapies
patient selection, 284 diuretic, 144
follow-up care and additional medications, 284 positive inotropic, 144
measurement of blood pressure, 279-281 Therapies, pacemaker, 386-397
anxiety-induced artifact, 281 components and types of pacing systems, 387-391
cuff size and placement, 279-280 pacemaker nomenclature, 389
environment, 280 pacing modes, 389-391
methods, 279 pacing with chronotropic competence, 388
patient selection, 279 rate responsiveness, 388
personnel, 280 single- vs. dual-chamber pacing, 388-389
record keeping, 280 indications for pacing, 386
techniques, 281 pacemaker complications, 393-394
white coat effect, 281 pacemaker implementation, 391-393
population at risk, 277-278 pacemaker programming and follow-up, 394-396
cats, 277 pre-implantation evaluation, 386-387
dogs, 277-278 Thiobarbiturates, 361
Third-degree AV block, 72
442 Index
Thoracic projection, pulmonary vascular anatomy in lateral, 32f Ultrasound, Doppler (Continued)
Thoracic radiographic projection, lateral, 25f dilated cardiomyopathy (DCM), 94-95
Thoracic radiographic projection of heart chamber , lateral, 30f hypertrophic cardiomyopathy (HCM), 95
Thoracic radiographic projection of heart, lateral, 29f, 30f pericardial disease, 95-97
Thoracic radiographic projection of pleural effusion echocardiographic measurements, 89-93
lateral, 28f aortic and pulmonic stenosis, 91-93
ventrodorsal, 29f aortic insufficiency, 91
Thoracic radiographic technique chart, small animal, 25t chamber dimensions, 89
Thorax diastolic function, 91
miscellaneous sounds auscultated in, 21-23 E point to septal separation (EPSS), 90
right lateral view of, 44f ejection fraction (EF%), 90
Thromboembolic disease, 354 end-systolic volume index (ESVI), 90
Thromboembolism, 342 index of sphericity, 89
Thromboembolism, pulmonary, 176-182, 177b, 197 LA diameter, 90
Thrombus LV diameter, 89
left atrial, 10f LV fractional shortening (FS%), 90
saddle, 10f LV wall thickness, 90
Thyroid hormone, altering basal serum, 245b mitral insufficiency, 91
Thyrotoxic heart disease, 170-172 systolic function, 90
ancillary tests, 171-172 systolic time intervals, 91
pathophysiology, 171 transmitral flow, 91
physical examination, 171 valve function, 91
present complaints, 171 echocardiographic technique, 87-88
prognosis, 172 echocardiographic views, 88-89
signalment, 171 types of imaging, 78-87
therapy, 172 applications, 83-87
Tiletamine, 363 color flow Doppler, 83
Tissue Doppler imaging (TDI), 83 continuous-wave (CW) Doppler, 81
Toad poisoning, 268 Doppler echocardiography, 78-81
Torbutrol (butorphanol), 307, 362 high-pulse repetition frequency Doppler, 81-83
Toxicity. See also Cardiotoxicity M-mode echocardiography, 78
chocolate, 269 pulsed wave Doppler, 81
oleander, 269 spectral Doppler echocardiography, 81
Trachea, dog with collapsed, 58f tissue Doppler imaging (TDI), 83
Tracheal palpitation, 13 two-dimensional echocardiography, 78
Tranquilizers, 360, 361-362, 364 Unclassified feline cardiomyopathies, 165-166
benzodiazepines, 361 ancillary tests, 166
buprenorphine, 362 pathophysiology, 165
butorphanol, 362 physical examination, 166
fentanyl, 362 presenting complaints, 166
hydromorphone, 362 prognosis, 166
morphine, 361-362 signalment, 166
neuroleptanalgesia, 362 therapy, 166
opioid-diazepam combinations, 362 Unipolar pacemaker, dog with malfunctioning, 395f
opioids, 361 Uremia, 260-261
oxymorphone, 362 cardiac pathophysiology, 260
Transvenous pacing lead in dog, 392f diagnosis, 260
Transvenous pacing leads, 387f prognosis, 261
Transvenous VDD pacing system, canine with, 390f therapy, 260-261
Traumatic myocarditis, 274-275 Urinary obstruction, hyperkalemia in cat with, 255f
Tricuspid valve dysplasia, 237f
Tricuspid valve replacement, 385 V
Trypanosomiasis (Chagas disease), 271-272 Valve dysplasia
Tumors artioventricular, 236-238
cardiac, 200-214 tricuspid, 237f
dog with heart base, 207f Valvular disease, acquired, 110-138
heart base, 209 degenerative mitral valve disease (MVD), 110-131
miscellaneous cardiac, 210 clinical presentation, 112-115
Two-dimensional echocardiography, 78 diagnostic findings, 115-124
etiopathogenesis, 111
U incidence, 110
Ultrasound, Doppler, 78-98 pathology, 111
common acquired cardiac conditions, 93-97 pathophysiology, 111-112
2 D changes, 93-94 prevalence, 110
degenerative mitral valve disease, 93 infective endocarditis, 131-137
Index 443
Valvular disease, acquired (Continued) Ventricular systolic function, echocardiographic evaluation of,
clinical presentation, 132-133 94-95f
diagnostic findings, 133-135 Ventricular tachycardia (VT), 73-74, 353-354. See also
etiopathogenesis, 131-132 Supraventricular tachycardia
incidence, 131 Ventricular tachycardia (VT), treatment of, 326-328
pathophysiology, 132 acute intravenous antiarrythymic therapy, 327
prevalence, 131 chronic oral antiarrythymic therapy, 327-328
prognosis, 137 Ventrodorsal thoracic radiographic projection of pleural
therapy, 135-137 effusion, 29f
Valvular disease, canine degenerative, 126t Verapamil, 302
Valvular insufficiency, 289 Vertebral heart sum (VHS), 137f
Vasodilator therapy, 300 Vertebral scale system of cardiac size, 31f
Vasodilators Vessel and chamber enlargement, 36f, 37f
arterial, 144-145, 302-303 Veterinary patients, performing CPR in, 337f
cardiac drugs and anesthetic drug interactions, 358-359 VHS. See Vertebral heart sum (VHS)
venous, 144 Viagra (sildenafil), 309
Vasopressin, 336 VPCs. See Ventricular premature complexes (VPCs)
VDD pacing system, canine with transvenous, 390f VSD. See Ventricular septal defect (VSD)
Veins, distended jugular, 12b VT. See Ventricular tachycardia (VT)
Venous vasodilators, 144, 303 VVIR pacemaker, bipolar, 390f
Ventricular arrhythmias, 326
Ventricular arrhythmias in canine patients, 317t W
Ventricular asystole, 74, 329-330 Waveforms, cardiac conduction and genesis of, 51-52
Ventricular cardiomyopathy, right, 140f Waveforms, evaluation of, 54-63
Ventricular diastolic function, echocardiographic P wave, 54-55
evaluation of, 87f PR interval, 55
Ventricular enlargement in dog, severe right, 58f QRS complex, 55-62
Ventricular enlargement, left, 142f QT interval, 62-63
Ventricular escape beat, 74-76 ST segment, 62
Ventricular escape rhythm, 76 T wave, 63
Ventricular fibrillation, 74, 330 Weakness and exercise intolerance, 7
Ventricular impulse formation, disturbances of, 73-74 causes of, 7b
ventricular asystole, 74 Weight, 3
ventricular fibrillation, 74 Weight loss, 8-9
ventricular premature complexes (VPCs), 73 Wireless ECG
ventricular tachycardia, 73-74 hand-held, 54f
Ventricular outflow tract of heart, left, 33f printout report, 55f
Ventricular papillary muscles, left, 119f, 120f Worms, echogenic, 192f
Ventricular pre-excitation in dog, 71f
Ventricular pre-expectation syndrome, 67-71
X
Ventricular premature complexes (VPCs), 73 X-ray film scanner, 46f
Ventricular septal defect (VSD), 231-235, 233-234f
anatomy, 231
Z
diagnosis, 232 Zolazepam, 363
diagnostic testing, 233-234
pathophysiology, 231-232
pathophysiology and genesis of clinical findings in, 232f
physical examination, 232
prognosis, 234-235
repair, 383
therapy, 234-235