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American Manual
of Examination
in Medicine
(2CK)
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Cardiology
American Manual
of Examination
in Medicine
(2CK)
Authors
Rafael Salguero
Alfonso Jurado
Roberto Martn
David Filgueiras
Javier de Juan
Grard Loughlin
Sem Briongos
Felipe Dez
Index
01. Physical Examination........................................................................ 1
1.1.
1.2.
1.3.
1.4.
02. Electrocardiogram................................................................................. 4
2.1.
2.2.
2.3.
2.4.
2.5.
3.1. Bradycardia..................................................................................................................................... 6
3.2. Tachycardia..................................................................................................................................... 8
4.1.
4.2.
4.3.
4.4.
Classification ............................................................................................................................ 18
Pathophysiology and Clinical Characteristics ......................... 18
Complementary Tests ................................................................................................. 19
Treatment of Heart Failure................................................................................... 20
09. Hypertension............................................................................................. 49
9.1. Essential Hypertension ............................................................................................. 49
9.2. Secondary Hypertension ....................................................................................... 52
9.3. Special Cases ............................................................................................................................ 52
Card iology
Aortic Aneurysm................................................................................................................. 67
Acute Aortic Syndrome ............................................................................................ 68
Deep Vein Thrombosis............................................................................................... 70
Peripheral Artery Disease...................................................................................... 72
Lymphedema .......................................................................................................................... 75
Shock ................................................................................................................................................... 77
Rheumatic Fever ................................................................................................................. 78
Myocarditis ................................................................................................................................. 78
HIV-Related Cardiomyopathy ......................................................................... 79
Bacterial and Parasitic Myocarditis.......................................................... 79
Giant Cell Myocarditis................................................................................................. 80
Radiation Myocarditis ................................................................................................. 80
Cardiac Tumors ..................................................................................................................... 81
Card iology
Physical
Chapter 01
Examination
CARDIAC INVOLVEMENT
OBSERVATION DATA
Sleepapneahypopnea
syndrome(SAHS)
Cor pulmonale
Atrial fibrillation
Bradycardia and tachycardia
Obesity
Short neck
Daytime sleepiness
Duchenne dystrophy
Steinert myotonic
dystrophy syndrome
Infra-Hisian AV block
Ventricular tachycardia
Kearn-Sayre
syndrome
Infra-Hisian AV block
Ophtalmoplegia
Unilateral ptosis
Pigmentary retinopathy
Marfans syndrome
Ascending aneurysm
Aortic insufficiency
Mitral prolapse
Ehlers-Danlos
syndrome
Rendu-Weber-Osler
disease
AV pulmonary fistulas
Carcinoid syndrome
Pulmonary or tricuspid
valvulopathy
Sarcoidosis
AV block
Cor pulmonale by
pulmonary involvement
Xanthelasma
Corneal arcus
Tendon xanthomas
Homocystinuria
Systemic, pulmonary or
coronary thrombosis
The third heart sound (S3) is produced by rapidly rushing blood flow
entering either the right or left ventricle, performing auscultation
over the apical impulse of each ventricle. S3 may be physiologic in
children or in young people (especially women) and in situations involving high cardiac output (fever, pregnancy). In adults, this may be
an indicator of disease (systolic dysfunction, ventricular dilatation,
serious ventricle-atrial regurgitation).
The fourth heart sound (S4) corresponds to an atrial contraction generated by sudden deceleration of the blood entering the ventricle with
decreased compliance (associated with hypertrophy because of high
blood pressure, aortic stenosis, hypertrophic cardiomyopathy, mitral
insuciency, ischemia, advanced systo-diastolic dysfunction, hyperdynamia). It is produced as a late diastolic sound but it does not occur
when atrial fibrillation exists. As S3, it is a low-frequency sound best
audible with the bell of the stethoscope in the apical zone of the affected ventricle.
1.2. Murmurs
Aortic focus
EFFECTS ON MURMUR
Pulmonary focus
MANEUVER
Accessory aortic
focus
P
Aa
Increase
Decrease
Most murmurs
Squatting
Most murmurs
Amyle nitrite,
vasodilatation
Handgrip,
vasoconstriction
Valsalva and
bipedestation
The wave of normal arterial pulse has a rapid climb (commonly called
percussion wave), with a detectable anacrotic notch in invasive records
of central pulses, though nonpalpable, reaching a unique well defined
ARTERIAL PULSE
ETIOLOGY
CHARACTERISTICS
Celer et magnus
or hyperkinetic
Hypokinetic
Bisferiens
Dicrotic pulse
Parvus et tardus
Alternating
Bigeminus
Paradoxic
Amplitude-diminished heartbeat,
possible tachycardia
Card iology
Louis angle
5 cm
a wave
v wave
Right atrium
y depression
x depression
45
1R
2R
ABSENT
Atrial fibrillation
DIMINISHED
Dilated RA
Cardiac
tamponade
Tricuspid
obstruction
Tricuspid stenosis
Pulmonary stenosis
Pulmonary
hypertension
Diastole
INCREASED
Hypertrophic
RA
Systole
The descent x wave initiates by atrium relaxation and is intensified by the bulging of the
tricuspid valve into the right atrium, at the beginning of ventricular contraction.
v wave is due to the filling of RA during ventricular contraction (closed tricuspid).
Upon start of ventricular diastole and opening
of the tricuspid valve, blood passes suddenly
from RA to RV, appearing y descent (diastolic collapse), which is less eminent and deep
than x descent.
The main anomalies of JVP are shown in Table 4.
Electrocardiogram
Chapter 02
V9
The normal QRS axis is between -30 and +150. An axis beyond -30
is a left-deviated axis (as in left anterior hemiblock [LAH]), whereas a
right heart axis (beyond +150) is deviated to the right (typical in left
posterior hemiblock [LPH]).
V8
V7
aVR 150
V6
aVL 30
V5
DI 0
aVF 90
DII 60
2.4. Intervals
V4
V3
V4R
DIII 120
A quick way to measure QRS axis is by searching the lead in the frontal
plane in which QRS is the most positive (highest). The axis has to be
situated near such a lead.
V3R
V1
V2
2.2. Rhythm
3 mm
3-5 mm
< 3 mm
< 440 ms
QT
QT
Card iology
Figure 6. Left bundle branch block (top) and Right bundle branch block characteristics
in precordial leads
in progression of acute pericarditis, in apical hypertrophic cardiomyopathy (giant negative T waves), and in V1-V3 leads in RV arrhythmogenic cardiomyopathy. Negative T waves may be normal in
V1-V3 leads, especially in women and children (child pattern) and in
DIII lead. Generally, T wave is negative in aVR.
Occasionally, flat T waves are detected, defined as unspecific alteration of repolarization, and they are usually a normal variant
(especially frequent following cardiac surgery), though it is recommended to rule out subjacent ischemia. Anxiety, physical exercising (including ergometry), hyperventilation, sustained tachycardia,
postprandial period, orthostatism, acute pancreatitis (aecting DII,
DIII and aVF), and acute CVA may flatten or even invert T waves.
Figure 7. ECG obtained from a patient suering biventricular dilated
cardiomiopathy. Hypertrophic changes are remarkable as RBBB and
repolarization abnormalities
DISEASE
Sinus nodal
dysfunction
ECG MANIFESTATIONS
There may exist:
Bradycardia (< 55 bpm)
Bradycardiatachycardia
Corrected QT interval shortens in hypercalcemia and, occasionally, under digoxin treatment, as well as in congenital short QT
syndrome. It prolongs in hypocalcemia, in hypokalemia and other
endocrine metabolic alterations, and in acute ischemia because of
the administration of drugs prolonging QT interval (class IA and III
anti-arrhythmic drugs, macrolide and quinolone antibiotics, tricyclic
antidepressants) or in congenital long QT syndrome. Negative or inverted U wave may indicate underlying ischemia, although it is not
a frequent finding.
Arrhythmias
Chapter 03
TREATMENT
Pacemaker in (DDD/R):
Symptoms
Symptomatic daytime
pauses > 3 s
Consider pacemaker
according to PR > 0.3 s
and symptoms
ASSOCIATION
Second-degree
block (Mobitz I)
AV node
Second-degree
block (Mobitz II)
Anterior AMI
His bundle
Pacemaker
Pacemaker
LOCATION
Card iology
Figure 8. Lead aVF ECG revealing characteristic signs of sinus dysfunction with signicant sinus bradycardia
more distal the block point the more severe it usually is (Figure 9 and
Table 6).
whether infra-Hisian or supra-Hisian, as well as the sinus node dysfunction. If electrophysiologic study results are inconclusive and, mainly, if
syncope recurrence is very sporadic, a subcutaneously implanted Holter
may be useful.
THIRD DEGREE
AV BLOCK
NODAL
(SUPRA-HISIAN)
INFRANODAL
(INFRA-HISIAN)
Escape rhythm
40-60 bpm
20-40 bpm
Response to atropine
QRS
Prognosis
Good
Poor
SITUATION
INDICATION
ALWAYS
Other situations
Medical treatment usefulness is limited in acute transient management; permanent pacemaker implantation is the required solution in
nonreversible cases (Table 7).
There are multiple causes, since in most cases it is the result of stress, anxiety, fever, anemia, hypovolemia, hypotension, exercise, thyrotoxicosis, hypoxemia, heart failure, pulmonary embolism, adrenergic stimulus. Thus, sinus tachycardia is, in most cases, a sign that should alert to the possibility of
the patient presenting a potentially severe illness. Therefore, the root cause
should be treated. Rare inappropriate sinus tachycardia, common among
female health personnel, does not have a recognizable triggering factor, and
may require the use of -blockers, calcium antagonists or ivabradine.
Figure 12. 12-lead ECG from a patient in sustained atrial brillation with
VVIR pacemaker implantation stimulating RV apex at 100 bpm
3.2. Tachycardia
Premature P wave
Normal QRS
Subsequent
Noncompensatory
pause (usually)
Atrial Fibrillation
VENTRICULAR
PREMATURE BEATS
Premature QRS
Wide QRS
Compensatory
Prevalence
Consequences
Usually few
Treatment
Sinus Tachycardia
This is sinus rhythm with a rate of over 100 bpm, with P waves identical
to the sinus (Figure 13). This arrhythmia starts and finishes gradually,
and its frequency may be slowed temporarily with vagal maneuvers.
Atrial fibrillation (AF) is the most common type of arrhythmia after premature beats and also the most frequent sustained chronic arrhythmia. ECG reveals disorganized atrial activity without P waves, which
are replaced with irregular waves of the T-QRS complex (f waves, at
350-600 bpm) showing variable and irregular (complete arrhythmia)
ventricular conduction (ventricular response; Figure 14).
Card iology
POINTS
CHA2DS2-VASC
SCORE
H (hypertension)
1.3
2.2
D (diabetes mellitus)
3.2
4.0
6.7
A (age 65-74)
9.8
Sc (female gender)
9.6
FACTOR
ANNUAL ADJUSTED
STROKE RISK RATE (%)
6.7
15.2
Table 9. Stroke risk calculation in atrial brillation according to score system CHA2DS2-VASc
valvulopathies, hypertensive heart disease, almost any structural heart
disease, chronic obstructive pulmonary disease, sleep apnea, constituting a part of the bradycardia-tachycardia syndrome.
AF may range from asymptomatic to result in hemodynamic intolerance
with syncope or acute pulmonary edema. Arrhythmia management involves assuming that its presence indicates a steep increase in stroke
risks, especially (although not exclusively) caused by the formation of
clots in the left atrial appendage that once detached are responsible
for strokes. It is thus necessary to assess in all cases the need for anticoagulant treatment, which will be necessary for almost every patient
with heart disease or underlying prosthetic cardiac valves, as well as
when suggested according to the CHADS-VASc score of calculated risk
(Table 9).
Currently, there are two potential treatment strategies for atrial fibrillation:
Rate control strategy. It does not aim to restore sinus rhythm but to mitigate potential complications which may result from a permanent AF.
Rhythm control strategy. Aimed at restoring sinus rhythm and sustaining it for the longest possible time.
Various clinical trials have shown that neither strategy is better than the
other in terms of mortality. Hence, a strategy will be selected based on
patient characteristics and arrhythmia tolerance.
The figure shows general management of a patient with atrial fibrillation (Figure 15, next page).
Atrial Flutter
The common typical flutter in an atrial tachycardia caused by a macroreentry around the tricuspid annulus, which cycles at 250-350 bpm
(in a counter-clockwise direction in the common type, clockwise in the
reverse type) and from which atrial depolarization takes place, showing in the ECG saw-toothed regular atrial activity (F waves, positive
in V1 and negative in inferior leads) with scarce mechanical activity
(Figures 16 and 17).
Common flutter
V1
aVF
Atypical flutter
V1
aVF
Figure 17. ECG of common utter and atypical utter in leads V1 and aVF
10
rate of over 90% in common flutter. In atypical cases, ablation efficacy is lower.
Card iology
Figure 18. Common and atypical utter circuits: atrial layout representing the placement of atrial macroreentry in common utter
and atypical utter because of atriotomy scar
Figure 20. Lewis diagram showing the start of common AV nodal reentrant tachycardia
Tachycardia starts and finishes abruptly, and may cause palpitations, hypotension, syncope. It is prevalent among middle-aged women.
ECG outside of crisis periods is normal, and during tachycardia it shows
a retrograde P wave almost simultaneous to QRS thus altering their final
11
Figure 21. ECG of the same patient in V1 and DII during sinus rhythm and common AV nodal
reentrant tachycardia, showing image of pseudoR in V1 and pseudoS in DII
Figure 22. Lewis diagram showing focal atrial tachycardia with irregular conduction to ventricles
because of varying block degrees in AV node
occasion, the AV node does not tolerate such a high rate and some of the
P waves cannot be conducted to the ventricles, even though the tachycardia
remains (Figure 22).
It may respond to -blockers or calcium antagonists (which also stop the
AV node and obtain a slower ventricular response during tachycardia),
catheter ablation of the anomaly is performed if it does not respond, antiarrhythmic agents may further be tried with moderate ecacy.
Pre-excitation Syndromes
This occurs when there is a congenital accessory conductive pathway
(in addition to the AV node) for electric communication between atria
and ventricles which, in sinus, causes early depolarization of ventricles
(it pre-excites them), causing a shortened PR, a slurred upstroke to
the QRS complex (the delta wave, showing the fragment of ventricles
depolarized through the accessory conductive pathway before the sinus
impulse goes through the AV node), and a broad QRS (Figure 23).
There may be evident pre-excitation (especially the right pathways
close to the sinus node) or be inapparent in the ECG (especially in
12
Card iology
well tolerated hemodynamically, treatment involves electrical cardioversion. If it is well tolerated, electrical cardioversion will be performed or
anti-arrhythmic drugs from the Ic group or procainamide will be applied.
Intravenous administration of digoxin, calcium antagonists (and probably
amiodarone) is contraindicated, since by slowing node conduction and/or
causing vasodilation with increased reflex in sympathetic tone they may
facilitate conduction through the accessory pathway and VF.
A definitive treatment of accessory pathways is percutaneous catheter ablation of the accesory pathway, which is more eective than
anti-arrhythmic drugs and has low risk, and is therefore the treatment
of choice for patients with tachycardia episodes. In subjects with asymptomatic pre-excitation, clinical observation is advisable, except for hazardous-activity professionals (professional drivers, sport players, etc.)
or according to the patients wishes, when ablation is recommended.
It is a very rare type of tachycardia, caused by an increase in automatism or triggered activity (afterpotentials) in the AV node. QRS are the
same as the patients basal and there is frequently AV dissociation or
VA conduction. It starts and ends gradually and heart rate varies with
maneuvers aecting the autonomic nervous system (increased with
vagolytic drugs, exercise or catecholamines and decreased with vagal
maneuvers or -blockers). Carotid sinus massage may transiently stop
tachycardia, but does not cause it to disappear.
It is characteristic of digitalis toxicity, catecholamines increase, acute lower
myocardial infarction or myocarditis. Treatment is aimed at the root cause;
electrical cardioversion should not be attempted, especially if the cause is
digitalis toxicity, since it is not eective as far as it is not caused by reentrant.
Ventricular Tachycardia
Ventricular tachycardia (VT) involves the presence of three or more
consecutive beats originating in the ventricles at over 100 bpm. A wide
QRS tachycardia is shown in the ECG (over 0.12 seconds), with AV dissociation (there can be some retrograde P waves), usually starting with
ventricular premature beats (Figure 24).
13
In the acute phase of the acute myocardial infarction, which does not
yet have a scar, arrhythmias are the result of myocardial irritability
due to ischemia, i.e., ventricular premature beats, ventricular fibrillation or accelerated idioventricular rhythm associated with reperfusion).
Other diseases causing intramyocardial scars (dilated cardiomyopathy, right ventricular dysplasia, Chagas disease, etc.) may likewise
present monomorphic ventricular tachycardia during their clinical
course.
Other monomorphic VT, called idiopathic, appear in patients without
structural heart diseases (they comprise 10% of VT and have better
prognosis), such as right ventricular outflow tract VT (sensitive to adenosine and -blockers, caused in general by a focus with triggered activity) or fascicular ventricular tachycardia (sensitive to verapamil, usually
caused by reentry between the left posterior fascicle and surrounding
myocardium), whose treatment in recurring cases or cases with poor
tolerance is VT focus or circuit ablation.
Faced with a common tachycardia with wide QRS, a dierential diagnosis between monomorphic sustained VT and supraventricular
tachycardia with bundle branch block (aberrancy) is important, since
prognosis is dierent. Verapamil should not be used to distinguish
them, since it could cause shock or even cardiac arrest in a VT (Table
10).
SUPRAVENTRICULAR TACHYCARDIA
If the bundle branch block is equal to the block prior to tachycardia
VENTRICULAR TACHYCARDIA
If QRS > 0.14 s
If there is AV dissociation or variable retrograde conduction
Channelopathies
A modern term which comprises a group of arrhythmic syndromes
caused by dysfunction of ion channels located in the membranes of cardiac cells in patients without structural heart diseases.
Long QT syndrome (LQTS: most frequent channelopathy). It is a
congenital or acquired disorder whereby membrane ion currents
lengthen the duration of the action potential shown in the ECG, consisting of a prolonged QT interval, which facilitates the appearance
of afterpotentials (premature beats) that are transmitted to the rest
of the myocardium with functional reentrant phenomena causing
polymorphic ventricular tachycardia with twisting of the points (Torsades de Pointes or helicoidal ventricular tachycardia), where QRS
are polymorphic, i.e., they vary in width and duration, causing an
oscillation pattern on the basal line similar to a helix (Figures 26
and 27). These tachycardia episodes are very fast and cause syncope
if self-contained, although they may evolve into VF and cause sudden death.
Figure 27. Torsades de Pointes episode in patient with severe sinus bradycardia, secondary long QT and ventricular premature beat with probable
afterpotentials that start the episode (evolved into VF and required debrillation)
14
Card iology
ISCHEMIA
ELECTROLYTIC
ALTERATIONS
ANTI-ARRHYTHMIC
DRUGS
PSYCHIATRIC DRUGS
Hypocalcemia
Hypokalemia
Hypomagnesemia
Class Ia
Class III
Tricyclic antidepressants
Haloperidol
Phenothiazine
INTRACRANIAL
PROCESSES
OTHER DRUGS
BRADYARRHYTHMIA
CONGENITAL
LONG QT
SUBTYPE
MUTATION
EFFECT
LQTS 1
Activity K
channels
Exercise
-blocker ICD
Stress
Swimming
LQTS 2
Activity K
channels
LQTS 3
Activity
Na+
channels
Tiredness
Fever
T WAVE
TRIGGER
TREATMENT
ICD
Group I drugs?
15
Figure 29. 12-lead ECG of a ventricular brillation. The rhythm strip (lower section) shows the recovery of sinus rhythm after a discharge
of the debrillator implanted on the patient
16
Card iology
When this occurs long after an AMI, it does entail a poor long-term
prognosis. In all other cases recurrence is frequent and a definite ethologic treatment must be scheduled or, where this is not possible, a defibrillator must be implanted.
Therapeutic hypothermia may improve the brain prognosis of some patients resuscitated after a sudden death event.
The implanted cardioverted defibrillator (ICD) is a very useful tool to
prevent arrhythmic sudden death. The current indications are detailed
in Table 13.
CLINICAL STATUS
Secondary Aborted sudden
prevention death
Sustained
monomorphic
ventricular
tachycardia (SMVT)
Primary
Nonsustained
prevention Ventricular
Tachycardia (NVT)
Special
cases
Documented VF or VT because of
irreversible causes
SMVT with hemodynamic
compromise or in patients with
ventricular dysfunction (LVEF
< 40%)
NVT in patients with ischemic
ventricular dysfunction (LVEF
< 40%) with induced SMVT or VF
in the electrophysiology study
Post-AMI left
ventricular
dysfunction
Systolic heart
failure
Channelopathies
Hypertrophic
cardiomyopathy
Dilated
cardiomyopathy
Heart Failure
Chapter 04
17
4.1. Classification
4.2. Pathophysiology
STAGE A
STAGE B
STAGE C
Ischemic C.,
cardiomyopathies,
etc.
Hypertrophy
apoptosis
fibrosis
Myocardial lesion
Lower O2 inflow
to tissues
(anterograde
symptoms)
Increased O2
requirement
Increased
postload
Perfusion
pressure
Activation
of neurohormonal
systems and inflammation
Renin-angiotensin
aldosterone
Endothelin
ADH
Sympathetic system
Hydrosaline
retention
Natriuretic
peptides
The reference to the nature of the predominant functional disorder enables researchers to dierentiate between systolic HF and diastolic HF,
even though the current trend is to replace systolic HF and diastolic
HF with HF with reduced systolic function (reduced LVEF) and HF
with a preserved systolic function (preserved LVEF). This dierence is
essential when it comes to deciding on the appropriate treatment for
each patient (Table 15).
preload
(retrograde
symptoms)
Prevalence
Greater (descending)
LVEF
< 50%
> 50%
Left ventricular
dilatation
Yes
No
Left ventricular
hypertrophy
Scarce
Frequent
Treatment
-blockers
Verapamil or diltiazem
Careful preload and afterload management
(diuretics and vasodilators)
Usual etiologies
Ischemic cardiopathy
Dilated cardiomyopathy
Valvular heart disease
Myocarditis
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Hypertension and diabetes
Pericardial disease
Table 15. Dierences between heart failure with depressed systolic function and heart failure with preserved systolic function
18
Card iology
Dyspnea;
Orthopnea;
Paroxysmal nocturnal dyspnea;
Acute pulmonary edema
Jugular distension
19
4.4. Treatment
of Heart Failure
20
Card iology
Symptomatic treatment
Symptomatic
dysfunction
ACE inhibitor
ARA II
Beta blockers
Diuretics
H. failure
Digoxin
Nitrates
Hydralazine
Spironolactone
Severe H. failure
Heart transplant
Prevention of deterioration
ACE inhibitor
Beta blockers
Ivabradine?
Advanced stages
Spironolactone
Cardiac resynchronization
Ventricular assistance
21
combination has also been proven to increase survival rates, especially among black patients, who have obtained better prognosis, in
addition to the treatment with ACE inhibitors and beta blockers in
patients who remain symptomatic.
Reduction of preload. Diuretics reduce the preload and the pulmonary and systemic congestion symptoms, whereby they are extremely useful in cases of decompensation. Figure 36 shows the
action mechanism of the dierent kinds of diuretics.
However, they have not been proven to increase survival rates (with
the exception of spironolactone, but not because of its diuretic effects, as mentioned above). The main kinds of diuretics are shown in
Table 16.
Torasemide has been shown to have antifibrotic eects in experimental
models.
It must be taken into account that the excessive use of these drugs
can exacerbate the sensation of weakness as the result of the lowered cardiac output (by excessively reducing the preload necessary
22
Card iology
DIURETIC
ACTION MECHANISM
INDICATIONS
CONTRAINDICATION
COLLATERAL EFFECTS
Thiazides (chlorothiazide,
xipamide, indapamide)
Inhibition of Na/Cl
channels in distal
convolute tubule
Hypo K
Hyperuricemia
Increased glucose and
lipids
Inhibition of the
Na+-K+-2Cl- symporter
(cotransporter) in the
thick ascending limb
of the loop of Henle
Anuria
Pregnancy
Hypersensitivity
K+ sparing agents
1. Aldosterone antagonists
(spironolactone)
2. Amiloride, triamterene
Hyper K
Associated with other
diuretics with edemas or HTN Renal failure
Treatment with K
Hyperaldosteronism not
supplements
correctible with surgery
Edemas with
hyperaldosteronism
(nephrotic syndrome, CHF,
cirrhosis)
Impotence,
gynecomastia
Hyper K
Same as above
Liddles syndrome
Hyper K
Refractory edema
Serious acute edemas
GF < 25 mL/min.
Serious HTN
Hypo K
Hypo Na
Hyperuricemia
Hypo Mg
Cytotoxicity
Digoxin. Has been traditionally used to treat combinations of atrial fibrillation and heart failure, even though no clinical trials have
proven its eects on survival rates. It has also not been proven to
increase survival rates in sinus rhythm, but does reduce hospitalization rates in cases of heart failure.
It must not be used in patients with HF and preserved ejection fraction (unless the patient needs their heart rate controlled by AF).
The beneficial eects of digoxin are believed to result, partially,
from the increase in vagal tone resulting from its use, since the
levels useful in treatment (between 0.6 and 1.2 g/mL) are more
related to this eect than to the increase in contractility. Its therapeutic margin is very low, so it is common for drug toxicity to occur
(Figure 37).
Sympathetic agonist drugs. Dopamine and dobutamine can be used
in decompensations in which patients do not respond to conventional therapy. Ibopamine is an oral dobutamine analogous drug
which alleviates symptoms but also worsens the prognosis of HF
patients, whereby it is not normally used.
Phosphodiesterase III inhibitors. They have also not been shown
to cause an assessable improvement in patients with heart failure.
Levosimendan. Calcium sensitizer which may be used instead of
sympathetic agonist drugs in cases of decompensations requiring
inotropic support.
Digoxin toxicity
No digoxinemia
Digoxinemia
Renal failure
Drugs
Digestives
Electrical
23
When diastolic function is impaired, the atrial contribution to ventricular filling becomes more important, therefore it is useful to treat
atrial fibrillation by maintaining sinus rhythm as long as possible.
In case it is necessary to implant a pacemaker, it should be a sequential
(bicameral) pacemaker in order to maintain atrioventricular synchrony.
Relaxation of the ventricular myocardium (lusitropic eect) may be
enhanced by decreasing the intracellular calcium concentration. This
may be indicated for patients with HF and preserved LVEF and can be
achieved with two types of drugs: beta blockers and calcium channel
blockers, verapamil and diltiazem (except for patients with systolic dysfunction). These drugs have an anti-angina eect, a relevant fact considering that an impaired diastolic function often appears as a consequence of myocardial ischemia.
Angiotensin receptor blockers, ARBs (candesartan) could contribute to
reduce hospitalizations. ACE inhibitors may also be used. Treatment
with diuretics and vasodilators should not be too rigorous for patients
with diastolic dysfunction as it is necessary to maintain an adequate
preload to prevent a decrease in cardiac output.
24
HF with depressed LVEF is the most commonly found underlying disease. In this case, treatment includes:
High-flow oxygen. Noninvasive or invasive mechanical ventilation
could be performed if necessary.
The patient should be seated, if possible, legs dangling.
Morphine sulfate improves the symptoms because of vasodilatory
and central sedative eects.
Potent diuretics should be used, such as furosemide, which also has
a vasodilatory eect.
Vasodilators should be used when blood pressure is not low (SBP
> 90-100 mmHg). Nitroglycerin is often administered intravenously,
but in cases such as pulmonary edema secondary to acute mitral or
aortic regurgitation, more powerful vasodilators are preferred, due
to their eectiveness on the arteries, such as intravenous nitroprusside, a drug that should always be used in an intensive care unit with
invasive monitoring of blood pressure.
Arterial hypotension may be treated with an intravenous positive
inotropic agent, such as dopamine, dobutamine or levosimendan.
Card iology
An intra-aortic balloon pump may be useful in some cases, especially when blood pressure is low.
Note that the use of sympathetic agonist drugs tends to worsen the
situation if the underlying heart disease is a condition with pure diastolic dysfunction, such as mitral stenosis or hypertrophic obstructive cardiomyopathy, and the triggering agent of the acute pulmonary edema is atrial fibrillation with rapid ventricular response (a
relatively frequent event). Nevertheless, beta blockers or calcium
channel blockers may be useful, as they prolong diastolic time by
slowing conduction through the AV node and have lusotropic eects.
However, an urgent electrical cardioversion is usually indicated in
this case.
With these devices, patients may be discharged in order to wait for their
heart transplant at home, or they may serve as therapy for patients not
eligible for transplantation. Nonetheless, their long-term use is associated with a significant risk of complications like bleeding, embolism and
infection (Figure 40).
25
Heart Transplantation
disease or sudden death. Other causes include tumors (skin cancer and
lymphoma being the most frequent) or acute rejection.
This is a very eective therapy for the treatment of end-stage heart failure. Results are good, not only regarding survival but also regarding lifequality (80% in functional class I). Current survival rates after one and
five years are over 80% and 70%.
Indications and contraindications are summarized in Tables 17 and
18.
According to the standard surgical technique, the donor heart is removed by severing the veins (cava and pulmonary) and large vessels
(pulmonary artery and aorta), therefore, the atria remains intact. The
heart of the recipient is removed by cutting o near the atrioventricular
groove, thus maintaining a portion of both atria. The implant is performed by the removal of donors posterior atrial wall and its subsequent suture to recipients atria. The pulmonary artery and the aorta
are subsequently sutured. Other less-used techniques exist, such as the
bicaval technique. Notwithstanding myocardial protection with cardioplegic solution (rich in potassium) and cold, ischemic times should be
below 5 h (see Figure 43).
The most common cause of death after heart transplantation is infection (17%). However, acute graft failure is the most common cause of
death during the first month, and, in the long term it is graft vascular
Hyperacute rejection is unusual and consists of severe endothelial injury due to preformed antibodies to HLA or AB0 systems.
Lymphocytic infiltration may occur upon acute rejection, which generally appears a week from transplantation and before the first year.
Although it may manifest as heart failure, outstanding clinical signs
are rare, and only minor symptoms may manifest, such as fatigue,
low-grade fever, arrhythmias, or the case may be even asymptomatic.
In most medical centers, acute rejection is studied by transjugular biopsy further spaced over time.
During transplantation follow-up, an endomyocardial biopsy is performed
periodically in order to supervise rejection. There is no other noninvasive
technique able to match the performance of endomyocardial biopsy.
Chronic rejection occurs further in time and involves damage to the
coronary circulation. Repeated rejection episodes seem to favor ocRELATIVE
ABSOLUTE
(Suitable patients in advanced functional class)
Refractory cardiogenic shock
Documented dependence on intravenous inotropic
support to maintain adequate tissue perfusion
Peak oxygen consumption below 10 mL/kg/min
once the anaerobic threshold has been reached
Uncontrollable ventricular arrhythmias despite all
possible therapeutic measures
Constraining ischemic symptoms, refractory
to therapeutic treatments (which include
revascularization)
Patients with congenital heart disease in advanced
functional class ineligible for surgical correction
INSUFFICIENT
AGE
AB0 INCOMPATIBILITY
INFECTIONS
MALIGNANT NEOPLASMS
LUNG DISEASES
26
Card iology
GROUP
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Cardiomyopathies
Chapter 05
TYPE
CAUSES
Familial/genetic
Nonfamilial/nongenetic
Obesity
Infant of diabetic mother
Overtraining syndrome
Familial/genetic
Nonfamilial/nongenetic
27
GROUP
TYPE
Restrictive cardiomyopathy
CAUSES
Familial/genetic
Nonfamilial/nongenetic
Anthracyclines (rare)
Metastasis
Cardiac lymphoma
Arrhythmogenic right
ventricularcardiomyopathy
Familial/genetic
Nonfamilial/nongenetic
Not reported
Nonclassifiable cardiomyopathy
Familial/genetic
Nonfamilial/nongenetic
Familial/genetic
Nonfamilial/nongenetic
Channelopathies
DILATED
LV volume
=//
LV thickness
= or (slight)
= or (slight)
Dysfunction
Diastolic
Systolic
Diastolic
Ejection fraction
=/
=/ (slight)
Clinical observations
Asymptomatic
SAD symptoms:
- Syncope and
sudden death
- Angina
- Dyspnea
Heart failure
symptoms
Mural thrombus
strokes
Arrhythmias
Angina episodes
are unusual
Effort dyspnea
Right heart failure
Strokes
28
Apparently, the phenotype of dilated cardiomyopathy may be secondary to genetic disorders (25%) or may as well be the final expression of myocardial damage produced by a large
amount of circumstances that converge in left
ventricular dysfunction and dilation; excessive alcohol consumption is the most frequent
cause of secondary dilated cardiomyopathy.
A considerable proportion of these patients respond to a history of viral myocarditis that may
Card iology
Treatment for this condition is the same as that of heart failure with
depressed systolic function (Chapter 4).
Peripartum cardiomyopathy and Chagas disease may manifest with
clinical evidence of dilated cardiomyopathy. Anthracyclines (adriamycin, doxorubicin, etc.) may cause dilated cardiomyopathy, thus it is important to reevaluate the systolic function with an echocardiography or
a radionuclide ventriculography before, during and after chemotherapy
cycles.
5.2. Hypertrophic
Cardiomyopathy
Complementary tests reveal cavity growth and systolic dysfunction (Figure 41).
Defined by an increase in ventricular wall thickness in the absence of
abnormal working circumstances (such as high blood pressure or heart
valve diseases) sucient to cause the anomaly (Figure 43).
Septal hypertrophy may result in flow acceleration of the left ventricle outflow tract causing a Venturi eect which, associated with abnormal location of mitral valve papillary muscles, forces the valves into systolic anterior
motions (SAM) and to move towards the septum. This causes dynamic left
ventricular outflow tract obstruction, which occurs at rest in one-third of
patients. Another third of patients does not present obstruction at rest,
29
Increases murmur
Ventricle contractility
(contraction with more strength)
Exercise
Isoprenaline
Digital
Calcium antagonists
-blockers
Volume expansion
Venous return
Raised legs
Contractility
Valsava
Sudden standing
Tachycardia
Nitroglycerin
Preload
Afterload
(less flow resistance)
Arterial vasodilators
Exercise
Squatting
Phenylephrine
Afterload
At macroscopic level, it is common to find significant asymmetric hypertrophy (> 15 mm), which
Decreases murmur
is septal in most cases. However, there are other
hypertrophy patterns, such as apical hypertrophic
Figure 45. Murmur variations in hypertrophic cardiomyopathy
cardiomyopathy (Yamaguchis disease, frequent
in Japan), with giant inverted T-waves in the precordial lead (Figure 44) or Likewise, an initially intense, bisferiens pulse is usually present and, if the
obstruction is severe, there is a double inverted splitting of the second
cases of concentric hypertrophy.
heart sound.
Anything decreasing preload (Valsalva maneuver, sudden standing, arrhythmias) and/or afterload (vasodilators, exercise) or increasing contractility (positive inotropes, physical exercise), increases the outflow
tract obstructive gradient and the murmurs intensity. On the contrary,
the murmurs intensity decreases with increased preload (squatting,
raising lower limbs, and volemia expansion) and/or afterload (vasoconstrictors such as phenylephrine, squatting) (Figure 45).
The ECG usually shows certain changes, such as varying degrees of left ventricular hypertrophy and left atrial growth. Abnormal Q waves in the left
precordial lead are characteristic in the absence of infarction. In apical form,
inverted giant T waves may be noted in the precordial lead (Figure 46).
Most patients remain asymptomatic or have mild symptoms. The most frequent symptom is dyspnea, followed by angina. Fatigue, lightheadedness
and syncope (because of various mechanisms, from neural mediation to
other severe, caused by left ventricular outflow tract obstruction or ventricular arrhythmias) are other symptoms. Very frequently symptoms are
heightened by exercise or during postprandial periods. Atrial fibrillation is
frequent during clinical course and usually results in a significant worsening
of symptoms.
Examination may be normal except for the presence of a fourth sound
and, occasionally, a double, prominent apical impulse.
In patients with left ventricular outflow tract obstruction a hard systolic murmur is heard, located in the apex and left sternal border, which may irradiate
to the hearts base but not to the carotids (unlike aortic valve murmur).
30
Card iology
Figure 47. Echocardiographic image in parasternal long axis (A) and short axis (B) of a patient with asymmetric septal hypertrophic cardiomyopathy,
showing excessive thickness of intraventricular septum (arrows)
Diuretics should be used with caution to avoid excessive preload decrease which would worsen the obstructive gradient; they are useful for
relieving pulmonary congestion.
Eective alternatives (in case of contraindications or inecacy) are disopyramide, verapamil or diltiazem. In refractory cases they may even be combined.
31
increase resistance to filling and cause symptoms to progress. Atrial fibrillation is very frequent, and up to one-third of patients suer stroke
episodes.
Further, physical examination is similar to what may be seen in constrictive pericarditis, with increased venous pressure, Kussmaul sign, decreased sound intensity, third or fourth extra sounds. A deep and quick y
descent wave predominates in the jugular venous pulse, an increased a
wave, of similar width to v, and an x descent wave that can also be quick
adopting a W morphology. Apical impulse is easily felt in restrictive
cardiomyopathy even if it is decreased, which does not occur in constrictive pericarditis.
Table 22 shows the main dierential diagnoses of restrictive cardiomyopathy.
Atrial fibrillation
Myocardial ischemia
Obstructive gradient
Unfavorable genotypes
Intense physical exercise
Under 30 years of age at
diagnosis
32
Significant (over 1,500 eosinophils/mm3), persistent (hypereosinophilic syndrome) eosinophilia may aect multiple organs (lungs, bone marrow, brain)
and especially the heart, where Loeers eosinophilic endocarditis with endomyocardial fibrosis may appear, key to determine the diseases prognosis.
In most cases it occurs in temperate countries and the cause is unknown.
Clinical features are the result of venous and pulmonary congestion secondary to impaired ventricle filling. The posterobasal region of the left
ventricle is frequently aected, involving the posterior leaflet and with
mitral valve regurgitation. Treatment is for diastolic heart failure and anticoagulation, corticosteroids and hydroxyurea or interferon may be added.
Surgery may obtain good results in certain cases with established fibrosis.
Endomyocardial Fibrosis
or Davies Disease
There is endomyocardial fibrosis, mainly in both ventricular outflow
tracts and in the right ventricular apex, leading to obliteration of cavi-
Card iology
Amyloidosis
It is rare for secondary amyloidosis (systemic amyloidosis [AA]) to affect the myocardium, while cardiomyopathy is the most frequent cause
of death in primary amyloidosis. Here (systemic amyloidosis [AL]), the
heart is involved in up to 90% of cases. It may be caused by any hematologic disease with clonal expansion of B-cells, since the protein that
is deposited is immunoglobulin light chain, and in up to 80% of cases
it occurs in relatively benign gammopathies. Organs other than the
heart are frequently aected. Transthyretin-related (TTR) amyloidosis
may cause familiar cases of heart amyloidosis.
Amyloidosis may cause restrictive cardiomyopathy (most frequently),
dilated cardiomyopathy in advanced stages, in some cases ventricular
hypertrophy (infrequent in other etiologies of restrictive cardiomyopathy), atrial or ventricular arrhythmias, conduction disorders or orthostatic hypotension. Sudden death is not exceptional. This disorder
shows a preference for right cavities, at least in early stages. Pericardial
eusion is very frequent.
A characteristic echocardiographic feature is a shiny speckled appearance of the myocardium with thickening of intraventricular septum.
Treatment for plasma cell dyscrasias may be eective on patients
during initial stages of the disease, although the general prognosis is
bleak.
Focal amyloid depositions frequently appearing in the heart of elderly
people (senile amyloidosis) lack clinical relevance.
Endocardial Fibroelastosis
This is a disease typical of fetus and infants, of unknown etiology, although it appears to be related to certain virus such as parotitis and
autoimmune phenomena, involving elastin and collagen depositions in
the endocardium, quickly progressing from a picture of initial restriction
to dilation with a very poor prognosis.
Hemochromatosis
This disorder should be suspected in patients with signs of heart failure associated with alterations of liver function, diabetes and increased
skin pigmentation. Cardiac damage may also occur in the nongenetic
secondary forms because of increased iron supply (e.g., from multiple
transfusions).
The clinical picture is usually a mix of systolic and diastolic dysfunction
with frequent associated arrhythmias. Iron depositions are predominant in the subepicardium. Repeated bloodletting and deferoxamine
may be helpful.
33
Endomyocardial biopsy, which is not usually necessary, confirms fibrofatty degeneration even when the segmented nature of the disease may result in false negatives.
An ECG is very useful even though it may be normal or near normal during initial stages. The most frequent anomaly is the presence of inverted
T-waves in right precordial leads (V1-V3) in people over 14 years of age
(prior to this, they may be normal) in the absence of right bundle branch
block. The most specific abnormality is the presence of epsilon waves
in V1-V3 (signs of low voltage in the final part of QRS, which is usually
slightly widened, a reflection of late activity of involved regions). Low
voltage is also frequent (Figure 48).
currence avoidance cannot be guaranteed. ICD is prescribed for sudden death survivors and high risk individuals (such as those showing
impaired left ventricle and those with ventricular tachycardia, especially
if it is recurrent in spite of anti-arrhythmic drug therapy and/or catheter
ablation).
Treatment of right-sided heart failure (diuretics, water deprivation) is
applied in advanced cases.
Spongiform Cardiomyopathy
(noncompacted myocardial)
There is a developmental defect in the growth of left ventricle myocardial wall sinusoids, which is therefore highly trabeculated and with large
intertrabecular recesses, resulting in a ventricular wall with spongy appearance. Patients may progress towards dilated forms, and the first
episodes may be strokes or arrhythmia. Very frequently it runs in the
family, with several involved mutations that have been reported. It may
occur both in isolation as well as accompanying complex congenital
heart diseases, Ebsteins anomaly, or neuromuscular disorders.
34
Card iology
Although its origin is unknown, it has been related to surges in sympathetic activity (stress cardiomyopathy) and usually returns within the first two
months. Treatment is empiric and customized, usually applying the treatment for acute coronary syndrome with ventricular dysfunction (beta blockers, ACE inhibitors). Prognosis is usually favorable and recurrences are rare.
Coronary Artery
Chapter 06
Disease
Heart failure
Ventricular arrhythmia and sudden death
6.1. Concepts
Aorta
Circumflex artery
Right coronary
artery
Atherothrombosis is a chronic inflammatory disease which commences with an endothelial dysfunction facilitating the flow of LDL cholesterol towards the subendothelial space, which is then oxidized and
esterified, and seeks to be phagocytized by macrophages obtained
from the bloodstream, but these are unable to fully digest such cholesterol and turn it into foam cells which finally commence their own
apoptosis.
Left anterior
descending
artery
Inferior wall
of the right
ventricle
Posterior,
lateral
and inferior
wall
His bundle
55%
90%
Sinoatrial node
AV Node
45%
10%
The release of cytokines attracts other inflammatory cells (monocytesmacrophages and lymphocytes), which multiply the release of cytokines and, among other phenomena, increase even more the endothelial permeability and dysfunction. Smooth muscle cells migrate towards
the subendothelial space and synthesize collagen, which attempts to
stabilize the increasing atheroma plaque with a higher or lower eciency, since the inflammatory cells produce enzymes that degrade the
matrix (metalloproteinase) and tend to destabilize it.
This generates the atheroma plaque, with a lipid core -formed by LDL
cholesterol esters- which is sometimes even crystalized, surrounded by
inflammatory cells, smooth muscle and collagen in dierent proportions, with the presence of vulnerable plaques (high contents of lipids
and inflammatory cells) and stable plaques (high fiber contents; Figure
51).
The presence of ruptures in the vulnerable plaques exposes the subendothelial material to the bloodstream and activates the platelets, which
attach and aggregate themselves, and set in motion the coagulation
cascade, thus producing the thrombosis of the atheroma plaque which
triggers the acute coronary syndromes (ACS), so that, if the occlusion is
complete, it produces an ACS with a persistent ST segment elevation in
the ECG (which causes a transmural infarction), and if the occlusion is
subocclusive, it originates an ACS without ST segment elevation (with
dierent variables ranging from the subendocardial infarction to the
unstable angina; Figure 52).
35
As an approximation, when a plaque occludes 70% of the arterial lumen, it produces an ischemia triggered by physical exertion, cold or
emotional stress, but not at rest. When the stenosis exceeds a value
of 80% to 90% (serious or severe), it can produce an ischemia at rest.
The main risk marker for cardiovascular diseases is age. Another important
marker is male sex. No action whatsoever is possible on these two factors,
i.e., they are nonmodifiable risk factors. The increase in life expectancy is,
therefore, one of the elements which has influenced a higher incidence and
prevalence of ischemic heart disease among the population.
Smoking, hypercholesterolemia (total cholesterol above 200-220 mg/
dL, LDL cholesterol above 160 mg/dL and/or HDL cholesterol below
35 mg/dL), hypertension, and diabetes mellitus are undisputed risk factors for ischemic heart disease (Table 23). An increased carotid intimamedia thickness, detected by means of a sonogram, is an important
marker of cardiovascular prognosis, despite the fact that its use as a
therapeutic target has not been broadly validated.
Recent studies on the eciency of various measures used in preventive
cardiology reveal that the prevalence of high cholesterol values is decreasing significantly. However, smoking or hypertension values experienced
no material modification, the prevalence of diabetes has increased, and
the prevalence of obesity has drastically increased (Table 24).
36
RISK FACTORS
Male sex
Hypertension
Tobacco consumption, especially cigarettes
Obesity, body mass index 30 kg/m2
Sedentary lifestyle
Dyslipidemia, high LDL cholesterol or low HDL cholesterol
Diabetes
Microalbuminuria
Estimated glomerular filtration < 60 mL/min
> 55 years of age in males and > 65 years of age in females
Family history of premature cardiovascular disease in men under 55
years of age and women under 65 years of age
Card iology
Perfusion
(with profusion)
initial event) imposes a marked limitation on the patients habitual activities is also deemed unstable (Table 27).
Nonrecoverable
AORTIC DISSECTION
Exercise
(dobutamine,
dipyridamole)
SPECT
Gammagraphy
(Tc, TI)
Stress echo
Healthy
Stunned Hibernating
myocardium myocardium myocardium Necrosis
No defects
Reversible defects
Irreversible defects
Rest
MITRAL PROLAPSE
PULMONARY
HYPERTENSION
ESOPHAGEAL SPASM
BILIARY DISEASE
PANCREATITIS
OSTEOMUSCULAR
PAIN
When a patient with stable angina shows symptoms at rest or for prolonged periods of time (up to 20 minutes), or more intense symptoms
with progressively lower eorts throughout a four-week period, the angina is said to have destabilized and is known as an unstable angina.
An angina which, having commenced recently (two months after the
37
II
ANGINA AT REST
III
IV
ANGINA OF
RECENT ONSET
ACCELERATED
ANGINA
Cardiovascular Society
The general treatment of a patient with stable angina is shown in Figure 55.
The diagnosis of chest angina is based on the patients medical history,
with its logic and limited sensitivity, and is complemented with additional tests, such as a baseline ECG and an ergometry.
With current treatment, the prognosis of patients with stable angina is
usually favorable. The historic annual mortality rate has been estimated
Suspected angina
Unstable angina
ACS management
Anamnesis
Physical exploration
ECG at rest
Lab tests
Chest XR, if applicable
Alternative diagnosis
Confirm and treat
Assess ischemia
Of choice: exercise testing
Stress test imaging procedure when:
- Inability to exercise
- Difficulties in reading ECG
- Inconclusive ergometric data
No
YES
Assessment of risk
Calculate LVEF
Low
Medical
treatment
Good
Medium
High
General measures
ASA or clopidogrel
Statin (goal LDL < 100 or < 70 in high-risk patients)
ACE inhibitor with confirmed cardiovascular disease (consider in all cases)
-blockers in patients with AMI or a history of heart failure
Anti-anginal treatment:
- Of choice: -blockers + sublingual nitroglycerin in crisis
- Association or alternative: calcium antagonists, prolonged action nitrates, ivabradine, others
(nicorandil, trimetazidine, ranolazine)
Assessment
of clinical response
Consider
coronarography
Coronarography
Poor
Coronarography
38
Card iology
The most physiologic way to induce ischemia, and the one providing
the most information, is physical exertion (exercise stress testing, stress
echocardiography or exercise nuclear cardiology). If the patient cannot
perform physical exercises, a pharmacologic stress must be induced
with dobutamine, adenosine or dipyridamole.
It is diagnostic test when the patient attains 85% of the maximum predicted heart rate. The global sensitivity of the test is 75%, which justifies the existence of false positives (especially in women) and negatives.
There is a series of criteria to identify patients with the worst prognosis
after an ergometry (Table 28).
CORONARY ANGIOGRAPHY
1. Stable angina with low exercise workload despite medical treatment
2. Poor prognosis data in diagnosis tests
3. In the non ST-segment elevation ACS in medium or high risk cases,
and, where positive results are obtained, in ischemia detection tests
in low risk cases
4. In the context of AMI
- Recurrent ischemia
- Cardiac failure or previously ignored diminished LVEF
- Primary PTCA
- Failed thrombolysis
- Mechanical complications
- Residual ischemia in diagnostic tests
5. Sudden death survivors, unless a definite diagnosis has been
reached other than ischemic heart disease (long QT, Brugada
syndrome, and so forth)
39
CORONARY ANGIOGRAPHY
6. Valvular heart disease preoperative period: when there is a risk of
coronary artery disease. Consider CT angiography as an alternative
to an invasive angiography
7. Assessment of the dilated cardiomyopathy to discard ischemic
causes. Consider CT angiography as an alternative to an invasive
angiography
8. Patients with chest pain requiring a certain diagnosis (professional
pilots, drivers). Consider CT angiography as an alternative to an
invasive angiography
PROVEN PROGNOSIS
IMPROVEMENT
ASA (or clopidogrel)
Statins
ACE inhibitors where there is a
confirmed cardiovascular disease
-blockers where there is a history
of AMI or ventricular dysfunction
Coronary revascularization if
indicated
SYMPTOMATIC
IMPROVEMENT
-blockers
Calcium antagonists
Nitrates
Ivabradine
Coronary revascularization
Nicorandil
Ranolazine
Trimetazidine
Molsidomine
Allopurinol?
Pain therapy
The main limitations of the PCI are the risk of suering a thrombosis (if
a stent is used in this cases, it extends over time and makes the use of
two stents mandatory, which causes an excessive scarring of the lesion resulting from the angioplasty). They only measure proven useful
to prevent restenosis (usually appearing as a progressive stress angina
three to six months after the CPI) is the use of stents (especially with
the new stents releasing antiproliferative agents). The use of drugeluting stents is recommended together with a double anti-aggregation to reduce the incidence of thrombosis from the stent for at least
six months or one year. On the contrary, when bare metal stents are
used, the use of drugs need only be maintained for one month.
PCI and surgery present similar mortality rates in cases of multivessel
disease, wherefore the disease can be indistinctively approached with
either technique (unless the patient is diabetic, in which case, surgery
will result in a better prognosis), even though more subsequent revascularization procedures are required after a PTCA and cerebrovascular
accident rates are higher after surgery.
The pathophysiology of Prinzmetal -or variant angina is coronary
spasm. The episodes usually occur at rest and preferably at night, and
cause elevation of the ST segment. The recommended treatment is the
use of calcium antagonists and nitrates. The intracoronary infusion of
acetylcholine or ergonovine enables physicians to induce spasms and
confirm the diagnosis.
Syndrome X (demonstrable angina and ischemia in detection tests with
normal epicardial coronary arteries) is usually the result of a dysfunction of the microvascular endothelium in patients with multiple cardiovascular risk factors.
Acute Coronary
Chapter 07
Syndrome
40
Card iology
Suspected NSTE-ACS
STE-ACS
Anamnesis
Physical exploration
ECG at rest (< 10 min) include V3R, V4R, V7-V9
Lab test: troponin, CPK-MB, hemoglobin, leukocytes, creatinine
Alternative diagnosis
Specific management
Medium-high risk
Low risk
No recurrence
No heart failure
No changes in the ECG
No increased troponins
Coronarography
< 72 h
Urgent
coronarography
Revascularization
Medical
management
Elective coronarography
Upon discharge:
Changes in lifestyle
Medical treatment
CVRF control
41
CLINICAL
ELECTROCARDIOGRAPHIC
ECHOCARDIOGRAPHY
LAB TESTS
Ventricular dysfunction
Extended contraction abnormalities
Assessment of markers:
- Necrosis (T or I troponins, CPK-MB)
- Inflammation (C-reactive protein)
- Neurohumoral activation (NT-proBNP, BNP)
Renal impaired renal function
OTHERS
42
No cardiac failure
II
III
IV
Cardiogenic shock
Card iology
ECG is not usually normal even during the first minutes of the AMI.
It is recommended to register additional leads to evaluate the
right ventricle AMI (V3R and V4R) or posterior wall (V7, V8 and
V9), mainly in patients with inferior AMI associated with those two
subtypes.
Changes may aect the following:
T wave (myocardial ischemic image):
Positive-peaked or isoelectric T: subendocardial ischemia.
Negative T: subendocardial or transmural ischemia.
ST segment (myocardial injury current; Figure 62).
Descended ST: subendocardial injury.
Elevated ST: subendocardial injury.
While necrosis is completed, ST segment tends to return to the isoelectric line. Simultaneously, Q waves (and loss of R wave) develop
in the leads in which ST segment occurs.
Inversion of T wave usually persists or normalizes after several
weeks or months. Persistence of ST elevation in leads in which necrosis waves have developed may indicate ventricular aneurysm
or segments with dyskinetic movements (paradoxic). However, in
some exceptional cases, a complete ECG normalization may occur.
T wave alterations generally take up more leads than STs, which, in
turn, take up more leads than Q waves (the ischemia area is greater
than the injury current area, and this is greater than the electric necrosis area).
In regions opposite to where AMI is localized, electrocardiographic
alterations reciprocal (opposite) to those appearing in the leads localizing the AMI are appreciated, although these changes may also
correspond to concomitant ischemia, in other regions, because of
other compromised coronary bundle branch (Figures 64 and 65).
43
Ischemia
Severe, acute or chronic cardiac insufficiency
Myocarditis or myopericarditis, complicates endocarditis
Myocardial damage by contusion, catheter ablation,
endomyocardial biopsy or electric cardioversion
Myocardial infarction in aortic dissection, aortic valvulopathy, severe
arrhythmias, hypertension episodes or pulmonary hypertension,
(pulmonary embolism, idiopathic, etc.)
Cardiomyopathy such as hypertrophic, tako-tsubo or infiltrating
Severe episode of sepsis or shock
Cardiotoxic chemotherapy (5-fluorouracil, anthracycline, herceptin)
OTHER CIRCUMSTANCES
STE-ACS suspicion
Anamnesis
Exploration
ECG (< 10 min)
SCASEST
Alternative
diagnosis
Consider ECG
and serial necrosis markers
Relevant
actions
Tests
Treatment
Persistent ST elevation,
left bundle branch block
ECG monitoring
Rest
Oxygen
Anti-emetic opiates
Watch AP and peripheral perfusion
ASA (prasugrel or ticagrelor or clopidogrel
should be added to ASA)
Reperfusion therapy
Yes
Primary
PTCA
Yes
No
Contraindications?
Thrombolysis
No
Consider
coronarography
3-24 h
Effective
Fibrinolysis
(In-hospital
or out-of-hospital)
Ineffective
Rescue
PTCA
44
Card iology
cialized team. It has been demonstrated that PTCA provides better clinical
results than in-hospital thrombolysis (less reinfarctions, artery reclusions,
and less residual ventricular dysfunction), and that it may even improve
by using stent, since the risk of the vessel reintervention is reduced.
Door-to-balloon time (the period from hospital arrival to angioplasty)
must not exceed 90 minutes; otherwise, it loses its advantage over fibrinolysis. If the patient presents cardiogenic shock or if fibrinolysis is contraindicated, PTCA is the treatment of choice, regardless of the delay.
Nowadays, in the acute phase, it is recommended to only act over the
artery responsible for the infarction and to consider complete revascularization, when indicated, by PTCA or surgery in a diered way, after
the patient has stabilized.
There follow some contraindications of thrombolytic medication (Table
34) to be checked before their administration to patients.
ABSOLUTE
CONTRAINDICATIONS
Active hemorrhage
(menstruation excluded)
History of intracranial bleeding
Ischemic ictus during the six
previous months
Known brain injury (e.g.,
neoplasia and traumatism)
Severe trauma, major surgery or
head injury in the three previous
weeks
Gastrointestinal bleeding in the
last month
Noncompressible punctures
(lumbar, hepatic biopsy, etc.)
Aortic dissection
Hemorrhagic abnormality
RELATIVE
CONTRAINDICATIONS
Transitory ischemic accident in
the previous six months
Oral anticoagulation
Active peptic ulcer
Pregnancy or immediate
puerperium (one week)
Refractory arterial hypertension
(> 180/110 mmHg)
Severe hepatopathology
Infective endocarditis
Prolonged or traumatic
resuscitation
PRIMARY PREVENTION
(always, at least, 40 days following
the AMI)
LVEF < 40%, VT nonsustained
and VT sustained inducible in
electrophysiologic study
LVEF < 35% and II-III functional
class of NYHA
LVEF < 30% and I functional class
of NYHA (indication IIa*)
SECONDARY PREVENTION
VF-produced sudden death
recovered outside the acute
phase
Sustained VT with poor
hemodynamic tolerance and
depressed LVEF
Sustained VT well tolerated
with normal LVEF (or almost
normal) (indication IIa*)
Changes in lifestyle
Diabetes control (HbA1c < 7%) and hypertension (AP < 140/90 mmHg)
Acetylsalicylic acid (ASA)
Prasugrel/ticagrelor or clopidogrel for 12 months
Anticoagulation if indicated for any other reason
-blocker
ACE inhibitors and ARAs
Statins
Eplerenone if LVEF < 40% or cardiac insufficiency
Consider ICD and TRS implants
Revascularization if indicated
7.3. Complications
of myocardial infarction
Arrhythmias
Tachyarrhythmias
Mechanisms producing ventricular arrhythmias in the acute phase of
an infarction (primary arrhythmias) dier from those appearing in the
chronic phase of the disease (in which there is an anatomic substrate
for the onset of anatomica re-entries in the scar). The main arrhythmias
are shown in Table 37.
Supraventricular Tachycardia
Sinus tachycardia generally indicates a major infarction with ventricular dysfunction and cardiac insuciency associated. It must not be treated as such.
Sinus bradycardia is common in the acute phase of inferior infarction
due to vagal hypertonicity, or secondary to opiates, and it appears in
25% of cases.
45
ARRHYTHMIA
TREATMENT
SECONDARY PREVENTION
PRIMARY PREVENTION
Defibrillation
Reperfusion
-blockers
Amiodarone 24-48h
Reperfusion
-blockers
VF or SMVT badly
tolerated beyond 48h
Defibrillation/cardioversion
Revascularization if indicated
ICD implant
Treatment of heart failure
Amiodarone or ablation in special
cases
Cardioversion
Anti-arrhythmics
(procainamide or amiodarone)
-blockers
VT ablation
Consider ICD
Amiodarone in special cases
Reperfusion
-blockers
Treatment of heart failure
Symptomatic NSVT
-blockers
Amiodarone in refractory cases
-blockers
Amiodarone in special cases
Valuate the indication of ICD implant
as primary prevention
Reperfusion
-blockers
Treatment of heart failure
Asymptomatic
NSVT or ventricular
extrasystole
-blockers
Avoid anti-arrhythmics of Ic group
-blockers
Treatment of heart failure
Valuate the indication of ICD implant
as primary prevention
Reperfusion
-blockers
Treatment of heart failure
Torsades de Pointes
Defibrillation if sustained
Reperfusion
Magnesium
Shorten QT (pacemaker,
isoproterenol)
Correct electrolytes
Reperfusion
Correct electrolytes
AIVR
No (indicates reperfusion)
Atropine if symptomatic
No
No
Reperfusion
-blockers
Treatment of heart failure
ICD implant :
- LVEF < 40%, SMVT and
inducible NSVT
- CF II-III and LVEF < 35%
- CF I and LVEF < 30%
Conduction disturbances
Almost 10% of STE-ACSs are found with AV block, and are more related
to mortality (due to the myocardial extension producing the block than
the block itself, since the block associated with the inferior infarction
has a good prognosis; Table 38).
SUPRA-HISIAN
It may be mild or turn into cardiogenic shock, and may increase mortality
in the short and long term. Symptoms, signs, diagnosis and treatment
are similar to other heart failure-related clinical situations. Killip and Forrester classifications are used to categorize the clinical situation.
The main causes of arterial hypotension in inferior wall STE-ACS are
shown in Figure 68.
INFRA-HISIAN
Heart rate
AMI Location
Inferior
Anterior
Atropine response
Responds
No response
Prognosis
Good
Poor
46
Inferior AMI
with hypotension
RV infarction
Liquids
Inotropes
Reperfusion
Cardiac rupture
Fluids
Pericardiocentesis
Surgery
Bradycardia
Atropin
Pump failure
Rare: diuretics
Inotropes
Contrapulsation
Reperfusion
Figure 68. Causes and treatment of inferior infarction with arterial hypotension
Card iology
Mechanical Complications
These are included in Table 39, and in Figures 69, 70, 71, 72 and 73.
COMPLICATIONS
TREATMENT
Anterolateral
Old woman
Hypertension
First infarction
Reperfusion and -blocker reduce
the risk
Electromechanical dissociation
High vein pressure
Echocardiography
Cardiopulmonary resuscitation
Immediate surgery
Ventricular septal
rupture
Mitral regurgitation
Reperfusion
In mild or moderate cases,
surgery is to be delayed
IABP
Diuretics
Vasodilators
Severe cases: immediate surgery
Ventricular aneurysm
Complications treatment
Pseudo aneurysm
Anterolateral
Thrombus-contained rupture
Chest pain
ECG
Immediate surgery
Right ventricular
infarction
Inferoposterior
Hypotension
High vein pressure and absence
of rales
Increased ST in V4R
ECG
Immediate surgery
IABP
Diuretics
Vasodilators
Reperfusion
Intravenous fluids
No diuretics, no vasodilators
Inotropes
47
Others
Postinfarction ischemia requires immediate intervention and an early
coronarography.
Thrombosis (apart from those related to supraventricular arrhythmias)
is commonly related to the formation of intracavitary thrombus present
in almost 5% of infarctions, mainly anterior infarctions.
Meta infarction acute pericarditis (epistenocardiac) produces ST elevation
and pericardial pain, requiring NSAIDs or colchicine for the treatment.
Figure 71. Mitral regurgitation correction by papillary muscle rupture
Conventional
suture
Dressler syndrome is defined by fever, pneumonitis and polyserositis (pleuropericarditis) probably immune-mediated. It is equivalent to the post pericardiotomy syndrome appearing, in some occasions, after cardiac surgery.
It generally occurs between the first and second week after infarction,
though it may be delayed. Treatment is similar to that of pericarditis.
Recurrence is frequent (especially in patients who have been administered glucocorticoids, which are very ecient in relieving symptoms).
Colchicine may be useful to prevent recurrence.
Dyslipidemia
Suture
in inverted T
Chapter 08
Although a comprehensive study of dyslipidemia is included in the Endocrinology chapter, some considerations must be mentioned.
Pericardial
patch
48
Card iology
CALORIES RELEASED
ACTIVE
CONTRIBUTION TO DIET (%)
IN COMPLETE
SUBSTANCE
OVER TOTAL CALORIES
OXIDATION
Carbohydrates 4.1 kcal/g
50% to 65%%
Fat
9.3 kcal/g
Saturated: < 10%
Polyunsaturated: < 10%
Monounsaturated: 10% to 15%
Cholesterol
< 300 mg/day
Proteins
4.3 kcal/g
10% to 20%
HIGH-INTENSITY
STATIN THERAPY
Daily dose lowers
LDL-cholesterol
on average,
by approximately
> 50%
Atorvastatin (40)80 mg
Rosuvastatin 20(40) mg
MODERATE-INTENSITY
STATIN THERAPY
Daily dose lowers LDLcholesterol on average,
by approximately
30% to 49%
LOW-INTENSITY
STATIN THERAPY
Daily dose lowers
LDL-cholesterol
on average,
by < 30%
Simvastatin 10 mg
Pravastatin 1020 mg
Lovastatin 20 mg
Fluvastatin 2040 mg
Pitavastatin 1 mg
Atorvastatin 10-(20) mg
Rosuvastatin (5)-10 mg
Simvastatin 20-40 mg
Pravastatin 40-(80) mg
Lovastatin 40 mg
Fluvastatin 40 mg bid
Pitavastatin 2-4 mg
Hypertension
Chapter 09
Hypercholesterolemia reduction is followed by a reduction in arteriosclerosis progression. The initial treatment of hyperlipidemia is a lowfat diet (< 30% to 35% of total caloric intake). Likewise, cholesterol in
saturated fatty acids and polyunsaturated acids must be poor. It is necessary that most fat be ingested by way of monounsaturated fatty acids
since they increase HDL levels (Table 41).
By consensus, adult high blood pressure (HBP) is defined as the presence of SBP over 140 mmHg (systolic HTN) and/or DBP over 90 mmHg
(diastolic HTN). However, these limits are arbitrary since there is a connection with cardiovascular risks at lower values, especially in patients
with high cardiovascular risk. Complete patient risk level should be determined, not only the BP level, to apply the correct therapeutic action
49
< 120
120-129
130-139
140-159
160-179
180
140
SBP (mmHg)
and
and/or
and/or
and/or
and/or
and/or
and
50
DBP (mmHg)
< 80
80-84
85-89
90-99
100-109
110
90
Card iology
GRADE I
GRADE II
Arteriovenous nicking
GRADE III
GRADE IV
Papilledema
Treatment
Hypertensive patients must comply with lifestyle and dietary instructions (low salt content, avoid overweight, perform exercise,
avoid anti-inflammatories) and monitor other cardiovascular risk
factors.
To decide when to start drug therapy for hypertension, systolic and diastolic pressure values alone are not enough in every case. It is advisable to assess the presence of established clinical or subclinical damage
of target organs and determine the overall cardiovascular risk (which
includes analyzing the presence and state of other cardiovascular risk
factors).
The latest recommendations for hypertension treatment published
by the Joint National Committee of United States are included in the
table below; there are slight dierences with other available guidelines
(Table 45).
The main target organs with damage caused by hypertension are the
central nervous system (typically strokes), heart (hypertrophy, myocardial ischemia or arrhythmia) see Figure 74. Also, kidneys (renal failure
because of nephroangiosclerosis) and the retina (hypertensive retinopathy), Table 44.
51
The therapeutic objective of hypertension treatment is to lower morbimortality of the patient; for this purpose an operational goal is followed
aimed at lowering blood pressure to values below 140/90 mmHg in
general, being lower in diabetic patients, and with more leniency with
regard to SBP in elderly patients.
The benefit of treatment is more closely related to lowering BP itself
than with a specific drug. For this reason, it is considered that all antihypertensive drugs are first line and all combinations are accepted,
except for ACE inhibitors with angiotensin II. However, the only drugs,
compared against placebos, which have been statistically shown to decrease morbimortality, are diuretics and beta blockers. Newer drugs
have not replicated this since it is unethical to design new studies
against placebo.
For patients with mild blood pressure elevation and low-moderate cardiovascular risk, treatment usually starts with a single drug in monotherapy and doses are subsequently adjusted or other drugs are combined to keep blood pressure values under control. However, patients
with markedly elevated blood pressure and high-very high cardiovascular risk usually require starting with antihypertensive therapy directly,
with a combination of two drugs and later adjustment of doses or addition of a third drug.
Table 46 shows the main cases for or against the use of each drug
group.
DRUG
-blockers
Thiazides
ADVISABLE
Coronary disease
Tachyarrhythmia
Heart failure
Hyperthyroidism
Pregnancy (second line)
Heart failure
Elderly
African American
Asthma
Bradyarrhythmia
Severe claudication
Diabetes risk
Metabolic
syndrome
Gout
Diabetes risk
Metabolic
syndrome
Pregnancy
Renal artery
bilateral stenosis
Hyperkalemia
Calcium
antagonists
Dihydropyridine
in monotherapy
for myocardial
ischemia
Constipation
-blockers
Benign prostatic
hypertrophy
Pheochromocytoma
Heart failure
Orthostatic
hypotension
52
Beta blockers are preferred in coronary patients, with atrial fibrillation or other tachyarrhythmias, hyperthyroidism, heart failure,
sometimes migraine or if there is essential tremor. They are not the
best option in case of high risk of developing diabetes (metabolic syndrome).
Calcium antagonists are preferred in cases of isolated systolic HTN
in the elderly, African Americans, angina with contraindication for
beta blockers, atrial fibrillation or, sometimes, for patients with migraine.
In resistant HTN cases, the application of potassium-sparing diuretics
such as spironolactone/eplerenone and amiloride or alpha blockers
such as doxazosin should be considered. In case medical treatment fails,
invasive procedures, such as renal denervation and carotid baroreceptor stimulation may be considered.
NOT ADVISABLE
ACE inhibitors
Heart failure
or angiotensin II Systolic dysfunction
Diabetes
Proteinuria
Chronic kidney failure
Renovascular HTN
Metabolic syndrome
Ventricular hypertrophy
Angina
Elderly
African american
Intermittent claudication
Metabolic syndrome
Ventricular hypertrophy
Pregnancy (second line)
ACE inhibitors are the drugs of choice in the presence of diabetes mellitus,
renovascular hypertension, and diabetic nephropathy -or from another
source-, ventricular systolic dysfunction or severe heart valve failure,
myocardial infarction history or high risk of developing diabetes. In case
of cough or angioedema caused by ACE inhibitors, the alternative is angiotensin II, which is useful when there is major ventricular hypertrophy.
The most frequent cause of secondary hypertension is renal (renovascular or renal parenchymaytous).
Kidneys are both involved as victims (they develop nephroangiosclerosis)
and executioners (pathogenesis involvement) in essential hypertension.
Many drugs (vasoconstrictors, hydrosaline retention facilitators such as
anti-inflammatories, and so forth) and endocrine and metabolic disorders (hyperthyroidism, Cushings syndrome, among others) cause hypertension.
Figure 75 lists the main causes of secondary HTN.
When HTN is secondary to an identifiable etiology, a treatment should
be conducted, if possible, according to the cause of the disease. For
instance, in case of renovascular hypertension, an angioplasty of the artery involved, or its surgical repair may be prescribed. However, medial
fibromuscular dysplasia (a nonatherosclerotic, noninflammatory vascular disease that causes abnormal growth within the wall of the renal
artery), HTN tends to remain stable and does not require mechanical
treatment if blood pressure is controlled by means of drug treatment.
When subadventitial fibrodysplasia is involved, this tends to be progressive and more frequently requires angioplasty or surgery.
Card iology
Neurogenic
alterations
Drugs
Hyperthyroidism
Aortic coarctation
Atherosclerosis
Arteriovenous
fistules
Aortic regurgitation
Suprarenal
alterations
Pregnancy
Kidney alterations
Pericardial Disease
Chapter 10
Figure 75. Main causes of secondary hypertension
For isolated systolic hypertension in advanced age, the drugs of choice
are calcium antagonists or thiazides. Nevertheless, other first-line
drugs may be used, avoiding abrupt BP falls and monitoring orthostatic hypotension with more lenient goals than with other hypertensive
patients.
In left-sided ventricular hypertrophy and in metabolic syndrome, the
drugs of choice are ACE inhibitors, ARB or calcium antagonists.
Alpha blockers (alpha-adrenergic-antagonists) are advisable for pheochromocytoma.
For benign prostatic hypertrophy, alpha blockers are advisable (although they may be less safe than other antihypertensives in monotherapy).
Patients with previous stoke may, in general, use any drugs. However,
treatment should be avoided during the first week after a stroke, unless
there is very high blood pressure.
Hospital admission is not required for hypertensive emergencies; initial treatment is applied with oral drugs such as captopril, furosemide
or amlodipine. Fast acting nifedipine should not be considered, since it
may cause hypotension and trigger myocardial ischemia.
Hypertensive emergencies require immediate treatment with intravenous drugs in an intensive care unit, being careful not to cause an
abrupt decline in BP to prevent hypoperfusion of vital organs. Nitroprusside, nitroglycerine, furosemide, urapidil and labetalol are highly
suitable drugs in this context.
With regard to pregnancy, it should be noted that during the second trimester BP values drop approximately 10-15 mmHg, returning
53
CAUSES
Idiopathic (over 80%)
Infectious
Virus: Coxsackie A and B, echovirus, adenovirus, infectious mononucleosis, chickenpox,
B hepatitis and HIV infection
Bacterial: tuberculosis, pneumococcus, Hemophilus, staphylococcus, streptococcus, gramnegative, Borrella and mycobacteria
Fungi: Histoplasma, Coccidioides and Candida
Others: amebiasis and toxoplasmosis
Transmural acute myocardial infarction
Chronic kidney disease
Malignancy
Metastatic neoplasms: lung cancer, breast cancer, lymphomas, leukemia and melanoma
Primary neoplasms: mesothelioma and lipoma
Post-radiotherapy syndrome
Autoimmune diseases: acute rheumatic fever, systemic lupus erythematosus, rheumatoid
arthritis, scleroderma, polyarteritis nodosa, Wegeners disease, Dresslers syndrome
and postpericardiotomy pericarditis
Inflammatory processes: sarcoidosis, amyloidosis and inflammatory bowel disease
Trauma: cardiac trauma, cardiopulmonary resuscitation, iatrogenic hemopericardium (implanted
pacemakers or defibrillators, angioplasty, endomyocardial biopsy, catheter ablation, etc.)
Drugs: hydralazine, procainamide, diphenylhydantoin, isoniazid, phenylbutazone, dantrolene,
doxorubicin, methysergide, penicillin, cromolyn and minoxidil among others
Other: myxedema, chylopericardium and aortic dissection
ECG
Speci ic forms
of pericarditis
Idiopathic pericarditis
ST
PR
Changes
T waves become inverted after the ST
in evolution segment becomes isoelectric
Pain
Fever
Idiopathic pericarditis is the most common cause of acute pericarditis and is usually caused by certain viruses, although no
systematic tests for their detection are performed. There are usually signs and symptoms
of infection of the gastrointestinal or upper respiratory tract during the previous days or simultaneous to the disease. It is characteristic
of young adults and is sometimes associated
with pleuritis and/or pneumonitis. It does not
usually evolve into pericardial eusion with
cardiac tamponade or constrictive pericarditis.
For treatment, NSAID (ibuprofen, ASA in high
doses and indomethacin) are prescribed for
several weeks with a gradual dose reduction.
In rare cases, glucocorticoids or colchicine
are required to treat inflammation and opioid
analgesics for pain. Anticoagulants should be
avoided because of the risk of hemorrhagic
transformation. It usually heals without sequelae.
Figure 76. Echocardiography image of severe pericardial eusion (PE) in apical (A) and subcostal
(B) four-chamber view
54
The major problem in this condition is the tendency to relapse (25% of cases). Colchicine is
the preferred drug for preventing relapse, administered during the acute phase and several
weeks later, in association with a NSAID, or
Card iology
Dresslers Syndrome
and Postpericardiotomy
The former usually occurs the first few weeks after myocardial infarction and the second after cardiac surgery or trauma. Both seem to
have an autoimmune etiology and are characterized by fever, pericarditis, pleuritis, pneumonitis and, sometimes, arthralgia. Anticardiomyocyte antibodies are frequently detected. Treatment is similar
to idiopathic pericarditis. Recurrence is also very common, especially
if glucocorticoids have been administered. A transmural infarction or
cardiac trauma can also lead to pericarditis with no autoimmune etiology, such as epistenocardiac pericarditis, during the early days of
the condition.
Other Etiologies
Connective tissue diseases especially systemic lupus erythematosus and rheumatoid arthritis, are frequently associated with asymptomatic pericardial eusion, although they may manifest as acute
pericarditis.
Acute rheumatic fever associated with pericarditis is often a manifestation of severe pancarditis.
Pyogenic pericarditis may occur after cardiothoracic surgery, in immunocompromised patients, esophageal rupture into the pericardium, by extension of foci of pyogenic infection of mediastinal or pulmonary origin, or within sepsis (sometimes sepsis is associated with
aseptic inflammatory pericarditis). Since pyogenic pericarditis has a
high mortality rate, early treatment with intravenous antibiotics is
required.
Tuberculous pericarditis manifests with pain (which is not usually
as intense as in idiopathic pericarditis), pericardial rub and fever.
There may be other signs of systemic tuberculosis infection (anorexia, weight loss, among others). Sometimes there is asymptomatic
chronic pericardial eusion, subacute or chronic pericarditis prone
to constriction. In addition to the tuberculosis treatment, NSAIDs
and, sometimes, corticosteroids are administered to prevent obstruction.
Uremic pericarditis is very common, appearing in about one-third
of patients with advanced kidney failure, especially in those undergoing dialysis. It is usually subacute and is frequently painless, although pericardial rub is often present. Fluid may be fibrinous or
hematic. Treatment includes anti-inflammatory drugs and hemodialysis. If there is cardiac tamponade, pericardiocentesis should be
performed. When pericarditis is recurrent or persistent, pericardiectomy may be indicated.
55
56
Card iology
incidence in global tamponades), and pericarditis with uremic and iatrogenic etiology (in interventional procedures or cardiac surgery).
Normal heart
(the pericardium facilitates
ventricular distention)
Decreased pulmonary vascularization
Arterial pulse
Cardiac tamponade
(pericardial fluid prevents
ventricular relaxation; it exerts
pressure on the septum)
B
PE
Expiration
Inspiration
Expiration
Inspiration
Complementary Studies
ECG. There is often reactive sinus tachycardia. Decreased amplitude of the QRS com-
Figure 81. Echocardiographic image (apical four-chamber view) showing severe pericardial
eusion (PE) in a case of cardiac tamponade (A). Doppler image of transmitral ow showing ample
respiratory variations in diastolic lling ow velocity (B)
57
Treatment
Expanding blood volume with serum or additional blood reduces collapse
of the cavities. Diuretics are contraindicated, since they reduce blood flow
volume and may increase collapse, which can induce shock. Treatment consists of evacuating pericardial fluid and, as a result, intrapericardial pressure
is reduced. In extreme cases, pericardiocentesis should be performed as
soon as possible. Drainage can be performed using two techniques:
Pericardiocentesis. Under local anesthesia, a long needle is inserted
between the xiphoid process and the left costal arch, guiding it toward the left shoulder. The puncture can be guided by ECG, echocardiography or fluoroscopy (Figure 82).
cardiac tamponade
A pericardial catheter can be placed and left for several hours or days,
enabling continuous drainage. In some cases, it may also be helpful for
intrapericardial treatment. There is risk of puncture of cardiac cavities,
pleura or other structures.
Pericardial window. This technique is indicated for patients who need
something more than a simple puncture. When there are frequent
relapses, septation, and purulent eusion or in cases of uremic etiology, this is the preferred procedure. It is performed using a subxiphoid
approach or left thoracotomy. This surgical drainage has the advantage that it is more complete and a biopsy of the pericardium can be
performed. Since it is performed under direct vision, it is easier to
remove adhesions and localized eusions. Risk is minimal and longterm outcome is better than that of performing a puncture.
Valvular heart
Chapter 11
disease
58
Card iology
59
SUMMARY OF VHD
In MR and AR, if LVEF < 30%: transplantation
MS
Rheumatic fever (RF)
ETIOLOGY
MR
RF (MS + MR)
Mitral valve prolapse
MI isolated
AS
< 30 years: unicuspid
30-70 years: bicuspid
>70 years: degenerative
Dyspnea
Angina
Syncope
Dyspnea (more frequent)
Diuretics
Digoxin
Nonvasodilators
ACE inhibitors
Nonvasodilators
ACE inhibitors/Dihydropyridine
calcium antagonists
Dilation of annulus:
Acute: aorta dissection
Chronic: Marfan syndrome
Dyspnea
Dyspnea
SYMPTOMS
MEDICAL TREATMENT
AR
Valvular:
Acute: endocarditis
Chronic: RF
Favorable anatomy:
PMBC
Unfavorable anatomy:
prosthesis
The deterioration risk is higher in cases of renal insuciency, hyperparathyroidism, people under 60-65 years of age, or hypercholesterolemia, Figure 85.
60
Biological prosthesis on the left side of the heart (mitral and aortic)
presents risk of deteriorating in the long run, thus requiring intervention. When in the right side of the heart, the risk is lower.
Card iology
MECHANICAL PROSTHESIS
BIOLOGICAL PROSTHESIS
No contraindications to chronic
anticoagulation
Patients with coagulation
indications for another reason
or with high embolic risk
(atrial fibrillation, mechanical
prosthesis in another valve,
severe left systolic dysfunction,
emboli family background,
hypercoagulability conditions)
High risk of valvular
deterioration
(hyperparathyroidism)
< 60 years of age
Patients with high reintervention
risk (left ventricular dysfunction,
prior bypass surgery, multiple
prosthesis)
Difficulties in or
contraindications for correct
chronic anticoagulation (high
hemorrhagic risk, lifestyle
or occupation, compliance
problems)
Resurgery because of prosthetic
thrombosis with proven poor
anticoagulation control
> 70 years of age
Young woman with pregnancy
desire
Express desire of informed
patient
LA-LV Gradient
LA Pressure
Pulmonary
congestion
Pulmonary
hypertension:
- Active
- Passive
RV
hypertrophy
LV Filling
Dilation
of LA
Blood
accumulates
Cardiac output
Atrial
fibrilation
Emboli
Right HF
In Figure 88, general guidelines for mitral stenosis are shown. Normally,
this disease progresses slowly over period of 10-20 years before producing symptoms. However, when symptoms appear, they progress in a few
years, which constitute a significant increase in mortality if no measures
are performed. This is why symptoms with ordinary activity are the base
of surgical indication. Likewise, in asymptomatic patients, percutaneous
mitral balloon commissurotomy (PMBC) can be performed in cases of atrial fibrillation, PCWP > 25 mmHg with exercise or in very severe stenosis.
61
PMBC
Periodic monitoring
Atrial Fibrillation
or area <1 cm2
Favorable for PMBC
Favorable for PMBC
PMBC
Yes
output (lack of blood flowing onwards since it flows back into the left
ventricle) are also included.
Chronic mitral regurgitation murmur is better auscultated in the apex
or armpit; it is systolic and generally larger when regurgitation becomes
more severe, Figure 89.
62
Mitral focus
radiates armpit
MT
AP
S3
MT
Hyperflux murmur
Card iology
Mild
or moderate
Follow-up
Define etiology
Primary MR
Symptoms
Surgery
(attempt of repair
if possible)
Secondary MR
Asymptomatic
EF 30% to 60%
and LESD <40 mm
or new onset AF
or PASP >50 mmHg
EF 30% to 60%
or LVESD 40mm
Symptomatic severe
MR with persistent
NYHA class III-IV
symptoms
Asymptomatic
severe MR
or progressive MR
Periodic monitoring
Likelihood of succesful
repair > 95% and expected
mortality < 1%
MV repair
MV surgery
(MV repair preferred)
Periodic monitoring
63
Mitral valve prolapse (Barlow syndrome) usually produces a midsystolic click followed by a mitral-regurgitation-produced murmur
(click-murmur syndrome). When preload decreases (Valsalva, bipedestation), the click comes earlier and murmur duration extends
(Figure 92).
S1
S2
C
S1
S2
C
S1
S2
C
Aortic stenosis is considered severe when the aortic valve area is < 1.0
cm2 (or indexed AVA 0.6 cm2/m2). If systolic function and cardiac output are normal, aortic stenosis is severe as long as the mean systolic
transvalvular gradient exceeds 40 mmHg.
Upon systolic dysfunction, the ventricle cannot open the valve completely. The aortic valve area may still be compatible with aortic stenosis. Dobutamine stress echo is used to determine the gradient growth
with poor increase of the valvular area in cases of true aortic stenosis.
Characteristic symptoms of severe aortic stenosis are triggered by effort (angina, syncope or dyspnea). Nowadays, the main predominating symptom is dyspnea. The risk of sudden death in aortic stenosis
increases exponentially when symptoms appear. The latter indicates
the need for aortic valve replacement.
Aortic stenosis murmur is auscultated in the aortic focus, radiating to
carotids and supraclavicular area (occasionally the apex: Gallavardin phenomenon). It is systolic and rhomboidal after aortic opening
(sometimes an opening click may be heard, mainly in bicuspid valves).
As the murmur lasts longer, its severity also increases (Figure 95).
64
Card iology
65
Symptoms combine both the eects of low anterograde flow with retrograde congestion.
Aortic Regurgitation
Severe AR
(stages C and D)
Vena contracta > 0.6 cm
Holodiastolic aortic
flow reversal
RVol 50%
ERO 0.3 cm2
LV dilation
Progresive AR
(stage B)
Vena contracta 0.6 cm
RVol < 60 mL/beat
RF < 50%
ERO < 0.3 cm2
LVEF 50%
LVEF 50%
LVEF < 50% Other cardiac
LVESD > 50 mm LVEDD > 65 mm
(stage C2)
surgery
(stage C2)
Low surgical risk
YES
NO
Periodic monitoring
AVR
Asymptomatic
(stage C)
AVR
AVR
AVR
LVEF 50%
LVESD 50 mm
LVEDD 65 mm
Erb focus
(aortic accessory)
Radiates to left
sternal border
AP
Hyperflux murmur
MT
Austin-Flint murmur
66
The presence of ascending aorta dilation along with severe aortic regurgitation implies concomitant operative intervention to repair the aortic
sinuses or replace the ascending aorta in patients with:
Bicuspid aortic valve if the diameter of the aortic sinuses or ascending aorta is greater than 4.5 cm.
Marfan Syndrome when the aorta reached 4.5 cm.
Patients with ascending aorta or aortic sinus diameter 4.5 cm or
greater.
Card iology
The most common cause of respiratory failure is pulmonary hypertension, usually secondary to left heart diseases.
Pulmonary valve disease murmurs are increased during inspiration
(Rivero-Carvallos sign).
Graham-Steeles murmur is the murmur of respiratory failure.
Treatment for severe pulmonary stenosis is usually by means of percutaneous catheter-balloon valvuloplasty.
For severe respiratory failure, an annuloplasty is performed concurrently with surgery on the originating left heart valve disease.
Vascular
STENOSIS
REGURGITATION
Most frequent
cause
Rheumatic
Functional:
pulmonary
hypertension
Organic: endocarditis
Symptoms
Of associated left-sided
valve disease
Systemic congestion
Of originating
disease
Systemic congestion
Jugular pulse
Increased A wave
Increased V wave
Decreased (reversed)
x sinus
Auscultation
Diastolic murmur
Increase during
inspiration
Systolic murmur
Increase during
inspiration
Severity
Medical
treatment
Surgery
instructions
Recommended for
patients with severe
tricuspid regurgitation
(TR) undergoing leftsided valve surgery
Mild, moderate, or
greater functional
TR at the time of leftsided valve surgery
with either tricuspid
annular dilation or
prior evidence of right
heart failure
Symptoms because
of severe primary
TR unresponsive to
medical therapy
Technique
Bioprosthesis
Commissurotomy
Percutaneous
valvuloplasty in some
cases
Prosthetic
De Vega
annuloplasty
Bioprosthesis
Chapter 12
Disease
67
often identified by chance during another addominal test. The main risk
factors for IAAA rupture are diameter, hypertension, active smoking, female sex and presence of symptoms (expanding aneurysm).
Ascending aorta thoracic aneurysm may appear because of cystic medial necrosis (typical with Marfan, Ehler-Danlos syndromes or associated
with bicuspid aortic valve) or tertiary syphilis.
Abdominal aortic aneurysm diagnosis is usually by means of abdominal ultrasound. However, in case of suspected complex aneurism or in
view of surgical intervention, CT angiography or magnetic resonance
angiography with contrast are more useful techniques. Opaque contrast aortography may underestimate the aneurysms diameter in
case of mural thrombus, but it is excellent for assessing adjacent arterial branches. Currently, an aortography is not usually required for
intervention, since CT and magnetic resonance angiography may provide sucient and accurate preoperative information.
Examination of these patients is key for the associated coronary disease; the latter may aect the prognosis and surgical risk of the patient.
Current treatment for this kind of aneurysms is shown in Figure 100.
Suspected abdominal
aorta aneurysm
Symptomatic
Asymptomatic
CT Angio
Consider:
RM Angio
Aortography
*Emergency
surgery
No smoking
Treat risk factors
Consider -blockers
> 5.5 cm
Low
surgical
risk
5.0-5.5 cm
High
surgical
risk
Programmed If not
feasible
surgery
Consider
intervention
if low surgical
risk
Consider
graft stent
4.0-5.5 cm
Follow-up every
6 to 12 months
using ultrasound
or CT scan
Growth
> 0.5 cm/year
*Preferrable
if there
is no rupture
68
Card iology
Thoracic
aortic aneurysm
Symptomatic
Asymptomatic
Emergency surgery
With high surgical
risk, consider graft
stent in descending
aorta
Ascending
Semi-annual size
follow-up
Treat risk factors
Avoid intense exercise
Beta blockers
Arch
Descending
Surgery
if > 5.5 cm
Surgery
if > 6 cm*
* With connective
tissue disease,
consider graft
stent if > 5.5 cm
* If high surgical risk,
consider graft stent
Yes
No
Consider surgery
if > 4-5 cm
Surgery
if > 5.5 cm
or growth
> 0.5 cm/year
Figure 102. Procedure for action in the event of thoracic aortic aneurysm
INTRAMURAL AORTIC
HEMATOMA
Etiopathogenesis Adventitia bleeding
towards the media
More frequent
in descending aorta
PENETRATING ULCER
Intima disruption
secondary
to atherosclerotic
damage
More frequent in
descending aorta
Epidemiology
Diagnosis
Treatment
Similar to aortic
dissection
in the corresponding
segment of the aorta
Similar to type B
dissection
Surgery if:
- Hemodynamically
unstable
- Pseudo aneurysm
- Acute rupture
- Continuous pain
- Distal embolization
perfusion deficits in the area involved. Typical findings of aortic dissection are asymmetric decrease of upper limb pulses and a diastolic
murmur of aortic valve regurgitation.
Stanfords classification (Table 54) divides acute aortic syndromes (and
aortic dissection) into type A or proximal: if the ascending aorta is involved (the most frequent, prognosis is poor, and requires surgical repair) and type B or distal: if they do not involve the ascending aorta (less
frequent, better prognosis, treatment is medical and it should be managed medically unless life-threatening complications develop).
Urgent and definitive imaging of the aorta using transesophageal echocardiogram, computed tomographic imaging, or magnetic resonance
imaging is recommended to identify or exclude thoracic aortic dissection in patients at high risk for the disease. Figure 103 shows recommendations for acute aortic syndrome management.
DE BAKEY CLASSIFICATION
I
II
III
A (proximal)
B (distal)
69
Patients undergoing orthopedic-traumatologic treatment either surgical or leading to immobilization are at risk of suering deep vein thrombosis. The main causes are shown in Table 55.
Diagnosis is usually confirmed by means of
Doppler ultrasound. Treatment consists of
rest, elevation of involved limbs to avoid edema, and anticoagulation to avoid progression
and development of pulmonary embolism.
Anticoagulation therapy must be commenced
and maintained for three months. However,
patients with recurrent episodes or nonreversible causes must be considered for indefinite anticoagulation.
Suspected
CT Angio + TEE
Medical
treatment
Type B
Urgent surgery
Consider after stabilization (24-72 hours)
only with
- Stable retrograde thrombosis dissection
- Stable intramural hematoma with aorta
< 50 mm and hematoma < 10 mm
Contraindicated with irreversible brain damage
Consider medical management if:
- Chronic dissection
- Stable and limited to arch
Yes
No
Close follow-up
70
Complete early ambulation, pneumatic compression stockings, and low doses of anticoagulants are used for prophylaxis of deep vein
thrombosis.
Card iology
Normal
venous flow
Normal vein
Varicose vein
71
Figure 109. Patient with edema on the face and upper limbs
72
Card iology
Intermittent claudication
STAGE I
STAGE II
Intermittent claudication:
IIa: nonincapacitating intermittent claudication
(for patients regular activity)
IIb: incapacitating intermittent claudication
(for patients regular activity)
STAGE III
STAGE IV
Aprox. Mortality
20% to 30% in five years
Prognosis
of involved limbs
Stable
75%
Advanced
claudication
aprox. 15%
Need
of surgery
aprox. 10%
Amputation
5%
Coronary disease
Cardiovascular
disease
No vascular history
Normal contralateral pulse
History of claudication
or vascular disease
Embolic heart
disease
Nonembolic
heart disease
Arteriography
Poorly-tolerated ischemia
(with motor and sensitive
changes)
Well-tolerated ischemia
(with no motor
or sensory changes)
limbs
Consider
Fibrinolysis
Surgery
Consider
if high risk
73
ARTERIAL EMBOLISM
Anamnesis
Rare
Frequent
Onset of symptoms
Sudden/Acute
Sudden/progressive (acute/subacute)
Predominant symptom
Pain
Pain/Paresthesia (+++)
Rare
Arteriographic findings
OBLITERATING
ATHEROSCLEROSIS
OBLITERATING
THROMBOANGIITIS
Age
Usually, over
50 years of age
Young, below
45 years of age
Blood pressure
Usually, hypertension
Often hypotension
Raynauds syndrome No
and migrating
phlebitis
Commonly present
Cholesterolemia
High
Normal or low
ESR (erythrocyte
sedimentation rate)
Normal
High
X-rays,
arteriography
Hard, calcified,
deformed, tortuous,
irregularly-sized
arteries
Atheromatous aorta
Quitting tobacco usually stops the progression of the disease; therefore, it is the most important step. The appearance of new lesions is a
sign that patient has not achieved cessation.
Administration of nicotine gum or patches may be sucient to maintain
the disease active. In certain cases, deviation of large vessels and local
debridement of lesions may be performed. Anticoagulant therapy has
not yielded the expected results and use of corticosteroids has not been
useful either. In some cases, amputation is necessary, usually more limited than with obliterating atherosclerosis.
In subclavian steal syndrome, the occlusion is in the subclavian artery
before the exit of the vertebral artery and causes symptoms of vertebrobasilar insuciency (Figure 116).
Raynauds phenomenon consists of recurrent episodes of vasoconstriction
aecting fingers most commonly, caused by exposure to cold or intense
emotions. It is important to dierentiate Raynauds disease from Raynauds
phenomenon. Raynauds disease is not the result of an underlying associated
medical condition (idiopathic); it comprises more than half the cases, being
predominant among young women and with usually milder manifestations.
74
RAYNAUDS DISEASE
Idiopathic
CONNECTING TISSUE
DISORDERS
BLOOD DYSCRASIA
TRAUMA
DRUGS
NEUROLOGIC
ALTERATIONS
Scleroderma
Systemic erythematosus lupus
Rheumatoid arthritis
Diabetes mellitus
Dermatomyositis
Cryoglobulinemia, macroglobulinemia
of Waldenstrom, myeloproliferative disorders
Hammer syndrome
Vibration lesions
Electric shocks
Ergotamine
-blockers
Bleomycin, vincristine, cisplatin
Syringomyelia
Carpal tunnel syndrome
Poliomyelitis
Card iology
Most patients with mild and infrequent episodes do not require special treatment. They should be instructed to avoid cold environmental
temperatures by using thick gloves and socks, and to avoid mechanic
microtrauma. Tobacco is contraindicated due to its potential vasoconstricting eect. In severe cases, vasodilator therapy with drugs may be
administered, calcium antagonists are advisable to this end, and if there
is no response, surgical sympathectomy may be considered, although
any benefits are usually temporary.
Syncope
Chapter 13
12.5. Lymphedema
The most common cause of lymphedema globally, and mostly in tropical Africa, is filariasis, which causes lymphatic obstruction due to nematodes and a corresponding inflammatory response, which leads to elephantiasis.
Frequent causes of lymphedema are tumors, both due to lymphatic
infiltration of malignant cells and treatment (surgery with lymph
node exeresis or fibrosis caused by radiation therapy to the lymph
system).
The clinical aspects are very important for diagnosis of this disease,
since lymphography is rarely used. Lympho-gammagraphy may be used
to detect the blocking point of lymphatic drainage, and it is a useful
technique in oncology to detect the sentinel ganglion where sick tissue is drained and in order to plan the surgery.
Lymphedema, unlike edemas with dierent etiology, has an orange
skin appearance on the surface area involved, it has a hard feel
(woody) and shows little response to diuretics or rest. In secondary
lymphedema, ducts are usually dilated and it is possible to determine
the occlusion level. On the contrary, in the primary form, lymph vessels
are absent or are hyperplastic or ecstatic.
The main goals of lymphedema treatment are to control edema
(superficial lymphatic massage, soft, and applied from a distal to
proximal direction, physiotherapy and other techniques; any element compressing the limbs, venous punctures, intense exercise
or trauma of the involved limb should be avoided, which should
be as long as possible above the heart level), maintain a healthy
and clean skin, and prevent complications such as cellulitis or erysipelas and lymphangitis. It is advisable to raise the feet while in
bed, use compression stockings and bandages after emptying the
edema by means of manual drainage; or use sequential pneumatic
compression boots during the day. Especially with lymphedema after breast surgery, good results have been shown with low-level
laser therapy.
Surgery is used in severe cases which do not respond to medical treatment and it consists of removing hypertrophied tissue and applying
There are some ECG alterations that indicate a high risk in case of syncope (Table 61).
75
RHYTHM
ALTERATIONS
QRS ALTERATIONS
REPOLARIZATION
ALTERATIONS
Pre-excitation
Branch block
Left-sided ventricular hypertrophy criteria
Pathologic Q waves
Epsilon wave
Table 61. ECG Alterations involving high risk in patients with syncope
If this initial assessment is enough to reach a diagnosis, patient
treatment follows. If not, it is known as syncope of unknown origin,
and other tests are necessary that should be considered only with
certain suspected clinical origins, such as Holter, echocardiography,
tilt test, electrophysiology study, stress test, cardiac catheterization
catheterization. Events loop recorder or implantable Holter are useful with syncope of unknown origin with suspected arrhythmic origin, especially when the frequency of syncope is very low (since in
this context it is rare for the conventional Holter to provide any data
of interest).
The figure below shows the general treatment of a patient with syncope
(Figure 117).
Vaso-vagal syncope is the most common type. It is triggered by seeing blood, prolonged standing, hot or tight environments, or even by
76
No
Yes
Was recovery spontaneous?
No
Metabolic alteration,
intoxication, RPC
Yes
Is it due to global brain hypoperfusion?
No
Yes
Yes
No
Suspected neuromediated
or orthostatic syncope?
Yes
Benign Syncope
No
Syncope with Unknown Profile
Yes
High Risk
No
Low Risk
Abnormal ECG
Card iology
Hypovolemic shock
Obstructive shock
Diaphoresis
Pneumothorax
Vomiting
Miscellaneous
Burns
Pulmonary embolism
Chapter 13
Tamponade
Bleeding
Cardiogenic
shock
14.1. Shock
Shock is a syndrome characterized by a decrease in tissue perfusion
below its metabolic demands. If the situation persists, organ dysfunction and tissue damage may be observed. Generally, compensation
mechanisms are activated (increase in adrenergic tone, increase in adrenergic tone, contractility and heart rate and with cutaneous, muscular and splanchnic vasoconstriction) to preserve vital organs (central
nervous system and heart). However, if these mechanisms extend in
time, they may be deletereous (Table 62).
TYPES OF SHOCK
VENOUS
CENTRAL
PERIPHERAL
CARDIAC
OXYGEN
VENOUS
VASCULAR
OUTPUT
SATURATION
PRESSURE
RESISTANCES
(%)
Hypovolemic
Cardiogenic
Obstructive
Septic Hyperdynamic
Hypodynamic
or late
Neurogenic
Anaphylactic
Distributive
shock
Intense internal
diuresis
77
MAJOR CRITERIA
Polyarthritis
Erythema marginatum
Subcutaneous nodules
Carditis
Chorea minor
MINOR CRITERIA
Fever
Arthralgia
Previous episode of FR
Previous episode of rheumatic
carditis
Elevated ESR or CRP
Prolonged PR interval
Anti-inflammatory treatment is important, acetylsalicylic acid is generally administered. Arthritis usually resolves within 24-48 hours.
Glucocorticoids are used only if NSAIDs are not enough or if there
are signs of carditis with moderate or severe heart failure.
It is not advisable to start treatment with anti-inflammatory drugs
until the diagnosis of rheumatic fever is clear. Arthralgias can be
treated with non anti-inflammatory analgesics while waiting to see
if the Jones criteria are met not to overestimate a rheumatic fever
diagnosis. Anti-inflammatory drugs are administered for several
weeks after normalization of ESR and C-reactive protein levels, followed by a gradual withdrawal. ASO levels take six months to decrease after initiation of treatment.
In cases of chorea minor, sedatives (especially diazepam) and rest
are very useful. Prolonged bedrest is not recommended, except in
cases of active carditis and persistent or severe heart failure.
Improvement of living conditions, early diagnosis and treatment of the
pharyngeal streptococcus infections are the most important factors for
the prevention of rheumatic fever.
Secondary prophylaxis is performed with an intramuscular injection of
benzathine penicillin G, administered on a monthly basis. Penicillins administered orally, erythromycin and sulfadiazine are a second option.
The last two can be used when the patient is allergic to penicillin.
The latest recommendations in regard to prophylaxis duration are presented in Table 64.
DURATION
CATEGORIES OF PATIENTS
Rheumatic fever without carditis
14.3. Myocarditis
78
Card iology
Symptoms are nonspecific, sometimes it is dicult to distinguish myocarditis from an acute coronary syndrome or acute pericarditis. Chest
pain is usually similar to pericardial pain due to frequent association
with viral pericarditis (myopericarditis), whose symptoms are more
prominent. However, when there is myocardial involvement, markers
for myocardial damage are elevated. During the previous days, there
may have been a nonspecific viral infection of the upper respiratory
tract or gastrointestinal tract. In some cases, myocarditis produces signs
and symptoms of heart failure because of ventricular dysfunction secondary to inflammatory infiltration of the myocardium and to microvascular damage, as well as arrhythmias that may cause sudden death,
especially in pregnant women and infants. It can also evolve into dilated
cardiomyopathy.
I.
II.
CLINICAL CRITERIA
14.4. HIV-Related
Cardiomyopathy
HIV-reacted cardiomyopathy appears relatively frequently in patients
with HIV and it is generally asymptomatic. Left ventricle aectation is
more frequent and in some cases it appears to be directly caused by HIV.
In other cases, myocarditis is due to opportunistic pathogens that take
advantage of immunosuppression. Nutritional deficiencies, toxic agents
or the medication used may also promote myocardial damage.
For treatment, rest is indicated as well as specific drugs for heart failure (diuretics, ACE inhibitors and beta-blockers). In subacute or chronic
cases that do not improve with standard treatment of heart failure, immunosuppressants (corticosteroids, azathioprine or cyclosporine) can
be administered.
Myocarditis
79
caused by S. aureus and enterococcus. In exceptional cases, hematogenous dissemination in sepsis, by almost any bacteria, may cause intramyocardial microabscesses often masked by other manifestations of
the disease.
Diphtheric myocarditis (C. diphtheriae). Cardiac involvement is
the most frequent cause of death in patients with diphtheria. It
can produce cardiomegaly with myocardial hypocontractility, as
well as arrhythmias and, typically, atrioventricular block (diphtheria toxin has particular anity for the cardiac conduction system).
Treatment consists of early administration of antitoxin and antibiotics.
Toxoplasma myocarditis (T. gondii) appears in immunocompromised adult patients (in children, it usually occurs as congenital
toxoplasmosis). In toxoplasma myocarditis, there is cardiac dilatation with heart failure, pericarditis with pericardial eusion and
rhythm and conduction alterations.
Lyme carditis (Borrelia burgdoreri) cardiac abnormalities develop
in up to 10% of cases, mainly atrioventricular block in the AV node,
condition that may require pacemaker implantation, but is usually
transient. Heart failure is exceptional.
Whipples disease (Tropheryma whippleii) can aect the heart
structures. The agent causing this disorder is located in the myocardium or coronary arteries. It is linked to macrovascular or microvascular ischemia. Myocarditis is usually mild, although there have
been reports of manifest heart failure.
Chagas disease (Trypanosoma cruzi). This disease is endemic in
Central and South America and it is a first order health problem,
as it is estimated that more than 20 million people are infected.
Immigration is a responsible factor for the increase in the number
of cases detected in our area. The protozoan Trypanosoma cruzi
is found in the digestive tract of the assassin bug that lives in
thatched roofs in rural endemic areas. At night, it comes down and
bites humans, mostly children, usually near the eyes. The bite itself
is not infectious, but contact with the feces of the bug with the sting
site or with conjunctival mucosa originates an acute infection by the
protozoan. Few patients with Chagas disease present an acute cardiac involvement (10%); however, when cardiac aectation occurs,
it can be fatal, with symptoms of acute fulminant myocarditis by
parasite migration to the myocardium and an intense local inflammatory response.
Usually, after a latency of 20 years, up to 30% of patients present clinical
symptoms because of damage of nerves and ganglia of the autonomic
system (the megaesophagus or megacolon are frecuent) and, cardiac
involvement. Myocardial damage appears to be caused by the parasite
itself and by the autoimmune response of the body that releases autoantibodies that act on the sarcoplasmic reticulum, the beta-adrenergic
receptor and other structures of the cardiac cells. Parasympathetic denervation as a result of ganglia involvement is a characteristic complication. Rhythm alterations are frequent.
Vegetative denervation usually produces sinus bradycardia and chronotropic incompetence, even in the presence of heart failure. Involvement of the conduction system with anterior hemiblock and right
bundle branch block are frequent markers of cardiac involvement.
Arrhythmia is relatively frequent, both atrial fibrillation and ventricular arrhythmia, related to physical activity in particular, and there can
be isolated extrasystoles, nonsustained or sustained tachycardia by
reentry through myocardial scars, which may lead to sudden death
(Figure 119).
80
Card iology
81