CARDIAC DISORDER c. PDA f.

Truncus Artreriosus

COURSE OUTLINE

Cardiac Disorders VALVULAR HEART

1. Valvular Heart Disease DISEASE

2. Cardiomyopathy  Mitral Valve Disease

3. Infectious Disorders of the Heart – Mitral Valve prolapse

a. pericarditis – Mitral Valve stenosis

b. myocraditis – Mitral Valve regurgitation

c. endocarditis  Aortic Valve Disease

d. RHF – Aortic Stenosis

4. Cardiac Tamponade – Aortic Regurgitation

5. Coronary Heart Disease  Tricuspid Valve Disease

6. Heart Failure  Pulmonic Valve Disease

8. Cardiac Dysrhythmias

9. Angina Pectoris MITRAL VALVE PROLAPSE

10. Myocardial Infarction  Occurs when the cusps of the mitral

valve billow upward into the atrium
during systolic contraction
Vascular Disorders
 Chorda tendinae lengthens and cusps
1. Hypertension may enlarge and thickens

2. Acute Arterial Occlusion  Diagnostics: echocardiography, stress

test, chest x-ray, cardiac
3. Arterial Ulcers catheterization
4. Aneurysms  Manifestations: asymptomatic; maybe
5. Raynaud’s Syndrome vague

6. Buerger’s Disease  Management: symptomatic

treatment (aspirin to prevent TIA,
7. Thrombophlebitis antibiotics, beta-blockers)

8. Varicose Veins MITRAL VALVE STENOSIS

9. Chronic Venous Insufficiency  Mitral valve becomes calcified and

immobile and the valvular orifice
10. Lymphedema
narrows
CONGENITAL HEART DISEASES
 Can result to heart failure and
a. ASD d. Tetralogy of decreased cardiac output
Fallot
 Manifestations: atrial fibrillation,
b. VSD e. Transposition of decreased exercise tolerance,
Great dyspnea, orthopnea, murmurs

Vessel  Management: oral diuretics and Na

– restricted diet in heart failure,
 anticoagulants, digitalis, beta-  Causes decreased cardiac output and
blockers increased right atrial pressure

MITRAL VALVE REGURGITATION  Manifestations: neck distention,

peripheral edema, murmurs
 Occurs when much pressure is
generated within the left ventricle to  Management: diuretics, digitalis
be generated to the aorta resulting to
backflow of blood to the left atrium

 Pressure is reflected back to the PULMONIC VALVE DISEASE

pulmonary veins and arteries
 Usually congenital defects
 Manifestations: asymptomatic until
 Causes: mitral stenosis, pulmonary
cardiac output falls, murmurs, atrial
emboli, chronic lung diseases
fibrillation, pulmonary manifestations
 Can lead to decreased cardiac output
 Management: restrict physical
activities, restrict sodium,  Manifestations: murmurs, fatigue,
diuretics, digitalis dyspnea
AORTIC STENOSIS
 Management: treat the underlying
cause
 Caused by calcification of the valve
and stiffening of the valve from Medical Management:
rheumatic heart fever
 Valve replacement may be necessary
 Results in decreased cardiac output for some patients
 Manifestations: initially  Long-term antibiotic therapy
asymptomatic, angina pectoris,
syncope, dyspnea  Penicillin – drug of choice

 Management: avoid vigorous  Erythromycin – for allergic people

physical activity, antibiotics,
digitalis, beta-blockers  Penicillin IM injections every 3 –
4 weeks for about 5 to 10 years

 High risk individuals and those

AORTIC REGURGITATION with recurrent infections,
prophylactic antibiotic
 Blood propelled into the aorta propels
treatment may be lifelong
back to the left ventricle through an
incompetent valve Nursing Management:

 Manifestations: initially  Teach patient about the

asymptomatic, palpitations, murmurs, disease and prevention as well
low BP as treatment modalities

 Management: same for aortic

stenosis
CARDIOMYOPATHY

 Unknown cause
TRICUSPID VALVE DISEASE
 3 major types
 Tricuspid stenosis or regurgitation
usually occurs after rheumatic heart – Dilated (congestive)
disease cardiomyopathy

– Hypertrophic cardiomyopathy
 – Restrictive cardiomyopathy  Manifestations: death (usually the
first sign), asymptomatic
 Risk factors
 Management: medications as
– Alcohol abuse
ordered, avoid alcohol
– Pregnancy Surgery: myotomy
– Hypertension

– Infections RESTRICTIVE CARDIOMYOPATHY

 Caused by fibrosis and thickening in

the heart that causes the ventricles to
lose their ability to stretch

 Frequently associated with

DILATED CARDIOMYOPATHY amyloidosis ( deposition of
eosinophilic fibrous protein in the
 Usually both ventricles dilate,
heart)
myocardial fibers degenerate and
replaced by fibrotic tissue  Management: no specific
interventions but goals are aimed to
 Can lead to heart failure with lethal
diminish heart failure
dysrhythmias and pooling of blood
with clot formation within the heart

 Associated with infections, metabolic INFECTIOUS DISORDERS OF

problems, neuromuscular problems,
THE HEART
toxins, pregnancy, connective tissue
disorders and genetic predisposition 1. PERICARDITIS

 Management: similar in heart  acute or chronic inflammation of the

failure pericardium

 Rest and avoid stress Assessment:

 Restrict sodium in diet • precordial pain

 Diuretics, nitroglycerin, • pain (inspiration, coughing &

anticoagulants, swallowing)
antidysrhythmics as ordered
• pain worse when supine
 Cardiac defibrillation
• pericardial friction rub
 Avoid alcohol
• fever & chills
 Heart transplant
• elevated WBC ct.

• cardiomegaly
HYPERTROPHIC
CARDIOMYOPATHY Caused by:

 Disproportionate thickening of the  bacterial (TB), viral (Flu / AIDS), or

myocardium that leads to obstruction fungal infection
of blood flow
 Trauma
 Causes: genetically transmitted,
idiopathic  acute MI ( usually 1 – 3 days post-MI)

 Neoplasms
 Uremia (kidney failure) Management:

 Radiation • Position: Bed rest / sitting up or

leaning forward
 Drugs (Procainamide, hydralazine,
Doxorubicin HCL) • Monitor pulse rate & rhythm

Management: • Admin. for fever & pain

• Position: side lying, high Fowler’s, • Limit activities

upright & leaning forward
• Admin. digoxin / antidysrhythmics /
• Admin. analgesic, corticosteroids, antibiotics as prescribed
NSAID’s
• NSAID’s / analgesics / salicylates
• Avoid aspirin & anticoagulants

• Antibiotics
3. ENDOCARDITIS
• Diuretics & digoxin
 - Inflammation of the endocardium;
• Monitor for complications: Cardiac platelets and fibrin deposit on the
Tamponade mitral and/or aortic valves causing
deformity, insufficiency or stenosis

2. MYOCARDITIS
Assessment:
 acute / chronic inflammation of the
myocardium
• fever, anorexia, wt loss, fatigue
Etiology:
• cardiac murmurs
• Bacterial : staphylococcus /
• Janeway’s lesions
pneumococcal
• Ossler’s nodes
• Viral : coxsackievirus / mumps /
influenza • Petechiae, splinter hemorrhages in
nailbeds
• Parasitic : Toxoplasmosis
• Splenomegaly
• Radiation / Lead
Management:
• Meds: Lithium / Cocaine
• balance activity w/ rest
Assessment:
• antiembolism stockings
• fever
• monitor emboli:
• pericardial friction rub
• Splenic – sudden abd. pain
• gallop rhythm
radiating to L shoulder /
• murmur rebound tenderness on
palpation
• pulsus alternans (regular alternation
of weak and strong beats without • Renal – flank pain radiating to
changes in cycle length) groin, hematuria & pyuria

• S/S of HF
4. RHEUMATIC FEVER / RHD
• Chest pain
 A pancarditis that follows exposure of
child to throat and skin infection
caused by Group A B-hemolytic
organisms
 Repeated bouts with permanent
scarring of the valvesà RHD à heart
failure
Management of RF/RHD :
 Aspirin or steroid
 Initially Penicillin for 10 days
 Secondary Prophylaxis: Penadur q 3-4
weeks
 Phenobarbital or haloperidol for
chorea
 Digoxin for heart failure
 Diuretics for heart failure
 Rest, adequate feeding and fluid
balance
JONES’ CRITERIA
2 Major or 1 Major and 1 Minor plus
the evidence of recent strep infection
 Major
– Carditis
– Polyarthritis
– Chorea
– Erythema marginatum
– Subcutaneous nodules
 Minor
– Fever
– Arthralgia
– Elevated Erythrocyte
Sedimentation Rate
– Positive C Reactive Protein
– Prolonged P-R interval
Supporting Evidence of Streptococal
Infection
 Increased Titer of Anti-Streptococcal
Antibodies ASO
 Positive Throat Culture for Group A
Streptococcus
 Recent Scarlet Fever
TERMS
 Chorea – a disorder causing
involuntary movement or spasms
 Janeway’s lesion - non-tender, small
erythematous or haemorrhagic
macules or nodules in the palms or
soles, which are pathognomonic of
infective endocarditis
 Ossler’s nodes - painful, red, raised
lesions on the finger pulps, indicative
of the heart disease subacute
bacterial endocarditis.
 Erythema marginatum - of pink rings
on the trunk and inner surfaces of the
arms and legs
 C Reactive Protein – a plasma protein
that increases during inflammation.
CARDIAC TAMPONADE
 pericardial effusion occurs when the
space bet. the parietal & visceral
layers of the pericardium fill with
fluid.
Etiology:
• stab wound
• tumor
• surgery
Assessment:
 Beck’s triad: distended neck veins /
muffled heart sounds / hypotension
 Paradoxical pulse
 Chest pain • syncope

 Cardiogenic shock • cough or hemoptysis

 Increased CVP • excessive fatigue

Management: Diagnostic Test :

• CCU for hemodynamic monitoring 1. ECG

• PERICARDIOCENTESIS 2. Cardiac Catheterization

• Admin. IV fluids as prescribed 3. Blood lipid level

Medical Management:

CORONARY ARTERY  Nitrates

DISORDERS  Antiplatelets

 Narrowing or obstruction of one or  Antilipemics

more coronary arteries as a result of:
 Beta-Adrenergic Blockers
– Atherosclerosis
 Calcium Channel Blockers
– Arteriosclerosis
 Surgery:
RISK FACTORS :
 Percutaneous Transluminal
Modifiable
Coronary Angioplasty – a
 Cigarette smoking balloon-tipped cathether is
usually inserted into the
 hypertension femoral artery and inflated
several times to reshape the
 Elevated serum cholesterol lumen
 Diabetes mellitus  Atherectomy – reduces
coronary stenosis by excising
 Physical inactivity
and removing atheromatous
 Obesity plaques

 Chronic stress – Type A personality  Coronary Artery Bypass

Grafting – involves the bypass
Non-modifiable of a blockage in one or more of
the coronary arteries using the
 Heredity and race – African saphenous veins, mammary
Americans artery or radial artery as
conduits or replacement
 Advancing age
vessels
 Gender – men and postmenopausal
 Intracoronary stenting –
women
tubes that act as mechanical
Signs and Symptoms : scaffold to reopen the blocked
artery .
• normal during asymptomatic period
 B. Nursing interventions:
• chest pain preoperative

• palpitations 1. Explain anatomy of the heart,

function of coronary arteries, effects
• dyspnea of CAD
2. Explain events of the day of
surgery
3. Orient to the critical and coronary
care units and introduce to staff
4. Explain equipments to be used
(monitors, hemodynamic procedures,
ventilators, ET, etc)
5. Demonstrate activity and exercise
6. Reassure availability of pain
medications
C. Nursing interventions: post-
operative
1. Maintain patent airway
2. Promote lung re-expansion
3. monitor cardiac status
4. maintain fluid and electrolyte
balance
5. maintain adequate cerebral
circulation
6. provide pain relief
7. prevent abdominal distension
8. Monitor for and prevent the ff.
complications:
a. Thrombophlebitis / pulmonary
embolism
b. Cardiac tamponade
c. arrhythmias
d. CHF
9. Provide client teaching and
discharge planning concerning:
a. limitation with progressive increase
in activities
b. sexual intercourse can usually be
resumed by 3rd or 4th week post-op
c. medical regimen
d. meal planning with prescribed
modifications
e. wound cleansing daily with mild
soap and H2O and report for any
signs of infection
f. Symptoms to be reported:
- fever, dyspnea, chest pain with
minimal exertion.
ANGINA PECTORIS
 chest pain resulting from myocardial
ischemia; a symptom of an existing
disease; no necrosis
Types :
1. Stable – triggered by a predictable
degree of exertion or emotion (eg.
Walking 20 feet)
2. Unstable – triggered by an
unpredictable degree of exertion or
emotion
3. Prinzmetal/variant – similar to classic
angina but longer and may occur at
rest
4. Intractable – unresponsive to
treatment
5. Nocturnal – associated with REM
sleep during dreaming
6. Angina decubitus – occurs when the
client reclines and lessens when the
client sits or stands up
7. Postinfarction – occurs after MI, when
residual ischemia may cause
episodes of
Causes: 5 E’s
• Exertion
• Emotion
• Exposure to cold
• Excessive smoking
• Excessive eating
Assessment:
• Pain pattern:
Mild – moderate
Retrosternal – choking, heartburn,
pressing, burning, squeezing
Radiating to the left shoulder and upper • retain saliva
arm and may travel down to the elbow,
wrist and fingers • keep in dark, airtight glass

Levine’s sign • burning sensation

Aggravated by activity • use gloves (ointment)

Relieved by rest • Patch: rotate sites, non-hairy

areas, avoid heat sources
3 – 5 mins.
• S/E: postural hypotension
Assessment:
Medication:
• Pallor
 Beta – Blockers – (-) inotropy / (-)
• Faintness
chronotropy = decreases O2 demand
• Palpitation
• propanolol (Inderal) / metoprolol
• Dizziness (Lopressor) / atenolol (Tenormin) /

Diagnostic Test: • Guidelines:

a. ECG 1. with food

b. Cardiac Catheterization 2. check HR & BP before giving

c. Exercise testing 3. C/I: Asthma & COPD

d. CT scan  Calcium Channel Blockers –

vasodilation & reduce myocardial
e. Myocardial scintigraphy contractility & spasm

f. Coronary angiography • nifedipine (Procardia), verapamil

(Calan), diltiazem (Cardizem)
Medication:
• assess HR & BP
 Nitrates – vasodilation; decreased
preload & afterload = dec. peripheral • admin. 1 hr ac or 2 hrs pc.
resistance

• isosorbide dinitrate (Isordil) /

nitroglycerin MYOCARDIAL INFARCTION
• transdermal nitrodisk (patch) / Nitrol,  sudden decrease of oxygenation due
Nitrobid (Ointment) to reduced coronary blood flow that
results to destruction of myocardial
Medication: Nitroglycerine
tissue in regions of the heart
• Form: Tablet / Patch / ointment
after 15 mins. = necrosis
Duration : 5 mins. (tab) / 24 hrs
Causes:
(patch)
 Thrombus
• Onset : 1 – 2 mins. Route : Sublingual
/ skin  Emboli
• Frequency : 3 tabs at 5 min. interval  Atherosclerosis
(tabs)
 Hypotension
• Guidelines:
Location:
• stop activity
 Left anterior descending artery –
anterior or septal wall MI or both
Circumflex artery– posterior wall MI or
lateral wall MI
Right coronary artery – inferior wall
MI
Diagnostic Studies :
1. Total CK levels
2. LDH
3. AST
4. ECG
a. T wave inversion (zone of
hypoxia)
b. ST elevation (zone of injury)
c. Pathologic Q wave (zone of
infarction)
Assessment :
• Pain pattern: severe crushing
substernal pain; knifelike that may
radiate to jaw, back & left arm
• Fever
• Nausea & vomiting
• Oliguria
• Pallor / cyanosis / coolness of ext.
Nursing Intervention :
a. Acute Stage:
 Admin. prescribed
medications : M. O. N. A.
(morphine, oxygen, nitrates,
aspirin)
• Lidocaine (Xylocaine)
• Beta-blockers (propranolol, timolol)
• Thrombolytics (streptokinase,
urokinase)
• Anticoagulants (heparin,
warfarin/coumadin)
• Oxygen @ 2 – 4 L/min
• Stool softeners & soft diet
• Diet: liquid / small frequent meals
(low fat, cholesterol, sodium diet)
• Semi-fowler’s
• Emotional rxns: anxiety, denial,
depression
• Monitor thrombolytic therapy
b. Following acute episode:
• maintain CBR
• provide ROM
• progress to ambulation
c. Rehabilitation:
• Early activity : 1 – 2 metabolic activity
on task
• Hospital Discharge: 14th day
• Resume ADL’s : 6 wks after
• Resume Sex : 4 – 8 wks after
Teaching Guidelines in resuming
sexual activity:
• Resume if able to climb 2 flights of
stairs
• Before: rest is impt. / avoid large
meals / wear loose fitting clothes /
nitro before sex / usual environment /
sex at room temperature / foreplay
• During: comfortable position / self-
stimulation / oral-genital / avoid anal
• Female position: side lying or rear
entry position
• Male Position : reverse missionary or
sitting position
HEART FAILURE
 inability of the heart to maintain
adequate circulation to meet the
metabolic needs of the body bec. of
an impaired pumping capability.
 Causes: 5. Provide client teaching and
a) Hypervolemia discharge planning

b) Arteriosclerosis 6. Monitor I & O

c) Myocardial Infarction 7. Monitor daily weight

d) Cardiomyopathies 8. Auscultate lung sounds

Types: 9. Monitor Vital signs

 Right-sided CHF (Systemic Sx) 10. Teach patient’s to monitor signs

of CHF – Pedal edema, Weight gain of
• Fatigue 1-2 kg / 2 day period, Dyspnea, Loss
of appetite and Cough
• distended jugular veins
Management :
• Ascites
• Diet modification
• pitting edema
• LOF
• Cyanosis
• Medications:
• hepatomegaly
Cardiac Glycosides – (+) inotropy /
• increased peripheral venous pressure (-) chronotropy
• anorexia / GI distress • digitalis / digoxin (Lanoxin) /
digitoxin (Crystodigin) /
• polyuria / wt. gain
lanatoside (Cedilanid-C)
 Left-sided CHF (Pulmonary Sx)
C. Medical Management of CHF:
• Cardiomegaly
1. determination and
elimination/control of underlying
• blood tinged sputum
cause
• Cough
2. Pharmacologic therapy:
• acute pulmo edema
 if MILD: VASODILATORS are
• Exertional dyspnea - started (like ACE inhibitors)

• cyanosis  If NO IMPROVEMENT and PRESENCE

of FLUID OVERLOAD: DIURETICS are
• Orthopnea given

• wt. Loss  If SYMPTOMS CONTINUE: DIGITALIS

Nursing Interventions:
1. Monitor respiratory status, and
provide adequate ventilation (when CHF
progresses to pulmonary edema) – give
Oxygen, place in Semi - Fowler’s position
and monitor ABG’s
are given
 If SEVERE: all THREE (3) are given
immediately
• Diuretics – H2O & Na+ excretion
• Loop diuretics – Furosemide (Lasix)

2. Provide physical and emotional rest • Thiazide diuretics – chlorthiazide

(Diuril)
3. Increase cardiac output
• Potassium sparing – spironolactone
4. Reduce & eliminate edema (Aldactone)
 • Inotropics – increases the  Premature Ventricular
strength of contraction such as Contraction
dopamine (Intropin),
dobutamine (Dobutrex)  Torsades de Pointes

• Vasodilators – ACE inhibitors – Conduction

• Rotating Tourniquet  First Degree AV block

Principles:  Second Degree AV block

apply 3 tourniquets  Third Degree AV block

inflate cuff 10 mm above – Reentry of impulses

diastolic pressure
 Atrial Flutter
rotate q 15 mins.
 Atrial Fibrillation
check distal pulses
 Ventricular Fibrillation
remove 1 at a time @ 15 mins.
Interval Clinical Manifestations :

o Cardiac surgery  Palpitations

 Syncope

 Pallor

 Diaphoresis

 Altered mentation

CARDIAC DYSRHYTHMIAS  Hypotension

 Abnormal heart rhythms often  Sluggish CRT

detected because of associated
manifestations of dizziness,  Decreased urine output
palpitations, and syncope
 ECG changes
 Dangerous because of reduced
2. Atrial dysrhythmias
cardiac output which can lead to
impaired cerebral perfusion  A.Premature Atrial complex (PAC)
 Most serious complication: sudden  B. Atrial Flutter
death
 C. Atrial Fibrillation
ETIOLOGY :
 D.Paroxysmal Atrial Tachycardia
 Disturbance in the 3 major
mechanisms:

– Automaticity 3. Ventricular dysrhythmias

 Sinus Tachycardia A. Premature Ventricular

 Sinus Bradycardia Contraction

 Premature Atrial B. Ventricular Tachycradia

Contraction
C. Ventricular Fibrillation

D. Ventricular Asystole
4. AV node Dysrhythmias
A. 1 degree heart block
B. Second degree heart block
a. Mobitz type 1
b. Mobitz type 2
C. Third degree heart block
SINUS TACHYCARDIA
 Rapid, regular rhythm at a rate of
100-180 bpm with normal P wave and
QRS complex
 Occurs in response to increased
sympathetic stimulation or decreased
parasympathetic stimulation,
medications (eg. Atropine, nitrates,
epinephrine), stress, caffeine,
nicotine, hyperthyroidism,
hypercalcemia, fever, heart failure,
fluid volume loss
 Management : aimed at treating the
underlying cause, bed rest, oxygen,
meds as ordered
 SINUS BRADYCARDIA SA node fires
less than 60 times per minute and the
P wave and QRS complex are normal
 Occurs in increased vagal stimulation,
drugs (eg. Digitalis, propanolol,
verapamil), MI, hypothyroidism
 Normal in some people (eg. Athletes)
 Management: treat the underlying
cause, increase the heart rate as
appropriate
PREMATURE ATRIAL CONTRACTION
 Early beats arising from ectopic atrial
foci interrupting the normal rhythm
 Associated with valvular disorders,
atrial chamber enlargment, stress,
fatigue, heart failure, MI, CAD,
pulmonary hpn
 P waves are premature and different
from the normal sinus P wave in
appearance, shape and size
 Management: Quinidine or
procainamide
PREMATURE VENTRICULAR
CONTRACTION
 Premature ventricular beats
associated with MI, acidosis, alcohol,
heart failure, CAD, nicotine,
hypermetabolic states
 Occur earlier than expected beat of
the underlying rhythm followed by a
compensatory pause
 Dangerous
 Management: lidocaine and other
antidysrhythmics
TORSADES DE POINTES
 Form of ventricular tachycardia in
which the QRS complexes appear to
be constantly changing
 Usually results from drug toxicity or
electrolyte imbalance
 Management: discontinuing the
offending agent and IV
magnesium sulfate
FIRST DEGREE AV BLOCK
 Delay in the passage of impulse from
the atria to ventricles usually occurs
at the level of the AV node
 P-R interval is prolonged but remains
constant
 Results from CAD, increased vagal
stimulation, congenital anomalies and
digitalis administration
 Requires observation and monitoring
since it can progress to higher-degree
AV block
SECOND DEGREE AV BLOCK
 More serious and some impulses are
blocked while others are not
 Develops from CAD, digitalis toxicity,
rheumatic fever, viral infections and
MI
 2 types:
 – Mobitz Type 1 Block  AV node cannot conduct all the atrial
(Wenckebach) impulses that bombard it

– Mobitz Type 2 Block  Management: Cardioversion, anti-

dysrhythmics (digitalis,
MOBITZ TYPE 1 BLOCK
quinidine, etc)
 Caused by a long refractory period
ATRIAL FIBRILLATION
that occurs at the AV node
 Rapid, chaotic atrial depolarization
 Due to increased vagal tone, digoxin
from a reentry disorder
administration and congenital
anomalies  400-700 bpm

 PR interval lengthens until a P wave is  AV node is bombarded with more

not conducted impulses than it can conduct

 Interventions is not required as long  Erratic of no identifiable P waves

as the ventricular rate remains
adequate for perfusion  Management: Antidysrhythmics,
beta-blockers, Defibrillation
MOBITZ TYPE 2 BLOCK
VENTRICULAR FIBRILLATION
 Level of the block is below the AV
node  Life-threatening dysrhythmia
characterized by rapid, erratic
 Results from ischemia, digitalis, impulse formation and conduction
quinidine or MI which causes abrupt cessation of
cardiac output
 Requires ECG monitoring
 Results from severe MI, electrocution,
 Management: administration of
digitalis toxicity, electrolyte
atropine, insertion of pacemaker,
imbalance
withholding cardiac depressant drugs
 No detectable P waves, QRS complex
THIRD DEGREE AV BLOCK
or T waves
 Complete absence of conduction of
 Management: initiate CPR until
electrical impulses due to a block in
Defibrillator is engaged
the AV node, bundle of His or bundle
branches

 2 halves of the heart are working

independently of each other

 Danger of ventricular standstill or

asystole

 Management: atropine,
pacemakers, catecholamine
infusion (epinephrine)

ATRIAL FLUTTER
VASCULAR DISORDERS
 “saw-toothed” atrial wave formation
caused by rapid reentry in the atria
HYPERTENSION

 Atrial rate ranges from 220-350 bpm

 abnormal elevation of BP above
140/90 mmHg based on at rest
 least 2 readings on same conditions.
TYPES OF HYPERTENSION
 Primary – essential or idiopathic;
etiology is multifactorial with no
identifiable cause
 Secondary – from identifiable causes
(eg. Diabetes)
 White coat – normotensive except
when BP is measured by a health
professional
 Isolated systolic – systolic is
140mmHg or above and diastolic is
normal
 Malignant –severe hpn when left
untreated and irresponsive to
treatment
Management:
a. Lifestyle modification:
• sodium restriction
• weight reduction
• alcohol restriction
• smoking cessation
• regular exercise
• Stress reduction
b. Drug Therapy
• Diuretics (Furosemide,
Spironolactone,
Hydrochlorothiazide)
• Beta-Blockers (Metoprolol,
Propanolol)
• ACE Inhibitors (Captopril,
Imidapril)
• Vasodilators (Hydrazaline)
• Calcium Channel Blocker
(Nifedipine)
• Alpha2 Agonists (Clonidine,
Methyldopa)
Major side-effects of
antihypertensive drugs:
• Orthostatic hypotension
• Dizziness
• Cardiac rate alteration
• Sexual disturbances
• Drowsiness
Health Teachings
• Emphasize compliance
• Therapy is usually for life
• Monitor BP
• Do not increase or decrease
dose w/o doctor’s order
• Do not abruptly discontinue
meds
• Avoid Tyramine rich foods
• Aged cheese
• Liver
• Beer
• Chocolate
• Yogurt
• Sausage
• Soy sauce
ACUTE ARTERIAL OCCLUSION
 Caused by trauma, embolism or
thrombosis and occurs mostly in the
limbs
 Manifestations: 6 Ps (Pain,
Pulselessness, Pallor,
Poikilothermia[coldness],
Paresthesias, Paralysis
 Management: Anticoagulants,
Thrombolytics, Embolectomy, place
patient in room temp with limb
slightly dependent.
ARTERIAL ULCERS
  Skin breakdown due to local pressure  Pulsating mass
or minor trauma in an ischemic
extremity  Shock

 Painful and heals poorly; forced to  Other manifestations:

undergo limb amputation if untreated
– Syncope
 Management: revascularization
– Light headedness
(arterial bypass surgery), skin
grafting to cover the ulcer, keep area – hypotension
free from pressure and irritation, bed
rest, debridement  Medical Management:
Antihypertensives as ordered,
ANEURYSMS ultrasonography q 6 months

 Permanent localized dilation of an  Surgical Management: Resection

artery that enlarges gradually and graft replacement.

 Causes: atherosclerosis, congenital RAYNAUD’S SYNDROME

malformations, infection, connective
tissue disorders, hypertension  vasospasm of the arterioles & arteries
of extremities.
 Complications: rupture, pressure on
surrounding structures, thrombosis Etiology:
and embolization
 cold
Classification of Aneurysms :
 stress
 Location
 Smoking
– Venous or arterial
 Caffeine
– Aortic, iliac, etc..
Manifestations :
 Etiology
 blanching of ext. followed by cyanosis
– Atherosclerotic, mycotic
(bacterial), anastomatic graft,  reddened tissue
syphilic
 numbness, tingling, swelling &
 Gross appearance coldness of ext.

– Fusiform (localized dilations of  Gangrene of the tips of the digits

an artery)
Management :
– Saccular (an outpouching of an
• stop smoking
artery where the medial coat is
thinned)
• Vasodilators and Calcium channel
– Dissecting (hematoma in the blockers
artery wall from a localized
• avoid precipitating factor
enlargement of the involved
artery) • warm clothing

 Complication: Rupture • avoid injuries to hands & fingers

– Triad manifestations of • Reduce stressful activities
rupture:

 Pain
BUERGER’S DISEASE
• Also called “Thromboangitis Management :
obliterans”
 Compression stockings
• occlusive disease of the median &
small arteries & veins accompanied  Surgery:
by clot formation.
– Sclerotherapy (injection of an
Etiology: agent into the varicose veins
that damages the vein and
 unknown endothelium causing
thrombosis that closes the
 smoking vein)

 males – Vein ligation ang Stripping

Manifestations :

 intermittent claudication

 ischemic pain occurring in the digits

while at rest

 cool, numb, tingling sensation

 diminished pulse at distal extremity

 Ulceration and gangrene

CHRONIC VENOUS
Management : INSUFFICIENCY

• Instruct to stop smoking  Group of disorders resulting from

faulty venous valves
• Monitor pulses
 Manifestations: swollen limbs, thick
• Avoid injury to extremities and brownish skin, venous stasis
ulcerations, itchy scaly skin
• Admin. vasodilators as prescribed
Management :
• Amputation (last resort)
 Elevate legs

 Sleep with foot of bed elevated

VARICOSE VEINS
 Encourage walking and exercises in
 Permanently distended veins that bed
develop due to loss of valvular
competence maybe due to prolonged Avoid:
standing
– Prolonged standing or sitting
 Common sites: greater and lower
saphenous veins and perforator veins – Crossing the legs

– Sitting in chairs that are too

 Incidence: higher in females
high
 Types:
– Wearing garters or too tight
– Primary – congenital/familial stockings
origin

– Secondary – from trauma,

obstruction, DVT or
LYMPHEDEMA
inflammation
 Swelling caused by impaired  Uncommon and cause is usually
transcapillary fluid transport and unknown
transportation of lymph
 Risk Factors:
 Classification
– Maternal infections (eg.
– Primary – according to age of Rubella)
onset
– Chromosomal abnormalities
 Congenital (Milroy’s (eg. Trisomy 21)
disease)
– Maternal diabetes
 Praecox (before age 35)
– Drugs
 Tarda (after age 35)
– Chronic alcohol use
– Secondary – due to damage
ACYANOTIC
of the lymphatic system by
another disease process AORTA DOES NOT GET
(filariasis, inflammation, UNOXYGENATED BLOOD
neoplasms, surgical excision)
 VETRICULAR SEPTAL DEFECT
Manifestations:
 ATRIAL SEPTAL DEFECT
 Bilateral or unilateral mild edema
 PATENT DUCTUS ARTERIOSUS
 Vesicles (blisters) filled with lymph on
the skin  COARCTATION OF THE AORTA

 Dull, heavy sensation  PULMONARY STENOSIS

 No pain  AORTIC STENOSIS

 Roughened skin CYANOTIC

 Limb becomes enlarged, AORTA GETS UNOXYGENATED

uncomfortable and unsightly BLOOD

Management :  TRANSPOSITION OF THE GREAT

VESSELS
 Physical therapy for affected arm or
leg  TETRALOGY OF FALLOT

 Diuretics  TRUNCUS ARTERIOSUS

 Elevate extremities Categories :

 Encourage ambulation  Left to Right shunting (acyanotic)

 Bed exercises for bed-ridden patients – Produces pulmonary

congestion/increased
 Monitor for infection pulmonary blood flow

 Emotional support – Ex: Ventricular Septal Defect,

Atrial Septal Defect, Patent
Ductus Arteriosus

CONGENITAL DISORDERS OF  Right to left shunting (cyanotic)

THE HEART
– Produces cyanosis/decreased
pulmonary blood flow
 – Ex: Tetralogy of Fallot,
Transposition of the Great
Arteries
GENERAL EFFECTS OF HEART
MALFORMATIONS
– Increased workload –
overloading of chambers
resulting in hypertrophy
– Pulmonary hypertension –
increased vascular resistance
resulting in dyspnea,
tachypnea, recurrent
respiratory infection
– Inadequate systemic cardiac
output resulting in exercise
intolerance and growth failure
– Arterial desaturation from
shunting of deoxygenated
blood directly into the systemic
circulation, resulting in
polycythemia, cyanosis,
clubbing of fingers, metabolic
acidosis, fatigue
– Production of murmurs
CHD - Left to Right Shunts
Defect Mechanism
VSD There is a hole within the
membranous or muscular
portions of the interventricular
septum that produces a left-to-
right shunt, more severe with
larger defects
ASD A hole from a septum secondum
or septum primum defect in the
inter-atrial septum produces a
modest left-to-right shunt
PDA The ductus arteriosus, which
normally closes soon after birth,
remains open, and a left-to-right
shunt develops.
VENTRICULAR SEPTAL DEFECT
(VSD)
 Abnormal opening between two
ventricles
 Pulmonary hypertension>decreased
cardiac output
 Manifestations
– Small - asymptomatic and
may close spontaneously
– Large – tachypnea,
tachycardia, poor feeding,
hepatomegaly, frequent URTI,
Failure to Thrive
 Hole within membranous or muscular
portions of IVS that produces a left-to-
right shunt, more severe with larger
defects
ATRIAL SEPTAL DEFECT (ASD)
 Abnormal opening between two atria
 Pathophysiology:
– Right Ventricular enlargement
and overload
– Elevated Pulmonary Artery
pressure
 Manifestations: usually
asymptomatic, may vary depending
on associated defects: Congestive
Heart Failure, Poor wt gain,
Decreased exercise tolerance
DIAGNOSIS OF ASD AND VSD
 2D echocardiogram
 Cardiac catheterization
 Murmurs
 May present heart failure
 Treatment:
 No medical management
 Increase calorie intake
 Surgery: usually before the 1st
year of life
 Complications
  Congestive Heart Failure

 Frequent Respiratory Tract

Infections
CORRECTIVE SURGERY: IF IN
 Failure to Thrive, Poor weight FAILURE!
gain
• OPEN HEART- defect is inside the
 Bacterial Endocarditis heart

• CLOSE HEART – defect is outside

the heart
PATENT DUCTUS ARTERIOSUS
ASD and VSD
(PDA)
- Surgical Dacron Patch
 Failure of the fetal structure to close, (open heart)
shunting blood from aorta to PA
- Non-surgical via
 Common in preterms less than 1500 cardiac catheter-
gms CARDIOSEAL
(Starflex/ Amplatzer)
 DA shunt blood from pulmonary
artery to aorta during intrauterine life PDA

 Persistence of ductus, which - Medical:

normally closes soon after birth, INDOMETHACIN
results in left-to-right shunt (prostaglandin
inhibitor)
 Lead to pulmonary hypertension.
- Surgical: LIGATION
Manifestations : via thoracotomy
(CLOSE HEART)
 Small to medium : asymptomatic
- VATS (Visual
 Large: CHF, decreased exercise Assisted
tolerance,poor feeding Thoracoscopic
Surgery)
 murmur à harsh, machinery-like at
upper L stenal border COA
 Bounding pulse - Resection with end to
end anastomosis
 Widened pulse pressure
- Balloon angioplasty
 Pulmonary congestion and RVH (non-surgical)

Aortic Stenosis
Treatment : - Aortic valvotomy
(OPEN HEART)
 Indomethacin – symptomatic
premature neonate – 0.1-0.25 - Balloon angioplasty
mgkgdose IV q12-24 H (non-surgical)
 Surgical ligation – via lateral Pulmonic Stenosis
thoracotomy
- pulm. valvotomy
 Coil occlusion if small, device closure (OPEN HEART)
if large
- Balloon angioplasty
(non-surgical)
 • gavage as necessary

MEDICAL/ NURSING MANAGEMENT Right to Left Shunts

Tetralogy of Fallot Pulmonary

stenosis results in
OBJ #1: PREVENT COMPLICATION- CHF right ventricular
1. IMPROVE CARDIAC OUTPUT hypertrophy and a
right-to-left shunt
CARDIAC GLYCOSIDE - DIGOXIN (increases across a VSD, which
strength of contraction) also has an overriding
aorta
2. PREVENT FLUID RETENTION &
PROMOTE

ELIMINATON OF EXCESS FLUIDS Transposition of

ACE INHIBITORS - CAPTOPRIL/ ENALAPRIL Great Vessels The aorta arises from
the right ventricle
DIURETICS- FUROSEMIDE and the pulmonary
trunk from the left
3. LOW SODIUM INTAKE
ventricle. A VSD, or
• LONALAC FORMULA ASD with PDA, is
needed for
• CLARIFICATION ON SOLIDS ALLOWED extrauterine survival.
There is right-to-left
• ***NOT ONLY THE SALTY FOODS ARE
shunting.
RICH IN SODIUM!
Truncus Arteriosus There is
incomplete separation
OBJ # 2: DECREASE OXYGEN DEMAND of the aortic and
pulmonary outflows,
• Cluster nursing care along with VSD, which
allows mixing of
• Quiet play activity
oxygenated and
• Control of environmental deoxygenated blood
temperature (avoid chilling) and right-to-left
shunting
• Decrease stress and anxiety level
(encourage mother to stay)

• Small frequent feeding TETRALOGY OF FALLOT

SYMPTOMS: Usually seen when

child is more active
0BJ 3: PREVENT RESPIRATORY because of increase
INFECTION oxygen demand

• Vitamin C-rich food • exertional dyspnea with cyanosis

(central)
• Avoid crowds
• activity induced “TET” spells relieved
• Promote immunization
by squatting

• clubbing of fingers
OBJ 4: PROMOTE NUTRITION
• stunted physical growth and delayed
• Small frequent feeding with development
nutritious allowed foods (low
sodium)
 • Pulmonic stenosis results in right  Treatment
ventricular hypertrophy and a right-
to-left shunt across a high VSD, which – Prostaglandin
also has an overriding aorta.
– Balloon atrial septostomy
• Most Common cause of Cyanotic
– Arterial switch
heart disease.
 The aorta arises from the right
Four Features :
ventricle and the pulmonic trunk from
 Displacement of the Aorta the left ventricle

 Right ventricular hypertrophy  A VSD, or ASD with PDA, is needed for

extrauterine survival
 Opening in the septum (VSD)
 R-to-L shunting
 Pulmonary stenosis
SYMPTOMS: In the Nursery
TREATMENT :
• PERSISTENT CYANOSIS INSPITE OF
• Palliative: BLALOCK-TAUSSIG VIGOROUS
CRYING
• Corrective: OPEN HEART
• HYPOXIA INSPITEOF OXYGEN
THERAPY
MEDICAL/ NURSING MANAGEMENT: TREATMENT :
1.Decrease O2 demand • medical: IV Prostaglandin E2
2. PROPANOLOL to prevent “tet” spells/ • Rashkind Procedure (Balloon
prophylactic antibiotic to prevent infective Septostomy)
endocarditis
• Surgical: Senning / Mustard
3. Monitor Hgb and Hct count- detects early Procedure (OPEN HEART)
POLYCYTHEMIA- phlebotomy as necessary.

4. Increase fluids/ Maintain IVF line as

necessary TRUNCUS ARTERIOSUS

5. Positioning during attacks- allow to squat/
knee-chest
6. Monitor activity tolerance/ LOC
 Both PA and aorta comes from a
single trunk that overrides both
ventricles
 there is cyanosis and congestion

 Tx: surgical correction is necessary

TRANSPOSITION OF THE GREAT
ARTERIES To repair:

 PA leaves the left ventricle while the  Close the VSD

aorta leaves the right ventricle
 Detach the PA
 there are 2 separate circulations
 Connect PA to the
 S/sx:
RV with a tube graft
– cyanotic at birth
TREATMENT :
– not compatible with life unless
there are other defects (PDA) - Rastelli Procedure :
that allow mixing of blood (closure of the VSD) with
excision of pulmonary
artery and aorta