CARDIOMYOPATHY

INTRODUCTION:- Cardiomyopathy include the subacute or chronic disorders of the myocardium.

It also refers to group of systemic diseases and processes that are toxic to or alter the myocardium. It is
an irreversible primary disease of the heart muscle. Cardiomyopathy along with myocardial layer can
also affect the endocardial, subendocardial, and pericardial layers.Heart muscle becomes enlarged or
rigid. Cardiomyopathy damages the muscle tone of the heart and reduces ability to pump blood to
body and can lead to heart failure, arrhythmias, fluid buildup specially in lungs or legs.

DEFINITION:-Cardiomyopathy as a heterogenous group of disease of myocardium, usually with

inappropriate ventricular hypertrophy or dilatation. [American Heart Association]
Or
Cardiomyopathy [CMP] constitutes a group of disease that directly affect the structural and functional
ability of the myocardium. [P. Hariprasath]

ETIOLOGY AND RISK FACTORS

 Hypertension- Hypertension causes vasoconstriction and left ventricle tries to work hard which
leads to compensatory hypertrophy.
 Heart valve problems- Incompetent or stenosis leads to increased workload on the left ventricle
and muscles are enlarged and causes hypertrophy and leads to cardiomyopathy. Heart loses
elasticity and efficiency.
 Heart tissue damage resulting into scarring from a previous heart attack
 Tachycardia causes impairment of the myocardium as workload increases on the heart to cope with
the reduced blood and hence oxygen supply and leads to hypertrophy.
 Metabolic disorders such as hypothyroidism or diabetes- Hypothyroidism cause diastolic
dysfunction and hemodynamic changes. Hypothyroidism causes bradycardia, mild diastolic
hypertension. Thyroid hormones act on the cardiac myocytes. This also causes mRNA
transcription of genes in contractile system. Thus altered thyroid hormones affect the functioning
of myocytes. Diabetes causes myocyte hypertrophy and also it causes the oxidative stress due to
impaired glycolysis and causes injury to the myocardial cells. Diabetes also causes autonomic
neuropathy and it leads to conduction problems.
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 Abuse of cocaine or antidepressant medication, such as tricyclic antidepressants- Cocaine
affects endothelial cells by stimulating the release of endothelin -1 a potent vasoconstrictor and
inhibiting the production of nitric oxide which is a major vasodilator. It stimulates cardiovascular
system and increases heart rate.
 Chemotherapy drugs:- Cytotoxic drugs damage the myocytes and cause their necrosis causing
disruption of conduction system leads to arrhythmia and cardiomyopathy.
 Viral infections:- Infection and inflammation causes the formation of scar tissue damaging heart
valves and cause regurgitation leading to cardiomyopathy.
 Deficiency of thiamine, calcium:- Anemia increases demand on heart muscles resulting in
compensatory hypertrophic cardiomyopathy.Hypocalcemia causes conduction abnormalities
leading to reduced ventricular functions.
 Hemochromatosis- Iron build up in the heart muscle causes not only toxicity and poisoning of
myocytes of heart but also cause myocardial ischemia and reperfusion injury. It is treated by
chelation therapy and phlebotomy.
 Sarcoidosis:- It causes inflammation and lumps of cells to grow in the heart and other organs
leading to inflammatory changes plus blood flow obstruction which may be a cause of
cardiomyopathy.
 Amyloidosis:- A disorder that causes the build-up of abnormal eosinophilic fibrous amyloid
protein which is otherwise healthy for heart but in excessive amount it leads to damage to the
blood vessels by plaque accumulation and disrupts the blood flow.
 Pregnancy complications- This is known as peripartum cardiomyopathy. The blood circulation
increases by around fifty per cent in pregnant women as a requirement to the growing foetus this
cause excessive increased workload on the left ventricle and may cause its hypertrophy causing the
cardiomyopathy.

CLASSIFICATION AND CAUSES OF CARDIOMYOPATHY:-

PRIMARY CARDIOMYOPATHY SECONDARY CARDIOMYOPATHY

The cause is known and secondary to another disease

 It is due to
unknown heart Dilated Restrictive
etiology. The Hypertrophic
 Cardiotoxic agents  Amyloidosis
only part  Hypertension
eg alcohol cocaine,  Sarcoidosis
involved is heart  Aortic
doxorubicin  Post radiation
muscles and stenosis
 Muscular dystrophy therapy
other cardiac  Genetic
 Hypertension  Endomyocardial
structures are
 Metabolic disorders fibrosis
unaffected.
 Myocarditis  Genetic
 It have genetic,
nongenetic or  Pregnancy  Ventricular
acquired cause.  Valve disease thrombus
 Ischemia [CAD]

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TYPES OF THE CARDIOMYOPATHIES:-
1. Dilated cardiomyopathy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy
4. Left ventricular non compaction cardiomyopathy
5. Arrhythmogenic right ventricular dysplasia

1. DILATED CARDIOMYOPATHY:- It is the most common type of the cardiomyopathyseen in

60% of all cases and the most common cause of the heart failure. Size of the ventricle cavity
enlarges with reduced cardiac output. Contractile function is decreased as myocardial tissue get
destroyed. It is characterized by diffuse inflammation and rapid degeneration of myocardial fibres
that result in ventricular dilation, impairment of systolic function and atrial enlargement. The
mortality rate for cardiomyopathy in male is twice that of females and for black 2.4 times that of
whites.

PATHOPHYSIOLOGY:-
Endotoxins from organism
Infecting organism(Coxsackie B virus)

Structural component

Plasma Monocyte macrophages Endothelial cells Neutrophils

Complement Cytokines Prostaglandin Lysosomes

activations  TNF Leukotrienes Oxygen free
and kinins  Interleukins Prostacyclin radicals
 Interferons Thromboxane Granulocyte
Platelet activating Endothelin colony
factors stimulating
Nitric oxide factors [G-CSF]

Release of endotoxins cause systemic inflammatory response

Further release of proinflammatory cytokines

 Tumour necrotic factor
 Interleukin-1

Endothelial damage
Myocardial depression

Decreased elasticity of the Intracellular lysosomes release digestive enzyme

blood vessels

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 Cell death, apoptosis leads to massive secretion of
proinflammatory substances such as TNF
Increased vascular resistance

Loss of myocytes, thinning of walls, increased

Increased demand on heart
size of chamber

Heart failure Blood moves more slowly from the ventricles

leading to clot formation

Stroke, lung emboli, deep vein thrombosis

CLINICAL MANIFESTATIONS:-
Cardiac symptoms:-
 Palpitation due to forceful contraction initially as compensation but later on contractility decreases
 Tachycardia or bradycardia depending upon the compensated or decompensated cardiomyopathy

 Peripheral edema and jugular venous distention due to increased hydrostatic pressure and venous
pooling

 Arrhythmias due to electrolyte imbalances and conduction failure due to loss of myocytes
 Decreased blood pressure and pulse pressure because of decreased stroke volume and cardiac
output
 S3 due to large amount of blood striking the compliant ventricle and S4 gallop due to large amount
of blood striking non-compliant ventricle.
 Moderate to marked cardiomegaly as compensation shown on chest X-ray
 Hepatomegaly due to portal hypertension secondary to compromised systolic function of heart.
 Atrioventricular valve incompetence specially mitral valve to due increased volume and pressure
in left atrium.
Respiratory manifestations:-
 Decreased physical capacity, Orthopnea, cough, paroxysmal nocturnal dyspnea due to
compromised tissue perfusion.
 Pulmonary crackles and edema due to fluid accumulation in alveoli.
 Pink tinged frothy sputum due to increased pulmonary congestion
Other manifestations:-
 Nausea, vomiting and anorexia due to irritation of vagus nerve thus hinder its normal functioning.
The chemicals produced due to cells death, apoptosis irritate the branches of vagus. And renal
failure leading to uremia may further lead to worsening of nausea and vomiting. [Mcheal A.
Smith ncbi.nlm.nih]
 Abdominal distention, right upper quadrant pain, secondary to systemic congestion

DIAGNOSTIC STUDIES:-Chest X-ray:- It may show cardiomegaly, pulmonary venous

hypertension and pleural effusion as less air filled spaces [i.e less black area] will be seen with more
white portion indicating fluid accumulation.

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 Doppler echocardiography:- It help to distinguish between dilated cardiomyopathy and other
structural abnormalities.
 ECG:- To rule out tachycardia and bradycardia and kind of dysrhythmia i.e atrial flutter[sawtooth
ECG i.e many P wave in between of QRS complex], fibrillation[absence of P wave and narrow
QRS complex], ventricular tachycardia etc. and type of conduction disturbances egComplete heart
block showing independent P wave and QRS complex.
 B type natriuretic peptide:- Increased value more than 100pg/ml indicate the heart failure due to
myocardia injury.
 Cardiaccatheterization to rule out the coronary artery disease.
 Endomyocardial Biopsy:- Sample can be taken at the time of catheterization to detect viral and
bacterial antigen in myocardial tissue. It can also help in diagnosis of amyloidosis,
hemochromatosis.

MANAGEMENT: Goals of management are:

 To reduce myocardial workload by using diuretics and vasodilators.
 Improve ventricular pump performance by Angiotensin converting enzyme inhibitors and positive
inotropes
 To maintain perfusion of vital organs.
 To prevent heart failure.

Supplemental oxygen
PHARMACOLOGICAL MANAGEMENT:
 Angiotensin converting enzyme inhibitors: e.g. Captopril, Benazepril and Enalapril
 Nitrates:- Enhance circulation to heart muscles by vasodilation. E.g. Nitroprusside, Nitroglycerine
 B-type Natriuretic peptide:- Reduces vascular resistance and increase natriuresis i.e excretion of
sodium in urine. e.g. Nesiritide
 Beta-adrenergic blockers:- To reduce the heart rate thus lowering the workload on myocardium.
E.g. Atenolol, Metoprolol, Propranolol
 Diuretics:- e.g. Furosemide, Torsemide (loop diuretics), Spironolactone (potassium sparing
diuretics)
 Positive inotropes: Digoxin, Dopamine, Dobutamine, milrinone etc. Digoxin has narrow window
of therapeutic index, serum level to be monitored and keeping range between 0.5-0.8ng/ml.
 Angiotensin II receptor blockers:- e.g. Losartan, Telmisartan, Valsartan
 Antidysrhythmic drugs: e.g. Amiodarone, diltiazem, Lidocaine.
 Anticoagulation Therapy eg Enoxaparin to prevent clot and emboli. Warfarin for long-term
anticoagulant therapy

NON-PHARMACOLOGICAL MANAGEMENT:- Dilated cardiomyopathy does not response to

pharmacological treatment and client experiencemultiple episodes of heart failure.
 Ventricular assist device:- Implantable cardioverter defibrillator used to maintain the electrical
activity of heart thus keeping the heart paced at sinus rhythm. They can be implanted to overcome
the conduction block.

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 Heart transplantation: When heart is irreversibly damaged and no longer function adequately,
cardiac transplantation is done. Cardiac transplantation has become an accepted therapeutic
procedure and shows 5 year survival of greater than 70% cases. 50% of heart transplant are
performed for treatment of cardiomyopathies.

2. HYPERTROPHIC CARDIOMYOPATHY:- Hypertrophic cardiomyopathy also known as

idiopathic hypertrophic subaortic stenosis, is asymmetric left ventricular hypertrophy without
ventricular dilationcharacterized by diastolic dysfunction.It can be of two types:-
a. Obstructive:-Septum thickens and bulges into the left ventricle. This bulge blocks flow of blood
out of the ventricle. It is known as hypertrophic obstructive cardiomyopathy or asymmetric septal
hypertrophy.
b. Non-obstructive:- Thickened heart muscle does not block the flow of blood out of the ventricle.
The entire ventricle may become thicker or only at the bottom of the heart i.eapical hypertrophy.
The for main characteristics of hypertrophic cardiomyopathy are:-
a. Massive ventricular hypertrophy
b. Rapid forceful contraction of left ventricle
c. Impaired relaxation i.e diastole dysfunction
d. Obstruction to aortic outflow

ETIOLOGY:- It occur due to mutations in genes encoding several cardiac sarcomere proteins.60% -
80% of cases are inherited through autosomal dominant transmission.

PATHOPHYSIOLOGY:-

Due to mutation in genes encoding sarcomere proteins i.e cardiac troponin

Myectom
y Loss of normal parallel alignment of myocytes i.e myocardial disarray

Asymmetrical septal hypertrophy Electrical conduction abnormalities

Left ventricular outflow Diastolic dysfunction Antiarrhyt

Dysrhythmias
obstruction due to inability to relax hmics, β
blockers
Increased HR,
Subaortic stenosis
Decreased blood filling Atrial fibrillation,
in left ventricle ventricular
Reduced cardiac output fibrillation and
Venous pooling behind ventricular
left ventricle tachycardia etc If not
Angina may occur due
to compression of treated
AV
microvascular of Increased hydrostatic pressure
myocardium pacing
leads to fluid shift
Diuretics,
vasodilators
Increased jugular 6 pressure,
pulmonary congestion,
impaired gaseous exchange,
shortness of breath
CLINICAL MANIFESTATIONS
 A systolic murmur heard at the lower left sternal border and apex. The murmur may occur with
obstruction i.e Left ventricle out flow obstruction or without obstruction.
 Dyspnea is the most common symptom and appears to be related to the elevated left ventricular
end-diastolic pressure.

 Fatigue, dizziness, syncope due to decreased cardiac output.

 Chest pain, , palpitations, to increased myocardium mass.

 Tall precordial R waves also reflect hypertrophy.

 Increased HR, Atrial fibrillation, ventricular fibrillation and ventricular tachycardia are the most
common forms of dysrhythmias.

DIAGNOSTIC EVALUATION:-
 Displace apical pulse to lateral due to increase in size of myocardium
 S4 heart sound and systolic ejection murmur between apex and the sternal border at 4 th intercoastal
space.
 ECG finding indicating ventricular hypertrophy i.e increased amplitude of R waved due to forceful
contraction.
 Echocardiogram showing thick ventricular wall.

MEDICAL MANAGEMENT:-
Pharmacological management:-
 Beta-adrenergic blockers:- To reduce the heart rate thus lowering the workload on myocardium.
E.g. Atenolol, Metoprolol, Propranolol
 Antidysrhythmic drugs: Used to treat the various arrhythmias. e.g. Amiodarone, diltiazem,
Lidocaine.
 Calcium channel blockers:- To slow down the movement of calcium in to cells reducing
contractility of heart.eg Verapamil, Diltiazem
 Angiotensin II receptor blockers:- e.g. Losartan, Telmisartan, Valsartan
 Diuretics:- e.g. Furosemide, Torsemide (loop diuretics), Spironolactone (potassium sparing
diuretics)

Non pharmacological management;-

 Atrioventricular pacing:- By pacing the ventricle from apex of the right ventricle, septal
depolarization occur first, allowing septum to move away from left ventricular thus reducing the
degree of obstruction to out flow.

 Myectomy:- Indication for the surgery include severe symptoms refractory to therapy with
marked obstruction to aortic flow. Surgery involve incision of hypertrophied septal muscles and

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 resection of some hypertrophied ventricular muscle. It result in symptomatic improvement and
increased physical tolerance.

 Alcohol induced percutaneous septal myocardial ablation[PTSMA]:- In this procedure alcohol

is administered to first septal artery branching off the left descending artery causes ischemia and
septal wall myocardial infarction. Its most common complication is conduction disturbancei.e in
10% of cases. Alcohol ablation is considered inferior treatment to myectomy there is need for
reintervention and pacemaker implantation however the cardiac death and mortality were found
low. [Pieter A. 2017, Journal of American College of Cardiology]

3. RESTRICTIVE CARDIOMYOPATHY:- It is the least common type of the cardiomyopathy. It

is the disease of heart muscle that impair the diastolic feeling and stretch as ventricles become
stiff and rigid due to replacement of the normal heart muscle with the abnormal tissue such as
scar tissue resulting in poor ventricle compliance.Systolic function remain unaffected.In end stage
restrictive cardiomyopathy the clinical manifestations are indistinguishable from chronic
constrictive pericarditis. So careful clinical diagnosis required to ensure the treatment options as
surgery can be opted for retrieve cardiomyopathy.

EPIDEMIOLOGY
Restrictive cardiomyopathy in India is sporadic disease, rare and occur in young. Prognosis of
restrictive is still worse than other cardiomyopathies.
[M. Kapoor, Journal of cardiovascular sciences]

ETIOLOGY:- The number of the pathological processes that are involved in the development of the
cardiomyopathy that are:-

Myocardial causes Endomyocardial causes

Non-infiltrative Infiltrative Endomyocardial fibrosis

 Idiopathic  Amyloidosis  Hypereosinophilic syndrome
 Familial  Sarcoidosis  Metastatic malignancy
 Hypertrophic  Gaucher’s disease  Radiation
 Scleroderma  Storage diseases  Chemotherapy toxicity
 Hemochromatosis  Drugs:-serotonin,
 Fabry’s disease methylsergide

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PATHOPHYSIOLOGY

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Other manifestations:-
 Physical intolerance, orthopnea, syncope and angina on exertion due to decreased coronary flow
 Palpitations as compensation
 Auscultation reveals AV valve regurgitation.

 Normal left ventricular systolic impulse and a prominent S3.

DIAGNOSTIC EVALUATIONS:-
 Chest X-ray:- In restrictive cardiomyopathy the X ray may be normal and may show hypertrophy.
Pleural effusion may be seen in patients with progression to heart failure.
 Electrocardiography:- May indicate tachycardia at rest, dysrhythmia like dysrhythmia are atrial
fibrillation indicated by irregular rhythm, absence of distinct P wave, presence of f waveand
atrioventricular block.

 Echocardiography:- Left ventricle normal sized with thickened wall, and dilated atria.

 Endomyocardial Biopsy:- To detect viral and bacterial antigen in myocardial tissue. It can also
help in diagnosis of amyloidosis, hemochromatosis.
 Blood tests:- To measure the iron levels[11-14%] to rule out hemochromatosis. Blood test to
measure B-type natriuretic peptide [FDA-<100pg/ml], a protein produced in the heart. The blood
level of BNP might rise when heart is in heart failure, which is a common complication of
cardiomyopathy.

MANAGEMENT:- There is no specific intervention for restrictive cardiomyopathy, so therapy is

supportive. It includes:-
 Oxygen therapy
 Diuretics:- e.g. Furosemide, Torsemide (loop diuretics), Spironolactone (potassium sparing
diuretics)
 Corticoids:- To reduce the inflammation in case of sarcoidosis. Eg Budesonide
 Vasodilators:- To reduce the systemic resistance. Eg Nitroprusside
 Angiotensin enzyme inhibitors:- . Captopril, Benazepril and Enalapril

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 Phlebotomy and chelation for hemochromatosis. One unit of blood i.e 350ml can be removed
usually for hemochromatosis 250ml of blood is removed and that help to reduce 250mg of iron.
After phlebotomy clients are advised to drink plenty of fluid to restore the blood volume.
Chelation therapy include several drugs that are deferoxamine, penicillamine dimercaprol. These
agents bind with the iron and help in excreting it out of body.
 Anticoagulant therapy if not contraindicated. Eg enoxaparin
 Digoxin:- Not used most oftenly but may be used in some cases.

SURGICAL MANAGEMNT:-
1. Implantable cardioverter-defibrillator:- Client with restrictive cardiomyopathy have
dysrhythmias refractory to antiarrhythmic drugs due to impaired conduction that can not be
restored. So ICD is inserted to maintain the rhythm of heart. This device monitors heart rhythm
and delivers electric shocks when needed to control abnormal heart rhythms.
2. Intra-aortic balloon pump:- It decreases the work of the heart during contraction.
3. Myectomy

4. Cardiac transplant;- Indications and contraindications for cardiac transplant are:-

INDICATIONS CONTRAINDICATIONS

 New York Heart Association [NYHA] class  Active systemic infections

III and IV symptoms  Active systemic disease egcollagen vascular
 Dilated cardiomyopathy disease.
 Ischemic cardiomyopathy  Active malignancy
 Ejection fraction less than <20%  Ongoing history of substance abuse eg
 Intractable angina or malignant cardiac alcohol, tobacco, drugs
dysrhythmia

DIFFERENCE BETWEEN DILATED, AND RESTRIVE AND HYPERTROPHIC

CARDIOMYOPATHY:-

Characteristic Dilated Restrictive Hypertrophic

Manifestations  Fatigue and  Dyspnea, fatigue  Dyspnea, angina
weakness  Right side heart  Fatigue
 Systemic or failure manifestations  Syncope
pulmonary
of systemic disease eg  Palpitations
emboli
hemochromatosis
 Heart failure
particularly left
sided
Physical  Moderate to  Mild to moderate  Mild cardiomyopathy
examination severe cardiomegaly S3, S4
cardiomegaly S3,  Apical systolic thrill
S4  AV valve and heave
regurgitation

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  Mitral valve  Increased inspiratory  Brisk carotid upstroke,
regurgitation v enous pressure systolic murmur that
manifested by increases with Valsalva
kussmaul’s sign maneuver

Chest study x-ray  LV enlargement  Mild cardiac  Mild to moderate

enlargement cardiac enlargement
 Pulmonary
venous  Pulmonary venous  Left atrial enlargement
hypertension hypertension

Electrocardiogra  Sinus tachycardia  Low voltage  Left ventricular

m hypertrophy
 ST and T wave  Intraventricular
abnormalities conduction defect  ST and T wave
intraventricular abnormalities
conduction defect
 Atrial and ventricular
dysrhythmia

4. LEFT VENTRICULAR NON COMPACTION CARDIOMYOPATHY :- It is also known as

fetal myocardium, honeycomb myocardium, hyper trabeculation syndrome. It occurs when
left ventricle does not develop correctly cardiac muscle in the left ventricle become thick and
appears spongy. Left ventricular noncompaction can be diagnosed at birth or adulthood. Two-
thirds of individuals with left ventricular noncompaction develop heart failure.

Epidemiology:- Left ventricular noncompaction  affect 8 to 12 per 1 million individuals per year.

Causes:- Mutation in MYH7 and MYBPC3 mutation in these genes causes 30% cases. These genes
codes for proteins that play a role in structures within muscle fibers called sarcomeres, necessary for
muscles to contract.
Clinical Manifestations:- Some individuals with left ventricular noncompaction experience no
symptoms at all where- as others have heart problems that include:-
 Sudden cardiac death
 Abnormal blood clots
 Arrhythmia
 Palpitations
 Exercise intolerance
 Dyspnea
 Fainting
 Lymphedema

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Diagnosis:- Echocardiography, Cardiac magnetic resonance imaging and computed
tomography to rule out the trabeculation.

Management:-
 Internal cardiac defibrillator to maintain the adequate cardiac output.
 Beta blockers eg Metoprolol to reduce the heart rate.
 Anticoagulation therapy eg Low molecular weight heparin 0.4mg S/c to reduce the risk of
stroke and other complications of thrombus formation.

5. ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA ;- It is also called as the right

ventricular cardiomyopathy. It is a rare type of cardiomyopathy. It occurs when muscle tissue in
the right ventricle destroyed and are replaced with scar tissue. This disrupts the heart's electrical
signals and causes arrhythmias. ARVD affects young adults and can cause sudden cardiac arrest.

COMPLICATIONS OF CARDIOMYOPATHY
 Heart failure:- Persistent increase in the workload of left ventricle may lead to heart failure.The
goal of the cardiomyopathy treatment is to prevent the development of heart failure.
 Heart valve regurgitation:- Increased ventricle pressure causing increased pressure on valve
leading to regurgitation.
 Edema:- Pulmonary edema and peripheral edema develop as result on increased hydrostatic
pressure and fluid shift.
 Arrhythmia:- Changes in structure and conduction leads to arrhythmia that may lead to asystole
and sudden death.
 Sudden cardiac arrest:- Dilated cardiomyopathy causes heart to suddenly stop beating.
 Emboli and thrombus:- Pooling of blood in left ventricle leads to formation of clots and emboli
that can cause stroke, pulmonary embolism.

NURSING MANAGEMENT:-
Nursing assessment:-
History taking- Obtain complete bio-demographical history related to:-
 Age because hypertrophic cardiomyopathy occur most commonly with increased age though it
may occur at any age.
 Gender as men are at greater risk of having dilated cardiomyopathy than women.
 Occupation as certain occupation predisposes the individuals to develop the cardiovascular
problems. Eg working in coal mines.
 Obtain complete past and present medical and surgical history.
 Review any medication history and complete family history to see its genetic predisposition.
 Obtain present chief complaints.
 Evaluate etiologic factors, such as alcohol abuse, pregnancy, recent infection, or history of
endocrine disorders.

Physical Assessment:
 Cardiovascular assessment:Inspection: Chest heaves specially in hypertrophic cardiomyopathy,
jugular venous distension may be seen due to increased pressure in vein.

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 Palpation: Increased heart size is common in patient with dilated cardiomyopathy. This cardiac
enlargement is detected by precordial palpation, with the apical pulse displaced laterally to the left
and downward.
 Percussion: Dull sound is percussed around precordial area due to accumulation of fluid. Pleural
effusion may be suspected.
 Auscultation: Determine rate, rhythm and characteristics of pulse.
 The pulse rate is usually elevated in response to low cardiac output.
 Pulsus alternans is characterized by an altering strong and weak pulse with normal rate and
interval. Pulsus alternans is associated with altered functioning of the left ventricle causing
variance in left ventricle preload.
 Third heart sound may occur that is associated with reduced ejection fraction and impaired
diastolic function. But not auscultated in hypertrophic cardiomyopathy.
 Fourth heart sound is reflection of decreased ventricular compliance.Common in three of the
cardiomyopathies.
 Pulmonary examination: Persistently elevated pulmonary artery pressures result in the
transudation of fluid from the capillaries into the interstitial spaces and alveolar spaces. The
accumulated fluid results in pulmonary crackle indicative of progressive heart failure.

1. Heart valve regurgitation:- Increased ventricle pressure causing increased pressure on valve
leading to regurgitation.
2. Edema:- Pulmonary edema and peripheral edema develop as result on increased hydrostatic
pressure and fluid shift.
3. Arrhythmia:- Changes in structure and conduction leads to arrhythmia that may lead to
asystole and sudden death.
4. Sudden cardiac arrest:- Dilated cardiomyopathy causes heart to suddenly stop beating.
5. Emboli and thrombus:- Pooling of blood in left ventricle leads to formation of clots and
emboli that can cause stroke, pulmonary embolism.
6. NURSING MANAGEMENT:-
7. Nursing assessment:-
8. History taking- Obtain complete bio-demographical history related to:-
9. Age because hypertrophic cardiomyopathy occur most commonly with increased age though
it may occur at any age.
10. Gender as men are at greater risk of having dilated cardiomyopathy than women.
11. Occupation as certain occupation predisposes the individuals to develop the cardiovascular
problems. Eg working in coal mines.
12. Obtain complete past and present medical and surgical history.
13. Review any medication history and complete family history to see its genetic predisposition.
14. Obtain present chief complaints.
15. Evaluate etiologic factors, such as alcohol abuse, pregnancy, recent infection, or history of
endocrine disorders.
16. Physical Assessment:
17. Cardiovascular assessment:Inspection: Chest heaves specially in hypertrophic
cardiomyopathy, jugular venous distension may be seen due to increased pressure in vein.

14
18. Palpation: Increased heart size is common in patient with dilated cardiomyopathy. This
cardiac enlargement is detected by precordial palpation, with the apical pulse displaced
laterally to the left and downward.
19. Percussion: Dull sound is percussed around precordial area due to accumulation of fluid.
Pleural effusion may be suspected.
20. Auscultation: Determine rate, rhythm and characteristics of pulse.
21. The pulse rate is usually elevated in response to low cardiac output.
22. Pulsus alternans is characterized by an altering strong and weak pulse with normal rate and
interval. Pulsus alternans is associated with altered functioning of the left ventricle causing
variance in left ventricle preload.
23. Third heart sound may occur that is associated with reduced ejection fraction and impaired
diastolic function. But not auscultated in hypertrophic cardiomyopathy.
24. Fourth heart sound is reflection of decreased ventricular compliance.Common in three of the
cardiomyopathies.
25. Pulmonary examination: Persistently elevated pulmonary artery pressures result in the
transudation of fluid from the capillaries into the interstitial spaces and alveolar spaces. The
accumulated fluid results in pulmonary crackle indicative of progressive heart failure.
26. Activity intolerance related to cardiac insufficiency and pulmonary congestion as evidenced
by dyspnea on exertion, shortness of breath, weakness and inability to perform activity of
daily living.
Expected outcome: The client will be able to perform the activities of daily living with less assistance
as evidensed by no or minimal exertion on physical activities.
Interventions:
 Encourage alternate rest and activity periods to reduce cardiac workload.
 Provide calming diversionary activities to promote relaxation to reduce oxygen consumption and
to relieve dyspnea and fatigue.
 Teach patient and significant other techniques of self-care that will minimize oxygen consumption
e.g. self-monitoring and pacing techniques for performance of activities of daily living.
Evaluation:- Improved daily living activities performance as evidensed by verbal report of client of
less fatigue.

HEALTH EDUCATION:
LIFE STYLE MODIFICATION:
 Educate patient to quit smoking as smoke injure the blood vessels and increase the systemic
resistance thus expose individual more to heart failure.
 Educate patient to maintain weight. Educate patient to notify heath care provider if he gain 3 or
more pounds in one day and 5 or more pounds in one week as this is sign of heart failure.
 Client is educated to notify the tightening of fingers in morning, periorbital edema, nocturia
suggestive of fluid accumulation and heart failure.
 Patient is educated to avoiding and limiting alcohol intake. Alcohol deteriorate the cardiac
functioning.
 Educated to avoid or limiting caffeine such as not more than a cup or two cup of coffee. Coffee
increases the heart work load.

15
ON MEDICATION:
 Follow a strict therapeutic regimen to avoid the chances of the heart failure.
 Take diuretics in day time to avoid the sleep disturbances at night.
 Always take the blood pressure reading before taking antihypertensive medicine, as blood pressure
readings vary depending upon the time of day.
 Educate patient to take pulse rate each day before taking medications and withhold medication
(digoxin used in some cases of restrictive cardiomyopathy) if heart rate is less than 60 b/min.Report
signs of digoxin toxicity anorexia, nausea, vomiting, yellow vision.
 Educate patient regarding sign and symptoms of digitalis toxicity such as anorexia, nausea, vomiting,
blurred vision. Visual halos, bradycardia, drowsiness etc.
 Discuss the signs and symptoms of the disease process, precipitating factors, and treatment. Stress
to patient the importance of treating disease symptoms and its complete treatment.
 Avoid over the counter medicines that may increase the heart workload and causing complication
as heart is already non-compliant.
 Antibiotic prophylaxis to be taken before any procedure to prevent the endocarditis.

ON DIET:
 Patient is educated to eat heart-healthy diet such as fruits and vegetables, whole grains, low fat
dairy products, skinless poultry fish, nuts and legumes. Heart- healthy fish such as salmon,
herring and tuna. These types of fish are high in omega- 3 fatty acids, which can help to lower
the cholesterol.
 Suggest available cookbooks (AHA) that may assist in planning and preparing foods.
 Patient is educated to limit saturated fat, trans fat, red meat etc.
 Unless fluids are restricted patient is encouraged to drink 6-8 glasses of water a day to maintain the
hydration.
 Patient is educated to avoid high sodium foods such as canned soups, processed meats, cheese,
frozen meals if hypertensive as in hypertrophic cardiomyopathy where-as salty soup may be
allowed as patient is on continuous on diuretics and antihypertensive medicines that may leads to
hyponatremia.
 American Heart Association recommended that hypertensive patient should consume <1.5 gm of
sodium per day that mean less than half of teaspoon of table salt.
 Potassium to be supplemented when on loop diuretics educate client to eat potassium rich foods
like banana, oranges, cooked spinach [but to be avoided in hemochromatosis],dry fruits etc.
 Client with hemochromatosis disease educated to avoid the iron rich food like green leafy
vegetables, spinach, lentil, nuts, dried fruits, pomegranate etc. and include citrus fruits that to
lower the clotting risk and boost immunity.
 Avoid heavy meals that may increase the mesenteric blood supply hence depleting the vital organs
from normal blood supply. Eg patient may develop syncope, angina etc. And avoid gas forming
foods eg cabbage, turnipetc as abdominal distention may also cause cardiac compression that may
compromise the function of heart.

ON EXERCISE:
 Patient is educated to perform regular but light exercises and avoidance of strenuous exercises.

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 Patient is educated to schedule physical activity at the same time every day so it becomes a regular
part of lifestyle.
 Patient is educated to manage stress by sit quietly for 15-20 min. and deep breathing, meditation
and yoga.
 Patient is educated to control anger and reducing stress by counting to 1 to 10 before responding.

ON FOLLOW UP:
 Patient and family members are educated to report any changes in patient’s condition such as
difficulty in breathing, especially with exertion, hacking cough, fatigue, weakness, dizziness etc.
 Patient and family members are educated how to monitor blood pressure at home.
 Encourage follow-up visits for control of diabetes, hypertension, and hyperlipidemia as these
condition may predispose the client to heart failure.
 Patients monitor their own blood pressure at home. Keep a log and to record blood pressure at the
same time each day. As BP reading may vary depending upon the time of the day.
 Take cuff to doctor to ensure that they are taking readings correctly and that the machine is
calibrated accurately.
 Patient is educated to avoid tight socks or stockings as this will impaired the blood flow results in
clot formation.
 Family members are demonstrated with cardiopulmonary resuscitation because sudden cardiac
arrest is possible.

EDUCATION REGARDING ICD:-

 Check pulse daily and note for any variation in pulse rate.
 Avoid electromagnetic inferences including household appliances, security system, external
electrical equipment, mobile phones.
 Consult physician before planning for pregnancy as it contraindicated mostly but studies have
proved the success of delivery with ICD.
 Regularly interrogate the device to know about its function, battery life and need.

REFERENCES

1. Woods S.L.et al. Cardiac nursing. Lippincott Williams & Wilkins. 2000
2. Lippincott Manual of Nursing Practice. 8th edition. Lippincott Williams & Wilkins Publishers;
2010. p. 68, 328-332, 361.
3. Smeltznner SC, Bare BG, Hinkle JL, Cheever KH. Brunner &Suddarth’s Textbook of Medical-
Surgical Nursing. 11th edition. Lippincott Williams & Wilkins Publishers; 2008. p. 789-805.
4. Longo et al.Harrisons principles of internal medicine.18(2):2012
5. Chintamoni Lewis LS et al.lewis’s medical surgical nursing:assessment and management of
clinical problems.7. New delhi.ELSEVIER;2011:
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6. https://www.ncbi.nlm.nih.gov/gtr/conditions/C1858725/

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