Nursing management of a patient with cardiomyopathy

CARDIOMYOPATHY Cardiomyopathy (CMP)is a primary disorder of the heart muscle that

causes abnormal myocardial performance and is not the result of disease or dysfunction of
other cardiac structures. ( K.V. Krishnadas)

CARDIOMYOPATHY A heterogeneous group of diseases of the myocardium

associated with mechanical and/or electrical dysfunction, which usually (but not
invariably) exhibit inappropriate ventricular hypertrophy or dilatation, and are due to
a variety of etiologies that frequently are genetic. ( Hurst’s text book of cardiology)

RELATED ANATOMY AND PHYSIOLOGY • Cardiac muscle (heart muscle)

involuntary striated muscle • The myocardium is the muscle tissue of the heart, and
forms a thick middle layer between the outer epicardium layer and the inner
endocardium layer

INCIDENCE • Dilated cardiomyopathy, the most common form, affects five in

100,000 adults and 0.57 in 100,000 children. • Hypertrophic cardiomyopathy, the
leading cause of sudden death in athletes, with an incidence of one in 500 persons. •
Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy are
rare, and their diagnoses require a high index of suspicion.

CLASSIFICATION OF CARDIOMYOPATHIES

WHO classification of cardiomyopathy(1995)

American Heart Association classification of cardiomyopathy

Primary secondary

Secondary cardiomyopathy • Infiltrative • Storage • Toxicity • Inflammatory •

Endocrine • Nutritional deficiencies • Consequence of cancer therapy • Autoimmune/
collagen

1. 10. Hypertrophic Cardiomyopathy

2. 11. Hypertrophic Cardiomyopathy • It is characterized by inappropriate left
ventricular hypertrophy, decreased cardiac output and outflow obstruction. •
Hypertrophic subaortic stenosis
3. 12. Common causes • Genetic(autosomal dominant) or familial • Hypertension •
Ischemia( coronary artery disease) • Aortic stenosis
4. 13. PATHOPHYSIOLOGY Four main characteristics • Massive ventricular
hypertrophy • Rapid, forceful contraction of the left ventricle. • Impaired relaxation(
diastole) • Obstruction to aortic outflow
5. 14. CLINICAL MANIFESTATIONS
6. 15. • Rapid, pounding heartbeat. • Chest tightness or pressure. • Fluid retention
resulting in swollen feet or ankles or unexplained weight gain.
7. 16. Diagnostic studies • History and physical examination • Palpation and auscultation
of the chest. • ECG findings • Echocardiogram • Chest X ray • Cardiac catheterization
8. 17. Management of hypertrophic cardiomyopathy
9. 18. GOAL • Improve ventricular filling. • Reduce ventricular contractility • Relieve
left ventricular outflow obstruction.
10. 19. Management of cardiomyopathy Lifestyle changes • Reduced alcohol
consumption, weight loss, exercise, smoking cessation, and a low-sodium diet.
11. 20. Management of cardiomyopathy • ᵦ adrenergic blockers • Calcium channel
blockers • Antidysrrhythmics • Implantable Cardioverter Defibrillator • Dual-
Chamber Pacing
12. 21. Symptomatic management Percutaneous Transluminal Septal Myocardial
Ablation(PTSMA)
13. 22. Surgical management • Ventriculomyotomy and myectomy
14. 23. Arrhythmogenic Right Ventricular Cardiomyopathy/ Dysplasia
15. 24. • It predominantly involves the right ventricle with progressive loss of myocytes
and fibrofatty tissue replacement, resulting in regional (segmental) or global
abnormalities. • Genetic defects of the part of the heart muscle, desmosome. • It
shows autosomal dominant inheritance
16. 25. • 80% of individuals present with syncope, palpitations or sudden cardiac death. •
Noninvasive tests • 12-lead ECG, signal-average ECG, echocardiography, right
ventricular angiography, CMR imaging, CT, and electroanatomic mapping of the
right ventricle
17. 26. • Endomyocardial biopsy Treatment • includes lifestyle alterations (i.e., avoiding
intense physical activity), antiarrhythmic drugs, and implantable cardioverter-
defibrillators in high-risk patients. • Cardiac transplantation
18. 27. ION CHANNELOPATHIES • Brugada syndrome • Long QT syndrome • Short
QT syndrome • SUNDS( Sudden Unexplained Nocturnal Death Syndrome) •
Idiopathic ventricular fibrillation.
19. 28. Brugada Syndrome • Associated with mutations in the gene (SCN5A)that encodes
for the sodium ion channel in the cellmembranes of the muscle cells of the heart (the
myocytes).
20. 29. • A distinctive ECG pattern consisting of right bundle-branch block and coved
ST- segment elevation in the anterior precordial leads (V1–V3).
21. 30. Management • Treatment of underlying arrhythmias • Implantable cardioverter
defibrillator • Quinidine class Ia antiarrhythmic.
22. 31. DILATED CARDIOMYOPATHY
23. 32. DILATED CARDIOMYOPATHY It is characterized by dilatation of the
ventricles with subsequent impairment of systolic function. Most common
cardiomyopathy
24. 33. ETIOLOGY • Idiopathic • Autosomal dominant , recessive and X- linked modes
of inheritance. • Gene mutation • Inflammatory and Infectious Myocarditis •
Autoimmunity
25. 34. OTHER CAUSES • Cardiotoxic agents- alcohol, cocaine, doxorubicin(
adriamycin) • Hypertension • Ischemia ( coronary artery disease) • Metabolic
disorders • Muscular dystrophy • Pregnancy • Valve disease
26. 35. PATHOPHYSIOLOGY Diffuse inflammation and rapid degeneration of
myocardial fibers. Ventricular dilation Cardiomegaly Impairment of systolic function
(contractile dysfunction) Atrial enlargement and stasis of blood in the left ventricle.
27. 36. Heart becomes weak and the chambers get large. Heart cannot pump enough
blood out to the body Decreased cardiac output
28. 37. • Chamber enlargement frequently leads to a dilation of the valvular orifice. •
Intracavitary thrombi located in the ventricular apices
29. 38. CLINICAL MANIFESTATIONS • Decreased exercise capacity • Fatigue •
Dyspnea at rest • Paroxysmal nocturnal dyspnea • Orthopnea
30. 39. As the disease progresses the patient may experience • Dry cough • Palpitations •
Abdominal bloating • Nausea • Vomiting • Anorexia
31. 40. Signs • Irregular heart rate with an abnormal S3 and/or S4 • Tachycardia or
bradycardia • Pulmonary crackles • Edema • Weak peripheral pulses
32. 41. • Pallor • Hepatomegaly • Jugular venous distension • Heart murmurs •
Dysrhythmias
33. 42. DIAGNOSTIC STUDIES • Doppler echocardiography • Chest X-Ray • ECG •
Elevated serum BNP( if heart failure) • Cardiac catheterization
34. 43. EMB (Endomyocardial biopsy)
35. 44. • Biochemical testing • Endocrine function • Radionuclide imaging (radionuclide
ventriculography) • Cardiac MRI • Multidetector computed tomography
36. 45. MANAGEMENT Goal • Enhance myocardial contractility • Decrease afterload.
37. 46. MANAGEMENT • Nitrates (eg: Nitroglycerin) • ACE inhibitors( Eg: captopril) •
ᵦ adrenergic blockers( Eg: metoprolol) • Aldosterone antagonists ( Eg: spironolactone)
• Diuretics to maintain the volume balance. • Cardiac glycosides( Eg: Digoxin)
38. 47. MANAGEMENT • Antiarrhythmics( Eg: Amiodarone) • Anticoagulation therapy
• Treatement of underlying disease process. • Continuous infusion of dobutamine
followed by aggressive diuresis.
39. 48. • Implantable cardiac defibrillators. • Biventricular pacemakers.
40. 49. SURGERY • Left ventricular reconstruction • Implantation of external restraint
devices
41. 50. • Left ventricular assist devices • Heart transplantation
42. 51. EMERGING SPECIFIC THERAPIES • Agents to eradicate persistent viral
infections and immunomodulatory agents. • Stem cells for cardiac regeneration and
gene therapy approaches are in clinical trials.
43. 52. RESTRICTIVE CARDIOMYOPATHY
44. 53. Restrictive cardiomyopathy • It is a disease of the heart muscle that impairs
diastolic filling and stretch. • Systolic function remains unaffected. • Least common of
the cardiomyopathic conditions. • The heart chambers are unable to fill with blood
because the heart muscle is stiff.
45. 54. ETIOLOGY • Amyloidosis • Scarring of the heart from an unknown cause. •
Myocardial fibrosis • Hypertrophy and infiltration
46. 55. Secondary causes includes • Endomyocardial fibrosis • Sarcoidosis • Neoplastic
tumor • Ventricular thrombus • Fibrosis of different etiology • Radiation to the thorax
47. 56. PATHOPHYSIOLOGY Increase in stiffness of the ventricular walls Impaired
diastolic filling of the ventricle Reducing preload and end-diastolic volume Heart
failure
48. 57. As the disease progresses Systolic dysfunction
49. 58. CLINICAL MANIFESTATIONS Classic symptoms of restrictive CMP are •
Fatigue • Exercise intolerance • Dyspnea
50. 59. Additional symptoms • Angina • Orthopnea • Syncope • Palpitations
51. 60. SIGNS OF HEART FAILURE • Dyspnea • Peripheral edema • Ascites •
Hepatomegaly • Jugular venous distension. • Kussmaul sign
52. 61. DIAGNOSTIC STUDIES • Chest x ray • ECG • Echocardiography •
Endomyocardial biopsy
53. 62. MANAGEMENT GOAL Improve diastolic filling Treatment of underlying
disease process
54. 63. • Treatment include conventional therapy for heart failure and dysrhythmias. •
Diuretics may help relieve symptoms • Calcium channel blockers. • Cardiac
transplantation
55. 64. COMPLICATIONS Embolus formation. Decreased ejection fraction allow
stasis of blood to occur in Lt ventricle. Thrombus may lodged in spleen kidney,
extremities, cerebral or coronary circulation. Dysarrhythmias. Sudden cardiac
death.
56. 65. Stress provoked (Tako-tsubo or Broken Heart Syndrome) • An acute
cardiomyopathy can be provoked by a stressful or emotional situation or exposure to
high doses of catecholamines (sympathomimetic drugs).
57. 66. Typical presentation • sudden onset of congestive heart failure • ECG changes
mimicking a myocardial infarction of the anterior wall. • Bulging out of the left
ventricular apex with a hypercontractile base of the left ventricle is often noted. •
"tako tsubo", or octopus pot in Japan.
58. 67. Treatment • Supportive management • Intra-aortic balloon pump • Fluids, and
negative inotropes such as beta blockers or calcium channel blocker • Aspirin
59. 68. • Common among middle-aged women • In most cases is fully reversible with
supportive care. • ECG fingings- myocardial infarction in the presence of left
ventricular dysfunction and absence of epicardial coronary stenoses should prompt the
diagnosis. • Endomyocardial biopsy is of value to exclude myocarditis.
60. 69. Peripartum Cardiomyopathy • Peripartum cardiomyopathy is defined as a
cardiomyopathy manifesting between the last month of pregnancy and 6 months post
partum.
61. 70. • Orthopnea • Dyspnea • pitting Edema • cough, frequent night-time urination, •
excessive weight gain during the last month of pregnancy (1-2+ kg/week; two to four
or more pounds per week), • Palpitations and chest pain.
62. 71. COMPLICATIONS • stroke, loss of circulation to a limb, even coronary artery
occlusion (blockage) with typical myocardial infarction
63. 72. Treatment • similar to treatment for congestive heart failure
64. 73. NURSING MANAGEMENT
65. 74. NURSING MANAGEMENT Nursing Assessment • Evaluate patient's chief
complaint, which may include fever, syncope, general aches, fatigue, palpitations,
dyspnea. • Evaluate etiologic factors, such as alcohol abuse, pregnancy, recent
infection, or history of endocrine disorders. • Assess for positive family history.
66. 75. • Auscultate lung sounds for crackles (pulmonary edema) or decreased sounds
(pleural effusion) • Assess heart size through palpation of chest for point of maximal
impulse (PMI), and auscultate for abnormal sounds. • Evaluate cardiac rhythm and
ECG for evidence of atrial or ventricular enlargement and infarction.
67. 76. Nursing Diagnoses • Decreased Cardiac Output related to decreased ventricular
function and/or dysrhythmias • Activity intolerance related to low cardiac output •
Fluid volume excess in related to ventricular dysfunction • Anxiety related to fear of
death and hospitalization • Fatigue related to disease process