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Cardio Myopathy.pptx
- 1. Adult Health Case:A 54-year old male self-presented to the emergency department with a 4-day history of awareness of irregularities of his heart rhythm. This was not accompanied by any chest pain but he revealed a one-month history of shortness of breath, tiredness, and leg swelling.
- 2. Cardio= Heart Myo= Muscle Pathy: Suffering/Disease WHO – 1980 – “Heart muscle disease of unknown cause” WHO & International Society and Federation of Cardiology Task Force – 1995 “Disease of the myocardium associated with cardiac dysfunction” AHA “ A heterogeneous group of disease of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardio-myopathies either are confined to the heart or are part of generalized systemic disorders, often leading to cardiovascular death or progressive heart related disability”
- 3. Genetic • HCM • ARCLD • LVNC • Conduction defects • Glycogen storage • Mitochondrial Myopathies Mixed • Restrictive (Non hypertrophied & non-dilated) • DCM Acquired • Inflammatory (Myocarditis) • Stress provoked (takotsubo) • Peripartum • Tachycardia induced CLASSIFICATION OF CARDIOMYOPATHY Ion Channel disorders LQTS Brugad SQTS CVPT Asian SUNDS
- 6. DILATED CARDIOMYOPATHY •Most common type • 5 to 8 cases per 100,000 people per year •Distinguished by significant dilatation of the ventricles without simultaneous hypertrophy •The size of ventricular cavity enlarges with reduced cardiac output •Impaired ventricular contraction leading to progressive left sided and later right sided failure
- 7. ETIOLOGY of DCMP 1. Cardiotoxicity agents 2. Coronary Artery Disease 3. Genetics (Autosomal dominant) 4. Hypertension 5. Metabolic disorder 6. Muscular dystrophy 7. Myocarditis 8. Valve disease 9. Pregnancy
- 8. Diffuse inflammation and rapid degeneration of myocardial fibers and cells Diminished contractile elements, muscle fibers Ventricular dilation, impaired systolic function, Atrial enlargement and stasis of blood Contractile dysfunction Functional MR and/or TR Progressive left sided Heart failure later right sided Heart failure Sudden Cardiac death
- 9. Symptoms -Decreased exercise capacity -Fatigue -Dyspnoea at rest -Paroxysmal nocturnal dyspnoea -Orthopnea As the disease progresses: -Experience dry cough -Palpitation -Abdominal bloating -Nausea/Vomiting -Anorexiaa Signs -Abnormal S3 or S4 -Dysrhythmia -Heart murmurs -Pulmonary crackles -Edema -Weak peripheral pulses -Pallor -Hepatomegaly -Jugular vein dilatation -Systemic embolization
- 10. showing dilated cardiomyopathy. Note the extremely dilated left ventricle. The left ventricular end-diastolic dimension was 5.9 cm, and the ejection fraction was 26%. LV, left ventricle ; RV, right ventricle ; LA, left atrium ; RA, right atrium. Two-dimensional echocardiography
- 11. • There is marked left ventricular hypertrophy with repolarisation abnormality (LV “strain” pattern) in V5-6. • LV dilatation has produced an interventricular conduction delay mimicking LBBB — however, this is not LBBB as the morphology is not typical and there are small Q waves in V5-6 (the presence of Q waves in V6 rules out LBBB). • There are some signs of left atrial enlargement — leftward deviation of the P wave axis (positive P waves in I and aVL, inverted in III and aVF) and prolongation of the terminal portion of the P wave in V1. • Right axis deviation in the presence of LVH suggests the possibility of biventricular enlargement. • The widespread downsloping ST depression may be due to LVH Electrocardiogram
- 12. Chest X-ray Cardiac Catheterization
- 13. Collaborative management • Focus on controlling HF • Pharmacological Management - Nitrates and Diuretics - ACE inhibitors - Β-Adrenergic blockers - Antidysrhythmics - Anticoagulation • Destination Therapy - Ventricular assist device - Cardiac resynchronization therapy - Implantable cardio-verter-defibrillator • Nutritional Therapy • Cardiac rehabilitation • Heart Transplantation
- 14. • Rare autosomal dominant condition • Occurs in men, women and Children • 0.05% to 0.2% of the population in US • 3% of death in young competitive athletes • Characterized by thick ventricle (symmetrical/asymetric al) and hypertrophy HYPERTROPHIC CARDIOMYOPATHY HCM is a clinically heterogenous, autosomal dominant heart muscle disorder due to primarily mutations in the genes encoding the cardiac sarcomere myofillament proteins. This culminates in the proteins altered structure and function with myofibrillar disarray, marked ventricular hypertrophy (frequently assy metric), diastolic dysfuction and in some patients, sudden cardiac death as its most devastating outcome.
- 15. ETIOLOGY OF HCM •Aortic stenosis •Genetic (Autosomal dominant) •Hypertension
- 17. • 1. 1. Left ventrical outflow obstruction 4. Mitral regurgitation Impaired contraction -High systolic contraction load -Ventricular contraction/relax ation not uniform -Accounts for exertional dyspnea -- Increased filling pressure -Increased Pulmonary venous pressure -Major determinant -Subaortic outflow obstruction - Systolic anterior motion (SAM) Physiological consequence -elevated intraventricular pressure - Prolongation of ventricular relaxation -Increased myocardial wall stress -Increased oxygen demand -Decreased cardiac output 2. Diastolic dysfunction 3. Myocardial Ischemia
- 18. Symptoms -Asymptomatic -Exertional dyspnea -Fatgue -Angina -Syncope -Palpitation Signs -Jerky pulse -Double or triple apex -S3, S4 sounds -Late systolic murmur (Outflow obstruction MR) -Atrial fibrillation
- 19. • Electrocardiogram (ECG) of the HCM subject showing normal sinus rhythm. ST segment abnormality and inverted T-wave in Leads I, II, III, V4, V5 and V6.
- 20. Echocardiography Chest X-ray Cardiac Catheterization Radionuclide studies MRI
- 21. Collaborative management • Goal of care are to improve ventricular filling by reducing ventricular contractility and relieving LV outflow obstruction. • Pharmacological management - β-adrenergic blockers - Antidysrhythmic medications - Anticoagulation - IE prophylaxis • Cardioverter defibrilator • AV pacing • Surgical management - Ventriculomyotomy and mectomy - Percutaneous transluminal septal myocardial ablation (PTSMA)
- 22. • characterized by impaired ventricular filling with normal ventricular wall thickness and systolic function • Abnormal diastolic function and dilated atrial chambers • Left sided ventricle involvement produces pulmonary venous congestion and dyspnea • Right sided presents with signs of systemic venous congestion • Classified as Primary and Secondary RESTRICTIVE CARDIOMYOPATHY
- 23. ETIOLOGY Of RCMP •Idiopathic •May be associated with -Amyloidosis -Endocarditis fibrosis -Neoplastic tumor -Post radiation therapy -Sarcoidosis -Ventricular thrombus
- 24. Physiology of RCMP Rigid myocardium Increased Diastolic Ventricular Pressure Jugular Venous distention Hepatomegaly Ascites Venous congestion Decreased Ventricular filling Decreased CO Weakness fatigue
- 25. • RCM is common type of CMP • Increased stiffness of the myocardium, substance fibrosis or scaring of endocardium • Impaired diastolic filling • Ventricular volumes are usually normal or reduced • Wall thickness is normal or mildly increased in some cm • Systolic function is typically preserved • Poor ventricular compliance • Intraventricular pressure rises precipitously with small increase in volume
- 26. Symptoms and signs Volume overload - Fatigue - Dyspnea - Orthopnea - Noctural dyspnea Arrhythmia - Palpitation - Syncope - Exercise intolerance Reduced Cardiac output - Exercise intolerance - Cognitive difficulties Angina, dyspnea, syncope-on exertion Sudden Cardiac death Pulse- tachycardia Hypotension Jugular venous pressure- raised Pulmonary crackles Kussmaul’s sign Pedal edema hepatomegaly
- 27. Chest X-ray - May be normal or show cardiomegaly from right and left atrial enlargement Electrocardiogram: - low voltage, conduction defect -Mild tachycardia at rest -Supreventricular (atrial fibrillation) -AV block
- 28. Echocardiogram : disproportionately enlarged atria, and the normal ventricular chamber size Endomyocardial biopsy: CT-scan
- 29. Collaborative Care • Aims to improve diastolic filling and the underlying disease process. • Conventional therapy for HF and dysrythmia • Heart transplantation may also be a considerable
- 30. Arrythmogenic Right Ventricular CMP • Occurs when the myocardium of the right ventricle is progressively infiltrated and replaced by fibrous scar and adipose tissue. • Initially, only localized areas of the right ventricle are affected, but as the disease progresses entire heart is affected. • RV dilates and develops poor contractility, RV wall abnormalities and dysrhythmias. • Palpitation or syncope may develop 15and 40 years of age • Should be considered in patient with VT originating in RV (LBBB) or sudden death among young athlets.
- 32. 1. Left Ventricular outflow tract - Myectomy - Mitral valvuloplasty 2. Latissimus Dorsi Muscle Wrap/Dynamic cardioplasty 3. Heart transplant 4. Mechanical Assisted devices - Ventricular Assist Device (VAD) - Total artificial heart
- 33. Myectomy
- 35. Heart Transplant
- 36. A. Ventricular Assist Device B. Total Artificial Heart
- 37. Nursing Management • Decreased CO related to structural disorders caused by cardiomyopathy • Ineffective cardiopulmonary cerebral peripheral secondary to renal perfusion related to decreased peripheral blood flow • Impaired gas exchange related to pulmonary congestion caused by myocardial failure • Activity intolerance related to decreased cardiac output • Anxiety related to change in health status secondary to role functioning.
- 38. Health Teaching to patient and caregiver
- 39. Pooja Prakash Cardiovascular and Thoracic Nursing