HEART FAILURE FROM ROBBINS AND HARSH MOHAN
- 2. • Congestive heart failure (CHF), is the common end point for many forms of cardiac disease. • Progressive condition with a poor prognosis.
- 3. • Heart failure may result from systolic or diastolic dysfunction. • Systolic dysfunction results from inadequate myocardial contractile function- • Ischemic heart disease • Hypertension.
- 4. • Diastolic dysfunction refers to an inability of the heart to adequately relax and fill- • Massive left ventricular hypertrophy • Myocardial fibrosis • Amyloid deposition • Constrictive pericarditis.
- 5. • One half of CHF cases are attributable to diastolic dysfunction. • Greater frequency seen in older adults, diabetic patients, and women. • Heart failure may also be caused by valve dysfunction (e.g., due to endocarditis) or following rapid increases in blood volume or blood pressure.
- 6. • Failing heart can no longer efficiently pump blood Increase in end-diastolic ventricular volumes increased end-diastolic pressures elevated venous pressures. • Inadequate cardiac output—forward failure. • Increased congestion of the venous circulation —backward failure
- 7. Compensatory mechanism • Frank-Starling mechanism- • Increased end-diastolic filling volumes dilate the heart. • Increased cardiac myofiber stretching. • Lengthened fibers contract more forcibly. • Increasing cardiac output.
- 8. • If the dilated ventricle is able to maintain cardiac output by this meansCompensated heart failure. • With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the body Decompensated heart failure
- 9. • Activation of neurohumoral systems- • Release of the neurotransmitter norepinephrine increases heart rate and myocardial contractility and vascular resistance. • Activation of the renin-angiotensin-aldosterone system water and salt retention (augmenting circulatory volume) and increases vascular tone.
- 10. • Release of atrial natriuretic peptide balance the renin-angiotensin-aldosterone system through diuresis and vascular smooth muscle relaxation.
- 11. • Myocardial structural changes, including augmented muscle mass- • Cardiac myocytes adapt to increased workload by assembling new sarcomeres. • Myocyte enlargement (hypertrophy).
- 12. • In pressure overload states (e.g., hypertension or valvular stenosis)- • New sarcomeres tend to be added parallel to the long axis of the myocytes, adjacent to existing sarcomeres. • Growing muscle fiber diameter thus results in concentric hypertrophy Ventricular wall thickness increases without an increase in the size of the chamber.
- 13. • In volume overload states (e.g., valvular regurgitation or shunts)- • New sarcomeres are added in series with existing sarcomeres. • Muscle fiber length increases. • Ventricle tends to dilate and wall thickness can be increased, normal, or decreased. • Heart weight—rather than wall thickness—is the best measure of hypertrophy.
- 14. Compensatory hypertrophy • The oxygen requirements of hypertrophic myocardium are amplified owing to increased myocardial cell mass. • Capillary bed does not expand in step with the increased myocardial oxygen demands. • Myocardium becomes vulnerable to ischemic injury.
- 15. • Pathologic compensatory cardiac hypertrophy is correlated with increased mortality • Cardiac hypertrophy is an independent risk factor for sudden cardiac death.
- 16. • Volume-loaded hypertrophy induced by regular aerobic exercise (physiologic hypertrophy) is accompanied by an increase in capillary density, with decreased resting heart rate and blood pressure. • These physiologic adaptations reduce overall cardiovascular morbidity and mortality.
- 17. • In comparison, static exercise (weight lifting) is associated with pressure hypertrophy and may not have the same beneficial effects. • Heart failure can affect predominantly the left or the right side of the heart or may involve both sides.
- 18. Left-Sided Heart Failure • Causes- • Ischemic heart disease (IHD) • Systemic hypertension • Mitral or aortic valve disease • Primary diseases of the myocardium (amyloidosis).
- 19. MORPHOLOGY • Heart- • Gross:- cardiac findings depend on the underlying disease process • Myocardial infarction or valvular deformities may be present. • Left ventricle usually is hypertrophied and can be dilated, sometimes massively. • Result in mitral insufficiency and left atrial enlargement. • Increased incidence of atrial fibrillation.
- 21. Microscopic changes Nonspecific Myocyte hypertrophy with interstitial fibrosis of variable severity. Superimposed on this background may be other lesions that contribute to the development of heart failure (e.g. recent or old myocardial infarction).
- 22. Lungs In acute heart failure- Rising pressure in the pulmonary veins transmitted back to the capillaries and arteries of the lungs. Increase in hydrostatic pressure in the venules of the visceral pleura. Results in congestion and edema as well as pleural effusion
- 23. • GROSS- • The lungs are heavy and boggy. • Microscopically- • Perivascular and interstitial transudates • Alveolar septal edema • Accumulation of edema fluid in the alveolar spaces.
- 24. Chronic heart failure Red cells extravasate from the leaky capillaries into alveolar spaces. Phagocytosed by macrophages. Breakdown of red cells and hemoglobin Appearance of hemosiderin-laden alveolar macrophages—heart failure cells.
- 25. Clinical Features • Dyspnea (shortness of breath) on exertion • Cough • Dyspnea when recumbent (orthopnea) • Paroxysmal nocturnal dyspnea • Cardiomegaly • Tachycardia • Third heart sound (S3) • Fine rales at the lung bases
- 26. • Mitral regurgitation • Systolic murmu • Atrial fibrillation- “irregularly irregular” heartbeat • Strokes and manifestations of infarction in other organs. •
- 27. • Diminished cardiac output leads to decreased renal perfusion. • Triggers the renin-angiotensin-aldosterone axis • Increasing intravascular volume and pressures • Prerenal azotemia
- 28. • Diminished cerebral perfusion may manifest as hypoxic encephalopathy • Irritability, diminished cognition, and restlessness that can progress to stupor and coma.
- 29. Treatment • Correcting the underlying cause- A valvular defect or inadequate cardiac perfusion. • Salt restriction • Pharmacologic agents that variously reduce volume overload (e.g., diuretics) • Increase myocardial contractility (“positive inotropes”) • Reduce afterload (adren ergic blockade or inhibitors of angiotensin-converting enzymes)
- 30. • Cardiac resynchronization therapy- • Exogenous pacing of both the right and left ventricles • Cardiac contractility modulation (exogenous stimulation of cardiac muscle)
- 31. Right-Sided Heart Failure • Consequence of left-sided heart failure. • Any pressure increase in the pulmonary circulation produces an increased burden on the right side of the heart. • Isolated right-sided heart failure is infrequent. • Occurs in patients with disorders affecting the lungs; hence it is often referred to as cor pulmonale.
- 32. • Besides parenchymal lung diseases, cor pulmonale also may arise secondary to disorders that affect the pulmonary vasculature- • Primary pulmonary hypertension • Recurrent pulmonary thromboembolism • Pulmonary vasoconstriction (obstructive sleep apnea).
- 33. • The common feature of these disorders is pulmonary hypertension. • Results in hypertrophy and dilation of the right side of the heart. • In cor pulmonale, myocardial hypertrophy and dilation are confined to the right ventricle and atrium. • Bulging of the ventricular septum to the left. • Reduce cardiac output by causing outflow tract obstruction.
- 34. MORPHOLOGY • Liver and Portal System- • The liver usually is increased in size and weight (congestive hepatomegaly). • Cut section: Prominent passive congestion, a pattern referred to as nutmeg liver • Congested centrilobular areas are surrounded by peripheral paler, noncongested parenchyma. • Left-sided heart failure- Severe central hypoxia produces centrilobular necrosis in addition to the sinusoidal congestion.
- 35. • Long-standing severe right-sided heart failure- • Central areas can become fibrotic, creating so-called cardiac cirrhosis. • Elevated pressure in the portal vein and its tributaries (portal hypertension), with vascular congestion producing a tense, enlarged spleen (congestive splenomegaly). • If severe, chronic passive congestion and edema of the bowel wall may interfere with absorption of nutrients and medications.
- 36. • Pleural, Pericardial, and Peritoneal Spaces. • Systemic venous congestion due to right-sided heart failure can lead to transudates (effusions) in the pleural and pericardial spaces. • A combination of hepatic congestion (with or without diminished albumin synthesis) and portal hypertension can lead to peritoneal transudates (ascites).
- 37. • Subcutaneous Tissues- • Edema of dependent portions of the body, especially the feet and lower legs, is a hallmark of right sided CHF. • In chronically bedridden patients, the edema may be primarily presacral.
- 38. Clinical Features • Hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. • Venous congestion and hypoxia of the kidneys and brain produce deficits comparable to those caused by the hypoperfusion of left- sided heart failure.
- 39. • Cardiac decompensation- Biventricular CHF, features of both right-sided and left-sided heart failure. • Patients may become frankly cyanotic and acidotic. • Consequence of decreased tissue perfusion • Resulting from both diminished cardiac output and increasing congestion.
Editor's Notes
- #19: EXCEPTION- mitral valve stenosis, restrictive cardiomyopathies