Pathology of Heart Failure PDF

8- Pathology of heart failure. By Dr. Amal Noor Edeen Allithy Professor of pathology Medicine program RC- M3 BMC Topic/Subject Ø Describe etiology, pathophysiology and morphology of congestive heart failure Ø Describe clinical features of heart failure Subtopics Ø Pathogenesis of HF Ø Morphology...

8- Pathology of heart failure. By Dr. Amal Noor Edeen Allithy Professor of pathology Medicine program RC- M3 BMC Topic/Subject Ø Describe etiology, pathophysiology and morphology of congestive heart failure Ø Describe clinical features of heart failure Subtopics Ø Pathogenesis of HF Ø Morphology and clinical features of left-sided HF Ø Morphology and clinical features of right-sided HF HEART FAILURE • CHF occurs when the heart cannot generate sufficient output to meet the metabolic demands of the tissues. • In a minority of cases, heart failure can be a consequence of greatly increased tissue demands, as in hyperthyroidism, or poor oxygen carrying capacity as in anemia (high-output failure). • Heart failure generally is referred to as congestive heart failure (CHF). • CHF is the common end point for many forms of cardiac disease and typically is a progressive condition that carries an extremely poor prognosis. qEtiology: • Most cases of heart failure are due to systolic dysfunction— inadequate myocardial contractile function, characteristically a consequence of ischemic heart disease or hypertension. • Alternatively, CHF also can result from diastolic dysfunction— inability of the heart to adequately relax and fill, such as in massive left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, or constrictive pericarditis. • Finally, heart failure also can be caused by valve dysfunction (e.g., due to endocarditis). Pathophysiology of CHF •Chronic heart failure: In many cases CHF develops gradually and insidiously owing to the cumulative effects of chronic work overload or progressive loss of myocardium. •Acute heart failure: Onset can be abrupt, as in the setting of a large myocardial infarct or acute valve dysfunction. • Forward failure: the failing heart can no longer efficiently pump the blood delivered to it by the venous circulation. The result is an increased enddiastolic ventricular volume, leading to increased enddiastolic pressures and, finally, elevated venous pressures. Thus, inadequate cardiac output is almost always accompanied by increased congestion of the venous circulation—that is, backward failure. Left-Sided Heart Failure qHeart failure can affect predominantly the left or the right side of the heart or may involve both sides. qThe most common causes of left-sided cardiac failure are: • Ischemic heart disease (IHD), • Systemic hypertension, • Mitral or aortic valve disease, and • Primary diseases of the myocardium (cardiomyopathy). qThe morphologic and clinical effects of left-sided CHF stem from diminished systemic perfusion and the elevated backpressures within the pulmonary circulation. qMORPHOLOGY §Heart. The gross cardiac findings depend on the underlying disease process, for example, myocardial infarction or valvular deformities may be present. §Lungs. Rising pressure in the pulmonary veins is ultimately transmitted back to the capillaries and arteries of the lungs, resulting in congestion and edema as well as pleural effusion due to an increase in hydrostatic pressure in the venules of the visceral pleura. •The lungs are heavy, and microscopically show perivascular and interstitial transudates, alveolar septal edema, and accumulation of edema fluid in the alveolar spaces. In addition, variable numbers of red cells extravasate from the leaky capillaries into alveolar spaces, where they are phagocytosed by macrophages. The subsequent breakdown of red cells and hemoglobin leads to the appearance of hemosiderin-laden alveolar macrophages—so-called heart failure cells—that reflect previous episodes of pulmonary edema. CVC, lung (left sided heart failure) Clinical Features • Dyspnea (shortness of breath) on exertion is usually the earliest and most significant symptom of left-sided heart failure; • Cough also is common as a consequence of fluid transudation into air spaces. • As failure progresses, patients experience dyspnea when recumbent (orthopnea); this occurs because the supine position increases venous return from the lower extremities and also elevates the diaphragm. • Paroxysmal nocturnal dyspnea awakening patients from sleep with extreme dyspnea bordering on feelings of suffocation. • Other manifestations of left ventricular failure include an enlarged heart (cardiomegaly), tachycardia, and fine rales at the lung bases, caused by the opening of edematous pulmonary alveoli. Right-Sided Heart Failure qEtiology: ØRight heart failure usually is the consequence of left-sided heart failure, since any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart. ØIsolated right-sided heart failure also can occur in a few diseases. vThe most common of these is severe pulmonary hypertension, resulting in right-sided heart pathology termed cor pulmonale. vPrimary pulmonic or tricuspid valve disease, vCongenital heart disease, such as with left-to-right shunts causing chronic volume and pressure overloads. qClinical picture: The major morphologic and clinical effects of pure right sided heart failure differ from those of left-sided heart failure in that engorgement of the systemic and portal venous systems typically is pronounced and pulmonary congestion is minimal:ØElevated pressure in the portal vein and its tributaries (portal hypertension), with vascular congestion producing a tense, enlarged spleen (congestive splenomegaly). ØChronic passive congestion of the bowel wall with edema can be severe enough to interfere with absorption of nutrients and medications. ØChronic venous congestion of the liver: Leading to enlarged tender liver and may progress to liver cirrhosis (cardiac cirrhosis) ØPleural, Pericardial, and Peritoneal Spaces. Systemic venous congestion due to right heart failure can lead to transudates (effusions) in the pleural and pericardial spaces. ØA combination of hepatic congestion and portal hypertension leads to peritoneal transudates (ascites): The effusions into the various body cavities typically are serous, with a low protein content, and lack inflammatory cells. ØSubcutaneous Tissues. Peripheral edema of dependent portions of the body, especially ankle (pedal) and pretibial edema, is a hallmark of right heart failure. In chronically bedridden patients, the edema may be primarily presacral. In particularly severe cases, generalized massive edema (anasarca) may be seen. Clinical Features • Pure right-sided heart failure typically is associated with very few respiratory symptoms. Instead, the clinical manifestations are related to systemic and portal venous congestion, including hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. • Venous congestion and hypoxia of the kidneys and brain due to right heart failure can produce deficits comparable to those caused by the hypoperfusion caused by left heart failure. • In most cases of chronic cardiac decompensation, patients present with biventricular CHF, encompassing the clinical syndromes of both right-sided and left-sided heart failure. High output failure qIn a minority of cases, heart failure can be a consequence of greatly increased tissue demands, as in hyperthyroidism, or poor oxygen carrying capacity as in anemia (high-output failure). qEtiology: • Arteriovenous (AV) fistulas cause a decrease in peripheral vascular resistance because they allow shunting of blood from high-pressure arterial circulation to the low-pressure venous system. This shunting causes a decrease in systemic vascular resistance (hypotension) results in elevated heart rate and decreased effective circulating volume, thereby triggering activation of the reninangiotensin-aldosterone system (RAAS). RAAS activation, in turn, causes retention of sodium and water, resulting in increased cardiac filling pressures with elevated cardiac output, which may culminate in a state of high-output heart failure. • Other causes include pregnancy, anemia, hyperthyroidism. Thank You