Presentation on theme: "Congestive Heart Failure Inability of the heart to handle the volume of blood returned to it."— Presentation transcript:
Congestive Heart Failure Inability of the heart to handle the volume of blood returned to it
Congestive Heart Failure To learn the etiologic factors of congestive heart failure To learn the effects of heart failure
Types of Heart Disease Four categories of disease account for about 85 to 90% of all cardiac deaths: (1) ischemic heart disease (responsible for the great majority of the cardiac deaths) (2) hypertensive heart disease and pulmonary hypertensive heart disease (cor pulmonale); (3) certain valvular diseases–calcific aortic valve stenosis, mitral valve prolapse, infective endocarditis, and rheumatic heart disease; and (4) congenital heart disease.
Any one of the causes mentioned above, when sufficiently severe or advanced, may ultimately impair cardiac function and render the heart unable to maintain an output sufficient for the metabolic requirements of the tissues and organs of the body, producing congestive heart failure (CHF).
Etiology Either the heart muscle cannot pump because of intrinsic disease, or the heart must pump against excessive resistance, or the heart must pump a preposterously large amount of blood
Pathophysiology In summary: CHF occurs (1) either because of a decreased myocardial capacity to contract "forward failure" (i.e., inability to perfuse the arteries), (2) because of an inability to fill the cardiac chambers with blood. "backward failure" (i.e., congestion and its problems).
Difference "Cardiogenic shock" is a term reserved for the acute situation (usually a myocardial infarct), “Failure" can simply mean inability to handle the ordinary venous return.
Most instances of heart failure are the consequence of progressive deterioration of myocardial contractile function (systolic dysfunction), as often occurs with ischemic injury, pressure or volume overload, or dilated cardiomyopathy.
Sometimes, however, failure results from an inability of the heart chambers to expand sufficiently during diastole to accommodate an adequate ventricular blood volume (diastolic dysfunction), as can occur - with massive left ventricular hypertrophy, - myocardial fibrosis, - deposition of amyloid, or - constrictive pericarditis.
Cardiac Hypertrophy: Pathophysiology and Progression to Failure Cardiac hypertrophy is the compensatory response of the myocardium to increased work. Myocardial hyperfunction induces increased myocyte size (cellular hypertrophy through addition of sarcomeres, the contractile elements) that causes an increase in the overall mass and size of the heart. Because adult cardiac myocytes cannot divide, augmentation of myocyte number (hyperplasia) cannot occur in the adult heart.
The pattern of hypertrophy reflects the stimulus. Concentric hypertrophy : Pressure-overloaded ventricles (e.g., hypertension or aortic stenosis) develop concentric hypertrophy, with an increased ratio of wall thickness to cavity radius. Eccentric hypertrophy : In contrast, volume- overloaded ventricles (e.g., mitral regurgitation) develop hypertrophy with dilatation (eccentric hypertrophy), with proportionate increases in ventricular radius and wall thickness.
Geometry, structure, and composition (cells and extracellular matrix) of the hypertrophied heart are not normal. It should not be surprising that cardiac hypertrophy often evolves to cardiac failure. Besides predisposing to CHF, left ventricular hypertrophy is an independent risk factor for cardiac mortality and morbidity, especially for sudden death and ischemic heart disease.
Cardiac hypertrophy 350 gm... Normal upper limit of weight for an adult 1.5 cm... Normal upper limit of thickness for an adult left ventricle 0.5 cm... Normal upper limit of thickness for an adult right ventricle
Whatever the underlying basis for CHF, a variety of compensatory mechanisms come into play when the hypertrophied heart can no longer accommodate the increased demand. The heart begins to dilate, thereby stretching the sarcomeres and increasing the force of contraction and secondarily the stroke volume. Myocardial hypertrophy may become increasingly detrimental because of the increased metabolic requirements of the enlarged muscle mass.
The downward slide of stroke volume and cardiac output often ends in death. Thus at autopsy, the heart of patients having CHF is generally characterized by increased weight, progressive wall thinning, chamber dilatation, and microscopic changes of hypertrophy.
Nevertheless, because the vascular system is a closed circuit, failure of one side cannot exist for long without eventually producing excessive strain on the other, terminating in total heart failure.
Congestive Heart Failure : Left-Sided Heart Failure Left-sided heart failure is most often caused by (1) ischemic heart disease, (2) hypertension, (3) aortic and mitral valvular diseases (particularly calcific aortic stenosis and rheumatic heart disease), and (4) myocardial diseases.
The common effects of left-sided failure Dyspnea (from pulmonary edema and total-body hypoxia) paroxysmal nocturnal dyspnea ("cardiac dyspnea"); on lying down for a while, fluid redistributes itself in the body, resulting in pulmonary edema. The lungs become heavier (i.e., congestion, edema) their weight presses on the pulmonary veins which in turn makes them more congested. Patients may throw the windows open at night, or learn to sleep on various numbers of pillows; you the physician will hear rales; the pathologist may see "brown induration" and hemosiderin-laden "heart failure" macrophages. Cough ("from the left atrium pushing on the bronchus"; this is common in mitral valve disease even in the absence of failure) Prerenal azotemia
Hypoxic encephalopathy Sodium overload and systemic dependent edema (from hypoperfused kidneys; these patients may also have nocturia ) High-output failure is a special situation, in which the heart fails because it must pump an excessive among of blood. The causes: Anemia Hyperthyroidism High fever Shunts between an artery and a vein Beriberi (arterioles open) Paget's disease of bone (abnormal bone vasculature) Iatrogenic (i.e., shunts in dialysis)
Left ventricle is usually hypertrophied and often dilated, sometimes quite massively. Secondary enlargement of the left atrium is frequently present. Atrial fibrillation (i.e., uncoordinated, chaotic contraction of the atrium) often results.
A fibrillating left atrium carries an increased risk of embolic stroke. The distant effects of left-sided failure are manifested most prominently in the lungs, although the function of the kidneys and brain may also be markedly impaired.
Lungs in Left-Sided Heart Failure With the progressive damming of blood within the pulmonary circulation, pressure in the pulmonary veins mounts and is ultimately transmitted retrogradely to the capillaries. The result is pulmonary congestion Edema (heavy, wet lungs).
Lung : hyperemia&edema
The lung changes include: (1) a perivascular and interstitial transudate, particularly in the interlobular septa; (2) progressive edematous widening of alveolar septa; and (3) accumulation of edema fluid in the alveolar spaces. (4) Transferrin in edema fluid and hemoglobin from erythrocytes, which leak from congested capillaries, are phagocytosed by macrophages and converted to hemosiderin. Hemosiderin-containing macrophages in the alveoli (called heart failure cells) denote previous episodes of pulmonary edema.
Heart failure cells
Kidneys in Left-Sided Heart Failure With left-sided heart failure, the decreased cardiac output causes a reduction in renal perfusion, which activates the renin-angiotensin-aldosterone system, inducing retention of salt and water with consequent expansion of the interstitial fluid and blood volumes. In kidneys already suffering from hypoperfusion, the reduced cardiac output may lead to ischemic acute tubular necrosis. If the perfusion deficit of the kidney becomes sufficiently severe, impaired excretion of nitrogenous products may cause azotemia, known as prerenal azotemia.
Brain in Left-Sided Heart Failure In far-advanced CHF, cerebral hypoxia may give rise to hypoxic encephalopathy (ischemia, and infarction ), with irritability, loss of attention span, and restlessness, which may even progress to stupor and coma.
Congestive Heart Failure : Right-Sided Heart Failure Right-sided heart failure occurs in pure form in only a few diseases. Usually it is a consequence of left-sided failure because any increase in pressure in pulmonary circulation incident to left-sided failure inevitably produces an increased burden on the right side of the heart. Pure right-sided failure most often occurs with cor pulmonale, i.e., right ventricular pressure overload induced by intrinsic disease of the lungs or pulmonary vasculature.
In these cases, the right ventricle is burdened by increased resistance within the pulmonary circulation; dilatation is generally confined to the right ventricle and atrium. This can be acute with right-sided dilatation and thinning in massive pulmonary embolism. In chronic right-sided overload (e.g., owing to chronic obstructive pulmonary disease), right ventricular and atrial hypertrophy is usually present.
The major morphologic and clinical effects of pure right-sided failure differ from those of left-sided failure in that pulmonary congestion is minimal, whereas engorgement of the systemic and portal venous systems is pronounced. The major organs affected by right-sided heart failure are the liver, spleen, kidneys, subcutaneous tissues, and brain as well as the entire portal area of venous drainage.
Liver in Right-Sided Heart Failure The liver is usually slightly increased in size and weight; a cut section displays the prominent “nutmeg” pattern of chronic passive congestion of the liver. When left-sided failure is also present, the severe central hypoxia produces centrilobular necrosis along with the sinusoidal congestion. If the right-sided failure is severe and rapidly developing, rupture of sinusoids produces central hemorrhagic necrosis. With long-standing severe right-sided cardiac failure, the central areas in time can become fibrotic, creating the so-called cardiac sclerosis.
“Nutmeg” pattern of chronic passive congestion of the liver
Chronic passive congestion of the liver
Cardiac sclerosis (cirrhosis )
Kidneys in Right-Sided Heart Failure Congestion of the kidneys is more marked with right-sided heart failure than with left- sided failure, leading to greater fluid retention, peripheral edema, and more pronounced azotemia.
Portal System of Drainage in Right-Sided Heart Failure Right-sided heart failure leads to elevated pressure in the portal vein and its tributaries. Splenic congestion produces a tense, enlarged spleen. Microscopically there may be marked sinusoidal dilatation, accompanied by areas of recent hemorrhage. With long-standing congestion, the enlarged spleen may achieve a weight of 500 to 600 gm (normal, approximately 150 gm), and the long-standing edema may produce fibrous thickening of the sinusoidal walls, to create the firm organ characteristic of congestive splenomegaly. In addition, abnormal accumulations of transudate in the peritoneal cavity may give rise to ascites.
Subcutaneous Tissues in Right-Sided Heart Failure Peripheral edema of dependent portions of the body, especially ankle edema, is a hallmark of right-sided failure. In severe or long-standing cases, edema may be quite massive and generalized, a condition termed anasarca.
Pleural and Pericardial Spaces in Right-Sided Heart Failure Effusions may appear, particularly in the right thoracic cavity.
Brain in Right-Sided Heart Failure Symptoms essentially identical to those described in left-sided failure may occur, representing venous congestion and hypoxia of the central nervous system.
Brain: venous congestion
In summary The effects of pure left-sided heart failure are largely due to pulmonary congestion and edema. Right-sided heart failure induces essentially a systemic (and secondary portal) venous congestive syndrome, with hepatic and splenic enlargement, peripheral edema, pleural and pericardial effusions, and ascites.