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HEART FAILURE AND DISORDERS OF PERICARDIUM The physiology of heart failure involves interplay between two factors: the inability of the failing heart to maintain sufficient cardiac output to support body functions and the recruitment of compensatory mechanisms designed to maintain the cardiac reserve. CARDIAC OUTPUT The cardiac output is the amount of blood that the heart pumps each minute. It reflects how often the heart beats each minute (i.e., heart rate) and how much blood the heart pumps with each beat (i.e., stroke volume) and can be expressed as the product of the heart rate and stroke volume. The normal value is 5 L per minute. Heart rate is regulated by balancing sympathetic, or adrenergic, activity, which accelerates heart rate, with parasympathetic, or vagal, activity which slows it down. Stroke volume is a function of preload, afterload, and cardiac contractility. COMPENSATORY MECHANISMS In heart failure, the cardiac reserve is largely maintained through compensatory mechanisms, the most important of which are: • Frank - Starling mechanism • increased sympathetic nervous system activity • renin-angiotensin mechanism • atrial natriuretic peptide • myocardial hypertrophy The healthy and the failing heart may use the same compensatory mechanisms. In the failing heart, early decreases in cardiac function may go unnoticed because these compensatory mechanisms maintain the cardiac output. This state is called compensated heart failure. Unfortunately, these mechanisms were not intended for long-term use. In severe and prolonged decompensated heart failure the compensatory mechanisms may themselves worsen the failure. FRANK -STARLING MECHANISM The Frank - Starling mechanism increases stroke volume by means of an increase in ventricular end-diastolic volume (i.e., preload). With increased diastolic filling, there is increased stretching of the myocardial fibres, more optimal approximation of the actin and myosin filaments, and a resultant increase in the force of the next contraction. In heart failure, the Frank-Starling mechanism helps to support the cardiac output. Cardiac output may be normal at rest in persons with heart failure because of increased ventricular end-diastolic 1

volume and the Frank-Starling mechanism. However, this mechanism becomes ineffective when the heart becomes overfilled and the muscle fibres are overstretched.

INCREASED SYMPATHETIC NERVOUS SYSTEM ACTIVITY Stimulation of the sympathetic nervous system plays an important role in the compensatory response to decreased cardiac output and to the pathogenesis of heart failure. Both cardiac sympathetic tone and catecholamine levels are elevated during the late stages of most forms of heart failure. By direct stimulation of heart rate and cardiac contractility and by regulation of vascular tone, the sympathetic nervous system helps to maintain perfusion of the various organs, particularly the heart and brain. In persons with more severe heart failure, blood from the skin, kidneys, and 2

gastrointestinal tract is diverted to the more critical cerebral and coronary circulations. The negative aspects of these adaptations include an increase in vascular resistance and the afterload against which the heart must pump. There is also evidence that prolonged sympathetic stimulation may exhaust myocardial stores of norepinephrine and may lead to destruction of sympathetic nerve endings. RENIN-ANGIOTENSIN MECHANISM One of the most important effects of a lowered cardiac output in heart failure is a reduction in renal blood flow and glomerular filtration rate, which leads to salt and water retention. Normally, the kidneys receive about 25% of the cardiac output, but this may be decreased to as low as 8% to 10% in persons with heart failure. With decreased renal blood flow, there is a progressive increase in renin secretion by the kidneys along with parallel increases in circulating levels of angiotensin II. The increased concentration of angiotensin II contributes to a generalised and excessive vasoconstriction and provides a powerful stimulus for aldosterone production by the adrenal cortex. Aldosterone increases tubular reabsorption of sodium with an accompanying increase in water retention. Because aldosterone is metabolised in the liver, its levels are further increased when heart failure causes liver congestion. Angiotensin II also increases levels of antidiuretic hormone (ADH), which serves as a vasoconstrictor and inhibitor of water excretion. Angiotensin II is also thought to contribute to the myocardial hypertrophy that occurs in heart failure, possibly acting as a growth factor. Angiotensin-converting enzyme (ACE) inhibitor drugs, which block the conversion of angiotensin I to angiotensin II, have become common therapy for heart failure. MYOCARDIAL HYPERTROPHY Myocardial hypertrophy is a long-term compensatory mechanism. Cardiac muscle, like skeletal muscle, responds to an increase in work demands by undergoing hypertrophy. Hypertrophy increases the number of contractile elements (i.e., actin and myosin) in myocardial cells as a means of increasing their contractile performance. Heart diseases that increase resistance to the ejection of blood from the ventricles provide the greatest stimulates for hypertrophy. For example, the wall of the left ventricle may increase to six times its normal size in severe aortic stenosis. If portions of the heart muscle are damaged and replaced with scar tissue, the undamaged part of the myocardium often hypertrophies as a 3

means of improving the pumping capacity of the ventricle. Cardiac hypertrophy improves cardiac function by increasing ventricular wall thickness, which normalises wall stress so that the heart contracts more efficiently.

CONGESTIVE HEART FAILURE Heart failure occurs when the pumping ability of the heart becomes impaired. Congestive heart failure is heart failure that is accompanied by congestion of body tissues. After an initial compensatory period, the clinical manifestations of heart failure become complicated with pulmonary congestion of systemic venous congestion. Heart failure may be described as high-output or low-output failure, systolic or diastolic failure, and right-sided or left-sided failure. HIGH - OUTPUT AND LOW - OUTPUT FAILURE An uncommon type of heart failure that is caused by an excessive need for cardiac output is often referred to as high-output failure. With high-output failure, the function of the heart may be supranormal but inadequate owing to excessive metabolic needs. Causes of high-output failure include severe anemia, thyrotoxicosis, conditions that cause arteriovenous shunting. Lowoutput failure is caused by disorders that impair the pumping ability of the heart, such as ischemic heart disease and cardiomyopathy.

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RIGHT - SIDED HEART FAILURE The right heart pumps deoxygenated blood from the systemic circulation into the pulmonary circulation. Consequently, when the right heart fails, there is accumulation or damming back of blood in the systemic venous system. This causes an increase in right atrial, right ventricular end-diastolic and systemic venous pressures. The clinical result is manifested in development of oedema in the peripheral tissues and congestion of the abdominal organs. Manifestations of right - sided heart failure: • Fatigue • Dependent oedema • Distension of the jugular veins • Liver engorgement • Ascites • Anorexia and complaints of gastrointestinal distress • Cyanosis • Elevation in peripheral venous pressure

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LEFT-SIDED HEART FAILURE The left side of the heart pumps blood from the low-pressure pulmonary circulation into the high-pressure arterial side of the systemic circulation. With impairment of left heart function, there is a decrease in cardiac output; an increase in left atrial and left ventricular end-diastolic pressures; and congestion in the pulmonary circulation. When the pulmonary capillary pressure (normally about 10 mm Hg) exceeds the capillary osmotic pressure (normally about 25 mm Hg), there is a shift of intravascular fluid into the interstitium of the lung and development of pulmonary edema.Manifestation of left-sided heart failure: 6

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Dyspnea Orthopnea - shortness of breath occurs when a person is supine Cough Blood - tinged sputum Cyanosis Elevation in pulmonary capillary wedge pressure

DISORDERS OF THE PERICARDIUM The pericardium is a two-layered membranous sac that isolates the heart from other thoracic structures, maintains its position in the thorax, and prevents it from overfilling. The mechanisms that control the movement of fluid between the capillaries and the 7

space that separates the two layers of the pericardium are the same as those that control fluid movement between the capillaries and the interstitial spaces of other body tissues. The pericardial sac normally contains 30 to 50 ml of clear, straw-colored fluid. Although 1 L or more of fluid may accumulate, volumes of more than 500 ml are uncommon. Conditions that produce edema in other structures of the body, such as kidney disease and heart failure, may also produce an accumulation of fluid in the pericardial sac. This is called pericardial effusion. TYPES OF PERICARDIAL DISORDERS Acute pericarditis Acute pericarditis represents an acute inflammatory process and is usually characterised by chest pain, pericardial friction rub, and serial ECG abnormalities. Acute pericarditis can be classified according to cause (e.g., infections, trauma, rheumatic fever) or the nature of the exudate (e.g.,serous, fibrinous, purulent, hemorrhagic).Causes: 1. Infectious – viral (echo, coxsacki and others); bacterial (tuberculosis, staphylococcus, streptococcus) and fungal. 2. Immune and collagen disorders - rheumatic fever, rheumatoid arthritis, systemic lupus erythematous. 3. Metabolic disorders - uremia and dialysis, myxoedema. 4. Ischemia and tissue injury - myocardial infarction, cardiac surgery, chest trauma. 5. Physical and chemical agents - radiation therapy, hydralazine. Cardiac tamponade Cardiac tamponade is cardiac compression caused by excess fluid or blood in pericardial sac. It can occur as the result of trauma, cancer, uremia, cardiac rupture due to myocardial infarction or diagnostic procedures, or dissecting aneurysm. A rapid accumulation of fluid results in an increase in central venous pressure, a decrease in venous return to the heart, distention of the jugular veins, a decrease in cardiac output despite an increase in heart rate, a decrease in systolic blood pressure, and signs of circulatory shock.

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Constrictive pericarditis In constrictive pericarditis, fibrous scar tissue develops between the visceral and parietal layers of the serous pericardium. In time, the scar tissue contracts and interferes with diastolic filling of the heart, at which point cardiac output and cardiac reserve become fixed. Pericardial effusion Pericardial effusion refers to the presence of fluid in the pericardial cavity. Its major threat is compression of the heart chambers. The amount of fluid and the elasticity of the pericardium determine the effect the effusion has on cardiac function. Small pericardial effusions may produce no symptoms or abnormal clinical findings. Even a large effusion that develops slowly may cause few or no symptoms, providing the pericardium is able to stretch and avoid compressing the heart.

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