Details Descriptions About :: Heart Failure

 A syndrome rather than a disease, heart failure occurs when the heart can’t pump enough blood to meet the metabolic needs of the body. Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion. Age Alert Incidence of heart failure rises with age. About 1% of people older than age 50 and 10% of those older than age 80 experience heart failure.

Causes for Heart Failure

Causes Abnormal cardiac muscle function Myocardial infarction Cardiomyopathy Abnormal left ventricular volume Valvular insufficiency High-output states: chronic anemia, arteriovenous fistula, thyrotoxicosis, pregnancy, septicemia, and hypervolemia Abnormal left ventricular pressure Hypertension Pulmonary hypertension Chronic obstructive pulmonary disease Aortic or pulmonic valve stenosis Abnormal left ventricular filling Mitral valve stenosis Tricuspid valve stenosis Constrictive pericarditis Atrial fibrillation Hypertension

Pathophysiology Heart Failure

Pathophysiology Heart failure may be classified according to the side of the heart affected or by the cardiac cycle involved. Left-sided heart failure: decreased left ventricular contractile function. Cardiac output falls, and blood backs up into the left atrium and then into the lungs. Right-sided heart failure: ineffective right ventricular contractile function. Blood backs up into the right atrium and into the peripheral circulation. Systolic dysfunction: left ventricle can’t pump enough blood out to the systemic circulation during systole; the ejection fraction falls. Blood backs up into the pulmonary circulation, pressure rises in the pulmonary venous system, and cardiac output falls. Diastolic dysfunction: left ventricle can’t relax and fill during diastole. The stroke volume falls. All causes of heart failure eventually reduce cardiac output and trigger compensatory mechanisms that improve cardiac output at the expense of increased ventricular work. Increased sympathetic activity enhances peripheral vascular resistance, contractility, heart rate, and venous return. It also restricts blood flow to the kidneys, causing them to secrete renin, which, in turn, converts angiotensinogen to angiotensin I to angiotensin II—a potent vasoconstrictor. Angiotensin causes the adrenal cortex to release aldosterone, leading to sodium and water retention and an increase in circulating blood volume. If the renal mechanism persists unchecked, it can aggravate heart failure. The increase in end-diastolic ventricular volume causes increased stroke work and volume during contraction, stretching cardiac muscle fibers. The muscle becomes stretched beyond optimum limits and contractility declines. In heart failure, the body produces counterregulatory substances (prostaglandins, atrial natriuretic factor, and brain natriuretic peptide [BNP]) to reduce the negative effects of volume overload and vasoconstriction. When blood volume increases in the ventricles, the heart makes these compensations: Short-term: As the end-diastolic fiber length increases, the ventricular muscle dilates and increases the force of contraction Long-term: Ventricular hypertrophy increases the heart muscles’ ability to contract and push its volume of blood into the circulation. With heart failure, compensation may occur for a long time before signs and symptoms develop.

Signs and symptoms Heart Failure

Signs and symptoms Left-sided heart failure Dyspnea, orthopnea, paroxysmal nocturnal dyspnea Nonproductive cough, crackles Hemoptysis Tachycardia; S3 and S4 heart sounds Cool, pale skin Right-sided heart failure Jugular vein distention Hepatojugular reflux and hepatomegaly Right upper quadrant pain Anorexia, fullness, nausea Weight gain, edema, ascites, or anasarca Dyspnea, orthopnea, paroxysmal nocturnal dyspnea

Diagnostic Lab Test results

Diagnostic test results Chest X-rays show increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly. Electrocardiography shows hypertrophy, ischemic changes, or infarction and may also reveal tachycardia and extrasystoles. BNP assay, a blood test, may show elevated levels. Echocardiography reveals left ventricular hypertrophy, dilation, and abnormal contractility. Pulmonary artery monitoring typically shows elevated pulmonary artery and pulmonary artery wedge pressures, left ventricular end-diastolic pressure in left-sided failure, and right atrial pressure or central venous pressure in right-sided failure. Radionuclide ventriculography reveals an ejection fraction less than 40%; in diastolic dysfunction, the ejection fraction may be normal.

Treatment for Heart Failure

Treatment Treatment of the underlying cause, if known Angiotensin-converting enzyme inhibitors (for patients with left ventricular dysfunction) digoxin, beta-adrenergic blockers, diuretics, nitrates, morphine, or oxygen Dobutamine, milrinone, nesiritide Lifestyle modifications to reduce risk factors Coronary artery bypass surgery, angioplasty, or heart transplantation NORMAL CARDIAC CIRCULATION

 

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