Atlas of pathophysiology, 2 Edition

Part II - Disorders

Cardiovascular disorders

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.


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


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

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 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 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







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