Comparative analysis

CAUSE EXAMPLES

Abnormal cardiac muscle function Myocardial infarction Cardiomyopathy Abnormal left ventricular volume Valvular insufficiency

High-output states:

chronic anemia arteriovenous fistula thyrotoxicosis

pregnancy septicemia beriberi

infusion of large volume of intravenous fluids in a short time period 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 Atrial myxoma

Constrictive pericarditis Atrial fibrillation

Impaired ventricular relaxation:

hypertension

myocardial hibernation myocardial stunning

Systolic dysfunction. Systolic dysfunction occurs when the left ventricle can't pump enough blood out to the systemic circulation during systole and the ejection fraction falls. Consequently, blood backs up into the pulmonary circulation and pressure rises in the pulmonary venous system. Cardiac output falls; weakness, fatigue, and shortness of breath may occur. Causes of systolic dysfunction include myocardial infarction and dilated cardiomyopathy.

Diastolic dysfunction. Diastolic dysfunction occurs when the ability of the left ventricle to relax and fill during diastole is reduced and the stroke volume falls. Therefore, higher volumes are needed in the ventricles to maintain cardiac output.

Consequently, pulmonary congestion and peripheral edema develop. Diastolic dysfunction may occur as a result of left ventricular hypertrophy, hypertension, or restrictive cardiomyopathy. This type of heart failure is less common than systolic dysfunction, and its treatment is not as clear.

All causes of heart failure eventually lead to reduced cardiac output, which triggers compensatory mechanisms such as increased sympathetic activity, activation of the renin-angiotensin-aldosterone system, ventricular dilation, and

hypertrophy. These mechanisms improve cardiac output at the expense of increased ventricular work.

Increased sympathetic activity — a response to decreased cardiac output and blood pressure — enhances peripheral vascular resistance, contractility, heart rate, and venous return. Signs of increased sympathetic activity, such as cool extremities and clamminess, may indicate impending heart failure.

Increased sympathetic activity also restricts blood flow to the kidneys, causing them to secrete renin which, in turn, converts angiotensinogen to angiotensin I, which then becomes 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. This renal mechanism is helpful; however, if it persists unchecked, it can aggravate heart failure as the heart struggles to pump against the increased volume.

In ventricular dilation, an increase in end-diastolic ventricular volume (preload) causes increased stroke work and stroke volume during contraction, stretching cardiac muscle fibers so that the ventricle can accept the increased intravascular volume. Eventually, the muscle becomes stretched beyond optimum limits and contractility declines.

In ventricular hypertrophy, an increase in ventricular muscle mass allows the heart to pump against increased resistance to the outflow of blood, improving cardiac output. However, this increased muscle mass also increases the myocardial oxygen requirements. An increase in the ventricular diastolic pressure necessary to fill the enlarged ventricle may

compromise diastolic coronary blood flow, limiting the oxygen supply to the ventricle, and causing ischemia and impaired muscle contractility.

In heart failure, counterregulatory substances — prostaglandins and atrial natriuretic factor — are produced in an attempt to reduce the negative effects of volume overload and vasoconstriction caused by the compensatory mechanisms.

The kidneys release the prostaglandins, prostacyclin and prostaglandin E ₂, which are potent vasodilators. These vasodilators also act to reduce volume overload produced by the renin-angiotensin-aldosterone system by inhibiting sodium and water reabsorption by the kidneys.

Atrial natriuretic factor is a hormone that is secreted mainly by the atria in response to stimulation of the stretch receptors

in the atria caused by excess fluid volume. Atrial natriuretic factor works to counteract the negative effects of sympathetic nervous system stimulation and the renin-angiotensin-aldosterone system by producing vasodilation and diuresis.

Signs and symptoms

Early clinical manifestations of left-sided heart failure include:

dyspnea caused by pulmonary congestion

orthopnea as blood is redistributed from the legs to the central circulation when the patient lies down at night

paroxysmal nocturnal dyspnea due to the reabsorption of interstitial fluid when lying down and reduced sympathetic stimulation while sleeping

fatigue associated with reduced oxygenation and a lack of activity nonproductive cough associated with pulmonary congestion.

Later clinical manifestations of left-sided heart failure may include:

crackles due to pulmonary congestion

hemoptysis resulting from bleeding veins in the bronchial system caused by venous distention

point of maximal impulse displaced toward the left anterior axillary line caused by left ventricular hypertrophy tachycardia due to sympathetic stimulation

S₃ heart sound caused by rapid ventricular filling

S₄ heart sound resulting from atrial contraction against a noncompliant ventricle cool, pale skin resulting from peripheral vasoconstriction

restlessness and confusion due to reduced cardiac output.

Clinical manifestations of right-sided heart failure include:

elevated jugular venous distention due to venous congestion

positive hepatojugular reflux and hepatomegaly secondary to venous congestion right upper quadrant pain caused by liver engorgement

anorexia, fullness, and nausea may be caused by congestion of the liver and intestines nocturia as fluid is redistributed at night and reabsorbed

weight gain due to the retention of sodium and water edema associated with fluid volume excess

ascites or anasarca caused by fluid retention.

CULTURAL DIVERSITY In the Chinese culture, disagreement or discomfort isn't typically displayed openly.

Direct questioning and vigilant assessment skills are necessary to ensure that a patient's quiet nature doesn't mask signs and symptoms that may be life-threatening.

Complications

Acute complications of heart failure include:

pulmonary edema acute renal failure arrhythmias.

Chronic complications include:

activity intolerance renal impairment cardiac cachexia metabolic impairment thromboembolism.

Diagnosis

The following tests help diagnose heart failure:

Chest X-rays show increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly.

Electrocardiography may indicate hypertrophy, ischemic changes, or infarction, and may also reveal tachycardia and extrasystoles.

Laboratory testing may reveal abnormal liver function tests and elevated blood urea nitrogen and creatinine levels.

Echocardiography may reveal left ventricular hypertrophy, dilation, and abnormal contractility.

Pulmonary artery monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial pressure or central venous pressure in right-sided heart failure.

Radionuclide ventriculography may reveal an ejection fraction less than 40%; in diastolic dysfunction, the ejection fraction may be normal.

Treatment

Correction of heart failure may involve:

treatment of the underlying cause, if known

angiotensin-converting enzyme (ACE) inhibitors to patients with left ventricle dysfunction to reduce production of angiotensin II, resulting in preload and afterload reduction

AGE ALERT Older adults may require lower doses of ACE inhibitors because of impaired renal clearance.

Monitor for severe hypotension, signifying a toxic effect.

digoxin for patients with heart failure due to left ventricular systolic dysfunction to increase myocardial contractility, improve cardiac output, reduce the volume of the ventricle, and decrease ventricular stretch

diuretics to reduce fluid volume overload and venous return

beta-adrenergic blockers in patients with New York Heart Association class II or class III heart failure caused by left ventricular systolic dysfunction to prevent remodeling (See Classifying heart failure.)

diuretics, nitrates, morphine, and oxygen to treat pulmonary edema

lifestyle modifications (to reduce symptoms of heart failure) such as weight loss (if obese); limited sodium (to 3 g/day) and alcohol intake; reduced fat intake; smoking cessation; reduced stress; and development of an exercise program. Heart failure is no longer a contraindication to exercise and cardiac rehabilitation.

CULTURAL DIVERSITY Asian Americans consume large amounts of sodium. Encourage an Asian patient to substitute fresh vegetables, herbs, and spices for canned foods, monosodium glutamate, and soy sauce.

coronary artery bypass surgery or angioplasty for heart failure due to coronary artery disease

cardiac transplantation in patients receiving aggressive medical treatment but still experiencing limitations or repeated hospitalizations

other surgery or invasive procedures may be recommended in patients with severe limitations or repeated hospitalizations, despite maximal medical therapy. Some are controversial and may include cardiomyoplasty, insertion of an intra-aortic balloon pump, partial left ventriculectomy, use of a mechanical ventricular assist device, and implanting an internal cardioverter-defibrillator.

AGE ALERT Heart failure in children occurs mainly as a result of congenital heart defects. Therefore, treatment guidelines are directed toward the specific cause.

Hypertension

Hypertension, an elevation in diastolic or systolic blood pressure, occurs as two major types: essential (primary) hypertension, the most common, and secondary hypertension, which results from renal disease or another identifiable cause. Malignant hypertension is a severe, fulminant form of hypertension common to both types. Hypertension is a major cause of cerebrovascular accident, cardiac disease, and renal failure.

Hypertension affects 15% to 20% of adults in the United States. The risk of hypertension increases with age and is higher for blacks than whites and in those with less education and lower income. Men have a higher incidence of hypertension in young and early middle adulthood; thereafter, women have a higher incidence.

Essential hypertension usually begins insidiously as a benign disease, slowly progressing to a malignant state. If

untreated, even mild cases can cause major complications and death. Carefully managed treatment, which may include lifestyle modifications and drug therapy, improves prognosis. Untreated, it carries a high mortality rate. Severely elevated blood pressure (hypertensive crisis) may be fatal.

Causes

Risk factors for primary hypertension include:

family history advancing age

AGE ALERT Older adults may have isolated systolic hypertension (ISH), in which just the systolic blood pressure is elevated, as atherosclerosis causes a loss of elasticity in large arteries. Previously, it was believed that ISH was a normal part of the aging process and should not be treated. Results of the Systolic Hypertension in the Elderly Program (SHEP), however, found that treating ISH with antihypertensive drugs lowered the

incidence of stroke, coronary artery disease (CAD), and left ventricular heart failure.

race (most common in blacks)

CULTURAL DIVERSITY Blacks are at increased risk for primary hypertension when predisposition to low plasma renin levels diminishes ability to excrete excess sodium. Hypertension develops at an earlier age and, at any age, it is more severe than in whites.

obesity tobacco use

high intake of sodium high intake of saturated fat excessive alcohol consumption sedentary lifestyle

stress

excess renin

mineral deficiencies (calcium, potassium, and magnesium) diabetes mellitus.

Causes of secondary hypertension include:

coarctation of the aorta

renal artery stenosis and parenchymal disease brain tumor, quadriplegia, and head injury

pheochromocytoma, Cushing's syndrome, hyperaldosteronism, and thyroid, pituitary, or parathyroid dysfunction oral contraceptives, cocaine, epoetin alfa, sympathetic stimulants, monoamine oxidase inhibitors taken with tyramine, estrogen replacement therapy, and nonsteroidal anti-inflammatory drugs

pregnancy-induced hypertension excessive alcohol consumption.

Pathophysiology

Arterial blood pressure is a product of total peripheral resistance and cardiac output. Cardiac output is increased by conditions that increase heart rate or stroke volume, or both. Peripheral resistance is increased by factors that increase blood viscosity or reduce the lumen size of vessels, especially the arterioles.

Several theories help to explain the development of hypertension, including:

changes in the arteriolar bed causing increased peripheral vascular resistance

abnormally increased tone in the sympathetic nervous system that originates in the vasomotor system centers, causing increased peripheral vascular resistance

increased blood volume resulting from renal or hormonal dysfunction

an increase in arteriolar thickening caused by genetic factors, leading to increased peripheral vascular resistance abnormal renin release, resulting in the formation of angiotensin II, which constricts the arteriole and increases blood volume. (See Understanding blood pressure regulation.)

Prolonged hypertension increases the workload of the heart as resistance to left ventricular ejection increases. To increase contractile force, the left ventricle hypertrophies, raising the oxygen demands and workload of the heart.

Cardiac dilation and failure may occur when hypertrophy can no longer maintain sufficient cardiac output. Because hypertension promotes coronary atherosclerosis, the heart may be further compromised by reduced blood flow to the myocardium, resulting in angina or myocardial infarction (MI). Hypertension also causes vascular damage, leading to accelerated atherosclerosis and target organ damage, such as retinal injury, renal failure, stroke, and aortic aneurysm and dissection.

The pathophysiology of secondary hypertension is related to the underlying disease. For example:

The most common cause of secondary hypertension is chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal artery stenosis interferes with sodium excretion, the renin-angiotensin-aldosterone system, or renal perfusion, causing blood pressure to rise.

In Cushing's syndrome, increased cortisol levels raise blood pressure by increasing renal sodium retention, angiotensin II levels, and vascular response to norepinephrine.

In primary aldosteronism, increased intravascular volume, altered sodium concentrations in vessel walls, or very high aldosterone levels cause vasoconstriction and increased resistance.

Pheochromocytoma is a chromaffin cell tumor of the adrenal medulla that secretes epinephrine and norepinephrine.

Epinephrine increases cardiac contractility and rate, whereas norepinephrine increases peripheral vascular resistance.