Heart failure
A syndrome characterized by myocardial dysfunction, heart failure leads to impaired pump performance (reduced cardiac output) or to frank heart failure and abnormal circulatory congestion. Congestion of systemic venous circulation may result in peripheral edema or hepatomegaly; congestion of pulmonary circulation may cause pulmonary edema, an acute, life-threatening emergency.
Pump failure usually occurs in a damaged left ventricle (left-sided heart failure) but may occur in the right ventricle (right-sided heart failure) either as a primary disorder or secondary to left-sided heart failure. Sometimes left- and right-sided heart failure develop simultaneously.
Although heart failure may be acute (as a direct result of myocardial infarction), it’s generally a chronic disorder associated with sodium and water retention by the kidneys. Advances in diagnostic and therapeutic techniques have greatly improved the outlook for patients with heart failure, but the prognosis still depends on the underlying cause and its response to treatment.
Causes
Heart failure may result from a primary abnormality of the heart muscle (such as an infarction), inadequate myocardial perfusion due to coronary artery disease, or cardiomyopathy. Other causes include:
❑ mechanical disturbances in ventricular filling during diastole when there’s too little blood for the ventricle to pump, as in mitral stenosis secondary to rheumatic heart disease or constrictive pericarditis and atrial fibrillation
❑ systolic hemodynamic disturbances such as excessive cardiac workload due to volume overloading or pressure overload that limit the heart’s pumping ability.
These disturbances can result from mitral or aortic insufficiency, which causes volume overloading, and aortic stenosis or systemic hypertension, which results in increased resistance to ventricular emptying.
Reduced cardiac output triggers three compensatory mechanisms: ventricular dilation, hypertrophy, and increased sympathetic activity. These mechanisms improve cardiac output at the expense of increased ventricular work.
Cardiac dilation
In cardiac dilation, an increase in end-diastolic ventricular volume (preload) causes increased stroke work and stroke volume during contraction, stretching cardiac muscle fibers beyond optimum limits and producing pulmonary congestion and pulmonary hypertension, which lead in turn to right-sided heart failure.
Ventricular hypertrophy
In ventricular hypertrophy, an increase in muscle mass or the diameter of the left ventricle allows the heart to pump against increased resistance (impedance) to the outflow of blood.
An increase in 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 myocardial contractility.
Increased sympathetic activity
As a response to decreased cardiac output and blood pressure, increased sympathetic activity occurs by enhancing 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, which respond by reducing the glomerular filtration rate and increasing tubular reabsorption of sodium and water, in turn expanding the circulating blood volume. This renal mechanism, if unchecked, can aggravate congestion and produce overt edema.
Chronic heart failure may worsen as a result of respiratory tract infections, pulmonary embolism, stress, increased sodium or water intake, and failure to comply with the prescribed treatment regimen.
Signs and symptoms
Heart failure is usually classified by the site of failure (left-sided, right-sided, or both). It may also be classified as systolic or diastolic. These classifications represent different clinical aspects of heart failure, not distinct diseases.
Left-sided heart failure primarily produces pulmonary signs and symptoms; right-sided heart failure primarily produces systemic signs and symptoms. However, heart failure often affects both sides of the heart.
Left-sided heart failure
Clinical signs of left-sided heart failure include dyspnea, orthopnea, crackles, possibly wheezing, hypoxia, respiratory acidosis, cough, cyanosis or pallor, palpitations, arrhythmias, elevated blood pressure, and pulsus alternans. Symptoms are due to decreased left ventricular output, which results in fluid accumulation in the lungs.
Right-sided heart failure
Clinical signs of right-sided heart failure include dependent peripheral edema, hepatomegaly, splenomegaly, jugular vein distention, ascites, slow weight gain, arrhythmias, hepatojugular reflex, abdominal distention, nausea, vomiting, anorexia, weakness, fatigue, dizziness, and syncope. Right-sided heart failure is often caused by disorders that increase vascular resistance (such as pulmonary embolism or stenosis, or hypertension).
Systolic failure
Systolic failure occurs when the heart’s ability to contract effectively decreases. This causes a decrease in the cardiac output and the ejection fraction. Clinical signs of systolic dysfunction include an S3 gallop, normal or low blood pressure, and an ejection fraction of less than 40%.
Diastolic failure
Diastolic failure occurs when the heart has a problem relaxing. The heart can’t properly fill with blood because the muscle has become stiff and noncompliant. Clinical signs of diastolic failure include an S4, elevated blood pressure, and a normal or near normal ejection fraction.
Complications
Complications of heart failure typically include pulmonary edema, venostasis with a predisposition to thromboembolism (associated primarily with prolonged bed rest), cerebral insufficiency, and renal insufficiency with severe electrolyte imbalance. (See Pulmonary edema: How to intervene.)
Diagnosis
The following tests are used to diagnose heart failure:
❑ Electrocardiography reflects heart strain, enlargement, and ischemia. It may also reveal atrial enlargement, tachycardia, and extrasystole.
❑ Chest X-ray shows increased pulmonary vascular markings, interstitial edema, pleural effusion, and cardiomegaly.
❑ Pulmonary artery monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, elevated left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial pressure or central venous pressure in right-sided heart failure.
❑ Echocardiography demonstrates left ventricular dysfunction with a reduced ejection fraction.
❑ Brain natriuretic peptide (BNP) assay detects abnormal hormone levels produced by failing ventricles.
❑ Cardiopulmonary exercise testing determines oxygen consumption and severity of heart failure.
Treatment
The aim of therapy is to improve pump function by reversing the compensatory mechanisms that are producing the symptoms. Heart failure can be controlled by treatment consisting of:
❑ diuresis to reduce total blood volume and circulatory congestion; spironolactone, a potassium-sparing diuretic, and nesiritide, a recombinant form of human BNP, are helpful
❑ vasodilators and angiotensin-converting enzyme inhibitors to increase cardiac output by reducing the impedance to ventricular outflow (afterload)
❑ digoxin to strengthen myocardial contractility
❑ beta-adrenergic blockers to improve ejection fraction and reduce morbidity and mortality
❑ dietary restrictions, such as restricted sodium and limiting fluid intake to 2 L/day
❑ biventricular pacemaker to control ventricular dyssynchrony
❑ antiembolism stockings to prevent venostasis and thromboembolus.
UNDER STUDY: An innovative approach to heart failure that remains under investigation is cellular cardiomyoblasty, the transplantation of autologous ex-vivo expanded cells into the myocardium. The transplanted muscle cells promote heart muscle regeneration.
Special considerations
During the acute phase:
❑ Place the patient in high Fowler’s position, and give him supplemental oxygen to help him breathe more easily.
❑ Weigh the patient daily, and check for peripheral edema. Carefully monitor his I.V. intake and urine output, vital signs, and mental status. Auscultate the heart for abnormal sounds (S3 gallop) and the lungs for crackles or rhonchi.
❑ Frequently monitor levels of blood urea nitrogen and serum creatinine, potassium, sodium, chloride, and magnesium.
❑ The patient should have continuous cardiac monitoring during acute and advanced stages to identify and treat arrhythmias promptly.
❑ To prevent deep vein thrombosis due to vascular congestion, assist the patient with range-of-motion exercises. Enforce bed rest and apply antiembolism stockings. Check regularly for calf pain and tenderness.
❑ Allow adequate rest periods.
Before discharge:
❑ Advise the patient to avoid foods high in sodium, such as canned or commercially prepared foods and dairy products, to curb fluid overload.
❑ Explain to the patient that the potassium he loses through diuretic therapy must be replaced by taking a prescribed potassium supplement and eating potassium-rich foods, such as bananas, apricots, and orange juice.
❑ Stress the need for regular checkups.
❑ Emphasize the importance of taking digoxin exactly as prescribed. Tell the patient to watch for and immediately report signs of toxicity, such as anorexia, vomiting, and yellow vision.
❑ Tell the patient to promptly report any pulse irregularities. He should also report dizziness, blurred vision, shortness of breath, persistent dry cough, palpitations, increased fatigue, paroxysmal nocturnal dyspnea, swollen ankles, decreased urine output, and rapid weight gain (5 to 21 lb [2.5 to 9.5 kg] in a week).
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
Other Book Chapters Related to Heart symptoms
Read excerpts from these other book chapters related to Heart symptoms:
Medical Books Excerpts
- Cardiomegaly
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright Details: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.
More About Causes of Heart symptoms
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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