Heart failure is a syndrome in which the heart is unable to pump an adequate supply of blood to meet the body’s metabolic needs. To compensate for decreased cardiac output, there is an increase in sympathetic nervous system activity and stimulation of renin-angiotensin-aldosterone output and ADH release. These neurohormonal compensatory mechanisms temporarily aid in maintaining an adequate cardiac output but are thought to contribute to cardiac remodeling (changes in the structure of the ventricle [e.g., dilation, hypertrophy]). The increase in fluid volume that results from increased aldosterone and ADH causes elevated pressure in the cardiac chambers, which stimulates the release of natriuretic peptides (atrial natriuretic factor [ANF] and brain natriuretic peptide [BNP]). These hormones counteract the effects of the increased levels of norepinephrine, renin, angiotensin II, and aldosterone and promote sodium and water excretion and vasodilation. Chronic distention of the heart chambers eventually exhausts stores of these natriuretic hormones and the effects of norepinephrine, renin, aldosterone, and ADH prevail, leading to heart failure.
Numerous conditions can lead to heart failure including coronary artery disease, myocardial infarction, cardiomyopathy, cardiac valve malfunction, hypertension, congenital heart defects, and systemic conditions that increase the metabolic rate (e.g., thyrotoxicosis, infection) or cause prolonged or severe hypoxia. Heart failure can be classified in a number of ways. It is often classified as left-sided or right-sided, backward or forward, and/or systolic or diastolic failure. A functional classification system based on the relationship between symptoms and the amount of activity needed to provoke the symptoms was developed by the New York Heart Association and is commonly used by many practitioners. In this system, which has 4 levels or classes, a person is said to have Class I heart failure if no symptoms are experienced with ordinary physical activity and Class IV failure when symptoms occur with any physical activity and possibly at rest.
Signs and symptoms of heart failure are dependent on which side of the heart is failing as well as whether there is forward or backward failure. Symptoms of forward failure are caused by low cardiac output. Symptoms of backward failure are associated with the ventricle failing to empty completely, which results in blood flow backup. In left-sided failure, there is reduced emptying of the left ventricle, which results in decreased systemic tissue perfusion as well as blood flow backup in the left atrium and pulmonary vasculature. Pulmonary vascular congestion leads to pulmonary edema with symptoms such as tachypnea, dyspnea, cough, and abnormal breath sounds. In right-sided failure, the effect of reduced function and emptying of the right ventricle is decreased pulmonary blood flow and backup of blood in the right atrium. This results in systemic venous congestion, which is manifested by peripheral edema and signs of major organ enlargement and dysfunction. Initially only one side of the heart may fail (more commonly the left side), but as failure progresses, both sides are usually affected.
The focus of treatment is to improve performance of the failing heart. Diuretic therapy and an angiotensin converting enzyme (ACE) inhibitor remain the cornerstone of treatment. A positive inotropic agent is often added to ameliorate symptoms. Recent studies have shown that the addition of a beta-adrenergic blocking agent and spironolactone also improve the clinical status of many persons with chronic heart failure. It is thought that ACE inhibitors, beta blockers, and spironolactone interfere with the compensatory neurohormonal activity that occurs with heart failure and alter the course of cardiac remodeling, subsequently slowing disease progression. The pharmacological treatment of heart failure varies somewhat depending on whether the client has systolic failure (an impaired inotropic state characterized by inadequate ventricular emptying) or diastolic failure (impaired filling of the ventricle). Positive inotropic agents are contraindicated for treatment of diastolic failure.
As long as the body’s compensatory mechanisms and/ or treatment measures are able to maintain cardiac output that is sufficient to prevent or relieve symptoms, a state of compensated heart failure exists. If the myocardium is severely damaged and intrinsic compensatory mechanisms and treatment measures fail to maintain adequate cardiac output and tissue perfusion, a state of decompensated heart failure exists. When this state persists and is no longer responsive to medical treatment, it is termed intractable or refractory heart failure.
Decreased cardiac output
Impaired respiratory function
ineffective breathing pattern
ineffective airway clearance
impaired gas exchange
Risk for imbalanced fluid and electrolytes
fluid volume excess
third-spacing of fluid
Imbalanced nutrition: less than body requirements
Risk for impaired tissue integrity
Disturbed sleep pattern
Risk for falls
acute pulmonary edema
Deficient knowledge, Ineffective therapeutic regimen management, or Ineffective health maintenance
Disturbed thought processes