PATHOPHYSIOLOGY OF HEART-FAILURE

Citation
Jh. Patterson et Kf. Adams, PATHOPHYSIOLOGY OF HEART-FAILURE, Pharmacotherapy, 13(5), 1993, pp. 190000073-190000081
Citations number
29
Categorie Soggetti
Pharmacology & Pharmacy
Journal title
ISSN journal
02770008
Volume
13
Issue
5
Year of publication
1993
Part
2
Pages
190000073 - 190000081
Database
ISI
SICI code
0277-0008(1993)13:5<190000073:POH>2.0.ZU;2-L
Abstract
Heart failure, a major contributor to cardiovascular disease morbidity and mortality, is newly diagnosed in approximately 400,000 patients e ach year, and is particularly prevalent in individuals over age 65 yea rs. Average mortality rates 5 years after diagnosis are 45-60%, and ma y be as high as 50% after 1 year for those with New York Heart Associa tion class IV heart disease. Heart failure occurs when myocardial musc le dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechan isms are overwhelmed or maladaptive. Pathologic classifications are br oadly based on the presence of systolic (dilated cardiomyopathy) or di astolic (hypertrophic or restrictive cardiomyopathies) dysfunction. Th e etiologies of heart failure may include inadequate coronary blood fl ow, pressure or volume overload, cardiomyopathy, or pericardial diseas e. Coronary artery disease, idiopathic dilated cardiomyopathy, and hyp ertension are the most frequent causes, and certain drugs may also wor sen myocardial function. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may i nduce fluid retention to compensate for the perceived low output and r educed circulating blood volume. Fluid retention in turn causes preloa d or filling pressure to increase and symptoms of pulmonary congestion to emerge. Depressed contractility also results in a reduction in blo od pressure, leading to compensatory neurohormonal activation and vaso constriction, which significantly elevate afterload and further reduce stroke volume. The overall approach to heart failure includes definin g the etiology, identifying precipitant factors, and assessing the sev erity of myocardial dysfunction and clinical symptoms. By carefully ch aracterizing the patient with congestive heart failure, the most effec tive plan of nonpharmacologic and pharmacologic interventions can be i nitiated.