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Pathophysiology of Congestive Heart Failure

The syndrome of CHF arises as a consequence of an abnormality in cardiac structure, function, rhythm, or conduction. In developed countries, ventricular dysfunction accounts for the majority of cases and results mainly from myocardial infarction, hypertension, or in many cases both. Degenerative valve disease, idiopathic cardiomyopathy, and alcoholic cardiomyopathy are also major causes of heart failure. Heart failure often occurs in elderly patients who have multiple comorbid conditions (eg, angina, hypertension, diabetes, and chronic lung disease). Some common
comorbidities such as renal dysfunction are multifactorial (decreased perfusion or volume depletion from overdiuresis).



The determinants of cardiac output include heart rate and stroke volume. The stroke volume is further determined by the preload (the volume that enters the left ventricle), contractility, and afterload (the impedance of the flow from the left ventricle). These variables are important in understanding the pathophysiologic consequences of heart failure and the potential treatments.


The pathophysiology behind CHF includes not only a structural abnormality; it also includes the cardiovascular response to poor perfusion with the activation of the neurohumoral system.10 Activation of the renin-angiotensin system attempts to increase preload by stimulating retention of salt and water, increasing vasoconstriction (and, thus, afterload), and augmenting cardiac contractility.