Cardiac (or myocardial) failure of acute onset or of chronic duration is the result of a structural and/or biochemical remodeling of the myocardium. This, in turn, compromises the contractile performance of the myocardium. The hypertrophic growth of myocytes and the architectural transformation of ventricular chamber size and shape--while initially useful compensatory responses--do not prevent the inevitable appearance of pump failure where oxygen delivery to the metabolizing tissues becomes inadequate. Indeed, the severity of cardiac failure can be judged from the level of oxygen consumption that elicits this state of impaired oxygen supply and demand. A better understanding of the mechanical behavior of the ventricular chamber, including its elastic and resistive properties, together with recent advances in our ability to measure instantaneous ventricular pressure and volume, may prove useful in identifying pathologic features of hypertrophy and dilatation in individual patients. In grading the severity of failure and comparing groups of patients, a normalization of the mechanical parameters by differences in chamber size, shape, and mass is necessary. Symptomatic cardiac failure, based invariably on inadequate oxygen delivery and/or pulmonary congestion, is more commonly the result of ventricular systolic dysfunction. Abnormalities in diastolic function, including ventricular relaxation and filling, while less common and often associated with preserved systolic pump function, do occur. Finally, it must be recognized that the failing ventricle carries an additional hydraulic load that arises from the arterial circulation to which it is coupled.(ABSTRACT TRUNCATED AT 250 WORDS)