In low-output failure the cardiac output is often maintained by increases in heart rate, chamber size, and muscle mass. Stroke volume usually falls unless severe bradycardia is present. Acute compensation occurs via sympathetic activation of heart rate. However, over days to weeks, progressive ventricular dilatation increases end-diastolic volume, thereby helping to maintain stroke volume in the face of a falling ejection fraction. By the Laplace law, dilatation will increase systolic wall stress; this is partially offset by a remodeling process in which functioning myofibers hypertrophy. The resultant increase in muscular mass permits an increase in cardiac work, although not at the expense of wall stress. Hypertrophy is a slow compensatory process which will nevertheless adversely affect diastolic function, ventricular compliance, and the end-diastolic pressure-volume relationship.
The left ventricle can be considered an elastic chamber which periodically increases its volume elastance Ve to a value equal to the slope of the relationship between end-systolic pressure and end-systolic volume. The arterial load property is measured as arterial elastance Ea, i.e. the slope of the relationship between arterial end-systolic pressure Pes and stroke volume. The end-systolic elastance Ees varies in response to ventricular contractility, while Pes varies inversely with stroke volume SV for a given end-diastolic volume Ved:
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