Cardiac Function During Hypovolemia

Abstract

Shock is defined by an impaired tissue perfusion which causes malfunction of vital organs. An inadequate cardiac output and/or maldistribution of blood flow can induce shock providing that vital organs are underperfused. An inappropriate cardiac output may result from an inadequate filling of the heart and/or an impairment of pump function. Restrictive changes of the heart walls or obstruction within the cardiac chambers may jeopardize cardiac filling, but the most common cause of heart failure in shock is a reduction of venous return due to absolute or relative hypovolemia. Changes in autonomic function which occur with hypovolemia limit many of the detrimental effects of reduced cardiac output. If the hypovolemia is severe or persists over a long period of time, the compensatory changes of cardiac function may deteriorate to progressive cardiac failure. Cardiac output is determined by four physiologic parameters: preload (end-diastolic fiber length), afterload (ventricular wall tension during ejection), contractility, and heart rate (Weems and Downey 1992; Guyton 1991). The changes in the cardiac factors induced by lack of intravascular volume and the associated systemic response of the organism are primarily dependent on the amount of volume loss (Table 1).