Circulatory or distributive shock occurs when blood volume is abnormally displaced in the vasculature—for example, when blood volume pools in peripheral blood vessels. The displacement of blood volume causes a relative hypovolemia because not enough blood returns to the heart, which leads to subsequent in-adequate tissue perfusion. The ability of the blood vessels to con-strict helps return the blood to the heart. Thus, the vascular tone is determined both by central regulatory mechanisms, as in blood pressure regulation, and by local regulatory mechanisms, as in tis-sue demands for oxygen and nutrients. Therefore, circulatory shock can be caused either by a loss of sympathetic tone or by re-lease of biochemical mediators from cells.
The varied mechanisms leading to the initial vasodilation in circulatory shock further subdivide this classification of shock into three types: (1) septic shock, (2) neurogenic shock, and anaphylactic shock.
The different types of circulatory shock cause variations in the pathophysiologic chain of events and are explained here separately. In all types of circulatory shock, massive arterial and venous dila-tion allows blood to pool peripherally. Arterial dilation reduces sys-temic vascular resistance. Initially, cardiac output can be high in circulatory shock, both from the reduction in afterload (systemic vascular resistance) and from the heart muscle’s increased effort to maintain perfusion despite the incompetent vasculature secondary to arterial dilation. Pooling of blood in the periphery results in de-creased venous return. Decreased venous return results in de-creased stroke volume and decreased cardiac output. Decreased cardiac output, in turn, causes decreased blood pressure and ulti-mately decreased tissue perfusion. Figure 15-6 presents the patho-physiologic sequence of events in circulatory shock.