Hypotension and shock

Cardiovascular collapse is the most common life-threatening manifestation of anaphylaxis. It is associated with vasodilation and peripheral pooling of blood, reducing venous return and cardiac output. In addition, plasma loss occurs in many patients.

The precise role of cardiac depression in anaphylaxis is controversial, but there is no doubt that myocardial depression is an unusual primary feature.

The situation with respect to 'cardiac anaphylaxis' can be summarized as follows. The human heart possesses histamine receptors and is responsive to histamine, interleukins, and other mediators. Histamine infused into the heart produces an increase in rate and a reduction in filling pressures, systemic blood pressure, left ventricular end-diastolic pressure, pulmonary artery pressure, and systemic and pulmonary vascular resistance ( Levi 1988) The human heart in vitro has reduced contractility when exposed to histamine. However, depression of cardiac function is rarely described, possibly because the myocardial function is supported by the endogenous catecholamine response. Drugs modifying cardiac function or the sympathoadrenal response make the reaction more severe. The integrity of the myocardium and the myocardial blood supply is a major factor in the response of the heart to both anaphylactic mediators and their effects; patients with cardiac disease are more likely to develop arrhythmias and cardiac failure than those with normal hearts. The cardiac filling pressures in humans rise after type I hypersensitivity, with severe pulmonary vasoconstriction and right ventricular failure occurring in aggregate anaphylaxis and some protamine reactions. The volume deficit in anaphylaxis may be severe; up to half the plasma volume may leak into the periphery within minutes ( FisherJ986).

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