Vasoplegic Syndrome

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Vasoplegic syndrome (VS) is a well-known form of vasodilatory shock that occurs in up to 44% of patients after cardiac surgery employing cardiopulmonary bypass (CPB)(1). CPB is often associated with a systemic inflammatory response and transient vascular dysfunction that results in profound and persistent vasodilation, leading to a decrease in systemic vascular resistance that grounds severe hypotension refractory to proper fluid resuscitation, and an increased requirement for vasopressors despite of high or normal cardiac outputs (2).

Although the exact mechanisms that lead to the development of VS are unknown, it is thought that it may be related to depletion of natural vasopressors during CPB (3), excessive complement activation (4), and the development of systemic inflammatory response syndrome (SIRS) (5, 6).
SIRS post cardiac surgery is believed to be induced by factors such as surgical trauma, changes in body temperature, blood exposure to non-physiologic surfaces, endotoxin release and ischemia-reperfusion of the myocardium (7, 8).

When blood passes through the CPB equipment, plasma proteins are immediately absorbed to biomembranes generating a
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These acute responses abide as CPB be continues. However, transfusion of blood from the salvage mechanism (cell saver) contributes to the pathogenesis of cardiac vasoplegia. This blood has hemolyzed erythrocytes, denatured proteins, fat globules and platelet and leukocyte aggregates. These fragments potentially stimulate inflammatory responses. Additionally, an ischemia-reperfusion syndrome occurs after aortic cross clamp, causing neutrophils to adhere to endothelial cells and the release of free radicals, which can cause direct damage to the tissues. The result is increased capillary permeability, interstitial edema and reduced intravascular volume

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