Treatment of this syndrome is usually limited to the initiation of vasopressors to maintain adequate perfusion pressures via the targeting of a specific mean arterial pressure (MAP). These criteria are relatively non-specific and found in other disease states such as sepsis, adrenal insufficiency, and hepatic failure, among others, with the distinction being the etiology of the shock (infection in the case of sepsis and exposure to extracorporeal circulation in the case of vasoplegia). The exact definition has varied but typically is considered when shock occurs within 24 h of CPB in the setting of a cardiac index (CI) is greater than 2.2 L/kg/m 2 and SVR less than 800 dyne s/cm 5. Vasoplegia is characterized by a normal or augmented cardiac output with low systemic vascular resistance (SVR) causing organ hypoperfusion. The present review discusses the pathophysiology of vasoplegic syndrome and evaluates the various treatment options with insight from personal experience with novel non-catecholamine therapies. Research describing the use of agents in refractory vasoplegic syndrome is limited primarily to case series and case reports. The need for escalating vasopressors is associated with a higher incidence of morbidity and mortality. A large number of patients require vasopressors post-operatively to maintain adequate tissue perfusion. The pathophysiology of vasoplegic syndrome is similar to that of sepsis. Vasoplegic syndrome, a form of vasodilatory shock following cardiopulmonary bypass (CPB), may affect up to half of all patients undergoing major cardiovascular surgery.
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