Management of vasoplegia

Abstract

Vasoplegia and vasoplegic syndrome (VS) are common sequelae of the inflammatory system following sepsis, anaphylaxis, intoxication, pancreatitis, different states of shock and procedures such as cardiopulmonary bypass (CPB). During CPB, 5–25% of patients may have this complication. It presents with decreased systemic vascular resistance, high cardiac output, increased fluid demand, all symptoms often intractable. This apparent paralysis of the vascular system is a result of activation of vasodilator mechanisms coupled with resistance to innate and exogenous vasoconstrictor mechanisms. Predominantly, the is overactivity of nitric oxide (NO) and deficiency of vasopressin.¹