Abstract
Following cardiopulmonary bypass (CPB) surgery, patients may experience vasoplegic or vasogenic shock syndrome. This condition has a variable incidence, reaching up to 44% in high-risk patients, with mortality rates ranging from 30% to 50%, primarily due to multiple organ failure. This complex condition is characterized by low arterial pressure, unresponsive vascular collapse to high doses of vasopressors, and biochemical signals of cellular oxygen debt. The cardiac output can either be low or abnormally elevated. A fundamental aspect of the pathophysiology of vasogenic syndrome after CPB is related to the dysfunction of vascular smooth muscle cell contraction. This syndrome is often associated with complex cardiac surgery such as reoperations, long periods of bypass and aorta clamping, and excessive blood transfusion. Some potential triggers that might lead to this condition include the preoperative use of antagonists of the renin-angiotensin system, calcium blockers antagonists, and chronic renal disease. Recent literature has advocated treating vasoplegic syndrome after bypass using oxide nitric synthase inhibitors, such as methylene blue and hydroxocobalamin, along with the progressive escalation of potent vasopressors and intravascular volume adjustment.