Vasodilatory shock occurs in 5% to 25% of patients after cardiac surgery and results in poor outcomes. 1 It is treated with vasopressor that leads to vasoconstriction of the splanchnic and skeletal circulation, resulting in end-organ hypoperfusion. 2 Although catecholamine vasopressor therapy, its duration, and number of vasopressors used are associated with an increased risk of adverse cardiac and noncardiac events, vasopressin appears to have a more effective and safer profile in the treatment of vasodilatory shock after cardiac surgery. 1,2 Vasopressin, a naturally occurring peptide, produces vasoconstriction by activating V1a receptor, blocking the opening of potassium adenosine triphosphate channels in vascular smooth muscle, and reducing nitric oxide production. 3,4 Vasopressin depletion and decreased circulating levels of vasopressin are fundamental mechanisms responsible for vasodilatory shock after cardiac surgery. 3,5,6 As such, vasopressin is commonly used to treat and prevent vasodilatory shock after cardiac surgery. In a prospective randomized controlled trial, Hajjar and colleagues 1 showed that the use of vasopressin after cardiac surgery is associated with a reduction in 30-day mortality, postoperative renal failure, and postoperative atrial fibrillation compared with norepinephrine. Other investigators previously demonstrated that vasopressin is effective in treating vasodilatory shock after cardiac surgery, sepsis, and other vasodilatory conditions, decreasing catecholamine use with no increase in adverse events. [7][8][9] Low ejection fraction, prolonged cardiopulmonary bypass (CPB), left ventricular assist device insertion, and preoperative use of angiotensin-converting enzyme inhibitors and beta-blockers are predictors of vasodilatory shock after cardiac surgery. 3,6 Despite the profound microvascular dysfunction seen in diabetes, diabetes has not been identified clinically as a risk factor for vasoplegia. However, diabetes is associated with poor outcomes after cardiac surgery. Some of those adverse outcomes can be explained by the microvascular and macrovascular dysfunction seen in diabetic patients, which are exacerbated by CPB. 10