Vasoplegic Syndrome (VS)

Recognize it by the numbers, not the feel - Hypotension with a normal-to-high cardiac index and a low SVR while vasopressor doses keep climbing. If the pressure is low and the pump is fine, this is a tone problem — not a volume problem and not a contractility problem.

Know who is going to do it - Rates are highest in patients on ACE inhibitors (44%), calcium channel blockers (47%), and with heparin exposure (55%). ACE inhibitors taken within 8 to 24 hours of general anesthesia make intraoperative hypotension considerably more likely, and there is no ACC/AHA guideline telling you whether to hold them, so practice varies.

Conventional therapy first - Fluid plus phenylephrine or norepinephrine restores hemodynamics in most patients. Vasoplegic syndrome is the subset that does not respond.

Do not just keep adding catecholamine - High-dose vasopressor causes limb and mesenteric ischemia, tissue necrosis, and metabolic acidosis, and norepinephrine reduces pulmonary, cutaneous, renal, and splanchnic blood flow. Vasopressor-dependent patients run higher lactate and creatinine, need renal replacement therapy more often, and stay longer in the ICU.

Vasopressin - Relative vasopressin deficiency is part of the syndrome. It acts on V1 receptors independent of adrenergic signaling, does not provoke arrhythmias, and keeps working in an acidic environment where catecholamines fail. It reduces catecholamine requirement and shows synergy with corticosteroid.

Methylene blue - A guanylyl cyclase inhibitor that interrupts the nitric oxide-cGMP vasodilation pathway. Typical dosing is 1 to 2 mg/kg IV (given over about 5 minutes, or 2 mg/kg infused over 20 minutes) followed in some protocols by 0.25 mg/kg/hr for 48 to 72 hours; maximum 7 mg/kg. It raises SVR and MAP and spares catecholamine. It can be given pre-, intra-, or postoperatively, with postoperative the most common timing. Treat it as an adjunct once you have made the diagnosis, not as a last resort. Dosing varies by institution.

Methylene blue contraindications - Hold it in G6PD deficiency (hemolytic anemia with jaundice and Heinz bodies on smear), in pregnancy (FDA class X, associated with intestinal atresia and fetal death after intra-amniotic injection), and with known hypersensitivity. Use caution in renal failure because it reduces renal blood flow, and in pulmonary hypertension, where reports of its pulmonary vascular effect conflict.

Methylene blue and serotonin - It is a monoamine oxidase inhibitor. Combined with SSRIs, SNRIs, MAOIs, or TCAs it can precipitate serotonin syndrome — diaphoresis, clonus, tremor, altered mental status, autonomic hyperactivity. The threshold reported is around 5 mg/kg, well above therapeutic dosing, but ask about serotonergic drugs before you push it. There is no antidote for methylene blue toxicity.

Expect the blue - Bluish-green urine, limb pain with IV administration, and a significant but transient drop in the pulse oximeter reading. The SpO2 fall is an artifact: the dye interferes with infrared absorption, not with oxygenation. Do not chase it.

Fix the substrate while you treat the tone - Correct hypocalcemia (calcium chloride bolus raises vascular tone and MAP without raising cardiac output). Correct acidemia — vasopressor responsiveness collapses below arterial pH 7.15. Consider hydrocortisone 100 mg every 8 hours or 50 mg every 6 hours for inflammation-mediated vasodilation and relative adrenal insufficiency.

Minimize sedation - Sedatives worsen the hypotension through systemic vasodilation and myocardial depression. In a ventilated patient with vasoplegia, less sedation is part of the hemodynamic plan.

Vasoplegic syndrome (VS) is hypotension with a preserved or high cardiac output, a low systemic vascular resistance, and an escalating vasopressor requirement — classically after cardiac surgery on cardiopulmonary bypass (CPB). There is no consensus threshold, but the working picture is MAP under 65 mmHg, SVR under 700 dyn·s·cm-5, and cardiac index above 2.5 L/min/m2 while running high-dose vasopressor infusions.

The problem is loss of vascular smooth muscle tone: excess nitric oxide driving cyclic GMP-mediated vasorelaxation, relative deficiency of endogenous vasopressin and cortisol, and activation of ATP-sensitive potassium channels by hypoxia, metabolic acidosis, and elevated lactate, which blocks the calcium entry that vasoconstriction requires. Incidence after cardiac surgery runs 5% to 25%. Vasoplegia persisting 36 to 48 hours carries 25% to 28.6% mortality.