Vasopressin deficiency contributes to the vasodilation of septic shock

Background The hypotension of septic shock is due to systemic vasodilation. On the basis of a clinical observation, we investigated the possibility that a deficiency in vasopressin contributes to the vasodilation of septic shock. Methods and Results In 19 patients with vasodilatory septic shock (systolic arterial pressure [SAP] of 92+/-2 mm HE [mean+/-SE], cardiac output [GO] of 6.8+/-0.7 L/min) who were receiving catecholamines, plasma vasopressin averaged 3.1+/-1.0 pg/mL. In 12 patients with cardiogenic shock (SAP, 99+/-7 mm Hg; CO, 3.5+/-0.9 L/min) who were also receiving catecholamines, it averaged 22.7+/-2.2 pg/mL (P<.001). A constant infusion of exogenous vasopressin to 2 patients with septic shock resulted in the expected plasma concentration, indicating that catabolism of vasopressin is not increased in this condition. Although vasopressin is a weak presser in normal subjects, its administration al 0.04 U/min to 10 patients with septic shock who were receiving catecholamines increased arterial pressure (systolic/diastolic) from 92/52 to 146/66 mm Hg (P<.001/P<.05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187 dyne . s/cm(5); P<.001). Furthermore, in 6 patients with septic shock who were receiving vasopressin as the sole presser, vasopressin withdrawal resulted in hypotension (SAP, 83+/-3 mm Hg), and vasopressin administration at 0.01 U/min, which resulted in a plasma concentration (approximate to 30 pg/mL) expected for the level of hypotension, increased SAP from 83 to 115 mm Hg (P<.01). Conclusions Vasopressin plasma levels are inappropriately low in vasodilatory shock, most likely because of impaired baroreflex-mediated secretion. The deficiency in vasopressin contributes to the hypotension of vasodilatory septic shock.