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Management of Vasodilatory Shock After Cardiac Surgery: Identification of Predisposing Factors and Use of a Novel Pressor Agent

M. Argenziano MD, JM Chen MD, AF Choudhri BS, S. Cillinane BA, E. Garfein BA, AD Weinberg MS, CR Smith, Jr. MD, EA Rose MD, DW Landry MD, PhD, MA Oz MD. J Thorac Cardiovasc Surg 1998;116:973-980.

Reviewer: Jane C.K. Fitch, M.D.

Baylor College of Medicine

The Methodist Hospital

Houston, Texas

Summary: This investigation reports on a novel treatment for profound vasodilation encountered following cardiopulmonary bypass (CPB). This vasodilatory hypotension is a manifestation of the inflammatory response to CPB. The investigators translated their knowledge of the role of arginine vasopressin (AVP) in vasodilatory shock states to its use postCPB. 145 cardiac surgery patients were studied prospectively and an additional group of patients receiving arginine vasopressin for vasodilatory shock after LVAD or heart transplantation (OHT) were studied retrospectively. Vasodilatory shock was defined as MAP < 70 mmHg, CI > 2.5 L/min and dependence upon norepinephrine. Logistic regression analysis was used to investigate predictors of vasodilatory shock. The criteria for vasodilatory shock were met in 11/145 patients (8%). EF < 35% and ACE inhibitors were independent predictors of postCPB vasodilatory shock based on both univariate regression and multivariate analysis. Serum arginine vasopressin concentrations were low in cases of vasodilatory shock, at 12.0 6.6 pg/mL. Blood pressure was enhanced and catecholamine requirements were decreased in cases of vasodilatory shock treated with arginine vasopressin. The arginine vasopressin dose administered was 0.01 to 0.1 U/kg, yielding plasma concentrations of 150 pg/mL. This is 10 to 25% of the dose usually administered to patients with cirrhosis to control esophageal variceal bleeding.

Discussion: CPB induces a total body inflammatory response, mediated by endothelial injury, cytokine release, and other inflammatory mediators. Interleukins promote vasodilation through increased levels of intracellular cGMP. Ischemia/reperfusion injury contributes to vasodilation by activating potassium channels and inhibiting calcium channels. Catecholamines are most commonly used to treat this syndrome, however, patients frequently develop catecholamine resistance and potentially toxic side effects. These mediators cause a vasodilatory shock syndrome, which, in this study, is associated with arginine vasopressin deficiency. Atrial natriuretic peptide (ANP) is known to inhibit arginine vasopressin secretion. In addition, autonomic dysfunction is known to contribute to arginine vasopressin deficiency. It is hypothesized that the efficacy of arginine vasopressin is dependent upon its ability to counteract vasodilatory mechanisms. This is also a possible mechanism explaining the restoration of catecholamine sensitivity frequently encountered following arginine vasopressin administration. This study provides compelling data that we may now have another drug in our armamentarium to use to treat postCPB vasodilatory shock. It remains to be seen if this state, based on arginine vasopressin levels, can be predicted and thus treated prophylactically.