Vasopressin and Postcardiopulmonary Bypass Refractory Hypotension

To the Editor: Overand and Teply [1] recently described a patient with intractable hypotension after cardiopulmonary bypass (CPB) who improved dramatically after the administration of vasopressin (VP). We wish to make a few comments regarding experimental and clinical data suggesting that VP is a promising therapeutic tool. First, in addition to its potent vasoconstricting effects, VP stimulates the endothelial release of prostaglandins and nitric oxide (NO) in the pulmonary, coronary, and mesenteric vascular beds [2,3]. Hence, the regional heterogeneity in VP receptor density and the balanced relaxant/constrictive effects of VP contribute to maintain cardiac circulatory output with minimal risk of myocardial ischemia. Second, although deficient release of VP has been documented in some patients with septic shock or with a ventricular assist device, reversal of vasodilatory hypotension with VP has been achieved regardless of the plasma concentration of VP [4]. Third, VP inhibits interleukin-1 beta-induced NO production in vascular smooth muscle, leading to restoration of vascular reactivity to endogenous contractile mediators such as endothelin, thromboxane A2, and catecholamines [5]. Taken together, these data lend support to the hypothesis that VP can partially reverse the adrenergic hyporesponsiveness associated with sepsis and circulatory bypass. Likewise, because the renin-angiotensin system modulates the central release of VP [6], we hypothesize that the impaired adrenergic response often observed in patients chronically treated with angiotensin-converting enzyme inhibitors [7] can be normalized with subpressor doses of VP. Finally, in the case of combined surgical procedure (aortic and mitral valve replacement) and prolonged CPB (>6 h), one may question whether ultrafiltration could prevent the occurrence of vasodilatory hypotension through attenuation of the systemic inflammatory response elicited by CPB and surgical trauma. Intraoperative ultrafiltration reduces the circulating levels of several biological markers of inflammatory cascade and could contribute to lesser postoperative blood loss, better hemodynamic control, and earlier extubation after cardiac surgery [8].