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Vasopressin‐induced changes in splanchnic blood flow and hepatic and portal venous pressures in liver resection
Author(s) -
Sand Bown L.,
Ricksten S.E.,
Houltz E.,
Einarsson H.,
Söndergaard S.,
Rizell M.,
Lundin S.
Publication year - 2016
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.12684
Subject(s) - vasopressin , splanchnic , medicine , splanchnic circulation , portal venous pressure , anesthesia , blood volume , central venous pressure , hyperdynamic circulation , cardiac output , hemodynamics , blood flow , cardiology , vascular resistance , blood pressure , portal hypertension , cirrhosis , heart rate
Background To minimize blood loss during hepatic surgery, various methods are used to reduce pressure and flow within the hepato‐splanchnic circulation. In this study, the effect of low‐ to moderate doses of vasopressin, a potent splanchnic vasoconstrictor, on changes in portal and hepatic venous pressures and splanchnic and hepato‐splanchnic blood flows were assessed in elective liver resection surgery. Methods Twelve patients were studied. Cardiac output ( CO ), stroke volume ( SV ), mean arterial ( MAP ), central venous ( CVP ), portal venous ( PVP ) and hepatic venous pressures ( HVP ) were measured, intraoperatively, at baseline and during vasopressin infusion at two infusion rates (2.4 and 4.8 U/h). From arterial and venous blood gases, the portal (splanchnic) and hepato‐splanchnic blood flow changes were calculated, using Fick′s equation. Results CO , SV , MAP and CVP increased slightly, but significantly, while systemic vascular resistance and heart rate remained unchanged at the highest infusion rate of vasopressin. PVP was not affected by vasopressin, while HVP increased slightly. Vasopressin infusion at 2.4 and 4.8 U/h reduced portal blood flow (−26% and −37%, respectively) and to a lesser extent hepato‐splanchnic blood flow (−9% and −14%, respectively). The arterial‐portal vein lactate gradient was not significantly affected by vasopressin. Postoperative serum creatinine was not affected by vasopressin. Conclusion Short‐term low to moderate infusion rates of vasopressin induced a splanchnic vasoconstriction without metabolic signs of splanchnic hypoperfusion or subsequent renal impairment. Vasopressin caused a centralization of blood volume and increased cardiac output. Vasopressin does not lower portal or hepatic venous pressures in this clinical setting.