OBJECTIVE: To assess the effects of arginine vasopressin (AVP) on hemodynamic, clinical, and laboratory variables and to determine its adverse side effects in advanced vasodilatory shock. DESIGN: Retrospective study. PATIENTS: A total of 316 patients. INTERVENTIONS: AVP infusion (4 units/hr). MEASUREMENTS AND MAIN RESULTS: Cardiocirculatory, laboratory, and clinical variables were evaluated before, 0.5, 1, 4, 12, 24, 48, and 72 hrs after administration of AVP. AVP increased mean arterial pressure, systemic vascular resistance, and stroke volume index. Heart rate, central venous pressure, mean pulmonary arterial pressure, norepinephrine, milrinone, and epinephrine requirements decreased. There was no difference in the hemodynamic response between patients with septic shock, postcardiotomy shock, or systemic inflammatory response syndrome. Cardiac index decreased in 41.1% of patients during AVP treatment. In patients with hyperdynamic circulation before AVP, cardiac index decreased, whereas it remained uncharged or tended to increase in patients with normodynamic or hypodynamic circulation. During the course of AVP treatment, liver enzymes (28.5% of patients) and total bilirubin concentrations (69.3% of patients) increased, whereas platelet count decreased (73.4% of patients). Simultaneous hemofiltration significantly contributed to the decrease in platelet count (p < .001) and increase in bilirubin (p < .001). Whereas patients with an increase in bilirubin were more likely to die, a decrease in cardiac index or platelet count and an increase in liver enzymes did not affect mortality. Systemic inflammatory response syndrome as admission diagnosis, a high degree of multiple organ dysfunction, and norepinephrine requirements of >0.5 microg x kg x min before AVP treatment were independent risk factors for death from advanced vasodilatory shock treated with AVP. If norepinephrine dosages exceeded 0.6 microg x kg x min before AVP treatment, a substantial increase in mortality occurred. CONCLUSIONS: Supplementary AVP infusion improved cardiocirculatory function in advanced vasodilatory shock, but an increase in liver enzymes and bilirubin, and a decrease in platelet count occurred during AVP therapy, particularly during simultaneous hemofiltration. Initiation of AVP infusion before norepinephrine requirements exceeding 0.6 microg x kg x min may improve outcome.
OBJECTIVE: To assess the effects of arginine vasopressin (AVP) on hemodynamic, clinical, and laboratory variables and to determine its adverse side effects in advanced vasodilatory shock. DESIGN: Retrospective study. PATIENTS: A total of 316 patients. INTERVENTIONS: AVP infusion (4 units/hr). MEASUREMENTS AND MAIN RESULTS: Cardiocirculatory, laboratory, and clinical variables were evaluated before, 0.5, 1, 4, 12, 24, 48, and 72 hrs after administration of AVP. AVP increased mean arterial pressure, systemic vascular resistance, and stroke volume index. Heart rate, central venous pressure, mean pulmonary arterial pressure, norepinephrine, milrinone, and epinephrine requirements decreased. There was no difference in the hemodynamic response between patients with septic shock, postcardiotomy shock, or systemic inflammatory response syndrome. Cardiac index decreased in 41.1% of patients during AVP treatment. In patients with hyperdynamic circulation before AVP, cardiac index decreased, whereas it remained uncharged or tended to increase in patients with normodynamic or hypodynamic circulation. During the course of AVP treatment, liver enzymes (28.5% of patients) and total bilirubin concentrations (69.3% of patients) increased, whereas platelet count decreased (73.4% of patients). Simultaneous hemofiltration significantly contributed to the decrease in platelet count (p < .001) and increase in bilirubin (p < .001). Whereas patients with an increase in bilirubin were more likely to die, a decrease in cardiac index or platelet count and an increase in liver enzymes did not affect mortality. Systemic inflammatory response syndrome as admission diagnosis, a high degree of multiple organ dysfunction, and norepinephrine requirements of >0.5 microg x kg x min before AVP treatment were independent risk factors for death from advanced vasodilatory shock treated with AVP. If norepinephrine dosages exceeded 0.6 microg x kg x min before AVP treatment, a substantial increase in mortality occurred. CONCLUSIONS: Supplementary AVP infusion improved cardiocirculatory function in advanced vasodilatory shock, but an increase in liver enzymes and bilirubin, and a decrease in platelet count occurred during AVP therapy, particularly during simultaneous hemofiltration. Initiation of AVP infusion before norepinephrine requirements exceeding 0.6 microg x kg x min may improve outcome.
Authors: Matthias Lange; Christian Ertmer; Sebastian Rehberg; Andrea Morelli; Gabriele Köhler; Tim G Kampmeier; Hugo Van Aken; Martin Westphal Journal: Inflamm Res Date: 2010-12-29 Impact factor: 4.575
Authors: Stefan Jochberger; Corinna Velik-Salchner; Viktoria D Mayr; Günter Luckner; Volker Wenzel; Gerda Falkensammer; Hanno Ulmer; Nils Morgenthaler; Walter Hasibeder; Martin W Dünser Journal: Intensive Care Med Date: 2008-09-30 Impact factor: 17.440
Authors: Andrea Morelli; Christian Ertmer; Sebastian Rehberg; Matthias Lange; Alessandra Orecchioni; Valeria Cecchini; Alessandra Bachetoni; Mariadomenica D'Alessandro; Hugo Van Aken; Paolo Pietropaoli; Martin Westphal Journal: Crit Care Date: 2009-08-10 Impact factor: 9.097
Authors: Nameet Jerath; Helena Frndova; Brian W McCrindle; Rebecca Gurofsky; Tilman Humpl Journal: Intensive Care Med Date: 2008-03-19 Impact factor: 17.440