Vasopressor stays vasopressor and inotrope stays inotrope! 英文参考文献.docVIP

Available online /content/12/2/415 Letter Vasopressor stays vasopressor and inotrope stays inotrope! Günter Luckner1, Walter R Hasibeder2 and Martin W Dünser1 1Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse, 6020 Innsbruck, Austria 2Department of Anesthesiology and Critical Care Medicine, Krankenhaus der Barmherzigen Schwestern, Ried im Innkreis, Austria Corresponding author: Martin W Dünser, Martin.Duenser@i-med.ac.at Published: 14 April 2008 Critical Care 2008, 12:415 (doi:10.1186/cc6850) This article is online at /content/12/2/415 ? 2008 BioMed Central Ltd See related research by Müller et al., /content/12/1/R20 We should like to comment on the interesting work reported by Müller and colleagues [1]. We feel that the results of their experiment were predictable and that arginine vasopressin shock will subsequently develop an additional vasodilatory component [2]. Although they require an inotrope at early stages, a vasopressor may be useful to restore a (sub)normal vascular tone at later stages. (AVP) was not indicated in that setting. Infusing a vasoconstrictor without relevant inotropic potential in an acute low flow state with maintained or increased vascular tone must further augment organ vascular resistance and thereby reduce cardiac output. In the critical care setting, a We therefore believe that this experiment does not appropriately reflect the clinical situation and does not support the conclusion that AVP, as a rule, should not be applied in patients with myocardial infarction and cardiogenic shock. Indeed, preliminary clinical experience suggests that when overwhelming systemic inflammation translates into vasodilatation in some patients with cardiogenic shock, the addition of AVP (attaining plasma levels as observed after AVP withdrawal