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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 (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 vasopressor can only be beneficial in patients with pathological vasodilatation, whereas patients with low systemic blood flow and maintained vascular tone require either fluids and/or an inotrope. In their report Müller and colleagues indiscriminately interchange vasodilatory and cardiogenic shock. However, these forms of shock must be strictly separated when considering the use of a strong vasopressor such as AVP. Some patients with cardiogenic 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. 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 by Müller and coworkers [1]) can decrease high catecholamine dosages, thus attenuating adrenergic stress and myocardial oxygen demand [3].

Vasopressor stays vasopressor and inotrope stays inotrope!