Abstract
In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow. Depending on the infusion rate, this vasoconstriction also reduces coronary blood flow despite an increased coronary perfusion pressure. In a porcine model of transitory myocardial ischemia-induced left ventricular dysfunction, Müller and colleagues now report that the AVP-related coronary vaso-constriction may impede diastolic relaxation while systolic contraction remains unaffected. Although any AVP-induced myocardial ischemia undoubtedly is a crucial safety issue, these findings need to be discussed in the context of the model design, the dosing of AVP as well as the complex direct, afterload-independent and systemic, vasoconstriction-related effects on the heart.
Highlights
How does Müller and colleagues’ study compare with the existing literature? The observed cerebral and renal vasoconstriction confirms findings by Malay and colleagues: incre
In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow
In the previous issue of Critical Care Müller and colleagues reported that arginine vasopressin (AVP) after porcine myocardial ischemia reduced the cardiac output and the brain, coronary and kidney blood flow [1]
Summary
How does Müller and colleagues’ study compare with the existing literature? The observed cerebral and renal vasoconstriction confirms findings by Malay and colleagues: incre-. In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow.
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