On sepsis, troponin and vasopressin: the bitter truth

Ilse Gradwohl-Matis,Martin W Dünser

doi:10.1186/cc12772

Ilse Gradwohl-Matis, Martin W Dünser

Open Access

https://doi.org/10.1186/cc12772

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Journal: Critical Care	Publication Date: Jan 1, 2013
Citations: 2	License type: cc-by

Affiliation: Paracelsus Medical University

Abstract

One of the rationales for the use of vasopressin in septic shock has been its potential cardioprotective mechanisms. Lower heart rates, higher arterial pressures, and fewer norepinephrine doses during vasopressin therapy were hypothesized to protect the heart from myocardial ischemia. In a prospective sub-study of the VASST (Vasopressin in Septic Shock Trial) project, Mehta and colleagues specifically evaluated this hypothesis but failed to find lower cardiac biomarkers or fewer ischemic electrocardiogram changes in patients receiving vasopressin compared with subjects receiving norepinephrine alone. After recent evidence of a lacking survival benefit, the present study results further challenge the future role of vasopressin as a vasopressor in septic shock.

Highlights

One of the rationales for the use of vasopressin in septic shock has been its potential cardioprotective mechanisms
During a time when the intensivists’ belief in the beneficial effects of vasopressors andnormal arterial pressures on tissue perfusion remained unchallenged, vasopressin was propagated as a non-adrenergic vasopressor in various shock states
*Correspondence: m.duenser@salk.at Department of Anesthesiology, Perioperative and General Intensive Care Medicine, Salzburg General Hospital and Paracelsus Private Medical University, Müllner Hauptstrasse 48, 5020. This hypothesis was tested by Mehta and colleagues in a prospective sub-study of the randomized controlled Vasopressin in Septic Shock Trial (VASST) [1]

Summary

Introduction

One of the rationales for the use of vasopressin in septic shock has been its potential cardioprotective mechanisms. During a time when the intensivists’ belief in the beneficial effects of vasopressors and (sub)normal arterial pressures on tissue perfusion remained unchallenged, vasopressin was propagated as a non-adrenergic vasopressor in various shock states.

Results

Conclusion