Searching for non-invasive markers of tissue hypoxia

Juan Puyana,Michael R Pinsky

doi:10.1186/cc5691

Abstract

Tissue hypoxia is a common end product of circulatory shock and a primary target for resuscitation efforts. In this issue Podbregar and Mozina show that thenar tissue O2 saturation (StO2) and mixed venous O2 saturation (SvO2) co-vary in patients in left ventricular failure, but in patients with sepsis StO2 was higher than SvO2. Although StO2 may co-vary with SvO2 they have different determinants such that after shock StO2 may increase well before SvO2 as a result of increased O2 demands to repay O2 debt incurred during hypoperfusion. Thus, the use of StO2 alone to define the endpoint of resuscitation may be misleading.

Highlights

Severe shock is characterized by inadequate O2 delivery relative to metabolic demands [2]
In this issue of the journal Podbregar and Mozina propose the use of tissue oxygen saturation (StO2), monitored noninvasively with near-infrared spectroscopy of the thenar muscle, as a surrogate measurement of tissue perfusion [1]
StO2 was significantly higher in patients with both left ventricular (LV) failure and sepsis than in normal volunteers

Summary

Introduction

Severe shock is characterized by inadequate O2 delivery relative to metabolic demands [2]. In this issue of the journal Podbregar and Mozina propose the use of tissue oxygen saturation (StO2), monitored noninvasively with near-infrared spectroscopy of the thenar muscle, as a surrogate measurement of tissue perfusion [1]. They measured StO2 in patients with left ventricular (LV) failure and with or without sepsis.

Results

Conclusion