Open Access

Searching for non-invasive markers of tissue hypoxia

Critical Care200711:116

https://doi.org/10.1186/cc5691

Published: 23 February 2007

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.

In this issue of the journal Podbregar and Mozina propose the use of tissue oxygen saturation (StO2), monitored non-invasively 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. They reasoned that StO2 would discriminate between patients with low cardiac output and preserved or unimpaired O2 extraction ratio (not present in septic patients) from those septic patients with poor ventricular function and low O2 extraction ratio as assessed by SvO2 [1]. Not unexpectedly, they found the lowest StO2 values in patients with LV failure without sepsis. Interestingly, StO2 was significantly higher in patients with both LV failure and sepsis than in normal volunteers. Unfortunately, the authors did not address the fundamental differences between peripheral StO2 and SvO2 even though they suggest that SvO2 may replace StO2 in the absence of sepsis. These issues deserve comment.

Severe shock is characterized by inadequate O2 delivery relative to metabolic demands [2]. Unfortunately, present monitoring techniques for the assessment of O2 delivery and O2 utilization are invasive, impracticable, give an incomplete picture of the circulation, and may not be useful in guiding effective resuscitation, as documented by the poorer outcomes for SvO2-guided therapy in patients with established shock [3, 4]. Recently, however, early goal-directed therapy in patients with sepsis presenting to an emergency department improves outcome when central venous O2 saturation is used as one of the endpoints of resuscitation [5]. Still, neither SvO2 nor central venous O2 provide any insight on the state of oxygen utilization in tissues.

The relationship between StO2 and SvO2 is not always predictable. Although StO2 should decrease when tissues are starved of O2 relative to their needs, the physiological events dictating changes in StO2 and SvO2 are different. Ischemic tissues initially sustain metabolism by anaerobic respiration, leading to an 'O2 debt' shown by a transient increase in O2 consumption during reoxygenation. Similarly, StO2 must increase before SvO2 increases because its increase is the cause of the increase in SvO2. SvO2 may therefore remain low for a while despite normalization of StO2. Thus, with decreases in O2 delivery one would expect both SvO2 and StO2 to decrease in parallel, but with resuscitation StO2 should increase before SvO2.

Shock is a complex process with neurovascular, metabolic and inflammatory responses occurring simultaneously. Changes in StO2 capture the vasoconstriction associated with reduced cardiac output during progressive hypovolemia. In fact, StO2 is as good a predictor of multiple organ dysfunction syndrome in trauma patients as base deficit, with the advantage that StO2 is continuous and noninvasive [6]. Initially, the O2 extraction ratio in hemorrhagic shock is high, and cellular metabolism is not compromised. However, as flow decreases, extremity flow usually decreases first; therefore decreases in thenar StO2 should occur before significant visceral ischemia develops, and when thenar StO2 has recovered after resuscitation most other organs should also show resolution of ischemia. Unfortunately, when shock progresses to generalized mitochondial dysfunction, tissue wellness will not be captured by StO2 values alone. Therefore an ideal noninvasive monitoring platform for shock should indicate not only that O2 delivery is impaired but also the extent to which this has affected cell metabolism. Such parameters may include tissue pH, partial pressure of CO2, and ideally the levels of a mitochondrial function product such as NADH. Furthermore, many of these changes are dynamic and multidirectional depending on the integrity of the patient's compensatory response and the timeliness and effectiveness of the resuscitation.

It is necessary to understand the hysteresis of the StO2 response throughout the continuum of shock and resuscitation. Such information is lacking in the report by Podbregar and Mozina. However, a physiologic perturbation such as inducing a brief episode of forearm ischemia as a circulatory stress test, to note the rapidity of re-oxygenation upon release, may be more revealing about the physiologic reserve of the patient and the metabolic activity of the muscle. We have used this approach in a fashion similar to that of De Blasi and colleagues [7]. Our preliminary study [8] supports previously published findings that resting StO2 levels in both normal volunteers and patients with sustained circulatory shock are not dissimilar and thus cannot be used for early monitoring of tissue hypoperfusion [9]. However, by inducing an occlusion stress, emergent parameters can be defined that allow one to assess local metabolic demand and reperfusion reserve. Potentially, this approach might prove useful in clinical decision making. We are still searching for measures of circulatory adequacy, and non-invasive measures of StO2 reflect one exciting avenue of exploration. Let us use it to define the adequacy of resuscitation therapy in those in circulatory shock. Whether its value may or may not track SvO2 is less of an issue than its potential to define circulatory sufficiency.

Abbreviations

LV: 

left ventricular

StO2

thenar tissue O2 saturation

SvO2

mixed venous O2 saturation.

Declarations

Authors’ Affiliations

(1)
Associate Professor of Surgery and Critical Care, Innovative Medical & Information Technology Center, UPMC, Director Applied Research IMITs Center,F1265 Presbyterian
(2)
Professor of Critical Care Medicine, Bioengineering and Anesthesiology

References

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Copyright

© BioMed Central Ltd 2007

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