InSpectra St0

Hutchinson Technologies

Please see Bibliography of References for a list of abstracts, manuscripts and posters.

StO2 Proof of Concept

Effect of pharmacologic vasodilation on skeletal muscle oxygen extraction

Simon P, Mesquida J, Suffoletto B, Gomez H, Kellum J, Pinsky M. Crit Care Med.2009;37(12, Suppl):A88.

Introduction: Peripheral vaso-motor paralysis in septic shock impairs regional autoregulation of blood flow and may impair effective skeletal muscle O2 extraction. However, it is unknown whether abnormal O2 utilization is due to either failure of vasoregulation or cellular energetic function. We therefore studied the effect of pharmacologic vasodilation on the rate of tissue O2 saturation (StO2) decrease in response to stagnant ischemia.

Hypothesis: Pharmacologic vasodilation decreases regional O2 uptake independent of metabolic demand.

Methods: A topical 0.6 mg/hr nitroglycerin patch was applied to the thenar eminence of ten healthy volunteers. Using a wide gap near-infrared spectrometer (InSpectra 650, Hutchinson, 15 mm) placed over the same area, thenar StO2 kinetics and tissue hemoglobin index (THI) were recorded during a vascular occlusion test (VOT) of stagnant forearm ischemia to StO2 <40% and release 0,15 and 30 minutes after patch application. We compared the slope of StO2 deoxygenation (%/min) across runs using a paired Wilcoxon Sign-Rank test.

Results: The StO2 deoxygenation slope decreased from baseline to 30 minutes after topical nitroglycerin application (-8.3±1.3 to -6.8±1.4 %/min, p < 0.001). A small decrease was also noted in plateau THI over time (16.3±1.5 to14.9±1.3, p=0.008) and in local skin temperature. There was no significant difference across time points in StO2 reoxygenation slope with release of vascular occlusion, plateau StO2, THI deoxygenation/reoxygenation slope, heart rate, or mean arterial pressure. In 18 other volunteers without vasodilator neither StO2 deoxygenation slope or THI changed between similar sequential VOTs.

Conclusions: Topical nitroglycerin decreases the local rate of microvascular hemoglobin desaturation during stagnant forearm ischemia. Thus, pathologic vasodilation is a potential mechanism for the decreased tissue oxygen extraction seen in septic shock, possibly from supply-demand mismatch and microcirculatory shunt. The concomitant decrease noted in regional tissue hemoglobin content might result from microcirculatory shunting to vessels outside the window of our 15 mm probe.