INTRODUCTION: We assessed tissue O(2) saturation (StO(2)) and total hemoglobin (HbT) changes during a vascular occlusion test (VOT) as markers of O(2) consumption and cardiovascular reserve. METHODS: Using the non-invasive InSpectra near infrared spectrometer, we studied the effect of VOT to StO(2) < 40% then release on thenar eminence StO(2) and HbT in 15 normal volunteers (controls) and 10 trauma patients. We repeated the VOT four times in controls and twice in patients, with controls exercising during the last VOT, and correlated StO(2) with HbT changes by linear regression analysis. RESULTS: StO(2) started to decrease 3-28 s post-occlusion (latency) in controls and then decreased in a linear fashion (-0.18 +/- 0.04% O(2)/s, mean +/- SD), while post-occlusion StO(2) recovery was rapid (5.20 +/- 1.19% O(2)/s). Exercise decreased latency (0-5 s) and increased desaturation rate (-0.18 and -0.69% O(2)/s, P < 0.005) without altering recovery. Trauma patients showed similar StO(2) desaturation rates, but slower recovery (5.20 +/- 1.19 vs. 2.88 +/- 1.71%/s, P < 0.0001). Repeated VOT gave similar recovery results within study groups. The hyperemic response was variable in both groups and, if present, was associated with an increased HbT. HbT pre- and post-VOT were significantly different within each subject. Although HbT slope of recovery correlated significantly with StO(2) recovery in trauma patients (rho 0.76), it was not in controls. CONCLUSIONS: One VOT defines StO(2) deoxygenation and recovery. That StO(2) and HbT recovery co-vary only in trauma patients suggests that pre-existing vasoconstriction was unmasked by the ischemic challenge consistent with increased sympathetic tone.
INTRODUCTION: We assessed tissue O(2) saturation (StO(2)) and total hemoglobin (HbT) changes during a vascular occlusion test (VOT) as markers of O(2) consumption and cardiovascular reserve. METHODS: Using the non-invasive InSpectra near infrared spectrometer, we studied the effect of VOT to StO(2) < 40% then release on thenar eminence StO(2) and HbT in 15 normal volunteers (controls) and 10 traumapatients. We repeated the VOT four times in controls and twice in patients, with controls exercising during the last VOT, and correlated StO(2) with HbT changes by linear regression analysis. RESULTS: StO(2) started to decrease 3-28 s post-occlusion (latency) in controls and then decreased in a linear fashion (-0.18 +/- 0.04% O(2)/s, mean +/- SD), while post-occlusion StO(2) recovery was rapid (5.20 +/- 1.19% O(2)/s). Exercise decreased latency (0-5 s) and increased desaturation rate (-0.18 and -0.69% O(2)/s, P < 0.005) without altering recovery. Traumapatients showed similar StO(2) desaturation rates, but slower recovery (5.20 +/- 1.19 vs. 2.88 +/- 1.71%/s, P < 0.0001). Repeated VOT gave similar recovery results within study groups. The hyperemic response was variable in both groups and, if present, was associated with an increased HbT. HbT pre- and post-VOT were significantly different within each subject. Although HbT slope of recovery correlated significantly with StO(2) recovery in traumapatients (rho 0.76), it was not in controls. CONCLUSIONS: One VOT defines StO(2) deoxygenation and recovery. That StO(2) and HbT recovery co-vary only in traumapatients suggests that pre-existing vasoconstriction was unmasked by the ischemic challenge consistent with increased sympathetic tone.
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