Journal of Applied Physiology
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J Appl Physiol 104: 475-481, 2008. First published November 15, 2007; doi:10.1152/japplphysiol.00600.2007
8750-7587/08 $8.00
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Noninvasively determined muscle oxygen saturation is an early indicator of central hypovolemia in humans

Babs R. Soller,1 Ye Yang,1 Olusola O. Soyemi,1 Kathy L. Ryan,2 Caroline A. Rickards,2 J. Matthias Walz,1 Stephen O. Heard,1 and Victor A. Convertino2

1Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and 2U. S. Army Institute of Surgical Research, Fort Sam Houston, Texas

Submitted 5 June 2007 ; accepted in final form 13 November 2007

Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and fat corrected deep muscle oxygen saturation (SmO2) and pH to standard hemodynamic parameters for early detection of imminent hemodynamic instability. Muscle SmO2 and pH were determined with a novel near infrared spectroscopic (NIRS) technique. Heart rate (HR) was measured continuously via ECG, and arterial blood pressure (BP) and stroke volume (SV) were obtained noninvasively via Finometer and impedance cardiography on a beat-to-beat basis. SmO2 and SV were significantly decreased during the first LBNP level (–15 mmHg), whereas HR and BP were late indicators of impending cardiovascular collapse. SmO2 declined in parallel with SV and inversely with total peripheral resistance, suggesting, in this model, that SmO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand. Spectroscopic determination of SmO2 is noninvasive and continuous, providing an early indication of impending cardiovascular collapse resulting from progressive reduction in central blood volume.

tissue oxygen; near infrared spectroscopy; physiological monitoring; hemodynamic instability; lower body negative pressure



Address for reprint requests and other correspondence: B. R. Soller, Dept. of Anesthesiology, UMass Medical School, 55 Lake Ave North, Worcester, MA 01655 (e-mail: babs.soller{at}umassmed.edu)







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