Because of increasing curricular responsibilities, I am no longer conducting animal research. However, during 2009, I began to conduct modeling studies to examine  quantitatively the factors responsible for determining skeletal muscle hemoglobin oxygen saturation, particularly as occurs in shock and trauma patients. An abstract of this work that was recently presented at the 2009 Ohio Physiological Society meeting is found below:
 

A PHYSIOLOGICAL MODEL OF FACTORS THAT DETERMINE SKELETAL MUSCLE HEMOGLOBIN OXYGEN SATURATION 

Richard E. Klabunde, Department of Biomedical Sciences, Ohio University Heritage College of Osteopathic Medicine, Athens, OH 45701; klabunde@ohio.edu

With the advent of instruments utilizing near infrared spectroscopy (InSpectra™StO₂ Tissue Oxygenation Monitor, Hutchinson Technology Inc.) for the non-invasive measurement of hemoglobin oxygen saturation in tissues (StO₂), it is now possible to assess tissue oxygenation in shock for critically ill or traumatically injured patients. To better understand the significance of these clinical measurements, the present study utilized fundamental physiological principles to show how changes in systemic arterial pressure, vascular resistance, tissue blood flow, blood hematocrit, and O₂ consumption affect StO₂ in skeletal muscle. Predicted changes in StO₂ were then compared to changes in StO₂ measured in patients for the purpose of better understanding StO₂ measurements.

A mathematical model was derived from well-established principles of hemodynamics (Poiseuille’s equation) and oxygen balance (Fick principle), and from experimental data on skeletal muscle hemodynamics. The calculations assumed normal published values for muscle blood flow and oxygen consumption, and uniform tissue perfusion. Average StO₂ was approximated by calculating venous O₂ saturation. The relationship between hematocrit and relative blood viscosity was based on published studies from blood perfused dog limbs. The effects of low shear rate on apparent viscosity were not incorporated into the model (i.e., viscosity was assumed to be independent of flow).

The model shows that under resting conditions of muscle blood flow, arterial oxygen content and muscle oxygen consumption, StO₂ is about 85%, which agrees with human subjects in which StO₂ is measured in the thenar muscle of the hand. A 40% reduction in flow caused either by reducing perfusion pressure or increasing vascular resistance reduces StO₂ from 85 to 75%. Flow reductions greater than 40% cause large, disproportionate decreases in StO₂.  At any given flow, a change in oxygen consumption (VO₂) causes a reciprocal change in StO₂. For example, if blood flow is reduced by 50% and then VO₂ is increased two-fold (e.g., by muscle contraction), StO₂ decreases from 70 to 40%. If VO₂ decreases as flow decreases, which occurs in low flow states, a paradoxical increase in StO₂ may result. At a given perfusion pressure, increasing Hct from 40 to 60% has no effect on StO₂ because the increase in blood viscosity (which reduces flow) is offset by the increase in O₂ carrying capacity of the arterial blood; however, increasing the Hct to 80% leads to a reduction in StO₂ because viscosity is increased more than O₂ carrying capacity. Reducing Hct from 40 to 20% decreases StO₂ at a given perfusion pressure because O₂ carrying capacity is reduced more than viscosity is reduced.

The predictions of the model closely parallel clinical observations of thenar muscle StO₂ when monitored in shock patients. Therefore, the model helps to explain how changes in patient hemodynamic status before and during resuscitation efforts alter StO₂.