A physiological model of factors that determine skeletal muscle hemoglobin oxygen saturation

Abstract

A mathematical model for hemoglobin oxygen saturation (StO2) in skeletal muscle was derived from Poiseuille's equation, the Fick principle, and from published data on skeletal muscle hemodynamics and oxygen consumption (VO2). The model shows that StO2 is about 85% under resting conditions of blood flow, arterial oxygen content and VO2. 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. 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 hematocrit (Hct) from 40 to 60% has no effect on StO2; however, increasing the Hct to 80% reduces StO2 because blood viscosity increases more than blood O2 carrying capacity. Reducing Hct from 40 to 20% decreases StO2 because O2 carrying capacity decreases more than blood viscosity. The predictions of the model closely parallel clinical observations of thenar muscle StO2 when monitored in normal subjects and trauma patients. Therefore, the model helps to explain how changes in patient status before and during resuscitation alter StO2.