Myocardial venous O₂ saturation becomes more heterogeneous during hypoxic and carbon monoxide hypoxia

The hypothesis tested was that myocardial venous O₂ saturation (SvO₂) heterogeneity, a measure of microregional O₂ supply/consumption balance, would increase under hypoxic and CO-hypoxia conditions. Since we are able to determine both O₂ supply and the O₂ supply/consumption ratio, we could also determine whether regional myocardial O₂ consumption was heterogeneous. Twenty open-chest anesthetized dogs were studied under control and four hypoxic conditions, hypoxic hypoxia induced by ventilation with either an 8% O₂ (SaO₂ = 56%) or a 6% O₂ (SaO₂ = 40%) gas mixture for 20 min, or CO hypoxia induced by ventilation with a 1% CO gas mixture for either 7 min (SaO₂ = 67%) or 20 min (SaO₂ = 40%). Regional myocardial blood flow was measured using radioactive microspheres in 40 pieces (~ 0.5 g) of the left ventricular free wall. Arterial and venous O₂ saturations were determined with a four-wavelength microspectrophotometric method. A total of 28 veins (20-100 μm were examined to determine SvO₂ for each condition within each animal. The coefficient of variation (CV = SD/mean × 100), an index of heterogeneity, was calculated for both flow and SvO₂ under each condition. Flow increased with increasing severity of hypoxia but its heterogeneity did not change with hypoxic or CO hypoxia. However, SvO₂ heterogeneity significantly increased with increasing severity of hypoxia. A linear regression of SvO₂ CV and mean SvO₂ showed a significant correlation (CV = -0.84 (mean SvO₂) + 51.1, R = 0.59). All possible myocardial O₂ consumptions were calculated by multiplying all of the flows and O₂ extractions. In 53 subepicardial and subendocardial measurements, only 10% of the flow and O₂ supply/consumption heterogeneity observations could be explained by uniform O₂ consumption if our acceptance criterion was 0.06-0.1 ml O₂/min/100 g, and 50% could be explained with an acceptance criterion of 0.3-0.4 ml O₂/min/100 g. Therefore, there must be some regional myocardial O₂ consumption heterogeneity. The increase in venous O₂ saturation heterogeneity during hypoxia may be due to increased variation in regional myocardial O₂ consumption or variation in the control of O₂ supply/consumption coupling.