Myocardial Venous O 2 Saturation Becomes More Heterogeneous during Hypoxic and Carbon Monoxide Hypoxia

Abstract

The hypothesis tested was that myocardial venous O 2 saturation (SvO 2) heterogeneity, a measure of microregional O 2 supply/consumption balance, would increase under hypoxic and CO-hypoxia conditions. Since we are able to determine both O 2 supply and the O 2 supply/consumption ratio, we could also determine whether regional myocardial O 2 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% O 2 (SaO 2 = 56%) or a 6% O 2 (SaO 2 = 40%) gas mixture for 20 min, or CO hypoxia induced by ventilation with a 1% CO gas mixture for either 7 min (SaO 2 = 67%) or 20 min (SaO 2 = 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 O 2 saturations were determined with a four-wavelength microspectrophotometric method. A total of 28 veins (20-100 μm) were examined to determine SvO 2 for each condition within each animal. The coefficient of variation (CV - SD/mean × 100), an index of heterogeneity, was calculated for both flow and SvO 2 under each condition. Flow increased with increasing severity of hypoxia but its heterogeneity did not change with hypoxic or CO hypoxia. However, SvO 2 heterogeneity significantly increased with increasing severity of hypoxia. A linear regression of SvO 2 CV and mean SvO 2 showed a significant correlation (CV = -0.84 (mean SvO 2) + 51.1. R 0.59). All possible myocardial O 2 consumptions were calculated by multiplying all of the flows and O 2 extractions. In 53 subepicardial and subendocardial measurements, only 10% of the flow and O 2 supply/consumption heterogeneity observations could be explained by uniform O 2 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 O 2/min/100 g. Therefore, there must be some regional myocardial O 2 consumption heterogeneity. The increase in venous O 2 saturation heterogeneity during hypoxia may be due to increased variation in regional myocardial O 2 consumption or variation in the control of O 2 supply/consumption coupling.