Myocardial surface Po2 - an indicator of myocardial tissue oxygenation?

The validity of myocardial surface tissue Po2 (PtO2) as a reliable indicator of transmural myocardial tissue oxygenation was studied in six anaesthetised, open chest pigs. Epicardial surface Pto2 was correlated with other variables of myocardial tissue oxygenation such as regional blood flow, coronary venous Po2, O2 saturation, PCO2 and regional myocardial lactate extraction. The study design was based on an experimental model in which the effects of a pacing induced tachycardia on tissue oxygenation of ischaemic and normally supplied myocardium were measured. Two platinum multiwire surface electrodes were placed on the epicardium, on the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (CX). The LAD was constricted to reduce mean surface Pto2 in the LAD area to about 50% of its baseline value. This did not affect surface Pto2 in the CX area. The reduction of surface Pto2 in the LAD area was associated with decreases in coronary venous Po2 and O2 saturation and with increases in coronary venous lactate and PCO2. Subendocardial regional blood flow and the subendocardial to subepicardial flow ratio were significantly lower than in the CX area. Increasing the heart rate by pacing (+45 beats·min−1) led to an increased degree of ischaemia as shown by fall in surface Pto2 in the LAD area to values around zero kPa, by marked increase in coronary venous lactate and PCO2, by reduction in total (−10%) and subendocardial (−40%) LAD flow and by deterioration of the subendocardial to subepicardial flow ratio. The increased degree of ischaemia was not accompanied by an increase in O2 extraction. The marked decrease in surface Pto2 occurred in spite of a slight increase in the subepicardial regional blood flow (+10%); thus the increase in O2 delivery was not sufficient to meet the increase in O2 demand. Total flow was increased by 27% in the CX area without changes in the subendocardial to subepicardial flow ratio and in the surface Pto2 values. When pacing was stopped, surface values of Pto2 in the LAD area returned to prepacing values, as did lactate extraction and coronary venous PCO2. Clear and close relationships with surface Pto2 were found for regional lactate extraction, coronary venous PCO2 and the normalised subendocardial RBF. Poor or no correlations were found for the normalised subepicardial regional blood flow, the coronary venous O2 saturation and the absolute values of subendocardial and subepica