[Effects of tachycardia on ischemic canine hearts during nitrous oxide-oxygen-halothane anesthesia]

Effects of tachycardia on left ventricular function, myocardial metabolism and intramyocardial pH under nitrous oxide-oxygen-halothane anesthesia, were studied in 11 canine hearts with critical coronary stenosis. A comparison was made with coronary occlusion. Critical stenosis was produced using a screw occluder to limit the left anterior descending coronary artery blood flow to prevent reactive hyperemia after 10 second occlusion. The degree of ischemia was estimated by intramyocardial pH, arterio-venous lactate and potassium. Intramyocardial pH was measured with a hydrogen ion-selective electrode implanted in the subendocardium. Tachycardia was induced by right cardiac sympathetic nerve stimulation. After 7 min tachycardia in dogs with coronary stenosis, intramyocardial pH decreased significantly from 7.09 +/- 0.10 to 6.83 +/- 0.15, then tended to return toward control levels over a period of 20 min after cessation of tachycardia, although some did not return to the control level even after 30 min. Regarding LV function, LVP and positive LV dp/dt max did not increase. Negative LV dp/dt max decreased significantly. The time constant (T) was prolonged but not significantly, while LVEDP rose considerably from 8.2 +/- 4.1 mmHg to 14.6 +/- 6.8 mmHg. In contrast, after 7 min occlusion, intramyocardial pH decreased significantly from 7.14 +/- 0.08 to 6.72 +/- 0.15 and recovered after 15 min. LVP decreased slightly. Positive and negative LV dp/dt max decreased significantly. T was not prolonged initially, but after reperfusion prolonged significantly. LVEDP increased significantly from 7.9 +/- 3.3 mmHg to 11.9 +/- 6.3 mmHg. In summary, tachycardia in dogs with coronary stenosis under nitrous oxide-oxygen-halothane anesthesia caused regional ischemia. The degree of ischemia was slightly less than with occlusion, but LV diastolic dysfunction was more prominent.