Isoflurane reduced systemic arterial pressure to presternotomy levels within 6.9 ± 0.7 minutes, but induced myocardial lactate production in 2 of 22 patients, likely due to reflex tachycardia.
The effect of isoflurane on regional myocardial metabolism and blood flow, when used as an adjunct to fentanyl-nitrous oxide anesthesia, to control intraoperative hypertension was investigated. Twenty-two patients with two- or three-vessel coronary artery disease with an ejection fraction >0.5 and on beta-blockers up to the morning of surgery were studied during elective coronary artery by-pass grafting. Systemic and pulmonary hemodynamics, and regional (great cardiac vein, GCVF) myocardial blood flow and myocardial metabolic parameters were measured. In 10 patients, both GCVF and global (coronary sinus, CSF) myocardial blood flows were recorded. Measurements were made 1) after induction of anesthesia but prior to skin incision, 2) during sternotomy, and 3) during isoflurane administration after its use to reduce arterial pressure to the presternotomy level. The increase in systemic arterial pressure during sternotomy was due to an increase in systemic vascular resistance accompanied by increases in heart rate, pulmonary capillary wedge pressure, (PCWP) regional myocardial oxygen consumption and extraction, GCVF and total coronary vascular resistance. Isoflurane reduced systemic arterial pressure but not PCWP, to presternotomy levels within 6.9 ± 0.7 minutes at an end-tidal concentration of 1.5 ± 0.2%. Isoflurane induced a pronounced systemic and coronary vasodilatation and increases in cardiac index, heart rate and regional myocardial oxygen extraction while the GCVF/CSF ratio remained unchanged. While mean regional—MLE% values were not effected by sternotomy, in two patients myocardial lactate production was seen during sternotomy but not during isoflurane. In another two patients, isoflurane induced lactate production. The two latter patients differed from the group as a whole mainly because of their higher heart rates during isoflurane. We conclude that isoflurane may induce myocardial ischemia even in the abscence of hypotension. This in turn may be caused by an isoflurane-induced reflex tachycardia and not necessarily redistribution of coronary flow. On the other hand, isoflurane may also have beneficial effects on stress-induced myocardial ischemia.
Sahlman et al. (1989) studied Coronary artery disease (n=22). Isoflurane vs. Sternotomy without isoflurane was evaluated on Systemic and pulmonary hemodynamics, regional myocardial blood flow, and myocardial metabolic parameters. Isoflurane reduced systemic arterial pressure to presternotomy levels within 6.9 ± 0.7 minutes, but induced myocardial lactate production in 2 of 22 patients, likely due to reflex tachycardia.