Anaesthesia for abdominal vascular surgery in patients with coronary artery disease (CAD), part I: isoflurane produces dose–dependent coronary vasodilation

The effects of anaesthesia for major abdominal vascular surgery on coronary flow regulation and mechanisms of myocardial ischaemia were studied in 56 patients with CAD, using a randomized, partly double–blinded protocol. After induction with fentanyl (3 μg–kg^-1) and thiopentone (2–4 mg kg^-1) and tracheal intubation, principal anaesthetics were nitrous oxide/oxygen (60/40) with isoflurane (n = 20), halothane (n = 19) or fentanyl (15–20 μg kg^-1) (n = 17). Conventional invasive techniques and coronary venous retrograde thermodilution were used to assess systemic and coronary haemodynamics. Coronary vascular resistance was estimated from myocardial oxygen extraction. Myocardial ischaemia was diagnosed by 12–lead ECG and/or anterior wall motion abnormalities by cardiokymography and/or myocardial lactate production. When adjustment of anaesthetic dose was insufficient for haemodynamic control, iv phenylephrine and nitroglycerine were adminstered to treat hypotension and hypertension or cardiac failure respectively. Measurements were performed at four specific intervals; awake, before surgery and 10 and 30 min after abdominal incision. Comparable changes of systemic haemodynamics and myocardial oxygen consumption were observed in the three groups. Coronary vasodilation was evidenced in isoflurane patients only and was linearly dose–dependent (P < 0.001). Partial Least Squares Projections to Latent Structures modelling with cross validation confirmed this dose–dependency and ruled out a clinically measurable influence by intervention drugs or simultaneous systemic haemodynamic abnormalities. The incidence of myocardial ischaemia during anaesthesia and surgery was comparable in the three groups (35, 37 and 24%, respectively) and there was an association with systemic haemodynamic aberrations in 19 of the 27 ischaemic episodes. In contrast to ischaemic halothane and fentanyl patients, isoflurane patients with ischaemia had significantly lower myocardial oxygen extraction (P = 0.008 and P = 0.001, respectively), indicating that the oxygen extraction reserve was not utilized in a normal way during ischaemia.     

Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anaesthesia in man

Seven normoventilated and five hyperventilated healthy adults undergoing cholecystectomy and anaesthetized with methohexitone, fentanyl and pancuronium were studied with measurement of cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and quantified electroencephalography (EEG) under two sets of conditions: 1) 1.7% end-tidal concentration of isoflurane in air/oxygen; 2) 0.85% end-tidal concentration of isoflurane in nitrous oxide (N2O)/oxygen. The object was to study the effects of N2O during isoflurane anaesthesia on cerebral circulation, metabolism and neuroelectric activity. N2O in the anaesthetic gas mixture caused a 43% (P less than 0.05) increase in CBF during normocarbic conditions but no significant change during hypocapnia. CMRO2 was not significantly altered by N2O. EEG demonstrated an activated pattern with decreased low frequency activity and increased high frequency activity. The results confirm that N2O is a potent cerebral vasodilator in man, although the mechanisms underlying the effects on CBF are still unclear.