Nitrous oxide augments the systemic and coronary haemodynamic effects of isoflurane in patients with ischaemic heart disease.

The effects of 70% nitrous oxide, added to 1% end-tidal isoflurane and administered by intermittent positive pressure ventilation (IPPV), on coronary haemodynamics and myocardial oxygenation were investigated in 10 patients with ischaemic heart disease. Standard methods were used for determination of their central haemodynamic effects. Coronary blood flow was measured by the retrograde thermodilution technique and coronary sinus blood sampled for measurement of myocardial oxygen consumption and lactate extraction. One per cent end-tidal isoflurane decreased systemic blood pressure (-39%) by a combination of systemic vasodilation and reduction in cardiac performance. Coronary blood flow remained unaltered despite the fall in coronary perfusion pressure and myocardial oxygen consumption (-30%) and extraction (-30%) fell significantly. Ischaemic ECG changes parallelled by decreased myocardial lactate extraction or lactate production were recorded in 6 of the 10 patients during steady state isoflurane anaesthesia. When nitrous oxide was added to isoflurane there was a fall in heart rate (-13%), a further reduction in systemic blood pressure (-18%) and myocardial oxygen consumption (-31%) and extraction (-17%) whereas all other variables including coronary blood flow remained unaltered. The myocardial ischaemia was worsened in three of the six patients with ECG and metabolic signs of impaired oxygenation during isoflurane alone. It is concluded that nitrous oxide potentiates the systemic and coronary haemodynamic effects of isoflurane in patients with coronary artery disease. The mechanisms for myocardial ischaemia seem to be decreased coronary perfusion pressure and/or redistribution of coronary blood flow by direct coronary vasodilation.