The effects of
enflurane with and without
nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease.
Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC
enflurane-
nitrogen-
oxygen (70/30) to 1MAC
enflurane-
nitrous oxide-
oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%).
Enflurane-
nitrogen-
oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During
enflurane-
nitrous oxide-
oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during
enflurane-
nitrogen. During
enflurane-
nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with
nitrous oxide. It is concluded that
enflurane is a powerful coronary
vasodilator and in this respect slightly less potent than
isoflurane.
Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing
hypotension.
Nitrous oxide added to
enflurane depresses cardiac function and augments the coronary vasodilatory effect of
enflurane to a level at which coronary blood flow becomes totally pressure dependent.