- Email: [email protected]
THE CARDIOVASCULAR EFFECTS OF NITROUS OXIDE IN THE DOG
162
BRITISH JOURNAL OF ANAESTHESIA
CORRESPONDENCE THE CARDIOVASCULAR EFFECTS OF NITROUS OXIDE IN THE DOG
NORMAN W. B. CRAYTHORNE THOMAS D. DARBY
West Virginia University REFERENCE
Eckenhoff, J. E., Hafkcnschiel, J. H., Harmel, M. H., Goodale, W. T., Lubin, M., Bing, R. J., and Kety, S. S. (1948). Measurement of coronary blood flow by the nitrous oxide method. Amer. J. Physiol., 152, 356.
NOTICE REFRESHER COURSE IN ANAESTHESIA for General Practitioners and part-time Anaesthetists MAY 18
TO
MAY 21, 1966
Numbers limited to 30. Particulars from Dr. R. A. FISHER, Postgraduate Medical Centre, Royal Victoria Hospital, Bournemouth, Hampshire.
Printed in Great Britain by John Sherratt & Son Ltd.. Park Road. Aluincham
Downloaded from http://bja.oxfordjournals.org/ at Michigan State University on June 9, 2015
Sir,—We greatly appreciate Dr. Bloch's interest in our paper. However, we do not believe that the points to which he has taken exception are of great importance. Small changes in arterial Pco, cause significant changes in myocardial contractilixy. However, although the change in contractility is statistically significant, it is small and we do not believe that it would lead to any change in our conclusions. In some of the animals studied, sympathetic block was produced so that the role of the sympathetic nervous system during nitrous oxide anaesthesia could be determined. Following sympathetic block, blood pressure was maintained at normal levels with a slow infusion of methoxamine and when the rate of infusion had been titrated against the blood pressure and a "steady state" achieved; nitrous oxide was again administered. It is certainly possible that methoxamine might obscure the action of nitrous oxide on blood pressure. However, no change in blood pressure occurred. Our conclusion was that during nitrous oxide anaesthesia, blood pressure was not maintained by stimulation of the sympathetic nervous system. It is true that after 10 minutes of nitrous oxide inhalation, there will be some difference between the tension of nitrous oxide in myocardium and in the arterial blood. However, we do not believe that it is of great importance. Eckenhoff et al. (1948) have
pointed out that the brain is in equilibrium with the cerebral venous blood within 10 minutes and that, as the myocardium is approximately five times more vascular than the brain, the heart should reach equilibrium even more rapidly than the brain. We believe that in the dogs we studied, the depression of myocardium by nitrous oxide was compensated for by a change in the mechanics of the left ventricle. However, if nitrous oxide were administered to an animal in which the myocardium had already been depressed by other drugs, it would seem quite probable that haemodynamic changes would then appear. Occasionally, following cardiopulmonary bypass, we have seen hypotension with the administration of 75 per cent nitrous oxide in oxygen to patients on whom open heart surgery had just been completed and whose myocardium was impaired by disease, hypothermia and surgical trauma.
BRITISH JOURNAL OF ANAESTHESIA
CORRESPONDENCE THE CARDIOVASCULAR EFFECTS OF NITROUS OXIDE IN THE DOG
NORMAN W. B. CRAYTHORNE THOMAS D. DARBY
West Virginia University REFERENCE
Eckenhoff, J. E., Hafkcnschiel, J. H., Harmel, M. H., Goodale, W. T., Lubin, M., Bing, R. J., and Kety, S. S. (1948). Measurement of coronary blood flow by the nitrous oxide method. Amer. J. Physiol., 152, 356.
NOTICE REFRESHER COURSE IN ANAESTHESIA for General Practitioners and part-time Anaesthetists MAY 18
TO
MAY 21, 1966
Numbers limited to 30. Particulars from Dr. R. A. FISHER, Postgraduate Medical Centre, Royal Victoria Hospital, Bournemouth, Hampshire.
Printed in Great Britain by John Sherratt & Son Ltd.. Park Road. Aluincham
Downloaded from http://bja.oxfordjournals.org/ at Michigan State University on June 9, 2015
Sir,—We greatly appreciate Dr. Bloch's interest in our paper. However, we do not believe that the points to which he has taken exception are of great importance. Small changes in arterial Pco, cause significant changes in myocardial contractilixy. However, although the change in contractility is statistically significant, it is small and we do not believe that it would lead to any change in our conclusions. In some of the animals studied, sympathetic block was produced so that the role of the sympathetic nervous system during nitrous oxide anaesthesia could be determined. Following sympathetic block, blood pressure was maintained at normal levels with a slow infusion of methoxamine and when the rate of infusion had been titrated against the blood pressure and a "steady state" achieved; nitrous oxide was again administered. It is certainly possible that methoxamine might obscure the action of nitrous oxide on blood pressure. However, no change in blood pressure occurred. Our conclusion was that during nitrous oxide anaesthesia, blood pressure was not maintained by stimulation of the sympathetic nervous system. It is true that after 10 minutes of nitrous oxide inhalation, there will be some difference between the tension of nitrous oxide in myocardium and in the arterial blood. However, we do not believe that it is of great importance. Eckenhoff et al. (1948) have
pointed out that the brain is in equilibrium with the cerebral venous blood within 10 minutes and that, as the myocardium is approximately five times more vascular than the brain, the heart should reach equilibrium even more rapidly than the brain. We believe that in the dogs we studied, the depression of myocardium by nitrous oxide was compensated for by a change in the mechanics of the left ventricle. However, if nitrous oxide were administered to an animal in which the myocardium had already been depressed by other drugs, it would seem quite probable that haemodynamic changes would then appear. Occasionally, following cardiopulmonary bypass, we have seen hypotension with the administration of 75 per cent nitrous oxide in oxygen to patients on whom open heart surgery had just been completed and whose myocardium was impaired by disease, hypothermia and surgical trauma.