A departmental policy addressing chemical substance abuse.

Substance abuse is a major socioeconomic problem. However, the ready availability of potent narcotic and sedative drugs probably constitutes a unique risk for anesthesiologists. Until recently, few anesthesia departments were prepared to recognize or safely manage afflicted colleagues. Because we felt it important to educate our staff and residents and to have a response mechanism established prior to the advent of a substance abuse problem, a departmental committee was formed to develop a Substance Abuse Policy. The policy has served to increase our general awareness and to direct our actions effectively when dealing with physician impairment. It is presented here in the belief that other departments might find it useful in tailoring their approach to this problem.

Errors in measurement of oxygen uptake due to anesthetic gases.

Errors in measurement of exhaled gas volume, mixed expired oxygen and carbon dioxide concentrations, and inspired oxygen concentration and the presence of exhaled anesthetic agents cause errors in on-line calculated oxygen uptake that increase geometrically with increasing inspired oxygen concentration. No one has quantified the decrease in the magnitude of the error that might be realized if directly measured nitrogen concentration were included in the calculation. We used a computer model to evaluate this improvement, assuming an oxygen uptake of 200 ml/min and normal ventilatory parameters. Using a Monte Carlo technique, we generated 100 sets of data points, with random errors averaging 0.5% around the expected gas concentrations, and compared the accuracy of oxygen uptake calculated with and without inclusion of directly measured inspired and expired nitrogen concentrations. When the inspired oxygen fractions were 0.2, 0.5, and 0.8, the calculated oxygen uptakes +/- % standard deviation were 200 +/- 4.3, 200 +/- 12, and 196 +/- 21 when directly measured nitrogen was included versus 200 +/- 3.5, 196 +/- 16, and 205 +/- 71 when it was not. The procedure was repeated, assuming 50 ml/min of anesthetic excretion and the calculated oxygen uptakes were 200 +/- 4.6, 202 +/- 12, and 195 +/- 17 versus 212 +/- 3.8, 251 +/- 17, and 398 +/- 64. Including direct measurement of inhaled and exhaled concentrations of nitrogen or another insoluble inert tracer gas allows accurate measurement of oxygen uptake, even in the presence of exhaled anesthetic gases. It also decreases the error in oxygen uptake determination by a factor of nearly six when the inhaled oxygen fraction is 0.8.

Cerebral blood flow and metabolism during morphine--nitrous oxide anesthesia in man.

The effects of two levels of morphine-nitrous oxide anesthesia on cerebral blood flow (CBF) and cerebral metabolism (CMRO2) were measured in healthy male volunteers. CBF and metabolic measurements were made in the awake control state, after morphine, 1 mg/kg, with 70 per cent nitrous oxide and 30 per cent oxygen, and at a total dose of 3 mg/kg morphine with the same concentrations of nitrous oxide and oxygen. Ventilation was controlled and carbon dioxide added to inspired gas to maintain PaCO2 constant at 40 torr. CBF was 48.2 +/- 4.4 (SEM) ml/100 g/min during the control phase; 45.7 +/- 6.4 ml/100 g/min after 1 mg/kg morphine, and 44.3 +/- 4.9 ml/100 g/min after 3 mg/kg morphine. The latter values are not significantly different from control. Cerebral metabolic rates for oxygen, glucose, and lactate were normal in the control phase and did not change significantly when morphine was present at either level. It is concluded that morphine-nitrous oxide anesthesia produces no alteration of cerebral blood flow or metabolism in normal man at the two dose levels studies.

Postoperative respiratory effects of morphine and halothane anesthesia: a study in patients undergoing cardiac surgery.

Lung volumes, deadspace, ventilation, and ventilatory response to CO2 challenge were studied on the day before and for the first three days after corrective cardiac surgery. Ten patients underwent coronary artery bypass grafting and ten patients had mitral valve prostheses inserted. Half of the patients in each group received halothane as the major anesthetic, and the other half received morphine sulfate (1-2 mg/kg). Mitral valve-replacement patients anesthetized with morphine showed lower CO2 sensitivity on the first postoperative day than those who received halothane. Patients who had coronary artery bypass grafts tended to hyperventilate during the postoperative period, but this did not occur on the first postoperative day in those who received morphine anesthesia. Respiratory rate was always higher postoperatively, most markedly in patients who receivedhalothane for coronary artery bypass grafts. Vital capacity was diminished by 67 per cent in all groups postoperatively. VD/VT tended to increase during the first and second postoperative days and then decrease toward control values on the third postoperative day in all groups except valve-replacement patients who received morphine. Morphine anesthesia may increase the period of mechanical ventilation necessary after cardiac surgery partly as a result of impaired CO2 sensitivity.

Sodium bicarbonate and systemic hemodynamics in volunteers anesthetized with halothane.

The cardiovascular effects of acute metabolic alkalosis (NaHCO3) in normal male volunteers anesthetized with halothane were measured. Pure metabolic alkalosis was studied by maintaning the end-tidal carbon dioxide tension at 40 torr. In each subject, cardiac index increased and total peripheral resistance decreased after each dose of NaHCO3. The increased cardiac index was associated with increased central blood volume, left ventricular minute work index, stroke index, and heart rate. Systolic time intervals showed increased myocardial performance. NaHCO3 administered to volunteers whose hearts were depressed by halothane appeared to cause peripheral vasodilation, volume expansion, and myocardial stimulation. The authors conclude that NaHCO3 administered during halothane anesthesia decreases total peripheral resistance and may lead to severe hypotension.

Cardiovascular responses to calcium administered intravenously to man during halothane anesthesia.

Calcium chloride (7 mg/kg) was administered intravenously to six healthy volunteers anesthetized with halothane. Cardiovascular changes were measured during constant ventilation and anesthetic depth under three conditions: 1) respiratory alkalosis, 2) normocarbia, and 3) respiratory acidosis. At each Paco2, calcium infusion significantly increased cardiac index, left ventricular minute work index, and stroke index. Heart rate, total peripheral resistance, and cardiac pre-ejection period decreased. No significant change in mean arterial blood pressure or central venous pressure followed calcium administration, and no arrhythmias occurred. It is concluded that calcium administration increases myocardial performance, presumably by increasing the availability of intracellular calcium ion for actomyosin interaction.

Effects of morphine-nitrous oxide anesthesia on cerebral autoregulation.

The effects of morphine-nitrous oxide anesthesia on cerebral autoregulation were studied in healthy male volunteers. Anesthesia was morphine, 2 mg/kg, and 70 per cent nitrous oxide in oxygen. Ventilation was controlled and carbon dioxide added to keep Paco-2 constant at 40 torr. Cerebral blood flow was measured first at the subject's normal mean arterial blood pressure, than at 60 torr and at 120 torr in a randomly assigned balanced order. Last, in five subjects cerebral blood flow was measured again at normal mean pressure. Blood pressure alteration was accomplished using phenylephrine or trimethaphan. Cerebral blood flow was 38.9 plus or minus 6.4 (SEM) ml/100 g/min at normal mean pressure, 49.5 plus or minus 10.7 ml/100 g/min at 60 torr. These values are not different a P IS LESS THAN 0.05. The data were analyzed for the possible effect of time on cerebral blood flow, and no change could be domonstrated. It is concluded that with Paco-2 constant at 40 torr morphine-nitrous oxide anesthesia does not significantly affect cerebral autoregulation in normal man.