Harry Wollman

Complications of percutaneous radial-artery cannulation: an objective prospective study in man.

One hundred and five percutaneous radial-artery cunnulations were prospectively studied in 100 patients. The patients were examined daily for complications, utilizing physical examination and Doppler flow measurements. Forty of the 105 cannulations (38 per cent) resulted in radialartery thrombosis. Arterial occlusion occurred in 25 per cent of 43 vessels cannulated for less than 20 hours, in 50 per cent of 40 cannulations lasting 20 to 40 hours, and in 41 per cent of 22 cannulations lasting 40 to 144 hours. Radial arterial pulses, produced by retrograde ulnar-artery flow, were palpable distal to 73 per cent of the radialartery thrombi, and Doppler flow signals were audible distal to 90 per cent of the thrombi. Arterial occlusion was found at the time of decannulation in only 42.5 per cent of those vessels which eventually thrombosed. An additional 30 per cent of the total number of thrombi developed within 24 hours of decannulation. However, 27.5 per cent first occurred later than one day after decannulation. All of the 20 thrombosed vessels which were followed during return visits recanalized. The longest time taken for recanalization was 75 days. No major ischemic complication was observed in any patient, despite the high incidence of temporary thrombosis. Histologic specimens from three cannulated radial arteries were obtained at subsequent postmortem examinations; photomicrographs of these specimens showed a pathologic picture consistent with the clinical impression.

Cerebral Circulation During General Anesthesia and Hyperventilation in Man

Studies of cerebral circulation and gaseous metabolism were performed in six healthy young volunteers during anesthesia induced with thiopental and maintained with nitrous oxide and d-tubocurarine. The blood thiopental level was very low when measurements were made, and intravenous d-tubocurarine has been shown not to affect cerebral flow or metabolism. Therefore 70 per cent nitrous oxide was probably the agent chiefly responsible for the changes observed. When Paco2 was normal, cerebral blood flow remained normal, but cerebral oxygen uptake decreased 23 per cent. About one third of this decrease was caused by a small decline in body temperature, with the remainder most likely owing to nitrous oxide. When mean arterial Pco2 was decreased to 18.3 mm. of mercury, cerebral blood flow was halved, and mean jugular venous Pco2 declined to 19.8 mm. of mercury, a level generally assumed to be associated with suboptimal cerebral oxygenation. However, cerebral metabolic rate for oxygen did not decrease further at this low Paco2.

CEREBRAL CARBOHYDRATE METABOLISM DURING HYPOCARBIA IN MAN: STUDIES DURING NITROUS OXIDE ANESTHESIA.

Brain carbohydrate metabolism was studied in 11 healthy male volunteers during anesthesia induced with intravenous thiopental (5 mg./kg.) and maintained with 70 per cent N2O-30 per cent O2 and d-tubocurarine. When arterial PCO2 (PaCO2) was normal, oxygen and glucose consumption were reduced approximately 25 per cent from the normal value in conscious man; but no change in the pattern of glucose utilization was noted. A reduction in PaCO2 below 20 mm. of mercury was accompanied by a decreased aerobic and an increased anaerobic utilization of glucose. Mild, readily reversible changes in the EEG pattern also occurred when PaCO2 was less than 20 mm. of mercury. Clinical implications of these changes are discussed. The validity of several indices of cerebral carbohydrate metabolism is considered.

CEREBRAL CIRCULATION OF MAN DURING HALOTHANE ANESTHESIA: EFFECTS OF HYPOCARBIA AND OF D-TUBOCURARINE.

Cerebral circulatory measurements were made in 13 young normal male volunteers anesthetized with 1.2 per cent halothane in oxygen. Studies were performed at normal and at low PaCO2 with intravenous d-tubocurarine and at low PaCO2 without d-tubocurarine. During halothane anesthesia the cerebral vasculature was shown to constrict when PaCO2 was lowered, a response similar to that which has been observed in awake man. Halothane in the concentration studied was demonstrated to be a mild cerebral vasodilator. d-Tubocurarine was shown not to affect either cerebral blood flow, cerebral vascular resistance, or cerebral oxygen consumption. The relation of cerebral blood flow to the more easily measured jugular venous PO2 is demonstrated and discussed.

CEREBRAL CARBOHYDRATE METABOLISM IN MAN DURING HALOTHANE ANESTHESIA: EFFECTS OF PACO2 ON SOME ASPECTS OF CARBOHYDRATE UTILIZATION.

Cerebral blood flow and carbohydrate utilization were measured in healthy adult male volunteers during anesthesia produced by 1.2 per cent halothane in oxygen during hypocarbia, normocarbia, and mild hypercarbia. Cerebral oxygen consumption was unaffected by the rate of cerebral blood flow but was diminished by approximately 15 per cent in the presence of a 1°C. fall in body temperature. Metabolic alterations induced by 1.2 per cent halothane were slight or absent. Increased anaerobic metabolism was not demonstrated when cerebral blood flow was diminished during hypocarbia. Slight alterations in the pathways of glucose and oxygen metabolism were shown to be produced by changes in PaCO2.

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.

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) normocarbis, 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 intracelllular calcium ion for actomyosin interaction.

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.

A prospective random comparison of halothane and morphine for open-heart anesthesia: one year's experience.

In 128 consecutive operations, a prospective, randomized comparison of morphine and halothane as primary agents for cardiac valvular repair and/or replacement was made. During induction, average systolic and mean blood pressures were lower (9 torr and 6 torr, respectively) with halothane than with morphine. However, the incidences of serious hypotension with the two agents were similar. Six of 61 patients with halothane and seven of 67 patients with morphine reached systolic blood pressures of 70 torr or less before incision. Intraoperative hypertension was more frequent and more severe with morphine, necessitating frequent use of supplementary chlorpromazine. Cardiac output data suggest that the higher average blood pressure seen with morphine was related to increased peripheral vascular resistance rather than increased cardiac output. There appeared to be hemodynamic differences between the agents, but neither mortality rates nor durations of hospital stay or postoperative stay in the intensive care unit demonstrated a clear–cut advantage of either morphine or halothane for anesthesia during cardiac–valve operations.

Effects of Premedicant Drugs on Respiration and Gas Exchange in Man

The effects on pulmonary function of atropine, scopolamine, morphine, and a synthetic narcotic, AN-2227, were studied in a controlled double-blind randomized experiment. Atropine and scopolamine (0.5 mg. each) produced minimal changes except for a 22 to 25 per cent increase in the respiratory dead space. Compensatory increase in minute volume kept carbon dioxide tension approximately the same. Alveolar ventilation was unaffected. The respiratory response to increased carbon dioxide was insignificantly affected by cither atropine or scopolamine. Oxygen consumption and carbon dioxide production were unchanged. Morphine sulfate, 10 mg., and AN-2227, 4 mg., increased end-tidal carbon dioxide tension significantly and decreased alveolar ventilation 9 per cent and 22 per cent respectively. Respiratory response to carbon dioxide inhalation was significantly reduced by both morphine and the new narcotic, evidenced by displacements of 6 and 9 torr, respectively, in the CO2 response curve. Smaller doses of AN-2227 depressed respiration to a lesser extent, with 2 mg. of the new narcotic being equidepressant with 10mg. morphine. Oxygen consumption and carbon dioxide production did not change significantly, and lung volumes were unaffected.