S. Craighead Alexander

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 circulatory response to acute brain disease: Implications for anesthetic practice.

Acute brain injury produces not only abolition of neuronal function but also tissue acidosis, edema, and a state of vasomotor paralysis. This altered vasomotion first affects autoregulation to blood pressure changes and later all cerebral vasomotor control, resulting in paradoxical flow changes with alteration of PCO2. In the initial state, these changes are reversible, and often there is absolute hyperemia. More profound, irreversible brain damage is characterized by very low perfusion. Nevertheless, provided no mechanical obstruction to blood flow exists, as from edema, blood flow in both situations is in excess of metabolic need. This stereotyped derangement is seen with brain tumors, acute cerebro-vascular accidents, hypoxia, and severe trauma to the head, and following neurosurgical intervention. The clinical management of all these conditions must, therefore, follow a similar pattern, which consists of the maintenance of normal levels of perfusion pressure, the avoidance of cerebrovasodilatation from hypercapnia and general anesthetics, and the induction of respiratory alkalosis to offset cerebral acidosis.

TWO-COMPARTMENT ANALYSIS OF THE BLOOD FLOW IN THE HUMAN BRAIN

Twenty-one measurements of cerebral blood flow in normal young male volunteers have been subjected to two-compartment analysis. Cerebral blood flow was measured by the method of Lassen & Munck ( l ) , without correction for circulation time through the brain. Studies were performed in awake subjects, during air breathing and during hypoxia produced by the inhalation of 7.5 per cent oxygen with 3.5 per cent carbon dioxide. Additional data were collected in subjects anesthetized with nitrous oxide and d-tubocurarine, a t normal arterial Pcoz levels and during hyperventilation as well. Thus the analyses cover cerebral blood flows ranging from 16.0 to 90.3 mUlOO glmin. The method of calculation is as follows: The arterial concentration of K196 is represented by the function:

The Effects of Cyclopropane on Cerebral and Systemic Carbohydrate Metabolism

Cerebral and whole-body carbohydrate metabolism were studied in 12 normal men during four different levels of cyclopropane anesthesia. Each subject was studied while conscious and during anesthesia with either 13 md 37 per cent or 5 and 20 per cent cydopropane in oxygen. All received d-tubocurarine. The lungs were artificially ventilated, and Paco; was held constant at about 35 torr. Cyclopropane depressed cerebral oxygen consumption (CMRoc), but there was no corralation with depth of anesthesia and degree of depression. There was evidence of increased brain lactate prodoction during anesthesia with 5 per cent cyclopropane. Arterial glucose conembation increased with cyclopropane and is desaiied by the equation. a glucose = 2.53 CaH4 + 2.52 where A glucose is the increased concentration in mg/100 ml and CaH4 represents (the arterial cyclopropane concentration in vol per cent. Subjects who inhaled 13 nnd 37 per cent cydopropane had increased arterial blood Iactate concentrations. Arterial excess lactate did not increase in either group.

In Vitro Effects of Inhalational Anesthetics on Viscosity of Human Blood

Human blood was equilibrated with halothane (1.2 per cent), cyclopropane (20 per cent), nitrous oxide (70 per cent), and diethyl ether (4 per cent and 15 per cent). The remaining gas in each instance was 5 per cent carbon dioxide in oxygen (carbogen). Blood viscosity was measured before and after equilibration with anesthetic, or anesthetic-free carbogen, utilizing a specially adapted micro-cone plate viscometer. Clinical concentrations of the inhalational anesthetics produced no changes in whole blood viscosity. However, high concentrations of diethyl ether in the range of 250 mg./100 ml., produced a small but statistically significant increase in viscosity.