Halothane 저혈압마취가 뇌순환계에 미치는 영향

Abstract

[한글]

[영문]

An induced hypotension is employed as a useful technique for operations on intracranial aneurysms, brain tumors and other intracranial lesions to diminish operative bleeding and to decrease brain tension (Fazekas et al., 1956; McLaughlin, 1961). In aneurysm surgery under induced hypotension, the sac becomes softer and thus diminishes the risk of rupture when clips are applied (Hampton and Little, 1953: Hugosson and Hogstrom, 1973).

In 1946 Gardner used arteriotomy to lower blood pressure by decreasing the blood volume during brain tumor surgery, then gradually improved. Pharmacologically-induced hypotension soon became the dominant method of producing hypotension. Halothane and trimethaphan are the most popular drugs for this purpose

(Sarnoff et al., 1952: Murtagh 1960).

On the other hand, the risks of hypotension are obvious. These include decreased cardiac output, decreased cerebral blood flow, and low perfusion pressure exposing brain tissue to the risk of hypoxia thereby aggravating the effects of the circulatory disturbance present in the brain lesion (Hampton and Little, 1953: Larson, 1964).

In this situation the blood oxygen tension in jugular-bulb and lactate content in brain tissue have been found to be reliable indeces of degree of cerebral oxygenation (Viancos et al., 1966; Kaasik et al., 1970: Yashon et al., 1972).

Consequently, several investigators have studied the critical level of arterial blood pressure during hypotensive anesthesia and have accepted 60 mmHg of systolic pressure (40-50 mmHg of mean arterial pressure) as a clinically applicable level free from the danger of cerebral hypoxia (Rollason and Hough, 1960; Eckenhoff et al., 1963). Furthermore, Griffiths and Gillies(1948) postulated that systolic pressure over 30 mmHg would provide adequate tissue oxygenation. However, there are only a few reports concerning the adequacy of cerebral oxygenation under such low levels of arterial blood pressure.

The purpose of this study is to investigate ,cerebral hemodynamics and metabolism during halothane-induced hypotensive anesthesia and to find any evidence of cerebral hypoxia at the levels of 60 mmHg and 30 mmHg, of systolic blood pressure.

15 adult mongrel dogs, weighing 10-13 kg, were anesthetized with intravenous pentobarbital sodium. Endotracheal intubation was performed. One femoral artery was cannulated with a polyethylene tube for arterial blood sampling. The tube was connected to a Statham pressure transducer for continuous arterial blood pressure recording. The common carotid artery was exposed and a probe of square-wave electromagnetic flowmeter was placed on the vessel to record the carotid blood flow. An electrocardiogram and above two parameters were recorded simultaneously on a 4-channel polygraph. The internal jugular vein was cannulated and a catheter threaded up to the jugular-bulb for sampling of venous blood draining from the brain. The cisterna magna was punctured with an 18 gauge spinal needle to sample the cerebrospinal fluid.

The experiments were divided into control phase, induction phase, hypotensive phase Ⅰ, hypotensive phase Ⅱ, and recovery phase. Each chase was maintained for 30 minutes. Cerebrospinal fluid, arterial and venous blood were sampled at the end of each phase for analysis of gas tension and lactate content. 100% oxygen was inhaled during the induction phase. During the hypotensive phases, halothane/O^^2 was administered to lower the arterial blood pressure. In the hypotensive phase I and hypotensive phase Ⅱ systolic pressure was maintained at 60 mmHg and 30 mmHg, respectively. In the recovery phase, halothane was discontinued and 100% oxygen only was inhaled.

The results obtained are summarized as fellows:

1. The carotid artery blood flow, which represents the cerebral blood flow, decreased linearly during the decline of the arterial blood pressure. At the end of each phase there was no-difference in the carotid blood flow between hypotensive phase Ⅰ and Phase Ⅱ. Cerebral vascular resistance was markedly reduced in the hypotensive phase Ⅱ, which suggests cerebral vasodilatation.

2. Cerebral venous pO^^2 decreased significantly in the hypotensive phases, but the values still remained within normal limits. A marked reduction of arterial pCO^^2 was noted in the hypotensive phases. The values approach the lower limits of safety.

3. The most outstanding difference between hypotensive phase Ⅰ and phase Ⅱ is in the lactate content of cerebral venous blood and cerebrospinal fluid. There was a moderate increase of lactate content, and a slight reduction of cerebral venous pH in hypotensive phase Ⅱ, however, a significant degree of cerebral hypoxia and metabolic acidosis could be excluded.

4. Most of the changes in the cerebral metabolism and hemodynamics including arterial blood pressure, tend to return to normal at the end of the recovery phase.

From the result of this study, it is concluded:

1. Halothane-induced hypotensive anesthesia at 60 mmHg of systolic blood pressure (45 mmHg of mean arterial pressure) is a safe level without threat of cerebral hypoxia.

2. Although there is some possibility of a mild metabolic acidosis at 30 mmHg of systolic blood pressure (23 mmHg of mean arterial pressure), adequate cerebral oxygenation is maintained without difficulty.