저혈압마취시 뇌순환계의 변화 = The changes of cerebral hymodynamics during induced hypotensive anesthesia

다국어 초록 (Multilingual Abstract)

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. In aneurysm surgery under induced hypotension, the sac becomes softer and thus diminishes the risk of rupture when clips ire applied.
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 cominant method of producing hypotension. Halothane and trimethaphan are the most popular drugs for this purpose.
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.
In this situation the blood oxygen tension in jugular-bulb and lactate content in brain tissue have been found to be reliable indices of degres of cerebral oxygenation.
Consequently, several investigators have studied the critical level of arterial blood pressure during hypotensive anesthesia and have accepted 60㎜Hg of systolic pressure. (40-50 ㎜Hg of mean arterial pressure) as a clinically applicable level free from the danger of cerebral hypoxia.
Furthermore, Griffiths and Gillies (1948) postulated that systolic pressure over 30㎜Hg 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 ㎜Hg and 30 ㎜Hg, of systolic blood pressure.
15 adult mongrel dogs, weighing 10-13 ㎏, 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 phase was maintained for 30 minutes. Cerebrospinal fluid, arterial dvenous 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/O₂ was administered to lower the arterial blood pressure. In the hypotensive phase Ⅰ and hypotensive phase Ⅱ systolic pressure was maintained at 60㎜Hg and 30㎜Hg, respectively. In the recovery phase, halothane was discontinued and 100% oxygen only was inhaled.
The results obtained are summarized as follows;
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 differnece 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 vasodilation.
2. Cerebral venous pO₂ decreased significantly in the hypotensive phases, but the values still remained within normal limits. A marked reduction of arterial pCO₂ was noted in the hypotensive phases. The values approach the lower limits of safety.
3. The most outstanding difference between hypotensive phase Ⅰ and 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, tent to return to return to normal at the end of the recovery phase.
From the result of this study, it is concluded;
Halothane-induced hypotensive anesthesia at 60 ㎜Hg of systolic blood pressure (45 ㎜Hg of mean arterial pressure) is a safe level without threat of cerebral hypoxia. Although there is some possibility of mild metabolic acidosis 30 ㎜Hg of systolic blood pressure (23 ㎜Hg of mean arterial pressure), adequate cerebral oxygenation is maintained without difficulty.