The Changes of Cerebral Hymodynamics During Induced Hypotensive Anesthesia.

Chung, Sang Sup; Park, Kwang Won; Paik, Kwang Sae; Oh, Heung Keun; Lee, Hun Jae

Original Article

Journal of Korean Neurosurgical Society 1974;3(2): 27-40.

Sang Sup Chung, Kwang Won Park, Kwang Sae Paik, Heung Keun Oh, Hun Jae Lee

Yonsei University College of Medicine, Korea.

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 are applid. 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 degrees of cerebral oxygenation. 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. 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 cereral 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 10~13kg, 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 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/O2 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 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 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 cereral vasodilation. 2. Cerebral venous pO2 decreased significantly in the hypotensive phases, but the values till 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 cereral 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 mmHg of systolic blood pressure(45 mmHg of possibility of mild metabolic acidosis 30 mmHg of systolic blood pressure(23 mmHg of mean arterial pressure), adequate cerebral oxygenation is maintained without difficulty.