Bradycardia, hypotension and cerebral dysfunction after spinal anaesthesia

EDITOR: In the case report [1] of the 86-year-old patient who developed bradycardia and hypotension associated with a disturbance of cerebral function after a spinal anaesthetic for the transurethral resection of his prostate the author postulated that this was an important drug interaction. It would seem that such a conclusion was based on the fact that the patient was on long-term treatment for hypertension with the angiotensin-converting enzyme (ACE) inhibitor, captopril 25 mg twice daily and a powerful diuretic bendrofluazide in the very substantial dose of 25 mg once daily. It is possible that he is right but the evidence is weak and there is a simpler explanation. Those anaesthetists, myself included, who were taught in Edinburgh by Griffiths and Gillies [2] during the immediate post-war years to use spinal anaesthesia for the provision of a bloodless operating field soon became familiar with a pattern of marked bradycardia and profound hypotension after the onset of anaesthesia. A further outstanding feature of this pattern was the ease with which general anaesthesia was maintained and indeed it was suggested that at arterial pressures below 50 mmHg it was probable that the patients would remain asleep without any anaesthesia [3]. We also learned that during this period the circulation was relatively unstable and that before a patient's position was altered, for example from the lithotomy to the supine position, it was wise to give an intravenous injection of a vasoconstrictor drug such as methylamphetamine (Methedrine) or ephedrine to avoid a dangerous circulatory collapse. The circulatory changes are easy to explain. The selective paralysis of the sympathetic outflow by the spinal anaesthetic block leaves the heart under the influence of the vagal nerves to produce a bradycardia, and an associated reduction in the peripheral vascular resistance lowers arterial pressure by greatly increasing the capacity of the peripheral vascular bed: the greater the expansion of which the more profound is the fall in arterial pressure. On the question of the disturbance in cerebral function it was widely believed that the loss of consciousness was due to the reduction in cerebral blood flow and the consequent hypoxia. However, that interpretation was challenged by Purdon Martin [4] who pointed out that consciousness was maintained by an awareness of the body and of the environment, a view supported by Macintosh [5] who testified from personal experience that the higher analgesia spread after spinal block the more the awareness of the body was diminished. In the case under discussion interpretation is handicapped by the absence of a detailed anaesthetic record and the matter is further complicated by the fact that the circulatory collapse did not occur until immediately after the patient had been moved from the lithotomy to the supine position thus substantially increasing the size of the peripheral vascular bed. Nevertheless, two factors likely to have contributed to the patient's cardiovascular collapse are immediately obvious. First, he was anaemic preoperatively (Hb 105 g L−1) and it is surprising that despite this preoperative level, his advanced years and the planned elective surgery 10 days after his admission to hospital, it was not thought necessary to give a blood transfusion. Second, he was almost certainly hypovolaemic. Although his blood volume was not measured the fact that 3.5 L of fluid were needed to stabilize his circulation after his collapse speaks for itself, especially as it is claimed that his intra-operative blood loss was minimal. Moreover, the daily dose of the diuretic drug bendrofluazide, 10 times greater than normally recommended needs to be explained. Thus it is not necessary to seek a more esoteric explanation for the circulatory collapse the cause of which is essentially mundane. J. P.