Management of blood pressure during spinal anaesthesia

In reporting a patient who suffered a myocardial infarction during spinal anaesthesia, Khavandi et al. [1] recommend systemic nitrate therapy for coronary arterial spasm due to sympathomimetic drugs. In this they promote a ‘reactive’ approach to the patient’s condition and its management, but their report raises a number of issues: An healthy young patient suffered a significant complication yet no senior anaesthetist was involved (as judged from the authorship of the paper and the lack of any acknowledgement) in her management. Ten minutes after induction of anaesthesia a very modest decrease in blood pressure (120/72–105/65 mmHg) was the trigger for the administration of large doses (for this situation) of ephedrine (5 mg) and metaraminol (1 mg). Marked hypertension (180/120 mmHg) and ventricular ectopics were produced, a much more serious situation than the one that triggered drug administration. This modest hypotension was associated with bradycardia (60 beats.min−1), pallor and a feeling of faintness. These are not the features of sympathetic block, but those of parasympathetic over-activity, and a parasympathomimetic blocking drug such as atropine would have been more logical. However, I have long argued that a better option in such situations is to decrease vagal activity by using sedative drugs to obtund anxiety [2]. The patient was very anxious pre-operatively and was given iv midazolam before the procedure, the dose being described as ‘unusually large’. However, she received a mere 2 mg, an amount that I would consider tiny in a healthy, young, anxious patient, and administration of another 2 mg after the hypertension developed did not produce unconsciousness. Adequate sedation has an important role in preventing vagal overactivity [3]. The prophylactic administration of intravenous fluid for a procedure without significant blood loss is defended by reference to a review of caesarean section [4], a procedure where there is such blood loss. Pre-loading in other situations is of very dubious benefit [5]. I agree that sympathetic block will lead to venous dilation and sequential decreases in venous return, preload, cardiac output and blood pressure, but this can all be prevented by placing the patient in a slight head-down tilt. This will maintain venous return, and thus the circulation, but have minimal impact on the spread of a hyperbaric solution [3]. Finally, their discussion of this patient opens with the bald statement that neuraxial blockade ‘is associated with lower all-cause mortality and lower rates of serious complications than general anaesthesia’ and this is supported by reference to Rodgers et al.’s meta-analysis [6]. I would quote from that paper: ‘Our overview indicates that neuraxial blockade reduces major postoperative complications in a wide range of patients. However, uncertainty about the net benefits of neuraxial blockade is likely to remain… It is unclear whether the differences that we observed reflect the benefits of neuraxial blockade alone…’ Please note the uncertainty and lack of clarity about the relative benefits of regional and general anaesthesia. Regional anaesthesia has much to offer patients, but the reasons for using it and the way in which it is managed must be underpinned by careful interpretation of the evidence (for and against), a clear understanding of the physiology of its effects and appropriate therapy of any changes if benefits are to be gained, something which was not the case here.