We would like to thank Professor Wildsmith for his interest in our case report [1]. We would, however, like to address several of the comments he makes. There was a consultant anaesthetist present throughout the case. The case report was written by the cardiology team, with advice on the discussion from the corresponding author. The trigger for the administration of vasopressors was not the ‘modest’ fall in blood pressure, but the patient’s signs and symptoms of pallor and faintness. We believe that this was clear from the wording of the case report, but apologise if it was not. Pallor, faintness and a heart rate of 60 beats.min−1 cannot reliably be attributed to parasympathetic over-activity, and can equally be caused by decreased venous return due to vasodilation from sympathetic blockade. Our patient developed a modest bradycardia after induction of spinal anaesthesia. However, as we previously discussed, the mechanism for bradycardia during spinal anaesthesia is multifactorial, and not completely explained by cardiac sympathetic fibre blockade [2]. Parasympathetic over-activity should be considered, with optimal patient positioning and the judicious use of atropine if it is suspected. However, atropine should not be used for hypotension where the cause is not known to be vaso-vagal, because if the underlying problem is decreased venous return, stimulating an empty heart will increase myocardial oxygen demand without augmenting supply [2]. Ephedrine may therefore be the more appropriate agent, for its combined chronotropic and vasoconstrictor properties [2, 3]. We would also caution against the use of sedative drugs to treat parasympathetic over-activity, which may or may not be due to anxiety, in patients with cardiovascular compromise. Sedatives have an increased effect during spinal anaesthesia [4], presumably due to deafferentiation, and this phenomenon has been implicated in several cardiac arrests [5]. Deep sedation should therefore be avoided [6]. We agree that there is little evidence for prophylactic fluids before spinal anaesthesia for surgery other than caesarean section, and did not advocate their use. We included the Cochrane review on caesarean section [7] as part of a broader discussion on hypotension following regional anaesthesia. We agree that the maintenance of venous return is paramount during regional anaesthesia, and that a slight head-down tilt can help to treat any resultant hypotension [3]. However, we would disagree that head-down positioning can reliably prevent hypotension. We found only one randomised trial, which found no benefit [8]. We accept that the relative benefits of regional and general anaesthesia are not fully delineated, but would point out that before Rodgers et al.’s meta-analysis [9] did find that regional anaesthesia conferred mortality and morbidity benefits, and the authors concluded that their data ‘should result in more widespread use of spinal or epidural anaesthesia’. Professor Wildsmith suggests that we have not carefully interpreted the evidence and lack ‘a clear understanding of the physiology’ in this area. We believe that we have made reasonable and pragmatic recommendations, and provided a clear and accurate overview of some of the physiology and complications of regional anaesthesia, based on a comprehensive, up-to-date literature search. We feel supported in this by the very positive correspondence that we have received from several anaesthetists about our discussion of the case.
Read full abstract
May 24, 2012
Thorsten Steinfeldt 
Open Access