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Pharyngeal packing during ENT surgery

obstetrics. However, there are a number of aspects of the condition that we feel were unsatisfactorily covered and which require some clarification. Neurocardiogenic or vaso-vagal syncope is loss of consciousness caused by reduced arterial pressure and blood supply to the brain, mediated through neural mechanisms rather than primary cardiac dysfunction. Bradycardia and vasodilation are the underlying mechanisms of the systemic hypotension [2]. The trigger may be central, from psychological stress or pain, or may be initiated peripherally by a reduction in venous return to the heart. This commonly occurs while standing. Occasionally it may occur during anaesthesia, especially in the context of neuro-axial block, in hypovolaemic states and in obstetrics. There is also an overlap with the BezoldJarisch reflex, which causes a similar constellation of symptoms and is triggered by activation of parasympathetic afferents from the heart (non-myelinated C fibres) due to relative or absolute hypovolaemia. The relevance of this reflex has been extensively discussed in the anaesthetic literature [3, 4]. Although the baroreceptor reflex is the primary homeostatic mechanism regulating blood pressure, it is now thought that the Bezold-Jarisch reflex which is primarily cardio-inhibitory, interacts with the baroreceptor reflex and may explain the profound bradycardia which may occur during severe haemorrhage. Whatever the exact mechanism of the syndrome, the prompt treatment of the condition is important as any delay may result in permanent cerebral damage or death. Saqr and Kumar correctly state that the pre-operative treatment of the condition is controversial. Treatment of anxiety with anxiolytics is recommended. Beta-blockers have been used extensively and continue to be regarded as a first-line prophylactic. However, it may be assumed that despite increased awareness and the more extensive use of prophylaxis, cases will continue to present both in the obstetric and the wider surgical population. When a case presents for surgery with the relevant history, then additional precautions include careful monitoring of fluid balance and monitoring should be used. We feel, however, that it was not made sufficiently clear by Saqr and Kumar in their article that in the acute situation the primary aim of treatment is the re-establishment of adequate blood pressure and heart rate. In this regard the use of beta-blockade should not be included in any pharmacological stratagem used to treatment this condition. The best pharmacological treatment of neurocardiogenic syncope has been fully discussed elsewhere [3]. It is thought that the sequence of atropine, ephedrine, and adrenaline is the best compromise. Ephedrine is the most logical choice for a single agent to treat profound bradycardia or asystole, given the lack of vasoconstrictor effect of atropine and the potential for heart rate reduction with alpha-agonists. Cardiac arrest does occur during neuro-axial block [5]. If tragic unexpected death is to be avoided, a clear treatment regimen must be advocated.