• S M Kinsella and J P Tuckey.
• Sir Humphry Davy Department of Anaesthesia, St Michael's Hospital, Bristol, UK.
• Br J Anaesth. 2001 Jun 1;86(6):859-68.

AbstractReflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold-Jarisch reflex and neurocardiogenic syncope. The circulatory response changes from the normal maintenance of arterial pressure, to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return as well as through affective mechanisms such as pain or fear. It is probably mediated in part via afferent nerves from the heart, but also by various non-cardiac baroreceptors which may become paradoxically active. This response may occur during regional anaesthesia, haemorrhage or supine inferior vena cava compression in pregnancy; these factors are additive when combined. In these circumstances hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilation. Treatment includes the restoration of venous return and correction of absolute blood volume deficits. Ephedrine is the most logical choice of single drug to correct the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anaesthesia.

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