Vagal fibers to the heart predominantly innervate the sinoatrial node, atrial musculature, and A^ node. Direct vagal stimulation leads to sinus bradycardia which is abolished by administration of atropine.6 Heart rate responses to the Valsalva maneuver in our patient suggested normally functioning vagal efferents to the heart. Electrophysiologic measurements indicated normal function of the conduction system. Thus, vomiting-induced cardiac slowing in our patient was possibly related to excessive stimulation of the vagal afferents from the upper gastrointestinal tract. canadian neightbor pharmacy
Vomiting is associated with antiperistalsis of the upper gastrointestinal tract and forceful expulsion of gastric contents through the mouth. Atrioventricular block during vomiting could be provoked either by antiperistalsis or distension of the esophagus by gastric contents. The former is unlikely to be a precipitating stimulus, as retching which is also associated with antiperistalsis was not associated with any bradycardia or conduction disturbance. As complete AV” block could be reproduced by balloon inflation of the esophagus, sudden distension of the upper esophagus by gastric contents is likely to be the initiating factor.
Sinus bradycardia and atrioventricular block are well documented though rare complications of swallowing. When symptomatic, this has been called swallow syncope. These complications of swallowing have been shown to be due to hypersensitive vagal responses. In most of the reported cases of swallow syncope, balloon inflation of the esophagus has reproduced the rhythm disturbances. In two cases of paroxysmal AV^ block related to nausea and vomiting reported by Talwar et al,4 balloon inflation of the esophagus was not attempted, and thus, the mechanism of heart block was not proved. Distension of the esophagus in normal subjects is not associated with any change in cardiac rhythm.5 Such responses in our patient, and in previously reported cases of swallow syncope, are-abnormal. As there was no obvious functional or structural abnormality of the esophagus, an excessive response by stretch receptors in the wall of the esophagus, to moderate distension, was probably responsible for reflex sinus bradycardia and JN block.
The distension produced by normal swallowing was possibly inadequate to stimulate this response. Furthermore, the hyperactive response was limited to the upper esophagus as distension of the middle and lower esophagus did not provoke heart block and responses of cardiac rhythm to other vagal afferents (eg, carotid sinus, pharyngeal) were also normal. The long history in this patient may reflect a congenital abnormality or a postinflammatory neuronal damage of the upper esophagus as a cause for this abnormal reflex.