Recurrent Paroxysmal Complete Heart Block Induced by Vomiting

12 Feb
2015

Recurrent Paroxysmal Complete Heart Block Induced by VomitingVomiting is a protective reflex stimulated mainly by afferents from the gastrointestinal tract. The efferent control of vomiting is via the vagi and sympathetic system. It is normally accompanied by slight tachycardia or bradycardia. Unlike swallowing, symptomatic disturbances of cardiac rhythm have not been well documented with vomiting. buy antibiotics online
Case Report
A 52-year-old woman, who was otherwise in good health, was admitted following a fainting episode during vomiting which occurred after moderate alcohol intake. While being monitored in the casualty department, she again vomited and felt faint, and it was noticed that she developed transient complete AV block. She admitted to episodes of loss of consciousness, all associated with vomiting, since the age of 10 to 12 years. On admission, detailed clinical examination, including physical examination of the cardiovascular and nervous systems, chest x-ray film, and 12-lead electrocardiogram, did not disclose any abnormality.

An electrophysiology study showed normal atrioventricular conduction. The AH and HV intervals were 70 and 50 ms, respectively Incremental atrial pacing provoked AV nodal Wenckebach periodicity at a pacing rate of 160 bpm.
Vagal and other provocative maneuvers were performed after insertion of a temporary transvenous pacing system. Carotid sinus massage, eyeball pressure, and oropharyngeal stimulation did not provoke any conduction abnormalities. The heart rate and blood pressure response to the Valsalva maneuver were normal. Swallowing of a large bolus of food was not associated with any change in cardiac rhythm. Ipecacunahna, an emetic, was given to reproduce and further document the problem. Three bouts of ipecac-induced vomiting were associated with sinus bradycardia, complete AV block, and ventricular asystole each time lasting up to 20 s (Fig 1A). Ipecac provocation was repeated on the following day after pretreatment with intravenous atropine (1.2 mg). This resulted in sinus tachycardia and prevented heart block during all subsequent bouts of vomiting (Fig 1B). Barium swallow and upper gastrointestinal endoscopy did not reveal any functional or structural abnormality of the esophagus. The patient was treated by implantation of a permanent demand ventricular pacemaker which was programmed to a rate of 40 bpm.
To further investigate the mechanism of paroxysmal complete AV heart block, inflation of balloons at different levels of the esophagus with electrocardiographic monitoring was undertaken. Simultaneous inflation of two, 22-mm diameter balloons at the same level in the upper esophagus (22 cm from the incisors) provoked sinus bradycardia with complete JN block which subsided when the balloons were deflated (Fig 2). However, no conduction abnormalities were seen when the same balloons were inflated in the middle and lower esophagus (32 and 42 cm from the incisors, respectively). Interestingly, when partially inflated balloons were being withdrawn through the upper esophagus, the patient again developed AV heart block. The study was not repeated after atropine because the patient complained of moderate chest discomfort during each of the balloon inflations.

Figure 1 A. Electrocardiographic recording during induced vomiting. Onset of vomiting is shown by a bar Arrows indicate continuous recordings. Soon after the onset of vomiting, complete JN block developed with sinus bradycardia and ventricular asystole. Fixed rate ventricular pacing (20 bpm) was started after about 15 s. P is P waves; Y ventricular paced beats. B. Electrocardiographic recording during induced vomiting with prior administration of intravenous atropine (1.2 mg). There is sinus tachycardia and no conduction abnormality. Paper speed 25 mm/s.

Figure 1 A. Electrocardiographic recording during induced vomiting. Onset of vomiting is shown by a bar Arrows indicate continuous recordings. Soon after the onset of vomiting, complete JN block developed with sinus bradycardia and ventricular asystole. Fixed rate ventricular pacing (20 bpm) was started after about 15 s. P is P waves; Y ventricular paced beats. B. Electrocardiographic recording during induced vomiting with prior administration of intravenous atropine (1.2 mg). There is sinus tachycardia and no conduction abnormality. Paper speed 25 mm/s.

 

Figure 2. Electrocardiographic recordings during balloon inflation in the upper esophagus after implantation of a programmable permanent ventricular pacing system. Arrows indicate a continuous trace. Complete heart block is seen soon after balloon inflation which subsides with deflation. P is P waves; Y ventricular paced beats. Paper speed 25 mm/s.

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