Abstract 4135239: Pausing Under Pressure: Ocular Hypertension as an Atypical Cause of Heart Block

A 67-year-old male with a history of hypertension presented to the emergency department with abnormal cardiac monitor results. Prior to this, he was diagnosed with primary open-angle glaucoma by ophthalmology and underwent left-sided aqueous tube shunt placement, which was complicated by hypotony requiring revision and holding of all topical glaucoma medications. Concurrently, he was noted to have an irregular heart rhythm during a routine physical. In office ECG showed normal sinus rhythm, but subsequent 14-day continuous ECG monitor showed sinus bradycardia with nadir heart rate of 21 beats-per-minute and 114 ventricular pauses (longest 4.8 seconds) primarily due to second-degree atrioventricular (AV) block, Mobitz type 1, but also periods of high-grade AV block. He was sent to the emergency department for expedited pacemaker evaluation. On further review, heart block and ventricular pauses occurred exclusively over a 12-hour period that temporally coincided with a hospitalization for acute ocular hypertension following shunt revision. His intraocular pressure peaked at 56 mmHg (normal range 10-21 mmHg), then normalized to 21 mmHg after acetazolamide and anterior chamber paracentesis. Bradycardia resolved following ophthalmic intervention. Bradyarrhythmias were attributed to excess vagal tone from acute ocular hypertension via an atypical but recognized cause of the oculocardiac reflex, and pacemaker placement was avoided. The oculocardiac reflex is a reflex bradycardia involving the trigeminal and vagus nerves. Cardiac effects are consistent with other vagally-mediated bradyarrhythmias, including sinus bradycardia, AV block, and even asystole. This reflex occurs commonly during traction on extraocular muscles during strabismus surgery, but can be seen in other orbital and ocular stimuli. To our knowledge, this is the first documented case of ocular hypertension leading to atrioventricular block through this mechanism. This case illustrates the importance of (1) clinical context of abnormal events during extended cardiac monitoring, (2) understanding the oculocardiac reflex as a cause of bradyarrhythmias, and (3) ruling out reversible medical causes of dysrhythmias prior to permanent device implantation.