Patient information and presenting symptoms

A 53-year-old Hispanic male with a past medical history of palpitations and chronic marijuana use presents to the ED with complaints of three episodes of LOC. He denies any prodromal or postictal symptoms. He states he had two episodes of LOC one day prior to admission and one episode the night prior to admission. The patient states that he was sleeping and then woke up to go to the bathroom. He sat on the toilet to urinate and suddenly fainted with no prodromal symptoms. This occurred twice on the same day. He endorses a similar episode, which occurred the night before admission when he went to work for his night shift. At 1:30 AM, a witness stated that he saw the patient have LOC for two to three minutes. Upon waking, the patient returned to baseline immediately. He denied any chest pain, shortness of breath, headache, abdominal pain, incontinence, confusion, blurriness, or weakness. The patient reports his heart rate was 50 bpm at the time of the incident and that he slept 16 hours the prior day. The patient endorses feeling deprived of sleep since starting night shifts earlier in the year and has only been averaging four to six hours of sleep per night. He states he has had intermittent palpitations since he started working the job. The patient reports his palpitations cease spontaneously and are not associated with other symptoms. He also endorses a 15-pound weight loss in the past three months with no changes in diet. Upon entering the ED, the patient was asymptomatic. Vital signs were unremarkable, including orthostatics. The patient’s complete medical history includes depression, hemorrhoids, hepatitis, hiatal hernia, and pancreatitis. He also reported daily marijuana use; however, the quantity is unknown.

Diagnostics

To rule out common causes of syncope, as mentioned above, a complete metabolic panel was ordered in the ED, which was unremarkable, with no evidence of electrolyte abnormalities or hypoglycemia. To rule out cardiac etiologies, an EKG and troponins were ordered. Troponins were negative, ruling out an acute myocardial infarction. EKG showed a nonspecific intra-ventricular conduction block and a normal ventricular rate of 69 bpm (Figure 1).

EKG was repeated to confirm this finding, and the repeat EKG showed sinus bradycardia with a ventricular rate of 54 bpm with no change in the conduction block (Figure 2).

Another EKG was done two hours later to monitor changes, and it continued to show sinus bradycardia with a ventricular rate of 55 bpm, but it also showed the resolution of the conduction block (Figure 3).

A head computed tomography (CT) scan was also ordered to rule out any central neurological causes of the syncope, which was unremarkable. The patient was admitted for observation and further evaluation and placed on telemetry. Telemetry during the first night of admittance revealed an eight-second pause and a heart rate of 37 bpm at 2:00 AM, but the patient was reported to be asymptomatic. The patient endorsed poor sleep, as he had to go to the bathroom three times overnight to urinate, but he denies any episodes of LOC. The patient states he has been urinating more but has a weaker stream. He states he had a sensation of diffuse hyperspasticity, but his wife denies seeing any movement such as that overnight. On day 2 of admission, a repeat EKG was done, showing sinus bradycardia and incomplete right bundle branch block (RBBB) (Figure 4).

To further investigate cardiac etiologies, an EPS was conducted this day as well, which revealed a dual AV node (AVN) physiology but no accessory pathway. An echocardiogram was also conducted to identify any structural cardiac pathologies that may be causing the syncopal episodes; however, it was negative for any ventricular hypertrophy or valvular pathologies. An additional EKG was conducted on day 3 of admission to reassess any conductive pathologies, and it showed resolution of the conduction block that was present on the EKG during day 1 of admission (Figure 5).

Serial labs were also drawn to monitor the patient’s electrolyte status and hematological status (Table 1). 

Several differential diagnoses were discussed, and appropriate diagnostic measures were considered to rule out certain etiologies. Arrhythmias, as the primary cause of the LOC, were ruled out by serial EKGs, a Holter monitor, and a negative family history. Orthostatic hypotension was ruled out by the change of less than 10 mmHg in the blood pressure when the patient went from a supine to a standing position. Electroencephalography to rule out seizures was abnormal, with findings of bilateral cerebral dysfunction with increased activity in the frontal, central, and temporal derivations but no epileptiform patterns. Aortic stenosis was also considered but ruled out due to the absence of murmur and normal echocardiogram. A transthoracic echocardiogram was performed to rule out hypertrophic obstructive cardiomyopathy (HOCM); it revealed no valvular disease and a normal ejection fraction of 60-65%. Negative troponins, no ST changes, and no chest pain aided in ruling out a myocardial infarction. Narcolepsy was also considered; however, a cataplectic state constitutes being awake as opposed to this patient’s LOC episode. The patient also had a normal thyroid-stimulating hormone (TSH) level consistent with euthyroid state. The patient’s EPS findings of a dual AVN physiology were also explored further for a potential AVNRT. AVNRT was not inducible with isoproterenol. 

Management

Taking into consideration that the patient did not have any episodes of LOC during his hospital course, an implantable loop recorder (ILR) was implanted to monitor the patient’s cardiac rhythm while at home to potentially unveil the cause of this patient’s LOC. During a follow-up encounter conducted over the phone one month after discharge, it was discovered that the ILR recorded a six-second pause, at which time the patient reported feeling light-headed and dizzy, which prompted him to lie down. There were also episodes of bradycardia recorded the next day with a heart rate averaging 40 bpm; however, this occurred while the patient was sleeping. A few months later, the ILR noted two four-second pauses. The patient reported to be awake during these times due to his work shift. The patient reported dizziness during these episodes as well but denied LOC. Upon further investigation, a vagal etiology was suspected due to the progressive elongation of beats prior to the pause. The patient returned for a follow-up a few months later due to three episodes of pauses, with the longest pause lasting 6.1 seconds; the patient's wife reported that the patient was sleeping during this time. The patient had follow-up diagnostic work done, for which the EKG showed normal sinus rhythm with left axis deviation and a decreased T-wave amplitude in anterior leads. An echocardiogram revealed a normal left ventricular ejection fraction, and an EPS failed to show any electrical conduction abnormalities.

Outcome

This patient received a final diagnosis of recurrent syncope with unknown etiology. His condition was managed with the placement of ILR, as well as an extensive educational component on the adverse effects of chronic marijuana use and poor sleep hygiene, and avoiding AV blocking agents, such as beta-blockers, non-dihydropyridine calcium channel blockers, antiarrhythmics, and digoxin. The patient denied getting another episode of LOC after discharge from the hospital.