Case Presentation: A 51 year old Haitian male with a history of hypertension and what he described as “low sodium” presented to the emergency room with 4 days of dizziness, frontal headache, and nausea preceded by a 2 week onset of dry mouth and malaise. He had been prescribed hydrocortisone on a previous hospitalization, which he had taken up until 2 weeks prior to presentation because his new nephrologist had told him to stop and start taking losartan instead. He denied any other symptoms, including chest pain or history of syncope. He denied any changes in weight, appetite, urinary habits, or diet. Family history did not include any sudden deaths or cardiac arrests. Vital signs and physical exam were unremarkable.
Laboratory values on admission were notable for a sodium of 112 mmEq/L; potassium was 4.8, chloride 74, bicarbonate 23, creatinine 1.20, calcium 9.5, magnesium 1.7, and phosphorus 2.8. Electrocardiogram was notable for ST-segment coving (ST-segment elevation downsloping to inverted T-waves) in leads V1 and V2, consistent with a Brugada pattern; this was different from an ECG later obtained from the patient’s historical records, which was normal sinus rhythm. Cardiac enzymes were normal. The patient was admitted to the intensive care unit for close electrolyte and neurological monitoring in the setting of symptomatic severe hyponatremia. Additional laboratory studies revealed a serum osmolality of 229, urine osmolality of 256, urine sodium of 67, TSH of 2.95, and morning serum cortisol of 4.9. The patient’s home dose of hydrocortisone was restarted, with gradual resolution of his sodium level to 130. Serial ECGs showed a resolution of his Brugada pattern. No tachyarrhythmias were captured on cardiac monitoring prior to discharge from the hospital.
Discussion: The Brugada syndrome is a disorder marked by a prolonged cardiomyocyte refractory period, resulting in a predisposition to ventricular tachyarrhythmias and sudden death. Classically, mutations in the cardiomyocyte sodium channel genes that lead to a relative increase of the sodium outward current relative to the inward sodium current result in the destabilization of the membrane potential. This produces the ECG changes that were originally described. More recently, mutations in calcium channel proteins have also been implicated, suggesting various genetic etiologies for this particular phenotype.
Since being described in 1992, many observers have also noted that a variety of transient, non-genetic conditions can precipitate this pattern on ECG, and likewise can resolve when the offending insult is removed. These conditions include fever, hyperkalemia, hypercalcemia, cocaine (by mimicking a class-1 antiarrhythmic), and certain antipsychotics that act on sodium channels. To our knowledge, our case may be particularly notable in the literature in that the driving force for this Brugada-pattern appears to be a consequence of severe hyponatremia, as the ECG gradually normalized alongside the sodium. We suspect the mechanism may be due in part to serum sodium concentrations that may play on channel activity and cardiomyocyte membrane potential.
Conclusions: The Brugada-pattern on ECG remains under-recognized and may be a commonly missed hallmark of other conditions commonly encountered in hospitalized patients, such as hypercalcemia, hyperkalemia and hyponatremia. Similarly, the pattern does not necessitate that patient have an underlying channelopathy—hospitalists must maintain a differential when encountering this phenomenon in the wards.