You Never Know What You Gada Bru‐Ing

1Tulane University Health Sciences Center, New Orleans, LA

Meeting: Hospital Medicine 2013, May 16-19, National Harbor, Md.

Abstract number: 251

Case Presentation:

A 55‐year‐old previously healthy man presented with sharp and stabbing right‐sided chest pain occurring intermittently for 5 days. Pain was exacerbated by cough with no relation to movement or exertion. He reported 1 week of cough, congestion, malaise, and subjective fevers. He denies any history of smoking. Both parents were deceased with cardiac disease of unknown etiology. Temperature was 99.2, heart rate 108, and blood pressure 112/71. Regular heart rhythm was auscultated with no murmurs or gallops. Chest was nontender. Expiratory wheezes were more pronounced on the right side. No peripheral edema was present. Initial white blood cell count was 24 × 103/μL. Troponin I was <0.015 ng/mL on 3 occasions and pro‐BNP 269 ng/L Chest radiograph displayed no evidence of acute cardiopulmonary disease. CT of the chest revealed a right lower lobe consolidation, no evidence of pulmonary thromboembolism, and mild cardiomegaly. Electrocardiogram revealed sinus tachycardia, ST‐segment elevations in V1 and V2, and right bundle branch block. Serial EKGs were performed. By day 2 of admission, EKG changes had normalized, and he was afebrile.


Basic interpretation of EKGs in order to identify life‐threatening disease is an imperative skill for the hospitalist. The EKG findings described in this case are typical of the Brugada pattern, demonstrating a complete or incomplete right bundle branch block with ST‐segment elevations in leads V1–V3. There are several different alterations of the ST segment dividing the Brugada syndrome into 3 types based on T‐wave morphology. In the classic Brugada type 1 EKG, or “coved” type, the elevated ST segment (≥2 mm) descends to an inverted T wave. The type 2 and type 3 patterns have a “saddle back” configuration, in which the elevated ST segment rises to an upright or biphasic T wave. The ST segment is elevated ≥1 mm in type 2 and <1 mm in type 3. The Brugada pattern may be idiopathic and transient and caused by fever, cocaine use, alcohol, tricyclic antidepressants, lithium, or any drug that block sodium channels. In this case, it was likely displayed because pf fever related to pneumonia, with resolution on defervescence. These triggers may unmask an underlying Brugada syndrome. This syndrome is an inherited ion‐channel disorder in those with structurally normal hearts. The prevalence is 0.4% in the United States, with increased incidence in men and those of Asian descent. It manifests with polymorphic ventricular tachycardia often during sleep and syncope and cardiac arrest. The ST‐segment elevations seen in Brugada are thought to arise from differential expression of defective sodium channels in the right ventricle and not from acute ischemia.


It is important for the clinician to recognize the Brugada pattern, as it may be a predictor of sudden cardiac death. Those suspected of having Brugada syndrome should be placed on telemetry, undergo an echocardiogram, and be referred to cardiology.

To cite this abstract:

Wells A. You Never Know What You Gada Bru‐Ing. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 251. Journal of Hospital Medicine. 2013; 8 (suppl 2). Accessed May 26, 2019.

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