• Julián Ortega-Carnicer, Juan Benezet, Francisco Ruiz-Lorenzo, and Roberto Alcázar.
• Intensive Care Unit and Nephrology Service, Hospital Alarcos, Av Pio XII s/n, 13002 Ciudad Real, Spain. jortegacar@nexo.es
• Resuscitation. 2002 Nov 1; 55 (2): 215-9.

AbstractThe Brugada syndrome (BRS) is a hereditary cardiac condition (characteristically with a gene mutation affecting sodium channel function) identified by an elevated terminal portion of the QRS complex (prominent J wave) followed by a descending ST-segment elevation ending in a negative T wave in the right precordial leads, and malignant tachyarrhythmias in patients without demonstrable structural heart disease. We report a patient with a previous history of epilepsy treated with psychotropic drugs (with a sodium channel blocking effect) and chronic renal failure on haemodialysis who developed hyperkalaemia (6.6 mmol/l) and ECG findings resembling BRS. This condition was manifested by the prominent J wave, the coved-type ST-segment elevation and the negative T wave in the right precordial leads. These ECG changes disappeared after haemodialysis when the potassium became normal. Subsequently, a flecainide test did not reproduce ST-segment elevation. We conclude that hyperkalaemia associated with cardiac membrane active drugs may cause ECG changes mimicking the Brugada syndrome.Copyright 2002 Elsevier Science Ireland Ltd.

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