Brugada-like electrocardiographic changes induced by hypokalemia

CASE REPORT

^IServiço de Eletrofisiologia Cardíaca - Hospital São Lucas da PUCRS

^IIServiço de Medicina Interna - Hospital Nossa Senhora da Conceição, Porto Alegre, RS - Brasil

Mailing Address

Keywords: Brugada syndrome; bundle-branch clock; hypokalemic.

Introduction

Since its description in 1992, Brugada Syndrome has become the second cause of death among young adults in some countries¹. The Brugada syndrome is an autosomal dominant disease with incomplete penetrance, which may cause syncope and sudden cardiac death in young individuals with a normal heart. It is characterized by an electrocardiographic (ECG) pattern of complete or incomplete right bundle branch block (RBBB) and ST-segment elevation in leads V1-V3. The characteristic ECG findings are seen in some patients not affected by the syndrome². Several nongenetic factors have been mentioned in the literature as possible inductors of the Brugada ECG pattern³. It may be induced in some patients during febrile states, electrolytes abnormalities, cocaine use and drugs that have a sodium channel-blocking effect, such as antiarrhythmics, anesthetics, and tricyclic antidepressants, among others⁴. We describe a case of a 21-year-old man who presented with severe hypokalemia and dynamic electrocardiographic changes compatible with Brugada pattern⁵.

Case Report

A 21 year-old male, white, single, with diagnosis of hypokalemic periodic paralysis (a genetic disorder associated with potassium loss), presented to the emergency room with sudden-onset tetraparesis after several hours of sleep and two episodes of vomiting. There were no respiratory or swallowing difficulties. He had no family or personal history of sudden death nor had experienced any episodes of syncope. He was taking spironolactone and denied the use of other drugs or alcohol. On physical exam his pulse was regular, and blood pressure was 112/61 mmHg in both arms. The skin was cool and sweaty. No jugular venous distension, goiter or lymphadenopathies were observed. Heart examination showed regular rhythm, no murmurs and pulse of 95 bpm. Lung and abdomen assessment was unremarkable. There were no deformities or edema of the extremities and distal pulses were present and equal bilaterally. Neurologic examination showed flaccid paralysis of all extremities, which involved the proximal and distal muscles and included the hips and shoulders. Deep tendon reflexes were slightly diminished to 2 out of 4. Cranial nerve function was intact. Routine chemistry, liver enzymes and complete blood count were normal, except for a potassium level of 1.5 (3.5-5.5 mmol/). The analysis of thyroid function was normal.

The 12-lead ECG on admission showed sinus rhythm and incomplete RBBB with ST-segment elevation in leads V1-V2, with a coved-type ST segment elevation consistent with type 1 Brugada pattern (Figure 1). A chest radiograph showed a normal-sized heart. Six hours after initiation of intravenous potassium replacement, the patient's neurologic symptoms had completed resolved. Repeat ECG showed normal sinus rhythm and electrocardiographic abnormalities disappeared (Figure 2). Echocardiography was unremarkable.

Discussion

Several nongenetic factors have been mentioned in the literature as possible inductors of the Brugada ECG pattern. The basis of the Brugada ECG pattern and Brugada syndrome remains a topic of debate, with arguments claiming both repolarization and depolarization abnormalities as being responsible^6,7. In both events, decrease of inward sodium (Na+) current is generally accepted as being essential⁸. The list of drugs or conditions that can unmask or induce a Brugada ECG pattern is growing⁹. Factors that can unmask or modulate the Brugada ECG pattern are beta-blockers, tricyclic or tetracyclic antidepressants, lithium, local anesthetics, fever, hyperkalemia, hypercalcemia, hyponatremia, alcohol and cocaine toxicity^4,8,10,11. The clinical meaning and the risk of arrhythmias that induce Brugada ECG pattern are unknown. Recent researches describe the risk of cardiac events in patients with a Brugada ECG pattern, without the Brugada syndrome, during acute medical situations⁴. Juntilla et al⁴ collected data on 47 patients; 26 patients with the Brugada ECG pattern due to drugs or medications; 16 with this ECG pattern developed during a febrile episode and 5 related to electrolyte imbalances⁴. Of the 47 subjects with an acute Brugada ECG pattern, 24 (51%) had malignant arrhythmias, with 18 patients developed sudden cardiac death, 3 had ventricular tachycardia episodes, and 3 had syncope. Tsai et al¹² described the Brugada ECG pattern during a hypokalemic periodic paralysis in a man with thyrotoxicosis¹².

In patients with Brugada syndrome there also have been reports of induction of ventricular tachycardia and ventricular fibrillation associated with transient hypokalemia^13,14. Hypokalemia induces QT prolongation and several ventricular arrhythmias because of an elevation of the resting membrane potential, prolongation of action potential duration, and an increase in the automaticity in cardiac myocytes¹³. The loss of the action potential dome due to transient outward of potassium current (Ito)-mediated phase 1 in right ventricular epicardium generates a transmural voltage gradient that underlies ST-segment elevation, similar to that observed in Brugada syndrome¹⁴.

The most common electrocardiographic alterations induced by hypokalemia include increased U-wave amplitude, T-wave depression and rectification and increased duration of ST-segment, with consequent increase in QT interval¹⁵. These findings are also identified on the admission ECG, which exhibited the Brugada pattern (Figure 1), and could be useful for the differential diagnosis. Hypokalemia is usually well tolerated in the absence of structural heart disease, especially in the presence of normal QT on the ECG¹⁴.

The Brugada ECG pattern may be a transient phenomenon in individuals who do not have genetically determined disease and should not be considered benign. There is some evidence proposing that this transient ECG pattern is a risk factor for the development of life-threatening cardiac arrhythmias and should be aggressively treated.

There is no conflict of interest with any financial organization regarding the material discussed in this case report.

Author contributions

Conception and design of the research: Gazzoni GF, Bergoli LCC, Soares JLF, Kalil C, Bartholomay E; Acquisition of data: Borges AP, Bergoli LCC, Soares JLF; Analysis and interpretation of the data: Gazzoni GF, Borges AP, Bergoli LCC, Soares JLF, Bartholomay E; Writing of the manuscript: Gazzoni GF, Borges AP, Bergoli LCC, Kalil C, Bartholomay E; Critical revision of the manuscript for intellectual content: Gazzoni GF, Borges AP, Bergoli LCC, Soares JLF, Kalil C, Bartholomay E.

Potential Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Sources of Funding

There were no external funding sources for this study.

Study Association

This study is not associated with any post-graduation program.

References

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Brugada-like electrocardiographic changes induced by hypokalemia

Guilherme Ferreira Gazzoni^I; Anibal Pires Borges^I; Luis Carlos Corsetti Bergoli^II; José Luiz Flores Soares^II; Carlos Kalil^I; Eduardo Bartholomay^I

Publication Dates

• Publication in this collection
  15 Apr 2013
• Date of issue
  Mar 2013