Journal of the Practice of Cardiovascular Sciences

CASE REPORT
Year
: 2022  |  Volume : 8  |  Issue : 2  |  Page : 112--114

Hyperkalemia-induced brugada phenocopy: A rare electrocardiogram manifestation


Satyajit Singh, Chandra Prakash Thakur, Surendra Naik, Muneshwar Kumar 
 Department of Cardiology, AIIMS, Raipur, Chhattisgarh, India

Correspondence Address:
Chandra Prakash Thakur
House No. 11, Suryodaya Colony, Tatibandh, Near AIIMS, Raipur - 492 099, Chhattisgarh
India

Abstract

Hyperkalemia-induced Brugada ECG pattern is rare. Although the association of hyperkalemia with Brugada pattern is a known entity, it is also very important to be aware of this presentation as the treatment of this Brugada Phenocopy is different from Brugada syndrome . This case presented with a Brugada like ECG but had hyperkalemia. On correcting the hyperkalemia, the ECG settled to normal.



How to cite this article:
Singh S, Thakur CP, Naik S, Kumar M. Hyperkalemia-induced brugada phenocopy: A rare electrocardiogram manifestation.J Pract Cardiovasc Sci 2022;8:112-114


How to cite this URL:
Singh S, Thakur CP, Naik S, Kumar M. Hyperkalemia-induced brugada phenocopy: A rare electrocardiogram manifestation. J Pract Cardiovasc Sci [serial online] 2022 [cited 2022 Dec 2 ];8:112-114
Available from: https://www.j-pcs.org/text.asp?2022/8/2/112/354129


Full Text



 Introduction



Hyperkalemia is a common medical emergency. Renal association clinical practice guidelines define hyperkalemia as threshold serum potassium (K+) level of ≥5.5 mmol/L. It is further classified by severity into mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L), or severe (≥6.5 mmol/L).[1] The incidence of hyperkalemia in hospital patients ranges from 1.1% to 10%. In-hospital mortality is significantly higher in patients with hyperkalemia (18.1%) compared to those with hypokalemia (5.0%) or normokalemia (3.9%).[2] The electrocardiogram (ECG) is used to assess cardiac toxicity and risk of arrhythmias in patients with hyperkalemia and is the most readily available diagnostic tool. ECG abnormalities may reflect the severity and rate of rise of serum potassium levels.[3] In this report, we have discussed a patient with rare ECG manifestation – hyperkalemia-induced Brugada phenocopy (BrP).

 Case Report



A 57-year-old male presented to trauma and emergency with difficulty in breathing for the past 15 days. It was associated with decreased urine output. The patient was a known case of chronic obstructive pulmonary disease for which he was on inhaler therapy. He was also a known diabetic on oral antidiabetic agents. There was no history of chest pain, dizziness, or syncope in the past. There was no family history of sudden cardiac death (SCD). He had pulmonary tuberculosis 28 years ago for which he had completed antitubercular regimen for 6 months.

At presentation, his pulse was 88 beats/min, blood pressure was 130/70 mm Hg, respiratory rate was 30 breaths/min, oxygen saturation was 88% at room air, and temperature was 98°F. His respiratory system examination revealed bilateral wheeze. Cardiovascular and abdominal examinations were within the normal limits.

His laboratory investigations showed hemoglobin 10.3 g%, total leukocyte counts 19310 × 103/μl, serum urea 61 mg/dL, serum creatinine 3.29 mg/dL, serum sodium 143 mEq/L, and serum potassium 6.7 mEq/L. Other laboratory investigations showed serum calcium 6.8 mg/dL, serum phosphorus 8.7, and serum uric acid 5.9 mg/dL. His ECG was consistent with type 1 Brugada pattern on presentation [Figure 1]. Transthoracic echocardiography showed structurally normal heart with normal systolic and diastolic function. There were no features of pulmonary embolism in echocardiography.{Figure 1}

The patient was immediately started on anti-hyperkalemic treatment. The ECG changes got resolved after 12 h. However, the patient died after 2 days due to respiratory failure.

 Discussion



Brugada syndrome (BrS) is a channelopathy that is associated with a higher likelihood of developing malignant ventricular arrhythmias and SCD. It is characterized by two types of ECG patterns: A coved ST-segment elevation (≥0.2 mV) and subsequent T-wave inversion in the right precordial leads (Type I) and saddleback appearance (Type II).[4] The underlying mechanism of BrS according to the repolarization hypothesis is that there is an outward shift in the balance of transmembrane currents in the right ventricular outflow tract (RVOT) epicardium, due to reduced inward sodium current and prominent transient outward potassium current. Accentuation of action potential notch in the RVOT epicardium is thought to underlie the generation of ST-segment elevation in ECG.[5]

BrPs are clinical entities that are characterized by Brugada ECG patterns Type I and Type II in the absence of BrS. Diagnostic criteria for BrP are given in [Table 1].{Table 1}

A systematic approach is required for the correct diagnosis of BrP. Provocative drug challenge testing is an important step for differentiating BrS and BrP. A negative test supports the diagnosis of BrP. However, it should be emphasized that false-negative results were reported up to 23% and cases with delayed diagnosis of BrS were described previously in the literature.[6]

BrP has been previously described in association with inferior/right ventricular myocardial infarction, pulmonary embolism, metabolic/electrolyte abnormalities (hypokalemia, metabolic acidosis, hyponatremia, and hyperkalemia), and adrenal insufficiency. Although hyperkalemia produces classical electrocardiographic (EKG) manifestations, only small subsets of patients develop BrP. Thus, differentiating these two clinical entities is essential as implantable cardioverter-defibrillator is not warranted in BrP.[7]

Systemic hyperkalemia is most frequently found in patients with chronic and acute renal failure and/or concomitant treatments with nephrotoxic medications or K-sparing drugs. The classical EKG manifestations of hyperkalemia were first documented in the early 1950s by the presence of peaked T-waves, shortened QT interval, lengthening of the PR interval, loss of P waves, and widening of the QRS complex. Moreover, Levine et al. also described the presence of the “dialyzable” current of injury resembling acute myocardial infarction or pericarditis.[8] Potassium plays an important role in maintaining the electrical potential across the cellular membrane, as well as in the depolarization and repolarization of the myocytes. Alterations in serum potassium levels can have dramatic effects on cardiac cell conduction and may lead to EKG changes. If proper interventions are not instituted on time, it can also lead to death depending on the severity and rapidity of onset.[9] However, Littmann et al. reported the first consecutive series that recognized the similarities between the classic BrS ECG manifestations and those occasionally shown in the context of severe hyperkalemia.[10]

In this case, hyperkalemia was treated with intravenous calcium gluconate, insulin, and glucose. The transthoracic echocardiogram showed normal left ventricular systolic and diastolic function with no regional wall motion abnormalities. The ST-segment elevation was settled in the ECG taken after 8 h [Figure 2]. As the Brugada ECG pattern got settled after treating hyperkalemia, no provocative tests were performed. Furthermore, from history, there was no prior history of palpitations, unexplained syncope, or family history of SCD. The reversal of Brugada pattern after the correction of potassium is suggestive that the Brugada pattern was more likely due to hyperkalemia.{Figure 2}

This is the first case report describing hyperkalemia-induced BrP in ECG reported from this region of India.

 Conclusion



Hyperkalemia-induced Brugada ECG pattern is a very rare manifestation. Although the association of hyperkalemia with Brugada pattern is a known entity, it is also very important to be aware of this presentation as the treatment of BrS and BrPs are entirely different. BrP is often correctable (in this case needed correction of potassium). On the other hand, BrS needs proper investigations and may also require the International Classification of Diseases. A thorough history, clinical examination, and laboratory investigations will help to differentiate between the two entities.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Renal Association Clinical Practice Guidelines – Treatment of Acute Hyperkalaemia in Adults – July, 2020.
2Conway R, Creagh D, Byrne DG, O'Riordan D, Silke B. Serum potassium levels as an outcome determinant in acute medical admissions. Clin Med (Lond) 2015;15:239-43.
3Littmann L, Gibbs MA. Electrocardiographic manifestations of severe hyperkalemia. J Electrocardiol 2018;51:814-7.
4Bayés de Luna A, Brugada J, Baranchuk A, Borggrefe M, Breithardt G, Goldwasser D, et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: A consensus report. J Electrocardiol 2012;45:433-42.
5Wilde AA, Postema PG, Di Diego JM, Viskin S, Morita H, Fish JM, et al. The pathophysiological mechanism underlying Brugada syndrome: Depolarization versus repolarization. J Mol Cell Cardiol 2010;49:543-53.
6Chauveau S, Le Vavasseur O, Chevalier P. Delayed diagnosis of Brugada syndrome in a patient with aborted sudden cardiac death and initial negative flecainide challenge. Clin Case Rep 2017;5:2022-4.
7Baranchuk A, Nguyen T, Ryu MH, Femenía F, Zareba W, Wilde AA, et al. Brugada phenocopy: New terminology and proposed classification. Ann Noninvasive Electrocardiol 2012;17:299-314.
8Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956;13:29-36.
9Campese VM, Adenuga G. Electrophysiological and clinical consequences of hyperkalemia. Kidney Int Suppl (2011) 2016;6:16-9.
10Littmann L, Monroe MH, Taylor L 3rd, Brearley WD Jr. The hyperkalemic Brugada sign. J Electrocardiol 2007;40:53-9.