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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2020  |  Volume : 31  |  Issue : 2  |  Page : 524-527
Hyperkalemia mimicking brugada pattern in electrocardiogram: A rare case report from Nepal


1 Department of Nephrology, National Academy of Medical Sciences, Bir Hospital, Kathmandu, Nepal
2 Department of Cardiology, National Academy of Medical Sciences, Bir Hospital, Kathmandu, Nepal

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Date of Submission08-Apr-2019
Date of Acceptance20-May-2019
Date of Web Publication09-May-2020
 

   Abstract 


Hyperkalemia is one of the dangerous complications of renal impairment (acute kidney injury or chronic kidney disease). Hyperkalemia may present with the electrocardiogram (ECG) changes as nonspecific repolarization abnormalities. Here, we report a case of AKI with hyperkalemia and the Brugada pattern of ECG, which reverted to normal after effective management of hyperkalemia. A 55-year-old male reported to the Emergency Department of National Academy of Medical Sciences (Bir Hospital) with injuries in his lower limbs and spine after he had met an accident two days back. He also had decreased urine output for the last one day. On physical examination, he had injuries in the spine and lower limbs. His laboratory investigations showed impaired renal function parameters with serum sodium 130 mEq/L and serum potassium of 7.3 mEq/L. His ECG was consistent with Brugada pattern. Patient was treated with 10% calcium gluconate, insulin and dextrose, salbutamol nebulization, and sodium polystyrene sulfonate till hemodialysis was initiated. Hyperkalemia and acidosis can manifest with the Brugada pattern in ECG. Thus, a careful evaluation of hyperkalemia and its treatment must be instituted in such an ECG pattern.

How to cite this article:
Dahal K, Shrestha D, Hada R, Baral A, Sherpa K. Hyperkalemia mimicking brugada pattern in electrocardiogram: A rare case report from Nepal. Saudi J Kidney Dis Transpl 2020;31:524-7

How to cite this URL:
Dahal K, Shrestha D, Hada R, Baral A, Sherpa K. Hyperkalemia mimicking brugada pattern in electrocardiogram: A rare case report from Nepal. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2020 Jul 3];31:524-7. Available from: http://www.sjkdt.org/text.asp?2020/31/2/524/284030



   Introduction Top


Hyperkalemia is defined as a condition when serum potassium exceeds 5.5 mEq/L. Potassium levels ≥7 mEq/L can lead to significant hemodynamic and neurologic consequences, whereas levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal.[1] It is one of the complications of renal impairment [acute kidney injury (AKI) or chronic kidney disease] and may be seen in patients with an acute cell-tissue breakdown like rhabdomyolysis or crush injuries. Hyperkalemia may present with the electrocardiogram (ECG) changes as nonspecific repolarization abnormalities,“peaked” T-waves, and QRS widening as well as depression of ST-segment.[2] We report a case of rhabdomyolysis with AKI with hyperkalemia and Brugada pattern of ECG, which reverted to normal after effective management of hyperkalemia. Till date, 10 to 12 cases with hyperkalemia mimicking Brugada pattern have been published. However, no case has been reported from Nepal. In addition to highlighting the need to diagnose and treat the potentially life- threatening hyperkalemia as an emergency, this will also raise the awareness among the clinicians to investigate for ECG changes to assess Brugada phenotype in patients with hyperkalemia.


   Case Report Top


Informed consent was obtained from the patient before publishing the case.

A 55-year-old male reported to the Emergency Department of National Academy of Medical Sciences (Bir Hospital) with injuries in his lower limbs and spine after he had met with an accident two days back. He also had decreased urine output for the last one day. He had no known past comorbidities with no family history of sudden cardiac death.

On physical examination, he had injuries in the spine and lower limbs. His pulse was 88 beats/min, and blood pressure was 130/70 mm Hg, respiratory rate was 22 breaths/min, oxygen saturation was 96% at room air, and temperature of 98°F. His respiratory system examination, chest examination, and abdominal examination were within the normal limits but had weakness in both upper and lower limbs.

His laboratory investigations showed hemoglobin 11.4 gm%, serum urea 209 mg/dL, serum creatinine 6.3 mg/dL, serum sodium 130 mEq/L (normal level: 135-145 mEq/L), and serum potassium of 7.3 mEq/L (normal level: 3.5-5.5 mEq/L). Other laboratory investigations showed serum calcium 5.5 mg/dL, serum phosphorus 11.8, serum uric acid 10.4 mg/dL, serum LDH 1034 U/L, N-Acetyl cysteine creatinine phosphokinase 3700 IU/L.

His ECG was consistent with Brugada pattern as depicted in [Figure 1]. His echocardiography showed normal systolic and diastolic function and had no valvular or regional wall motion abnormality.

For hyperkalemia, patient was initially treated with 10% calcium gluconate, insulin and dextrose, salbutamol nebulization, and sodium polystyrene sulfonate till hemodialysis could be initiated. His ECG became normal after serum potassium level got corrected with hemodialysis.
Figure 1: Brugada phenotype electrocardiogram.

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   Discussion Top


Potassium is principally an intracellular cation, but disorders of potassium metabolism are mostly recognized by measurements of extracellular potassium. Maintenance of the distribution of potassium between the intra- cellular and the extracellular compartments relies on several homeostatic mechanisms.[3] Plasma potassium concentration changes dramatically as a result of transcellular shifts without necessarily any alteration of total body potassium. Clinical disorders are, therefore, classified based on serum potassium concentration, rather than of potassium depletion or excess.[1]

Potassium plays an important role in maintaining the electrical potential across the cellular membrane, as well as in depolarization and repolarization of the myocytes.[4] Alterations in serum potassium levels can have dramatic effects on cardiac cell conduction and may lead to electrocardiographic (EKG) changes. If proper interventions are not instituted on time, it can also lead to death depending on the severity and rapidity of onset.[4][5]

Hyperkalemia in milder levels are associated with acceleration of terminal repolarization, resulting in T-wave changes. These T-wave changes are described as“tenting” or“peaking” of the T-wave.[5] The“peaked” T-wave is generally considered the earliest sign of hyperkalemia. Mild to moderate hyperkalemia causes depression of conduction between adjacent cardiac myocytes, resulting in progressive prolongation of the PR and QRS intervals as there is an elevation in potassium level.[5],[6] At the cellular level, atrial myocytes are most sensitive to hyperkalemia. Hence, the P-wave amplitude becomes less prominent early in the course, and later, the P-wave may disappear altogether, even in the presence of continued sinus node activity. With the progression to more severe levels of hyper- kalemia, further depression of sinoatrial and atrioventricular conduction is seen, resulting in the appearance of escape beats and escape rhythms.[6] The QRS complex continues to widen and may eventually blend with the T- wave, creating a“sine-wave” appearance to the ECG, producing the sinoventricular rhythm. Progressive increase in the potassium level eventually results in ventricular fibrillation and asystole.[6] It is important to note, however, that the relationship between potassium levels and EKG changes may vary between different patients. It is also important to realize that the ECG, in contrast with common medical belief, is not always a reliable test for mild-to-moderate hyper- kalemia.[7]

Brugada syndrome (BrS) is considered as a familial sudden cardiac death syndrome concomitant with increased risk of lethal ventricular tachyarrhythmia.[8] The gene namely SCN5A gene of the sodium (Na+) channel mutation is evident in up to 30% of BrS cases. It is evident that making a diagnosis of BrS is of prime importance as it can aid in the determination of patient’s other siblings at risk and prevent the peril of sudden death.[8] Also, BrS is a congenitally inherited cardiac channelopathy characterized by Type 1 and Type 2 ECG patterns in leads V1-V3 that predisposes the patient to malignant ventricular arrhythmias and sudden cardiac death.[9] Two types of patterns are common: Type 1“coved” or the Type 2“saddle-back” patterns. The Type 1 pattern has a high take-off ST- segment elevation that is ≥2 mm followed by a down-sloping concave or rectilinear ST segment with a negative symmetric T-wave. The Type 2 pattern is defined as a high takeoff (r’) that is ≥2 mm from the isoelectric baseline, followed by ST-segment elevation that is convex with respect to the isoelectric baseline with elevation ≥0.05 mV, with variable T-wave in lead V1 and positive or flat T-wave in lead V2.

Brugada pattern is clinical entities that are etiologically distinct from true congenital BrS. While, Brugada pattern are delineated by ECG patterns similar to BrS, but the condition might be caused due to numerous clinical conditions such as metabolic conditions, mechanical compression, ischemia and pulmonary embolism, ECG modulation, myocardial and pericardial disease, etc.[10] To differentiate between BrS and other entities is not easy due to the identical and indistinguishable ECG patterns.[11] A case report by Postema et al exemplified a case of familial BrS uncovered by hyperkalemia and acidosis.[12] On presentation, ECG revealed Brugada Type 1 ECG pattern which was resolved with the treatment of hyperkalemia. In the present case report, we suspected hyperkalemia and acidosis have evoked the Brugada Type ECG pattern. Hyperkalemia and acidosis can decrease Na+ current magnitude through inactivating the cardiac Na+ channel. This was similar to the case reported by Littmann et al.[13] Due to the lack of resources, in the present study, no electrophysiological studies of the effect of Na+ channel blockade challenge after resolution of a Brugada sign was done. Further, researches are needed to investigate whether the patients with hyperkalemia and acidosis- induced Brugada ECG patterns have a hereditary incongruity in the Na+ channel predisposing them to ventricular arrhythmias. This is the first case report describing hyper- kalemia that mimic brugada phenocopy in ECG reported from Nepal. The case report highlights the importance of thorough history, clinical examination, and laboratory investigation, which will notify the clinicians that the presence of hyperkalemia and acidosis may be associated with a Brugada ECG pattern.


   Acknowledgment Top


The author would like to sincerely acknowledge Dr. Juju Shrestha for his help during the recruitment of data of the patient case.

Conflict of interest: None declared.

Conflict of interest: None declared.



 
   References Top

1.
Penney MD. Sodium, water and potassium. In Clinical Biochemistry Metabolic and clinical aspects. Edinburgh: Churchill Livingstone: Elsevier Publishers; 2014. p. 27-64  Back to cited text no. 1
    
2.
Lehnhardt A, Kemper MJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol 2011;26:377-84  Back to cited text no. 2
    
3.
Evans KJ, Greenberg A. Hyperkalemia: A review. J Intensive Care Med 2005;20:272-90  Back to cited text no. 3
    
4.
Diercks DB, Shumaik GM, Harrigan RA, Brady WJ, Chan TC. Electrocardiographic manifes-tations: Electrolyte abnormalities. J Emerg Med 2004;27:153-60  Back to cited text no. 4
    
5.
Campese VM, Adenuga G. Electrophysio- logical and clinical consequences of hyper- kalemia. Kidney Int Suppl (2011) 2016;6:16-9  Back to cited text no. 5
    
6.
Przybojewski JZ, Knott-Craig CJ. Hyperkalaemic complete heart block. A report of 2 unique cases and a review of the literature. S Afr Med J 1983;63:413-20  Back to cited text no. 6
    
7.
Mattu A, Brady WJ, Robinson DA. Electro- cardiographic manifestations of hyperkalemia. Am J Emerg Med 2000;18:721-9  Back to cited text no. 7
    
8.
Omar HR, El-Khabiry E, Dalvi P, Mangar D, Camporesi EM. Brugada ECG pattern during hyperkalemic diabetic ketoacidosis. Ther Adv Endocrinol Metab 2017;8:20-1  Back to cited text no. 8
    
9.
Bayes 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  Back to cited text no. 9
    
10.
Anselm DD, Evans JM, Baranchuk A. Brugada phenocopy: A new electrocardiogram phenomenon. World J Cardiol 2014;6:81-6  Back to cited text no. 10
    
11.
Gottschalk BH, Anselm DD, Brugada J, Brugada P, Wilde AA, Chiale PA, et al. Expert cardiologists cannot distinguish between Brugada phenocopy and Brugada syndrome electrocardiogram patterns. Europace 2016;18: 1095-100  Back to cited text no. 11
    
12.
Postema PG, Vlaar AP, DeVries JH, Tan HL. Familial Brugada syndrome uncovered by hyperkalaemic diabetic ketoacidosis. Europace 2011;13:1509-10  Back to cited text no. 12
    
13.
Littmann L, Monroe MH, Taylor L 3rd, Brearley WD Jr. The hyperkalemic Brugada sign. J Electrocardiol 2007;40:53-9.  Back to cited text no. 13
    

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Correspondence Address:
Kashyap Dahal
Department of Nephrology, National Academy of Medical Sciences, Bir Hospital, Kathmandu
Nepal
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DOI: 10.4103/1319-2442.284030

PMID: 32394928

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    Abstract
   Introduction
   Case Report
   Discussion
   Acknowledgment
    References
    Article Figures
 

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