Pathophysiology of Hyperkalemia Presenting as Brugada Pattern on Electrocardiogram (ECG)

Abstract

Patient: Male, 26-year-old Final Diagnosis: Acute encephalopathy • Brugada pattern • hyperkalemia Symptoms: Brugada pattern Medication:— Clinical Procedure: — Specialty: Toxicology Objective: Unknown ethiology Background: Brugada phenocopies (BrP) are clinical and electrocardiographic (ECG) entities elicited by reversible medical conditions speculated to have pathogenesis rooted in ion current imbalances or conduction delays within the myocardial wall. During an inciting pathologic condition, it produces ECG patterns identical to those of congenitally-acquired Brugada syndrome and subsequently returns to normal ECG patterns upon resolution of the medical condition. This case report describes a 26-year-old man presenting to the Emergency Department (ED) for suspected heroin overdose with a rare ECG consistent with BrP secondary to acute hyperkalemia. Case Report: A 26-year-old man with a history of substance abuse and a seizure disorder presented to the ED for acute encephalopathy secondary to a heroin overdose complicated by severe rhabdomyolysis and acute renal failure. Laboratory investigations showed acute hyperkalemia (potassium of 7.2 mmol/L) in addition to an elevated creatine kinase, severe transaminitis, and elevated creatinine. His ECG on admission revealed Brugada-like changes in leads V1-V2, with subsequent resolution upon bicarbonate administration and normalization of potassium. After initial stabilization, the patient was admitted to the Intensive Care Unit (ICU). His rhabdomyolysis and acute kidney injury improved after copious rehydration. He was found to have community-acquired pneumonia, with a negative infectious disease workup, that improved with antibiotics. Upon resolution of his hypoxemic respiratory failure and improvement in mentation, he was discharged from the hospital. Conclusions: Our case report adds to the growing literature on BrP and highlights the importance of recognizing its characteristic ECG pattern as a unique presentation of a common electrolyte derangement.

Kalium in der Intensivmedizin

“…In einer retrospektiven Untersuchung mit Kalium ≥ 6,5 mmol/l wiesen 71 % pathologische EKG-Befunde auf (T-Wellen-Abnormalitäten, PR-Verlängerung > 200 ms, QRS-Verlängerung, Bradykardie < 50/min, AV-Block > II ° oder III °, ventrikuläre Tachykardie). Die häufigste Kombination ist eine QRS-Verlängerung und T-Wellen-Erhöhung, aber auch ungewöhnliche Veränderungen wie bei einem Brugada-Syndrom sind beschrieben worden [40][41][42]. Helfen könnten zukünftig computerassistierte Systeme, die basierend auf einem 12-Kanal-EKG als Deep-Learning-Modell mit deutlich höherer Sensitivität und Spezifität Ärzten helfen, schwere Dyskaliämien frühzeitig zu erkennen und möglicherweise kardiale Ereignisse zu reduzieren [43].…”

Brugada Pattern Manifesting During Hyperkalemia, Diabetic Ketoacidosis, and Acute Alcohol Intoxication

“…The sodium channel derangements lead to early after depolarizations from the right ventricular outflow tract epicardium, ultimately leading to oscillations of potential QRS depolarizations, which can exceed the threshold, which triggers a true ventricular event such as ventricular fibrillation or tachycardia [ 13 ]. This slows the upstroke of the phase 0 cardiac action potential, and the L-type inward calcium channels and transient dependent outward current during phase 1 have also been implicated as a substrate for Brugada morphology and arrhythmias [ 14 ]. Bradycardia exacerbates these findings and increases the potential for these dangerous rhythms to prevail.…”