Key result
Electrolyte repletion restores sinus rhythm from bidirectional VT in severe traumatic brain injury.
Case Report (n=1)
No
In a hemodynamically stable organ donor with severe brain injury and bidirectional ventricular tachycardia, correcting underlying electrolyte abnormalities like severe hypokalemia is the primary step to restore sinus rhythm and preserve organ viability.
Answers are grounded in this paper and cite their sources.
Electrolyte correction warrants priority in brain-dead donors with tachyarrhythmias; leaves open whether standardized protocols improve organ viability.
This Spot the Diagnosis article refers to ‘Question: Rhythmic chaos amidst brain death’, by A. Prashanth et al., https://doi.org/10.1093/ehjacc/zuae094. C) Correct any electrolyte imbalances, particularly potassium and magnesium, to stabilize cardiac function and maintain organ viability. In managing a 30-year-old male with severe traumatic brain injury being prepared for organ donation who develops sudden tachycardia, the priority is correcting hypokalemia (potassium level of 2.4 mmol/L). Electrolyte imbalances can cause arrhythmias, so addressing this is crucial for stabilizing cardiac function and maintaining organ viability. His ECG (Figure 1A) shows regular wide QRS tachycardia with no visible P-wave activity and constant RR intervals. The ventricular depolarizations (QRS ) complex are braod, with durations alternating between 140 and 130 ms, and display alternating morphologies (qR complexes, indicated by the orange arrow, and rS complexes in V1, indicated by the blue arrow). The QRS axis alternates significantly, suggesting two foci likely originating from the aortomitral continuity and left coronary cusp. Both QRS morphologies satisfy the Brugada and Basel algorithms for diagnosing ventricular tachycardia (VT). The rhythm's beat-to-beat changes in QRS morphology and axis confirm the diagnosis of bidirectional VT. After treatment, the patient’s ECG (Figure 1B) returns to sinus rhythm with visible P-waves (black stars) and normal QRS morphology (black arrow). The CT brain revealed extensive injury involving regions like the insula and hypothalamus, which, along with neurogenic stunned myocardium syndrome and electrolyte imbalances, increase the risk of arrhythmias. A surge in catecholamines, particularly norepinephrine, heightens myocardial excitability and interferes with usual synchronous conduction, further contributing to the development of these dangerous arrhythmias.1–3 (A) Twelve lead electrocardiogram during initial tachycardia showing wide complex tachycardia, with two different QRS morphologies (orange and blue arrows), with alternating axis without any discernible P waves suggestive of bidirectional VT. (B) Twelve lead Electrocardiogram post-treatment, showing discernible p waves (black stars) and baseline QRS morphology (black arrow). While intravenous amiodarone (option A) may be needed if the arrhythmia persists after correcting the electrolyte imbalance, it should not be the first step. Synchronized cardioversion (option B) is for unstable arrhythmias needing immediate rhythm restoration, but the patient maintained haemodynamics. Genetic testing (option D) for ryanodine receptor, calsequestrin 2 mutations, and aconite levels are important for differential diagnosis but not the immediate priority. Consulting an electrophysiologist (option E) can help but is not as urgent as correcting the electrolyte imbalance. None. Data sharing does not apply to this article as no new data were created or analyzed in this study.
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Kidambi et al. (2025) conducted a case report in Bidirectional ventricular tachycardia secondary to hypokalemia and severe traumatic brain injury (n=1). Correction of electrolyte imbalances (potassium and magnesium) was evaluated on Resolution of bidirectional ventricular tachycardia to sinus rhythm. Correcting hypokalemia (K+ 2.4 mmol/L) restored sinus rhythm from bidirectional VT (QRS 130-140 ms) in a 30-year-old male organ donor with severe traumatic brain injury.
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