Abstract
Introduction: This study delves into the mechanisms through which severe hypernatremia may precipitate ventricular tachycardia, drawing from a clinical case involving a 14-year-old patient presenting with ventricular tachycardia in the context of hypernatremia. By using in silico modelling, we aim to decipher whether and how hypernatremia could favour such an event. We hypothesized that hypernatremia could increase late sodium current in a context of adrenergic stimulation, both being already known to favour early-after-depolarizations.Main symptoms: After a thorough investigation ruling out secondary causes, including clinical, electrocardiogram, and biological anomalies, as well as genetic factors, the focus turned to assessing whether hypernatremia alone could account for the ventricular tachycardia episode.Main diagnoses: Leveraging a numerical model of human ventricular action potential (TNNP model) integrated with late sodium current (INaLate), we demonstrated that severe hypernatremia, coupled with β-adrenergic stimulation indicative of sympathetic tone, could indeed trigger ventricular tachycardia.Conclusion: In silico modelling can help to predict arrhythmia risk and to select the best strategies. This case suggests a re-evaluation of cardiopulmonary resuscitation algorithms, favouring the preferential use of lidocaine over epinephrine and amiodarone in cases of critical hypernatremia-related cardiac arrest.