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The authors review the current data regarding the impact of COVID-19 on arrhythmias. Critically ill COVID-19 patients have an increased risk of arrhythmia, and this may be due to hypoxia, myocarditis, abnormal host immune response, myocardial ischemia, myocardial strain, electrolyte abnormalities, intravascular volume imbalances, and the side effect of drugs. Clinicians should be aware of potential drug–drug interactions and that monitoring the QT interval is necessary with select therapies. The exposure to potential COVID-19 can be reduced by using telemedicine and carefully assessing the need for intervention.
Further data are required to understand the pathophysiology of arrhythmia in patients with COVID-19 and to develop effective prevention and management strategies.
This abstract is available on the publisher's site.
Current understanding of the impact of COVID-19 on arrhythmias continues to evolve as new data emerges. Cardiac arrhythmias are more common in critically ill COVID-19 patients. The potential mechanisms that could result in arrhythmogenesis among COVID-19 patients includes hypoxia caused by direct viral tissue involvement of lungs, myocarditis, abnormal host immune response, myocardial ischemia, myocardial strain, electrolyte derangements, intravascular volume imbalances and drug sides effects. To manage these arrhythmias, it is imperative to increase the awareness of potential drug-drug interactions, to monitor QTc prolongation while receiving COVID therapy and provide special considerations for patients with inherited arrhythmia syndromes. It is also crucial to minimize exposure to COVID-19 infection by stratifying the need for intervention and using telemedicine. As COVID-19 infection continues to prevail with a potential for future surges, more data is required to better understand pathophysiology and to validate management strategies.