Typically heart rates are well below 100-120 bpm. Mechanistic explanation is likely due to direct pathogenic effects on the sinoatrial node and effects of inflammatory cytokines are among the proposed mechanisms. Despite management of bradycardia with temporary or permanent leadless pacemakers, there is a high rate of short‐term morbidity and death due to complications of COVID‐19.
Interleukin 6 (IL-6) is the cytokine reported to exhibit the strongest correlation with depressed heart rate variability, which in turn may predict relative bradycardia.
I managed last 2 days a patient with significant sinus bradycardia heart rate 30s to 40s, intubated on mechanical ventilation for COVID-19 pneumonia, but on norepinephrine (not hypothermic). She responded well to atropine and heart rate would go up to 75 bpm. However little effect was obtained from switching from norepinephrine to dopamine.
Below I linked several articles that refer to a very poor prognosis for patients that have early bradycardia and/or persistent bradycardia in the intensive care unit during SARS CoV-2 management.
I also attached an article that gives an overview of bradycardia management in general. This is from the European Society of Cardiology published in their 2015 guidelines.
Be aware that Aminophyllin or theophylline, particularly in elderly patients can be used as a temporary measure to manage brady- arrhythmias, provided there is no ischemia and can even placed on an oral regimen of theophylline . Temporary pacemakers in general should be discouraged. They have a significant complication rate and if patient meets pacemaker criteria, he or she should be managed like a STEMI and brought urgently to the EP lab for emergent permanent pacemaker implantation.
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