respiratory failure appeared much more vulnerable to hemodynamic compromise just after atrial tachyarrhythmia onset, suggesting an increased hemodynamic sensitivity of mechanically ventilated COVID+ individuals to loss of sinus rhythm relative to COVID- critically ill participants. Despite the known association of severe COVID-19 infection with cardiovascular comorbid diseases, COVID+ participants actually had a lower burden of chronic cardiac disease and valvular disease, and a higher ejection fraction compared to the COVID- group, arguing that structural heart disease is not the reason for their apparent hemodynamic sensitivity to the loss of sinus rhythm. Rather, our data suggest that the striking relationship of hemodynamic deterioration to new onset atrial tachyarrhythmia in COVID+ individuals may be related to cardiopulmonary interactions in severe acute respiratory distress syndrome (ARDS) and/or to the high degree of ventilator support that they require, including high PEEP support.

Previous studies have shown that increasing PEEP is associated with decreased cardiac output and mean blood pressure.24 We speculate that the loss of atrial contractility in individuals with COVID-19 ARDS may further decrease preload and cause hemodynamic decompensation. This is further supported by the high prevalence of mechanical ventilation and subsequent temporal decompensation observed at onset of atrial tachyarrhythmia. Moreover, recent studies have highlighted the importance of right ventricular longitudinal strain in individuals with ARDS as a