I’ve been thinking about this during a recent case. We saw recurrent VT/VF that didn’t respond to lidocaine, amiodarone, or shocks. The right radial PaO₂ looked fine. But what if the coronaries were perfused from below the mixing point, with native hypoxic blood?This article is a physiologic hypothesis, based on bedside observation and ECMO dynamics. I’m still early in my ECMO learning, so I’m putting it out there as a question:Are we missing coronary hypoxia as a cause of arrhythmias in peripheral VA ECMO?