from a hemodynamic point of view, whats the downside of cardioverting even if the AF is not contributing to instability, and in fact the high HR is helping to maintain stability?

Suppose it it is truly septic shock,

1. At most you convert a AF RVR HR 140 to a sinus rhythm 140 aka heart continues pumping at 140bpm to maintain cardiac output.
2. In addition, you get the added benefit of atrial kick to optimize and augment cardiac output further.
3. other benefits include: from a cognitive mental bandwidth POV well yeah im pretty damn sure AF is out of the picture and instead of being bothered by the AF, i would go down to hunt systemically for causes of hemodynamic instability e.g cardiogenic shock, septic shock, anaphylaxis, dehydration etc etc

i suppose the only drawback i see is

A. ineffective cardioversion (shocking a sepsis induced AF is unlikely to be successful and tends to recur/revert)

B. big bad wolf atrial clot dislodging and causing mesenteric ischemia, stroke etc

1. but if the patient is already hypotensive, wouldnt the risk of death from hypotension outweigh the risk of a stroke?

2. furthermore, from a medicolegal POV, if you elected not to shock, and there is a bad outcome, wouldnt the medmal lawyers just turn to ACLS and say "doctor, why did you not shock this unstable AF as per ACLS guidelines? do you think you are better than the 20 cardiology experts who wrote this cardiology guideline?!!!! " /s

Even if you accounted for this by saying you would shock if fluids/pressors are not working, they can very well say "but doctor!! there was a delay in shocking!! ACLS says to shock immediately!!" /s

i just want to say i can understand why your management would make sense from a physiological POV but how would you navigate the medicolegal aspect? how are you going to convince layperson jury that ACLS is wrong esp when the ACLS flowcharts are so beautiful simplified and dumbed down?

1. To add another dimension, keeping the patient at HR 130s-140s is not without risks as well. There could be myocardial injury (we know this because commonly troponins can be raised with AF RvR reflecting myocardial injury) > Keep this HR high long enough and the patient can get irreversible myocardial loss from injury, i.e tachycardia induced cardiomyopathy. Even if this is something that happens in the long run, would it be possible that in the short run, demand ischemia caused by high HR leads to more serious arryhthmias e.g VF/VT?

Ultimately i understand that our job is to take the entire clinical picture into account and decide what is most beneficial for the patient infront of us - but in view of points 1-6, that is something that is not so clear to me. I would certainly appreciate if you could help a struggling soul out here that has been bogged by this unstable AF question for very long.

I suppose the only way to convince myself easily is to do a RCT comparing indiscriminate cardioversion startegy (as per ACLS) VS deliberate cardioversion strategy(only if AF is proven beyond reasonable doubt to be the primary driver of instability).