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Monday, June 17, 2013

Atrial Fibrillation: Sure, you can cardiovert it! But should you? (Part 2)


  In the first half of this post I emphasized a few points about AF. It can be triggered by a variety of non-cardiac sources - hypovolemia, alcohol, and especially sepsis can all exacerbate chronic AF, or provoke a new episode. You can cardiovert a hypotensive AF patient with any of those problems, and it might (might) fix the rhythm, but it would be unlikely to correct the underlying issue.

Need another example? Alright, how about AF and an ECG that suggests STEMI?
 
AF and proven STEMIs - first case
The examples above weren't actually hypotensive, but this last patient was. 

An elderly patient with a history of paroxysmal AF was transported by EMS for acute onset dyspnea, chest and abdominal pain. Things got more complicated when she arrested right upon arrival in the ED. 

Not the patient - this is me when the patient arrests 10 seconds after arrival.
 Fortunately, this meant that the patient got full, immediate, and successful resuscitation. The post-ROSC ECG, however, was concerning:



The patient had a pressure of 80/50 - what should the team have done next? If you say cardioversion, what would you have done if the first attempt didn't work? (or the second?)

(Also, does it help if you know that the prehospital ECG looked like this?)

Anything jumping out at you?
Well, you need a plan B in atrial fibrillation! In this case, the team decided not to re-shock a patient who had just regained their pulse, and who was apparently undergoing a STEMI. During emergent cardiac cath, a complete occlusion of their left anterior descending artery was found, and successfully stented.
 
AF and proven STEMIs - second case
I've talked about this case before, so I'll be brief. Midlle-aged woman, acute onset chest symptoms:


However, once the medic brought the rapid ventricular response (RVR) down a bit, and the symptoms improved a little, the computer message disappeared when the repeat ECG was obtained...


... but not the ST elevations, nor their apparent reciprocal changes. Her old ECG showed very normal inferior ST segments, supporting the diagnosis of an acute STEMI. During the emergent PCI, they found that an old stent in her RCA was 100% occluded.

On the other hand...
Some physicians are fairly skeptical about ST changes that are found in AF with RVR. As with other arrhythmias, you can end up with a variety of ST changes that resolve with the tachycardia. PSVT very commonly produces ST depressions, even in young folks with no heart disease. 

For example, despite the dramatic ST depressions (and aVR elevation!), this patient... 
ECG from a great case at EMS 12-Lead
 ... never had a troponin increase - no MI - and the ST segments normalized after cardioversion.

Stephen Smith, of Dr. Smith's ECG blog, also voices wariness about calling a STEMI in AF with RVR. He has a great case at his site that illustrates the lesson that, if the patient is losing units of blood from their GI tract, the cath lab is probably not the best first stop, even if the ECG computer is trying to tell you otherwise!

Pictured: Not a cath lab candidate.
So, when do you activate the cath lab? Do you wait to make the call until you've loaded the patient with diltiazem, or do you do it first thing? How long do you look for other causes, versus get everyone moving to the lab?

Ah, good question, and I wish I had some hard and fast answers. I don't know of any research that looks at this issue, and the experts can disagree. It's often going to depend on the clinical context, as well as evolutions in the ECG findings, echocardiograms, and comparisons with old ECGs - all of which are hard to do in the back of a rig!

The Bottom Line
This is a cornerstone of emergency medicine - if the rhythm is fast, and the patient is not doing well, and you think they are not doing well because of that rhythm, then the patient should be cardioverted. 

(Repeat - "they are not doing well because of that rhythm..." Important!)

This is clearly supported in our SHCGB protocols:



But we have seen in these posts a number of examples where cardioversion probably wouldn't have been effective, since the underlying medical issues needed treatment. Cardioversion isn't going to treat low magnesium, hypovolemia, and especially not sepsis!


Cardioversion for hemodynamically unstable AF is reasonable, but this isn't as "simple" as ventricular fibrillation. You need to consider the causes and aggressively treat them, and be ready with a "plan B."

5 comments:

  1. Timely. I had this discussion with a student the other. The one about rate versus symptoms. The way I suggested that he think of it was "Is the rate causing the problem, or is the problem causing the rate?"

    The case I presented to him was a person with a SVT at 220 or so and chest pain.

    The decision he had to make was whether he should treat the chest pain with NTG or treat the chest pain by controlling the rate.

    Blood pressure was adequate, so he couldn't even use that to help him make the decision.

    I don't think that this sort of differential is well taught in EMS. From what I've seen some ED residents and even attending physicians have a hard time with the concept.

    Maybe we should rethink how we teach this at all levels.

    ReplyDelete
    Replies
    1. Perhaps part of the problem is that so many elements of ACLS are understood as absolutes, as Class 1 interventions that must ALWAYS be performed. E.g. all chest pain patients get nitro, and all narrow-complex tachycardias > 150 bpm get cardioversion if there is evidence of instability.

      As a result, we end up with PSVT getting nitro, and sinus tachycardia due to hemorrhage being cardioverted.

      Now, ACLS, in the body of the text, does point out the importance of figuring out the "rate causing the problem," but somewhere in the simplified diagrams and the teaching the subtleties are lost.

      Delete
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