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An outside the box look at managing atrial fibrillation in the ED.
A great episode to a very common problem. I am 1 year out of residency and at my community hospital without residents, I have adopted to rate-controlling with a dose of IV diltiazem and then discharging on oral metoprolol with PCP or Cardiology follow-up (this is for the stable afib patient, obviously that I plan on sending home anyway). This seems to be working well for me, however, the thought of just giving an oral dose of metoprolol in the ED and sending home regardless of rates seems crazy to me, as it seems to be completely different than what was practiced in residency, where most patients with afib with RVR were given diltiazem bolus, drip and then admitted.
My question for this same type of patient, which was not mentioned in the episode, involves ED work-up...are you routinely checking a CXR and labs, including the troponin?It seems to me that some patients presenting with afib with RVR usually have some type of chest discomfort that is documented as "pain", "tightness", "heaviness" somewhere in the chart where after my evaluation I clinically suspect a discomfort simply due to the RVR as after my evaluation as the chest discomfort does not sound like ACS. There are also the times where rate related ischemic changes are seen on the EKG that resolve after rate control. So most times, I will order a troponin. If normal will typically go home. The problem occurs with the slight troponin bump that is likely rate related. This then will lead to a snowball of things...a call to cardiology, who are typically not impressed, a delta troponin, and sometimes an admission. Any suggestions on what to do with this?
Hi Jason! Such great points you bring up here. I've sent it to Ran Ran to get his 2 cents, but here is my take. But before getting to that, curious as to why you rate control with an IV calcium Ch blocker and send home on a beta blocker.When I've done what you're talking about, I tried to keep the medications in a similar class when converting from the IV to the PO. I don't have evidence to say this is better or worse, just my practice.
Regarding sending rapid patients home with just an oral dose and calling it a day... I am with you in consternation. Even after speaking to Ran at length about this, I don't think my mind is in a place that would be ready to give up the IV dose to get the HR to a more palatable number. That might be physician self treatment, but my practice reflected what you are currently doing.
Regarding the workup.
I have surveyed dozens of docs about the chest x-ray in a patient with recurrent, uncomplicated atrial fibrillation. It's about a 50/50 spit for those who do and don't get them. That may very well very depending on practice patterns locally. If there's no shortness of breath, signs of CHF, hypoxia, Etc, I think it's probably low-yield. The longer I got in my career, the fewer X-rays I ordered on uncomplicated paroxysmal a-fib patients. If there was any question of new symptomatology or something that was out of sorts, I would for sure get one. That being said, in my first decade of community practice, I got a chest x-ray on absolutely every single one of these patients until I developed my own clinical sense and clinical comfort.
Regarding troponin, unless there is chest pain or EKG findings, I think it is a fool's errand, especially if there is a rapid rate. It's just like getting a troponin in patients with really fast supraventricular tachycardia. If it's elevated, how much is that actually going to benefit the patient versus harm them downstream, just as you allude to. So for me, for the run-of-the-mill paroxysmal atrial fibrillation with rapid ventricular response, routine troponin ordering was not part of the equation. I had to get burned by that a few times to really take that practice to heart.
When there are ischemic changes on the EKG, I think a troponin is not unreasonable. As far as the symptoms of chest pressure with RVR, there's so much clinical judgment to that. I will fully confess to erring on the side of getting a troponin when there was a chest pain or pressure aspect to it although that chest symptom is often so nebulous in these patients.
Thanks for the reply and looking forward to Ran's 2 cents into this. As far as your question as to why I discharge on metorplol even though I used diltiazem IV in the ED is mainly it was the practice I saw with the cardiologist's in residency. No specific evidence. I was in a 4 year residency program and during my cardiology rotation the majority of cardiologist's would transition to PO metoprolol instead of diltiazem for the patient's admitted on diltiazem infusions. I don't remember if they had evidence for this or if it was just their practice to do it.
Hey Jason, here is the response from Ran Ran...
The practice pattern this provider describes is common. But common doesn't mean right. I simply ask: what does the one time dose of IV diltiazem give you and what does it risk? It gives you immediate rate control for 2-6 hours and risks putting the patient into a decompensated state if the HR was actually compensating for an underlying pathology. The next question is: is that worth the risk? Does 2-6h of rate control really make a difference for preventing tachycardia mediated cardiomyopathy? If you do think it makes a difference, then why are most of us simultaneously so comfortable sitting on sinus tachycardia, sometimes for days to weeks. There is a double standard where a patient with Afib with HR >110 needs "emergent" rate control else they might "go into heart failure and die" but a patient with sinus tach with HR > 110 needs no therapy at all. The average R-R interval of sinus tachy at 150 is the exact same as R-R interval of afib at 150 so this really makes no sense from a diastolic filling perspective.
The ED workup completely depends on the patient's complaint. It's not the Afib that has me checking on a troponin. It's the complaint of chest discomfort that sounds like ACS. If it doesn't sound like ACS then I don't check troponin. If the troponin is high and you invoke demand ischemia, this is a case where more emergent rate control is indicated if global perfusion would not be compromised as a result. But notice how this practice is identical to if the patient was in sinus tach. A patient with pressure chest pain, tachycardic to the 130s, hypertension would first get analgesics, then venodilation with nitroglycerin/ISDN or lasix, then afterload reduction with captopril, and - if there were no signs of heart failure - b-blockers for antianginal therapy. You should treat Afib the same. In the case you described, the patient has essentially failed a "self induced" stress test and they would've failed if they were tachy with Afib or tachy with sinus.
The hard part of Afib is that the atrial kick simultaneously adds to stroke volume as it takes from venous pressure. This means that loss of atrial kick leads to decompensation in conditions where there is low preload (sepsis, hemorrhage, hypovolemia) as well as in conditions where there is high preload (heart failure). That's what makes the condition so hard. It is dangerous to think of it as a solitary disease with an algorithmic treatment. In the EP world, the most terrifying arrhythmia is sinus tachycardia because it is NOT a solitary disease with algorithmic treatment. In my world, the most terrifying arrhythmia is atrial fibrillation managed as if it was a solitary disease with algorithmic treatment by people who fail to appreciate the patient's physiology.
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