To give you the setting, a few weeks ago I’m working in a rural ER I work at occasionally. 2 hours from nearest hospital. It is pretty well stocked, although only with common medications used in an ER. It’s actually quite busy and have about 12 active patients, 5 of them are in the process of getting transferred, 3 of them to an ICU. Just as I am starting to relax, two new patients check in within a minute of one another. I get called to triage about one of them who is a gentleman that is diaphoretic, hypotensive, jaundiced, and his testicles are swollen (he is not who this case is about). I have him rushed back so we can resuscitate him immediately as it becomes obvious this guy has Fournier’s Gangrene and needs to get transferred out now. Meanwhile the second patient to check in gets sent to a room in the back and is being handled by a new nurse as the others are helping resuscitate the other gentleman who is actively trying to die. I get handed an ECG, rate of 148 which is the same rate of my Fournier’s guy, so I just briefly glance at it while I’m putting in orders and assumed that ECG was for him. Probably about 25 minutes after both those patients check in, I go to check on the second guy however, he is in XR (I had put in some cursory orders as I knew I would be held up with the first guy). I get a few calls from surgeons and intesivists and hospitalists about coordinating care for my guy with Fournier’s so it is another 20 minutes before I go back to check on the second patient.
When I walk in I find a 50-something year old gentleman who is diaphoretic, severely tachypneic, and tripoding. His HR is 150, he is sating 87% on 6L NC, BP is 170/110. He is afebrile. Has diffuse crackles on lung auscultation. He apparently has no medical history. He had been having SOB for a few days and it significantly worsened that evening. I quickly put him on bipap, give him a couple SL nitros and go find his ECG and realize that ECG with a rate of 148 is his. It’s regular, axis normal, intervals are normal, no evidence of ischemia, but p-waves are upright in aVR and V1, and inverted in all other leads. My first thought is obviously 2:1 flutter with buried p-waves in the QRS complex. I am now questioning whether to rate control someone that is in new onset heart failure as the classic teaching is to avoid BB in acute heart failure exacerbations (not quite sure on the evidence behind this), however, it is also recommended to avoid CCB in patients with systolic heart failure. I use our very outdated bedside US to find the patient has an EF of likely somewhere around 15-20%.
So I find myself in a predicament. It is possible that the patient’s HF is due to their tachydysrhythmia vs causing it. Also, is this patient in and out of flutter/fib? His symptoms have been going on for greater than 5 days. What would you do? I thought the best answer would be synchronized cardioversion, however, the patient and wife adamantly refused it further complicating issues. The only med I had for chemical cardioversion was amiodarone, which I don’t typically use due to the cardiologists and intensvists at the receiving hospital where I also work not typically liking amio. So I am back to BB vs CCB vs do nothing and hope for the best. I end up giving a half dose of diltiazem which brings his rate down to 125. I get a repeat ECG that shows that what I thought was a-flutter was actually a unifocal atrial tachycardia. The patient now looks much better, although probably more due to the bipap. I call the cardiologist at the facility accepting him and they recommend holding off on additional meds and they’ll figure it out when he arrives. The patient then ends up converting to NSR as he is about to be transferred a few hours later.
So how would y’all handle this case? I thought it would be interesting to hear varying opinions.
TL;DR – Working at rural hospital with limited resources. Pt has new onset systolic heart failure and unifocal atrial tachycardia rate of 150, refusing electrical cardioversion. What do you do?
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