Author: Lloyd Tannenbaum, MD (EM Attending Physician, APD, Geisinger Wyoming Valley, PA) // Reviewer: Brit Long, MD (@long_brit)
Hello and welcome back to ECG Pointers, a series designed to make you more confident in your ECG interpretations. This week, we feature a post from Dr. Tannenbaum’s ECG Teaching Cases, a free ECG resource. Please check it out. Without further ado, let’s look at some ECGs!
“Wow! I may actually get out of here on time for once!” you think to yourself. Only 45 minutes left in your shift and you’ve dispositioned almost all of your patients. Your relief should be here in 30 minutes and you’ll be free to go…
“CODE BLUE, ROOM 929, CODE BLUE ROOM 929!”
Well. So much for leaving on time. You and the code team hustle upstairs and are greeted by the nursing supervisor.
“Hey Doc, thanks for running up here so fast. You look kinda winded. Anyway, we have a 62-year-old male 18 hours out from a cardiac transplant. He just had a prolonged syncopal event and was out for 3-4 minutes. He never lost his pulse but was completely unresponsive. Vitals show a heart rate of 180, a blood pressure of 94/40, respiratory rate of 18, SpO2 of 99% on room air and a blood glucose of 95. He’s starting to come around a little bit now. Here’s the ECG we just performed:”
Well. Yikes.
Rate: Fast. Around 180-190 beats per minute
Rhythm: No obvious P waves, NOT sinus rhythm
Axis: Normal
Intervals: No PR interval since no P waves, Narrow QRS complexes, QTc seems reasonable
Morphology: Well, there’s ST segment elevation in aVR and diffuse ST segment depressions in the majority of the rest of the leads. This is consistent with a strain pattern. Or, put more bluntly, the heart is working too hard!
Final Read: This is a narrow complex, regular tachycardia consistent with SVT with strain
You finish interpreting the ECG and walk into room 929 to go evaluate this patient. It looks like the patient is still in SVT on the monitor. Luckily the pharmacy team came up with you to assist. “Scott! This looks like SVT. can you pull up some adenosine?” You see Scott’s eyes get wide and his head starts shaking a very aggressive NO. Before you have time to decipher Scott’s weird head shaking, you hear one of the ICU nurses ask you, “Doc, what are the chances a heart transplant patient goes into SVT and starts passing out? Pretty wild, huh?”
Well, what are the chances, indeed? Let’s take a second to review common dysrhythmias after a cardiac transplant and then get snarked at by Scott for my medication choices.
Let’s start with the basics. Transplant rejection can cause myocardial damage due to inflammation and edema. Both of these are bad, but in a transplanted heart, they are especially bad. Inflammation and edema lead to fibrosis and graft dysfunction which can cause atrial fibrillation, atrial flutter, other dysrhythmias, and sudden cardiac death. For those of us skimming, that last one (sudden cardiac death) is the really bad one.
But, how common are these dysrhythmias? Let’s run through some of the more common ones:
Let’s start with Atrial Fibrillation (AFib) and Atrial flutter (Aflutter). 10 – 25% of pts with a cardiac transplant develop AFib/Aflutter. Most patients will develop these dysrhythmias in the first few weeks following transplant. Be warned, in cardiac transplant patients presenting with AFib/Aflutter shortly after transplant you need to consider graft rejection.
What about AV re-entrant tachycardia (AVRT) or AV nodal re-entrant tachycardias (AVNRT)? (Side note, please be aware that I’m going to use the blanket term SVT to refer to AVRT and AVNRT.) Well, to be honest, SVT after a cardiac transplant is pretty uncommon. There was a study 2008 that looked at 729 heart transplant patients (the largest study to date) and it found that SVT occurred in less than 0.5% of patients. Interestingly, when SVT occurred, it was usually due to dual AV nodal physiology or an unknown accessory pathway that was present in the donor heart before transplantation. How wild is that?! Here’s your new heart, SURPRISE! It has a secret accessory pathway! Enjoy this side quest.
Also, please be aware that not all post-transplant dysrhythmias are going to be tachydysrhythmias. Sinus node dysfunction is common after cardiac transplant. It has been reported to be present in as high at 17.5% of transplant patients, but it is often transient and seen in the early post-op period. Occasionally these patients will require temporary pacing until the heart recovers. We can also see a variety of blocks, such as AV-nodal blocks or bundle branch blocks. Note that Right Bundle Branch Blocks (RBBB) is the most common conduction abnormality and is present in approximately 50% of cardiac transplant patients. On the other hand, AV-nodal blocks are present in around 10% of transplant patients and, please note, complete heart block may be a sign of acute rejection.
What about Ventricular Fibrillation (VF) or Ventricular Tachycardia (VTach)? Well, most transplant patients who experience sudden cardiac death usually experience bradyarrhythmias, asystole, and PEA rather than VF/VTach. Interestingly, there was a study that looked at transplant patients and tried to answer the question, “Should we prophylactically put ICD/pacemakers into transplant patients in case of VF/VTach?” The answer was no, however, the indications for an ICD/pacemaker in this population are severe allograft vasculopathy, unexplained syncope, cardiac arrest, VF/VTach, or severely decreased LV function. The most interesting part of that study, in my opinion, was that several of the patients who had an ICD and that ICD recognized VF/VTach and were shocked appropriately, were resistant to the shocks. These patients eventually degraded into asystole, so you may need to consider higher voltage for cardioversion/defibrillation in these patients.
“SCOTT! Where the hell is that adenosine? Or do you have any other recommendations on meds to use to help this heart transplant patient? This SVT isn’t going to fix itself…”
“Hey Lloyd! pharmacy here, just dropping by to save your ass. Regarding arrhythmias in heart transplant patients, the pharmacological treatment is very similar as their non-transplant counterparts. For acute management in the ED there are a few drugs that need to be avoided or dose adjusted:
1.) Adenosine dose should be reduced by AT LEAST HALF the recommended starting dose due to concern for prolonged AV block. Interestingly, adenosine use to be completely contraindicated in heart transplant patients, but recent studies have shown that very low dose adenosine is likely safe in these patients. But by all means, keep yelling at me for full dose adenosine, I love a good mega code.
2.) Digoxin most likely won’t work, due to poor parasympathetic innervation. Might as well push normal saline and call it digoxin for all the good it’ll do.
3.) Lastly, for bradycardia, atropine will not work due to the vagal nerve being severed during transplant. Seriously, don’t waste your time—you’d have better luck jumpstarting the heart with a triple espresso.
Overall, aside from the above medication considerations, the arrhythmia algorithm does not change for heart transplant patients. Beta-blockers are safe and generally first-line for pharmacologic intervention. The 2021 AHA guidelines suggest caution with calcium channel blockers due to potential interaction with anti-rejection meds, but they’re fine for acute ED use. Same goes for amiodarone, the “dirty drug.” Typically it isn’t first line, but again, for a one time dose in the ED, it’s probably fine.
As for our rhythm control medications, nothing changes—they require the same considerations as in non-heart transplant patients. These patients are usually stable, which gives us time to consult specialties and determine the best medication.
Oh, anticoagulation for AFib? Yeah, that all stays the same—follow your regular protocol. Just remember it’s SUPER important to check for drug-drug interactions. Most meds can be used once or for acute needs but prolonged use may require dose adjustments of anti-rejection meds.
So, the exciting takeaway? Treating arrhythmias in these folks is exactly like treating them in anyone else… except for a few crucial details that could lead to total disaster if you don’t pay attention. You’ve got this! (Maybe.)”
Right as you and Scott are discussing the optimal medication to give this patient, he looks at you and says, “Doc, I feel really funny” and starts to pass out again. His blood pressure is falling and he’s still in SVT. You charge the defibrillator and perform an emergent synchronized cardioversion, but, unfortunately, it has no effect.
“BP falling fast!” your nurses tell you. Scott hands you a stick of push dose pressors and you give the patient a few mLs as you charge the defibrillator higher and prepare to shock again. The second shock works. The patient is now back in sinus rhythm and his blood pressure is normalizing. Cardiothoracic surgery arrives and takes over management of the patient, you’re free to head back downstairs.
Recap:
- It is not uncommon for cardiac transplant patients to have dysrhythmias
- For tachydysrhythmias, Atrial Fibrillation and Atrial Flutter are the most common, likely due to damage to the native conduction system
- We can also see bradydysrhythmias such as sinus node dysfunction and complete heart block
- Some medications need to be adjusted or simply won’t work in a transplanted heart
- Adenosine can last SIGNIFICANTLY longer on a transplanted heart than on a native heart. You MUST use a decreased dose if you choose to use adenosine on a cardiac transplant patient
- Digoxin and Atropine likely won’t work on a cardiac transplant patient
- If you need to cardiovert or defibrillate, you may need to use a higher voltage of electricity
- A great ED Pharmacist is worth his/her weight in gold
Most of the info from this post came from a recent review by the American Heart Association: https://www.ahajournals.org/doi/10.1161/CIRCEP.120.007954, for the full PDF, click here! (https://www.ahajournals.org/doi/epub/10.1161/CIRCEP.120.007954)
Hit me up with any questions,
Lloyd
**Looking for a dynamic guest lecture on Emergency Cardiology for your Grand Rounds? Reach out here for a lecture request by Dr. Tannenbaum**
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**I’ll be lecturing in Montreal with Dr. Amal Mattu and several other friends at the Emergency Cardiology Preconference for the International Conference on Emergency Medicine in May, come say hi!**
