Extreme supraventricular bradycardia

by Dr. Bojana Uzelac

This was a case of extreme supraventricular bradycardia; caused most likely by medications (synergistic effect of Propafenon and Bisoprolol). 



Picture 1. Pre-hospital ECG (recording speed is 25mm/s).

When I saw these tracings for the first time, I couldn’t believe that patient is alive! Who can live on 14 beats per minute?? I’m not saying that this condition can last much longer; it was obvious she is not well. Still, it is amazing that she had enough brain perfusion and that she was able to speak in so severe bradycardia! But, this is reality in the EMS work: you can catch the moment when patient is not in cardiac arrest yet (so, no CPR); but still in critical condition. That means you MUST do something right NOW.

In this case, the attending physician (Dr Ivan Ristic) opened her IV line and tried with Atropine 1mg and put her on inotropic support with Dopamine. But, electrodes for TCP have already been placed; it was assumed that medications won’t help here. So, they tried to pace her; and they were in a rush, because she started to vomit and defecated (bad sign). After few attempts they had successful pacing and got good response and clinical improvement.



Picture 2. Unsuccessful attempt of TCP



Picture 3. Successful pacing

Her heart rate was 70/minutes; her skin has become pinker and she continued to answer on questions during transportation. At the admission in hospital, EMS team was asked to accompany patient to the cath lab. So, she was on TCP for about 30-40 minutes.




Picture 4. During switching with IV pacing

In the cath lab, TCP was replaced with temporary IV pacemaker and patient was hospitalized in the Coronary Care unit.




Picture 5. Temporary IV pacemaker was placed in hospital

In that moment, hospital staff didn’t know what caused her extreme bradycardia. They were prepared to put her on permanent pacemaker, if her native rhythm couldn’t recover (in case that Scleroderma caused her bradycardia).

Luckily, after two days her sinus rhythm was back again, and temporary pacemaker was removed.



Picture 6. Patient is in sinus rhythm

Patient is doing well; she is fully recovered and will be discharged from hospital in a few days.
I was very confused about origin of this bradycardia. What is the rhythm here, who is driving the ventricle? This was the lowest supraventricular rate in a living patient (meaning no PEA) I have ever seen. (My first thought was that this must be ventricular in origin, but morphology simply doesn’t fit.) If we compare limb leads there is a match with her sinus rhythm, so this must be supraventricular in origin.



Picture 7. QRS complexes in the sinus rhythm and in the bradycardia share similar morphology

In precordial leads, beats are conducted with RBBB, by my opinion. Despite poor technical quality, you can still see narrow QRSs in lead V6 .



Picture 8. Narrow QRS complexes in lead V6 (despite low technical quality)

I’m sorry I don’t have ECG with more beats in a row. Therefore, I can’t be 100% sure is this regular or irregular rhythm. If regular, than this must be junctional rhythm; if not, than this is extremely slow AF.  

The lowest junctional rhythm I have ever seen before was 24/minute (by H. Marriott), so this rate of 14/minute potentially could be the lowest JR rate ever recorded! If I only have a longer tracingJ     

  


2 comments:

  1. I think an electrophysiologic study will help her. Also, there are literature data about conduction disorders in scleroderma. Some use corticosterone with good effect. Usually a permanent pacemaker is implanted for safety. I wonder how much was LV EF during the bradychardia!

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