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
tracing… J
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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