This is the conclusion to our special feature Stump the Chumps: Atropine and Complete Heart Block. If you've not seen the case, I recommend you go back and read it over.
To recap, our crew had been dispatched to a 63 year old female who was lightheaded and happened to have a bit of a bradyarrhythmia.
Ok, she had a lot of bradyarrhythmia.
Let's review that first 12-Lead ECG:
We've got a wide complex, regular ventricular rhythm at a rate of 30. A regular atrial rhythm is present as well at a rate of 140. What is most interesting in this case is the degree of AV nodal conduction present. The PRi appears fixed at 0.16s for most of the strip, however, the first complex has a much shorter PRi.
After the administration of atropine, while prepping for transcutaneous pacing, we had two rhythm changes:
Reviewing the subsequent 12-Leads shows a progression to 2:1 AV Block, then 1:1 conduction and sinus tachycardia.
Here at EMS 12-Lead, we had come up with two competing theories for the first 12-Lead:
- Complete heart block
- 2nd Degree AV Nodal block Type II, 4:1 conduction
In favor of a complete heart block is a wide complex rhythm with morphology suggesting a left ventricular escape, large bizarre T-waves, inconsistent PR interval, and a change in morphology after the change to a 2:1 AV Nodal block.
In favor of a 4:1 heart block is the apparent fixed PR interval between all three ECG's, with a progression from 4:1 to 1:1 conduction after the administration of atropine.
This is a tough case!
The team here at EMS 12-Lead couldn't come to a definitive answer for you folks, so we branched out. Part of what makes EMS 2.0 great are the doctors who have made themselves available to answer these tough questions. In fact, Drs. Ken Grauer and Arnel C. provided their expert rhythm analysis on this case!
Shortly after we received it, I sent this case over to Dr. Mark Perrin (@EPFellow), an electrophysiologist fellow, to get his take. What was the rhythm? Why did it appear to change with atropine? Well, he had this to say:
These are interesting ECGs. I think the different manifestations are all explained by the sinus rate:ECG '0' at 9:50 pm – is sinus cycle length 470 ms (Ed: sinus cycle length is the P-P interval), CHB (PR differs on the first two beats, and the complex is more consistent with a ventricular focus, note the reversal of 'rabbit ears' in V1 – sometimes used to differentiate SVT from VT).ECG '1' 10:18 pm – sinus CL 520 ms, now 2:1 AV block and showing the morphology of conducted beats which is very different from the first ECG.ECG '2' 10:20 pm – sinus CL 580 ms. Now 1:1 conduction, with conduction disease LAFB, and RV delay/RBBB as in ecg '1'.So I think this is an example of acceleration dependent CHB.
In a tachycardia dependent complete heart block, the AV node fails to conduct often after the atrial rate increases beyond a critical rate. As the sinus rate in our patient slowed, the degree of AV block improved!
So, how did atropine help this patient? Dr. Perrin continued:
My interpretation is sick/sob for other reasons initially, increased sinus rate -> CHB, felt even more terrible and afraid, sinus rate increases further….friendly paramedic arrives, reassures, sinus rate slows, and conduction returns. I think the atropine did nothing. This is an example of why atropine can actually make this kind of heart block worse, It tends to increase sinus rate, and a high sinus rate can increase the severity of heart block. But the most common effect of atropine is to do nothing…as is probably the case here (unless you posit it somehow reducing the sinus rate) – the level of block is below the AV node.
Many of our readers acknowledged this to be the likely reason for our patient's improvement. In the hospital this patient should receive a permanent pacemaker. Unfortunately the patient was lost to follow-up to the EMS crew.
So there we go, positioning, fluid, and some tender love and care can go a long way in some patients!