Stump the Chumps – Atropine and Complete Heart Block

This great case was sent in by an anonymous reader posed as a question, the likes of which we had not seen before. So, to pay homage to a wonderful radio show signing off this year, we're calling this segment: Stump the Chumps!

Our reader was dispatched to back up a crew attending to a 63 year old female complaining of lightheadedness.

The original crew had found her to be confused, lethargic, with nearly absent radial pulses, and pale clammy skin. The patient denies chest pain and shortness of breath, and adamantly denies any cardiac history. Only history of note is a recent trip to Southeast Asia over a month ago.

Her vitals were as follows:

  • Pulse: 30 bpm, palpable at the brachial
  • BP: 80 mmHg systolic, unable to auscultate a diastolic (LP12 unable to acquire as well)
  • RR: 14, lung sounds clear and equal
  • SpO2: 98% r/a
  • BGL: 124 mg/dL (6.9 mmol/L)

The patient was hooked up to the cardiac monitor and a 12-Lead ECG was obtained. During acquisition of this 12-Lead, the crew established intravenous access.

Stump the Chumps - Initial 12-Lead

After acquisition, it was decided to begin transcutaneous pacing. While the procedure was explained to the patient, 0.5 mg of atropine was administered via IV and combo-pads were placed.

A few minutes after the administration of atropine, the crew noticed a change in the rhythm and acquired a second 12-Lead.

Stump the Chumps - Post Atropine 1

The patient's blood pressure and skin color improved.

A few more minutes pass and again a rhythm change is noted on the monitor. Another 12-lead is acquired.

Stump the Chumps - Post Atropine 2

At this point, the patient has improved significantly and transcutaneous pacing is no longer necessary. The remainder of the transport was uneventful and in the hospital the patient was recommended for permanent pacemaker insertion.

We're left with a number of questions:

  1. Is the first 12-Lead a complete heart block? And if so, why did atropine work?
  2. What does the second 12-Lead show?
  3. What does the third 12-Lead show?

So, before we attempt to answer these questions, we'd like to hear what you think!


    a review of the M2 muscarinic receptor subtype would also be helpful… ๐Ÿ˜‰

  • Shalom says:

    1) No complete heart block…The sinus is activating the ventricles
    -It's 2nd degree AV Block (non-Wenkebach) with 3:1 conduction, RBBB possibly LPFB
    -The bizarre T waves are generally normal during such severe bradycardias

    2) Same rhythm but now 2:1 condution, and LAFB
    3) SInus tachy and LAFB…

  • Jessica R. says:

    I’m not comfortable calling the 1st strip complete heart block. I feel a little more inclined to call it 2nd degree type 2 with 3:1 conduction. But then again, atropine isn’t really supposed to work on that either. As far as answering the rest of these questions, I’ll have to do that later as I’m at work and it’s hard to see these strips on my phone. :-p

  • Deuce says:

    I dont believe the initial EKG is a complete heart block. I interpreted the rhythm as a 2nd degree type two heart block with a Right BBB and inverted T-waves. The Atropine had a better chance of working than a third degree, however I most likely would have gone straight to pacing rather than drug therapy. Lucky for the patient the Atropine worked!  

  • Nick Adams says:

    It never was a CHB.  It's a 2nd Degree AVB (type II) with a 4:1 conduction.  Atrial rate of 125 and a ventricular rate of 31.  The second strip shows a 2nd degree AVB with a  3:1 conduction, an Atrial rate of 120, and a Ventricular rate of 60.  The third strip is a ST where all atrial impulses are conductingthrough to the ventricles.  Atrial rate of 107, and a ventricular rate of 107.  Since Atropine blocks vegas nerve stimulation and increases SA nadal discharge, I'd say that it didn't do anything for the patient.  I would think that O2 and the patient relaxing had alot to do with the patients outcome, while the SA nodal discharge actually slowed.  I think that the patient's AV junction is ischemic and is blocked with increased rates (rate dependant).  With the decrease in O2 demand and consumption, the AV node began to work more efficiently.
    A-125 with a V-30
    A-120 with a V-60
    A-107 with a V-107

    • Kidrocksbodydbl says:

      Maybe it did maybe it was the sympathetic impulses that was the problem and when those pulses were cut off from the SA node then the SA node took over again and did it’s job correctly …… so it is a possibility that the CNS actually caused the issue and not the SA node. The Atropine was the actual DDX and they didn’t see it.

  • Nick Adams says:

    OOPS……2nd strip is a 2:1 conduction (originally said 3:1).  Hence the doubled ventricular rate.

  • Gustavo Flores says:

    Atropine will theoretically work on high degree AV blocks when the escape complex arises closer to the Bundle of His.

  • Ken Grauer says:

    ืื ื™ ืžืกื›ื™ื ืขื ืฉืœื•ื – as well as with several other commenters – that this was never "complete" AV Block … It would have been nice to see a long lead II rhythm strip – but NO matter!

    The atrial rate is regular at 120-125/minute. The ventricular rhythm is regular at ~32/minute. The QRS is wide (0.12 sec). The reason it NEVER was CHB is that the PR interval preceding each QRS is fixed (normal at 0.16sec). Thus the rhythm disturbance is 2nd degree AV block – most probably Mobitz II. The reason we can NOT be certain from this surface tracing that this doesn't represent Mobitz I – is that you NEVER see 2 consecutively conducted complexes (on rare occasions – Mobitz I may show one or more consecutive non-conducted beats …). That said – given QRS widening and the normal PR in beats that do conduct – this is most likely high-grade AV block of the Mobitz II type. That said – clinically, it doesn't really matter- because there is high-grade block with inadequate heart rate (ergo pacing is needed if no response to other measures … ).

    QRS morphology is interesting. In Tracing #1 it manifests RBBB-LPHB morphology. In tracings #2 and #3 – there is a less complete form (rSr') of RBBB – with now LAHB instead of LPHB (marked left axis – instead of the marked right axis with very steep downward descent of the S in lead I for Tracing #1).

    Agree with Nick about his observation on the change in atrial rate – which is initially ~125/min – then 120/min – then 107/minute in Tracing #3. Atropine has at least a dual mode of action – in that in addition to increasing the rate of SA nodal discharge – it may improve conduction through the AV node. Which effect exerts the optimal balance in a given patient is sometimes a coin toss (ie, will conduction be "improved" more from that direct effect vs whether speeding up the atrial rate in itself leads to a greater degree of AV block). In this case – who knows what the mechanism – We only see the results which are positive. The atrial rate has slowed (perhaps as Nick suggests due to time and oxygen) – and AV conduction is better (either due to whatever slowed the atrial rate – and/or – to partial effect of the atropine – which by increasing the ventricular rate may have improved output, and therefore this may be what contributes to slowing the atrial rate …). Bottom Line: Patient is better after one dose of Atropine – and in Tracing #2 we now see 2nd degree AV block with 2:1 AV conduction with similar P wave morphology and PR interval for conducting (so presumably similar mechanism of AV block, but now better conduction).

    Presumably the patient improved more clinically in Tracing #3 – such that at a slower atrial rate (107/min) – there is now 1:1 conduction. We have NO IDEA if it is improvement in the "degree" of AV block that results in 1:1 conduction – vs – slowing of the atrial rate (as a result of clinical improvement). Again – there is now RBBB/LAHB; lat Q waves and probable LVH – but no suggestion of acute changes on Tracing #3.

    BOTTOM LINE: Episode of highly symptomatic high-grade AV block with inadequate rate – so after acute MI is ruled out, a permanent pacer is needed.

    ATROPINE was indicated – though our expectations for it to work given very slow rate and wide QRS were not high. However, there IS AV conduction in Tracing #1 (fixed PR interval preceding every 4th beat) – so Atropine MIGHT work – and this case very educational in showing for whatever reason (effect of Atropine, treatment with oxygen with overall improvement of patient's general condition) – a little bit of Atropine may sometimes facilitate a chain effect of surprising improvement (OR – alternative scenario that Nick suggests – perhaps the Atropine didn't do anything …. ).

    MY PREFERENCE: Who cares – the patient is better so the treatment worked! – GREAT CASE! FOR Anyone WANTING MORE on Diagnosis of AV Block – GO TO:

  • Nick Adams says:

    @ Ken – Your analysis of this was very thorough, and enjoyed reading your analysis.  Thank you for the shout outs.
    I would like to add some other points of interest that may explain a few things pertaining to the blocks.  #1 – In the first 12 lead with the 2nd degree Type II with a 4:1 conduction, the patients B/P was 80 systolic.  Assuming that the DBP is equally low, the CPP, or coronary perfusion pressure might be low as well.  Especially with the decrease in CO while CO=HRxSV.  This would cause reduced blood flow to the heart muscle and conduction system (ischemia); Hence the RBBB and inferior ischemia noted by inverted TW's in leads III and aVF, which resolved when the heart rate increased (12 lead #3).  The LAFB remained with the pathological LAD (Bifascicular block).  In the 3rd 12 lead, the RBBB morphology is still there, but is now incomplete with a QRS duration of less then 120 ms.  Also noted is LVH without strain and LAE.

  • Abe says:

    I am pleased that i was not the only one that didn't think that it was a CHB. but would have liked to see a longer strip of lead 2.

  • VinceD says:

    I've refrained from leaving a super-long comment for a while, but all good things must come to an end.

    Of note: The first PRi in strip #1 is short (120ms), so that's a bit weird. Every single PRi on all three strips is just about 160ms on the money, so I'm at a loss as there's no provable mechanism for why the QRS is a little early. Thinking positive, at least the otherwise constant PRi supports the notion that none of these strips demonstrate complete heart block.

    Now I'm about to play the "what-if" game, so let me start by saying that the patient obviously got better and that's the important thing. Also, I agree that the treatment the patient received was probably correct and that it's likely what I would have done in the same circumstance. But, looking at this from my computer with a couple of texts in front of me, I have to say…

    (more disclaimer) I don't direct this at Dr. Grauer, but since he has such a detailed analysis of the situation, I'll use his comment as a point of reference for the first paragraph:

    I agree with almost everything you wrote above and your understanding of electrocardiography is much deeper than my own, but although atropine may have been indicated and the patient got better, I still don't know if I believe it was the correct choice. What if this patient was someone who got greater SA effects than AV effects from the drug. Suddenly the sinus rate increases from 125 bpm to 135 bpm and the increased bombardment of the AV node increases the block from 4:1 to 5:1. Now, instead of a ventricular rate of 31, it's 27, which may not sound much worse, but it certainly isn't any better. Maybe it would go to 140 bpm with 6:1 conduction and a V rate of 23 bpm. Or, maybe it'd go to a sinus rate of 135 with 3:1 and a V rate of 45 bpm. We don't know, and that worries me.

    As a general comment, I think a lot of the trouble with the use of atropine in anything other than sinus bradycardia boils down to a fundamental misunderstanding of just how the heart gets blocked and how we categorize the findings we see on the ECG. We are all initially taught that there's only first degree block, second degree type I, second degree type II, and complete heart block. While that may be a tidy system to use in an ACLS course, those classes usually give we shallow definitions of type I and II AV block, in addition to glossing over the nuances behind topics like high-grade AV block, AV-dissociation, concealed conduction, and just how-the-heck Wenkebach phenomenon works.

    As a result, most folks are taught that we don't give atropine to anything other than sinus brady or type I AV block because it "doesn't work," while some may also be told that it "worsens the block" and may turn a second degree block into a third degree or third degree into asystole. While it's true that it may potentially worsen the situation (for the reasons I mentioned above), I haven't encountered any reasoning behind why it would fundamentally change the type of block present.

    Getting back to the case, what we have is a sinus rate of 126 bpm and 4:1 conduction (and one weird early QRS). This is a high-grade second-degree AV block, which, according to my teaching, is a distinct entity from true type I or type II AV block. A sinus rate of 126 bpm shouldn't be unreasonable for a 63yo with no cardiac Hx, so there must be something wrong and we have to imagine that a faster sinus rate would result in lower conduction ratios (5:1, 6:1, …). Also, we have to consider a cause for the arrhythmia. My bradycardia mnemonic is DIE (drugs, ischemia, electrolytes), and with no real Hx, chief in my mind are ischemia and infection (not in the mnemonic), especially with the preponderance of weird bugs in Southeast Asia that may lead to endocarditis and conduction defects.

    With all that in mind, I really wouldn't expect atropine to work, and if anything, would plan for an even slower ventricular rate. Depending on the sedation I could obtain and the exact clinical picture in front of me, I may or may not give it. In a perfect world I would just give dexmedetomidine and pace the patient, but no-one carries that and pacing isn't a guarantee, so even though the patient is obviously very sick, and I've just spent several paragraphs bad-mouthing it, atropine would probably be my go-to drug AFTER pacing pads were in place and my pacer was setup as an immediate escape-route should things turn sour. Sorry for the rambling, but this is a very nuanced and intriguing case. Thanks for sharing!!

    • Kidrocksbodydbl says:

      Back to my comment about the sympathetic involvement the early QRS could be the brain saying he is running a marathon but he actually isn’t so when the vegas nerves were cut from pulsing the SA node then the SA node did revert to normal pulsing so my bet is he could have been managed with meds not a pacer.

  • Arnel C. says:

    WOW elite comment here. I agree with all (Dr. Ken, Vince etc) … Anyway here is a short take on the strips…
    Strip # 1 (2150)-
    Agree that this is ST (CL 440 ms/136 per min) , advanced HB with 4:1 conduction with LPFB/LPHB configuration, Finally I saw one LPFB in flesh and not in books (tnx). 
    Strip # 2 (2218 or 28 minutes after strip 1)- 
     Agree also that ST (CL 520 ms / 115 per min), 2:1 AV block , prob Mobitz II mechanism, RBBB and LAFB/LAHB configuration. 
    Strip 3 (2219 or about a minute afte stip #2) – 
    Agree again ST (CL 560 / 107 per min) with LAFB/LAHB configuration. 
    It seems the P wave here is 120 ms and PRI remained constant at 150 ms.
    0.5 mg atropine 1 dose did all these or was it co-incidence? In a matter of about 25 minutes atropine allowed more supraventricular impulses to pass through the AV node. So as cited by articles did atropine a freak of nature here?
    Regarding paradoxic response of atropine, ref # 359 of 2010 guideline part 8 was in a group of post-casrdiac transplant patient and not this one..
    An article cited in the 2005 guideline by Brady et al would be interesting to dig in unfortunately I cannot get free access on-line – re: on atropine use prehospital ( . They lumped the whole population (brady and AVB (all degrees). It would be nice how advanced HB behaved there. So this result could not be true for all population. Also the response efficacy was measure at 1 minute. 
    Now this is interesting, in figure 39-49 in Braunwald's Text book of Cardiology, they gave atropine 0.6 mg in type 1 Wenckebach. At 5 minutes more P waves were blocked and AVD noted caused by a combination of AVB and enhanched junctional dicharge rate but at 8 minutes atropine improved AV conduction and 1:1 conduction occured. 
    I am from SE Asia and have not known a tropical disease that would cause this. This is an interesting case if that trip was a culprit of this arrhtyhmia…
    Back to atropine…So can atropine have a role in subgroups of  patients just as we see in this case? Very interesting case. 

  • Ken Grauer says:

    GO Vince! I'll try and be shorter (for a change … ) – and I totally appreciate (and basically agree) with all you say. The scenario given is one where "ya gotta be there". I don't think there is a "wrong" or a "right" approach – but a lot of gray. In general – my preference for treating bradycardic high-grade blocks with wide QRS is pacing asap (because atropine IS unlikely to work) – though it is sometimes a tad quicker to get a dose of atropine in while settting up the pacer – which sounds like the scenario in this case. I don't think that is wrong.

    Please read my ACLS Comments. I spent many hours reviewing each word on bradycardia in the ACLS provider manual – and trying to synthesize that into a practical approach within guidelines. GO TO:

    Otherwise – I decided to limit my already too long previous comment to "themes" rather than all fascinating details of this case. I did note that the 1st PR DOES look shorter – and there is slight variation in the R-R interval of the ventricular rhythm – and the QRS in lead V1 of Tracing #1 is not a typical "RBBB" (qRR' with taller left rabbit ear) vs a much more typical rSr' in V1 for Tracings #2 and #3 – with bottom line that WE DON'T KNOW exactly what is going on beyond "high-grade (but not complete) AV block with wide QRS and inadequate rate" on Tracing #1 – because there is NO simultaneous long lead II rhythm strip that would enable us to correlate which QRS might be ventricular vs conducted with advanced Mobitz II. But clinically – none of that matters at this point – because the "theme" (and initial treatment) is the same.

  • Ken Grauer says:

    @Nick – THANKS – and I agree with your comment – except that the RBBB on Tracings #2 and #3 ARE (in my opinion) "complete" RBBB. All that is needed for diagnosis of "complete" RBBB is a QRS of ≥0.11 sec vs the 0.12 sec required for "complete LBBB" (remember the RV is not as thick as the LV). That said – one uses the lead where the QRS is WIDEST for interval measurement – and I do measure a full 0.12 sec in Tracings #2 and #3 for QRS width.
    That said – QRS morphology is "closest" to "RBBB" in Tracings #2,3 (vs calling this nonspecific IVCD) – but admittedly NOT quite "typical" in that the S wave in lead I is very narrow, and the r' in V1 is not very tall …  But the LAHB pattern is textbook gorgeous – so I think (while admittedly not a perfect "fit") – that the best description is RBBB/LAHB. That said – I agree that you could say that both LVH and LAHB each contributed a bit to widening the QRS in the setting of an underlying "incomplete RBBB". It comes down to your semantic preference – and I bet expert electrocardiographers wouldn't agree on this one either …
    We could go one step further and ask IF the diagnosis of "LVH" can really be made in the setting of underlying LAHB (let alone in bifascicular block) – but that is another debate without unified answer …

  • David Baumrind says:

    @Ken, @Nick:

    I completely follow your reasoning regarding this not being CHB, but rather second degree type II. I do have a question for you though… in the first ECG, the PRI is not constant throughout. In the very first complex, the PRI seems to be notably shorter than the other complexes. 

    How would you explain this?

  • Nick Adams says:

    @ David.  It's been my experience that when a patient goes into a second (I or II), or a CHB, it isn't always a single block at all.  I've seen, and have strips, of pt's bouncing between a 2nd degree type I and type II, or a Type II and a CHB.  With a "sick" junction, anything is possible. 
    Thank you Ken for the additional information about RBBB's, and it not needing to be greater then 120ms.  Still learning every day, and was just going by what I had learned so far and what the 12 leads have said of the years.  When ever it's a RBBB morphology, but is <0.12 sec, the EKG usually says that the block is "Incomplete".  I took this as meaning that the inpulse is still getting through the Rt bundle, but it's taking longer then normal.  Also, it is my understanding that when you havea RBBB, the first rabbit ear is the depolarization of the LV and the second is the RV and it took longer because it couldn't use the Rt bundle secondary to the block, so it had to travel through the myocardial tissue itself, which takes longer then the "fast tracts" as I like to call it…….hence a widened QRS.  Am I wrong to think this way pertaining to a RBBB?, or should I consider it a complete block with a duration of greater then 110ms?
    I just love these dicussions……

  • Ken Grauer says:

    @Dave's Question (Why is the 1st PR in the 1st ECG slightly shorter than the others?) – I did address that previously (above) – but will repeat my thoughts:

    I did note that the 1st PR DOES look shorter – and there is slight variation in the R-R interval of the ventricular rhythm – and the QRS in lead V1 of Tracing #1 is not a typical "RBBB" (qRR' with taller left rabbit ear) vs a much more typical rSr' in V1 for Tracings #2 and #3 – with bottom line that WE DON'T KNOW exactly what is going on beyond "high-grade (but not complete) AV block with wide QRS and inadequate rate" on Tracing #1 – because there is NO simultaneous long lead II rhythm strip that would enable us to correlate which QRS might be ventricular vs conducted with advanced Mobitz II. But clinically – none of that matters at this point – because the "theme" (and initial treatment) is the same.  (THAT SAID – Christopher who posted this may have additional insights ….).

    @NICK (who asked about the reason for the rabbit ears with RBBB) – The KEY is to remember that the very first part of the ventricles to depolarize is the septum – and this goes left to right. This is why you normally write small "septal" q waves in one or more lateral leads (I,aVL,V4,V5,V6) – because initial activity moves AWAY from the left (since the septum is depolarizing from left to right).

    It is because of this left-to-right septal activation that you normally write a small thin r wave in V1 and/or V2. That is NOT lost with RBBB – because the right bundle goes down the right part of the septum (and initial activation is undisturbed with RBBB because it still starts on the left). This writes the initial "r" with RBBB – and it is typically small …

    Then the LV depolarizes – which writes the S in V1 with RBBB.

    Finally – after the large LV has depolarized – the activation impulse makes its way toward the 'blocked' RV – and this is what writes the R'. Even though the RV is tiny – you often have a large R' because the LV has already depolarized and the tiny RV is depolarizing by itsself (unopposed).

    NICK – I break this down slide-by-slide in an instructional PDF. GO TO:  – and download the link at the 1st bullet on that page (self-instructional PDF on BBB). Click on "RBBB- Activation Sequence" – and slides will walk you through the process … BEST though if you go through the sequence of Normal Activation on this PDF first. There are plenty of NOTES (callouts) in the PDF along the way to explain each step.

    Hope this helps! – : ) Ken

  • ilie2000 says:

    bav II + LBBC+ hbpg

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