EKG Interpretation: Puzzling Bradycardia

49 y m presents to the Emergency Department complaining of shortness of breath. He has a history of hypertension and high cholesterol but is placed in the asthma booth because he is thought to be having an asthma exacerbation. He receives an albuterol and is feeling clinically better but the medicine chief is suspicious that the lack of an asthma history may suggest his dyspnea is due to a different etiology. He gets the EKG found below. Click on the picture for an enlarged view.

49 Y M EKG

How would you interpret this EKG? How do you manage this patient? Let the conversation begin!

10 Comments on "EKG Interpretation: Puzzling Bradycardia"

  • Second degree heart block Wenkebach type 2 (2 P to 1 QRS) with escape ventricular beats. Dude has a large LA. If I’m correct, treatment would be atropine, pacer pads, cardiology consult for pacemaker.

  • Hold on, Al’ai hasn’t replied yet with a Resen-esque discussion? Must be working or traveling. Well, here is the short-ish version:

    Wenckebach 3p’s -> 2 QRS. The third (dropped) p is buried in the second (preceding) QRS each time. Almost looks like 3rd degree, but the pr intervals are regularly irregular and the three ps march out perfectly as a triplet, but not as individual p-p intervals (each p-p gets progressively longer until dropped and reset). Since he is symptomatic-ish (no one said how long he has been feeling this way or what he looks like), we can consider treating. However, I doubt there is a rush since he had time to sit in the asthma booth and there is no ischemia on the EKG and his ventricular rate is still 48. Luckily, he has HTN, so we probably already accidently started treatment by using a beta agonist to treat what I would guess is the culprit (beta blocker, Ca Channel blocker etc). If you needed more, trying atropine and pacing is textbook, but I’d check the med list and look for a digoxin level (if he is on it) and start beta-blocker reversal and giving calcium first. My hunch is a tincture of time was all that was necessary.

    FOR THE RESIDENTS, PLEASE PRACTICE THIS: Use the edge of a piece of paper, hold it up to the rhythm strip, put a mark on the piece of paper for four consecutive p’s starting with the p preceding the shortest p-r interval (this happens to nicely coincide with the left most p) and include a marking for every other QRS that looks a little different then the one without interference (dorks can label these marks p1,p2,p3 and p1 again). Now move the paper over just one cardiac cycle, so that your first marking overlies the very next p – the markings for the following p’s don’t line up as they would if the p’s were originating from the same source (they ARE here as told from their axis and morphology) AND conducted without second degree type I block. Now move your markings over to the next p again – your first marking should now be overlying a weird disturbance in the QRS and the other markings are still not lining up. Now one more over to the right – waa lah, all the markings line up with the p’s again. There can only be two fixed patterns like this that include a fixed p to QRS ratio and a regularly irregular p-r interval: the very much most like is wenckebach, and the very much less likely 3rd degree block with a repeating sinus arrhythmia (otherwise all 3rd degree block has, by definition, AV dissociation with the A doing its rate and V doing its rate, each marching out regularly but independently).

    Here’s the long (Medscape) version to the treatment to save a step for tired residents:
    Second-degree atrioventricular (AV) block in the asymptomatic patient does not require any specific therapy in the prehospital setting. If the patient is symptomatic, standard advanced cardiac life support (ACLS) guidelines for bradycardia, including the use of atropine and transcutaneous pacing, are indicated.[12, 31]

    No specific therapy is required in the emergency department (ED) for Mobitz I (Wenckebach) second-degree AV block, unless the patient is symptomatic. Patients with suspected myocardial ischemia should be treated with an appropriate anti-ischemic regimen. Second-degree block at the level of the atrioventriocular node (AVN) may be due to digoxin, beta-blockers, or calcium channel blockers. Decreasing the dose and/or discontinuing these medications may restore normal AV conduction.

    Mobitz II block is more likely to progress to complete heart block and thus requires a different approach. As with Mobitz I block, AV nodal agents should be avoided, and an anti-ischemic regimen should be instituted if ischemia is suspected.

    Permanent pacing is considered in accordance with the relevant guidelines (see Pacemaker Implantation). Except for the use of atropine in selected cases of transient AV block, permanent cardiac pacing has replaced medical interventions in the treatment of patients with symptomatic, otherwise untreatable, AV block.
    Mobitz I block
    Admit patients who have symptoms or who have concomitant acute myocardial ischemia or myocardial infarction (MI). Admission should be to a unit with telemetry monitoring, which has transcutaneous pacing capabilities.

    Symptomatic patients should be treated with atropine and transcutaneous pacing. However, atropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur in this situation.

    The goal of atropine administration is to improve conduction through the AVN by reducing vagal tone via atropine-induced receptor blockade. However, this goal will only be effective if the level of the blockade is at the site of the AVN. Patients with infranodal second-degree AV block are unlikely to benefit from atropine. In addition, in patients who have denervated hearts (eg, patients who have undergone a cardiac transplant), atropine is also not likely to be effective.

    Mobitz II block
    Admit all patients to a unit with monitored beds, where transcutaneous and transvenous pacing capabilities are available. The admitting cardiologist should determine whether permanent pacemaker implantation is indicated.

    Transcutaneous pacing pads should be applied to all patients with Mobitz II second-degree AV block, including those who are asymptomatic patients, because such patients have a propensity to progress to complete heart block. The transcutaneous pacemaker should be tested to ensure capture. If capture is not able to be achieved, then insertion of a transvenous pacemaker is indicated, even in asymptomatic patients.

    Urgent cardiology consult is indicated for patients who have symptomatic type II block and for those asymptomatic patients who are unable to achieve capture with transcutaneous pacing.

    Some institutions recommend insertion of a transvenous pacemaker for all new Mobitz type II blocks, although this practice varies greatly from institution to institution.

    Patients who are hemodynamically unstable for whom an emergency cardiology consult is not available should undergo placement of a temporary transvenous pacing wire in the ED. A chest radiograph is required to confirm position of the wire and to exclude complications, including hemothorax or pneumothorax.

    2:1 block
    In cases where there is a 2:1 block and one is unable to determine if there is a Mobitz I block or Mobitz II block, the patient should be admitted and cardiology consultation should be obtained. In such cases, it is safest to assume that a Mobitz II second-degree AV block exists.

    Hoping Al’ai hasn’t made me look stupid in the time it took me to type this…. aaaaaaand, post.

  • Allow me to be the first to tell me to insert my foot into my mouth. On second look, the disturbance at the end of the second QRS is consistent with a retrograde p, not a buried 3rd p (a buried p should create a deflection in the same axis as the sinus p’s, and the terminal deflection in the second QRS is in the opposite direction). The retrograde p must originate from a source below the atrium, in this case a junctional beat (not ventricular as the QRS is narrow and hence a morphology that looks nearly the same as the SA triggered beat). Therefore, I think Alan is right, the pattern is p–>pr segment –> QRS –> dropped p –> junctional escape with retrograde p causing the disturbance at the end of the junctional QRS. The only thing holding me back from being sure about this the regularity of it all – a very punctual junctional pacer, I guess. That would make this 2:1 Wenckebach (with a fortunate junctional escape). 2:1 Wenckebach is presumed Mobitz I until proven otherwise. I assume the same is true if a junctional escape is making it a weird 1p:1QRS ratio. Either way, treatment remains as I stated. Tincture of time if on the right anti-hypertensives, if necessary medical therapy, if really necessary pacer, then Cards, Admit tele vs. CCU depending on level of concern (tele if clinically ok, CCU if really scared of Mobitz I).

  • Also agree with Alan — was momentarily thinking 3′ but noted the ‘odd’ qrs vs the narrow conducted beats. Also curious about the ?long Q-t interval…


  • Ask yourself: Why do the QRS complexes look different?
    Why isn’t there a P wave in front of every QRS?

  • After having looked at this EKG multiple time I want to share my thoughts on it…
    I agree with the fact that this is a Second Degree Heart Block Mobitz I or II. The reason why it is a “I or II” is the fact that the rhythm doesn’t march out long enough (more than 2 beats) before a beat is dropped and an escape rhythm is appreciated. In other words if the rhythm marched out 3 beats we would be able to appreciate whether or not the PR interval was elongating or not to distinguish between Mobitz I and II. Because it only marches out 2 beats, we must assume that the rhythm is a Mobitz II which is more dangerous and admit the patient for fear of eventual complete heart block. I don’t believe it is complete heart block because the p waves do not consistently conduct independent of the QRS complexes and that there appears to be an association between the P and QRS in the first beat of the 2 beat rhythm pattern. The second QRS complex is likely a ventricular escape beat which has a different morphology. Tell me what you guys think.

  • One of the Jacobi Attendings threw their hat in the ring with this explanation:
    AV dissociation vs. Complete Heart Block

    A> Complete heart block (Third-degree heart block)
    -Atrioventricular block in which no AV conduction occurs.
    -VENTRICULAR rate controlled by junctional or idioventricular pacemaker at rate SLOWER than ATRIAL rate.
    -QRS complex narrow if pacer site above bifurcation of HIS bundle.
    -ETIOLOGY- Acute complete heart block
    (1) AMI- especially heart block
    (2) Drug toxicities—i.e. digitalis, B-blocker

    *** usually always bradycardia

    -often requires pacemaker.

    B> AV dissociation
    -atria and ventricles beat independently.
    -ventricular rate >> atrial rate
    -NO retrograde ventriculoatrial conduction occurs
    -can occur at any HEART RATE
    *** often converts to sinus rhythm.

  • This is neither second or third degree heart block.

    In second degree heart block, all the QRS look alike, and every QRS has a P. This is not the case here, so clearly, i cannot choose the heart block in front of me.

    In third degree heart block, all the QRS look alike, and the QRS complexes are regular and “march out”. This is not the case here, so clearly, i cannot choose the heart block in front of you.

    This is the answer according to my cardiology source: sinus bradycardia with atrial bigeminy. The APC is blocked and there is a junctional escape beat.
    – Do you call this heart block?
    No. The PAC is blocked, it’s not a sinus beat so by definition it can’t be heart block. There probably is some AV conduction disease because the PAC isn’t that early.

  • First P conducted normally (with first degree AV block), second P wave is blocked. Third P wave was never generated (Sinus block Type II), Fourth P wave was never generated because the escape beat reset the sinus node. Then it starts all over.

  • VERY interesting tracing. I agree with much of AndrewChertoff’s comments. I think this rhythm might best be explained by labeling and numbering beats which I have done – GO TO – https://www.dropbox.com/s/w6m39x9xglszeiw/ECG-Jacobi-Escape-Capture-Mobitz%20I-%283-16-2014%29.png

    What is confusing is the baseline ventriculophasic sinus arrhythmia – that is, variation in the P-P interval as a result of underlying AV block. This is a relatively common phenomenon – in which typically it is the P-P cycle that is sandwiches a QRS that has the shorter P-P (ie, the P-P sandwiching beats #1,3,5,7) – presumably because perfusion from the conducted beats (ie, beats #1,3,5,7) results in a shortening of the P-P interval. I was NOT at all certain that there was underlying sinus arrhythmia – because the P-P variation is fairly marked and virtually totally HIDDEN within the QRS complex of beats #2,4,6. The KEY for me was the presence of a DEFINITE P wave (BLUE arrow) just preceding beat #8 (verified by seeing a slight notch in simultaneously recorded leads V4 and V6, as well as in the long lead II rhythm strip). I then was able to “march out” (using calipers) where presumably the hidden P wave would be falling (see open red arrows). I do believe there is slight very subtle suggestion within the slightly changing S wave of beats #2,4,6 that something is hidden – but for me, it was the BLUE ARROW that solidified this presumption.

    With underlying sinus mechanism (ventriculophasic sinus arrhythmia) established – I then worked on the assumption that “common things are common” – ie, most of the time when you have grouped beats with narrow QRS and non-conducted P waves – there is 2nd degree AV Block, Mobitz Type I (= AV Wenckebach). That seems to be the case here – with an “escape-capture” phenomenon. That is – NOTE the constant PR preceding beats #1,3,5,7 – all of which are being conducted. The P waves following beats #1,3,5,7 are non conducted. There follows escape – with the preceding R-R interval before beats #2,4,6 and 8 virtually identical (corresponding to an escape rate ~48/minute). As a result of this “escape” focus set at 48/minute – the next P wave (open arrows for those hidden P waves) does not conduct – but the reason it doesn’t conduct is NOT AV block, but rather not having a chance to conduct because the escape beats (#2,4,6,8) came in before those open arrow P waves had a chance to conduct. Thus, there is only 1 non-conducted P wave per cycle – and what we have is 2nd degree AV block, Mobitz I with escape capture phenomenon. The overall heart rate = 45-50/minute – so IF this patient is not hemodynamically unstable – NO emergent treatment is needed – and perhaps just stopping any rate-slowing agents (beta-blockers, verapamil/diltiazem/digoxin) might be all that is needed for this problem to resolve. Agree with AndrewChertoff that there are no acute ST-T wave changes.

    Finally – the question arises as to WHERE the escape focus is arising from. Most often – it comes from the AV node – but note that escape beats in this case are wider and manifest complete RBBB morphology (rSR’ in V1 for beat #6 – and wide terminal S wave in leads I for beat #2 and in V6 for beat #8). I measure the QRS of these wider beats at 0.11 second, which IS enough to qualify as RBBB – but given this definite rbbb morphology and a not overly widened QRS – the escape focus is almost certainly coming from some part of the conduction system. So – possibilities for the site of the escape focus include: i) the AV node – with bradycardia-dependent rbbb aberration; ii) the HIS; or iii) the common left bundle branch.

    Hope the above makes sense – GREAT case for discussion!

Leave a Reply