The patient whose ECG is shown in Figure-1 is a man in his 50s who presented to the ED with new-onset chest pain.
- Unfortunately — there is no long lead rhythm strip ... There is also slight distortion of the complexes in this tracing due to some angulation when a photo of this ECG was made. That said — tracing quality is sufficient for accurate interpretation.
QUESTIONS Regarding ECG #1:
- HOW would you interpret the ECG in Figure-1?
- Is there a probable “culprit” artery?
- Is there AV Block? IF so — Is this complete AV Block?
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| Figure-1: ECG obtained from a man in his 50s with new chest pain (See text). |
MY THOUGHTS on ECG #1:
This wasn’t my patient. I thought it might be helpful to describe the sequence of my thought process for assessing this case based on the information I was given.
As always — I like to begin by first interpreting the cardiac rhythm. Only after I take an initial look at the rhythm — do I look at the rest of the 12-lead. The problem with this initial look at the rhythm in this case — is that there is no long lead rhythm strip. This limits us to looking at the 12 leads that are shown, with no single lead showing more than 6 or 7 consecutive beats.
- MY Approach: Since we lack a long lead rhythm strip — I look for a lead in which P waves are evident. Ideally, this would be lead II — since the presence of upright P waves with similar P wave morphology in lead II would define the underlying rhythm as sinus. On occasion, when P waves are not well seen in lead II — I’ll select another lead in which they are.
- For ECG #1 — P waves are well seen (and upright) in lead II. These P waves look to be fairly regular — and this suggests that the mechanism of the underlying rhythm is most likely to be sinus. The atrial rate is increased at ~130/minute.
- PEARL #1: This is a challenging arrhythmia! KEY to determining what the etiology of this arrhythmia is — is determining whether or not the atrial (P wave) rhythm is or is not regular (or at least almost regular). Using CALIPERS allows you do to this in less than 5 seconds. The reality is — that IF you do not regularly use calipers for rhythm interpretation — then you will never get good at interpreting complex arrhythmias. And, IF you do not yet use calipers — I guarantee that your skill in rhythm interpretation will instantly improve the moment you start to do so.
PEARL #2: The immediate question I had regarding the rhythm in this tracing — was whether some form of AV Block was present? This is why determining whether the atrial rhythm is regular is important — because AV Block is unlikely if P waves are not regular (or at least almost regular).
- NOTE: It is common with 2nd- and 3rd-degree AV Block for there to be slight irregularity in the P-P interval due to the presence of ventriculophasic sinus arrhythmia. This slight irregularity is felt to result from variable coronary perfusion due to the AV Block itself (ie, P waves that closely follow QRS complexes tend to occur a bit sooner than P waves that do not "sandwich" a QRS complex — because of better SA node perfusion). But the amount of P-P interval variation tends to be small, and significantly less than is seen with PACs or sinus pauses in a patient with sick sinus syndrome.
Continuing My Initial Assessment of the Rhythm:
- By the Ps, Qs & 3R Approach (See Audio Pearl #3) — The QRS complex is narrow everywhere in ECG #1 — so the mechanism of this rhythm is supraventricular.
- P waves are upright and fairly regular in lead II.
- The R-R interval is clearly not regular — but I did get the impression that there appeared to be a “regular irregularity” (ie, some form of group beating) in this tracing.
- Looking in those leads for which I was clearly able to identify P waves in (ie, lead II; lead V6, among others) — it seemed as if at least some of the PR intervals repeated! This repetition of some of the PR intervals is unlikely to be due to chance — and suggests there is conduction of at least some of the P waves!
- It also appears that at least some of the regularly-occurring P waves are not conducted (because they are not followed soon after by any QRS complex).
- NOTE: Because I used calipers and because I followed a systematic approach (ie, looking for Ps, Qs & the 3Rs) — I was able to make the above observations within seconds!
PEARL #3: Suggestion of group beating and a fairly regular atrial rhythm and — the fact that at least some of the regularly-occurring P waves are not conducting — tells us that some form of AV Block is likely.
- That said, we can already rule out 3rd-degree (ie, complete) AV Block — because the ventricular rhythm is clearly not regular and — repetition of several of the PR intervals tells us that some of the P waves are being conducted! (No P waves at all would be conducted if the rhythm was 3rd-degree AV block).
PEARL #4: By the “KISS” Method (ie, “Keep It Simple” Stupid) that I use for assessing the AV Blocks ... — IF an AV Block is present — and if we know the rhythm is not simple 1st-degree AV Block (because PR intervals in ECG #1 vary) — and IF we have ruled out 3rd-degree AV Block (as per Pearl #3) — then the type of AV Block must be a form of 2nd-degree AV Block.
PEARL #5: As discussed in Audio Pearl #4 (See ECG Blog #186) — There are 3 basic Types of 2nd-degree AV Block: i) Mobitz I ( = AV Wenckebach) 2nd-degree AV Block (in which there is gradual increase in the PR interval until a beat is dropped); ii) Mobitz II 2nd-degree AV Block (in which the PR interval remains constant until one or more P waves in a row are not conducted); and, iii) 2nd-degree AV Block with 2:1 AV Conduction (in which you can not tell IF the PR interval would increase if given a chance to — since you never see more than a single conducted P wave in a row because of the 2:1 block).
- The rhythm in ECG #1 is clearly not simple 2:1 AV Block (since the ventricular rhythm is irregular — and therefore doesn’t show strict 2:1 AV conduction).
- Mobitz II is rare! In my experience — over 95% of all 2nd-degree AV Blocks that I have seen in over 40 years of looking for AV blocks, turn out to be Mobitz I. The importance of recognizing those rare cases of Mobitz II that do occur — is that a pacemaker will usually be needed. This is because of the disturbing tendency of Mobitz II to suddenly develop a very high-grade form of AV block (ie, nonconduction of multiple P waves in a row). The QRS complex will almost always be wide with Mobitz II (because this more severe form of AV block usually arises from lower down in the conduction system) — and Mobitz II is usually associated with acute anterior MI (from acute LAD occlusion).
- In contrast, with Mobitz I — the QRS complex is usually narrow (unless there already was underlying bundle branch block) — the PR interval of the 1st conducted beat in any cycle will often manifest 1st-degree AV block — and, the site of acute MI will usually be inferior (because this generally less severe form of AV block tends to arise at the level of the AV node — which is regularly supplied by either the RCA or left circumflex coronary artery).
BOTTOM LINE Regarding My Thoughts thus Far: I’ll emphasize that I was not at all certain about the rhythm in ECG #1 at this point in time. That said — I definitely did suspect some form of Mobitz I 2nd-degree AV Block because:
- There was an underlying regular sinus rhythm.
- The QRS complex was narrow.
- There seemed to be group beating — with conduction of several beats (best seen in lead V6) that manifest a constant (and slightly prolonged) PR interval.
At this point in the process, even though I had not yet made a definitive diagnosis of the rhythm — I turned toward assessment of the rest of the 12-Lead ECG in Figure-1. Practically speaking — further clarification of the rhythm diagnosis at this point would not have altered initial management, and this patient did present with new-onset chest pain that needed to be assessed! Continuing on with assessment of the rest of the 12-lead ECG:
- The QTc interval in ECG #1 looks borderline.
- The frontal plane axis looks normal (about +20 degrees).
- There is no chamber enlargement.
Regarding Q-R-S-T Changes in ECG #1:
- Regarding Q waves — Considering the small size of the QRS complex in the inferior leads, a large (and wide) Q wave is present in lead III, and a smaller Q wave is seen in lead aVF.
- R wave progression is appropriate — with transition (where height of the R wave becomes greater than depth of the S wave) occurring normally between leads V3-to-V4.
The most remarkable findings in ECG #1 relate to ST-T Wave Changes:
- All 3 inferior leads show significant ST elevation (especially given the small size of the QRS complex in leads III and aVF). At the end of these elevated ST segments appears a small amplitude upright (ie, hyperacute) T wave.
- There is reciprocal ST depression in both of the high lateral leads (ie, in leads I and aVL).
PEARL #6: Did YOU appreciate that “magic” = mirror-image opposite picture for the SHAPE of the ST-T wave in leads III and aVL that I previously emphasized in ECG Audio Pearl #2?
- The fact that the shape of the ST elevation in lead III of ECG #1 is a “mirror reflection” of the shape of the reciprocal ST-T wave depression in lead aVL (within the small GREEN rectangle in Figure-2) — essentially confirms recent or acute inferior STEMI.
- Note that the same “magic” relationship exists for the shape of the ST depression in lead aVL — which is a “mirror reflection” of the shape of the ST elevation in lead III (within the small BLUE rectangle in Figure-2).
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| Figure-2: To facilitate visualization of the mirror-image opposite view in selected leads — I have flipped vertically (to create a mirror-image reflection) one QRST complex in leads III, aVL; V2 and V3 — and I show these mirror-image reflections within the colored rectangles (See text). |
In the Chest Leads:
- The ST segment in lead V1 of ECG #1 is flat (neither elevated nor depressed).
- There is J-point ST depression in each of the 5 remaining chest leads. The fact that the amount of this ST depression is maximal in lead V2 (in association with recent or acute inferior MI) is diagnostic of acute posterior involvement.
PEARL #7: Use of the Mirror Test facilitates visualizing the ECG signs of acute posterior MI.
- Flipping a few anterior leads upside-down provides an ECG picture of what is occurring in the “mirror-image” posterior wall — which now manifests deep Q waves, ST elevation and deep T wave inversion suggestive of acute posterior MI (within the RED rectangles in Figure-2).
PEARL #8: Normally with acute posterior MI — each of the anterior leads (ie, leads V1, V2, V3 and often V4) will show at least some ST depression. The fact that the ST segment in lead V1 is flat (instead of depressed) suggests that in addition to acute infero-postero MI — there is probably also acute RV involvement (ie, acute Right Ventricular MI often produces ST elevation in right-sided lead V1 — which may be attenuated or cancelled out by simultaneous ST depression from ongoing posterior MI).
- Right-sided chest leads would be needed to prove there is acute RV involvement in ECG #1 — but IF acute RV MI is present, this would confirm the RCA (Right Coronary Artery) as the “culprit” artery — because the LCx (Left Circumflex) coronary artery does not perfuse the right ventricle.
- NOTE: For more on the ECG diagnosis of acute RV MI — Please see ECG Blog #190.
PEARL #9: Acute coronary occlusion typically manifests with ST elevation over the affected lead areas — and reciprocal ST depression in opposite lead areas. Reperfusion of the acutely occluded artery (either following thrombolytic therapy or angioplasty — or occurring spontaneously) — is usually heralded by T wave inversion in leads that initially showed ST elevation.
- The mirror-image of T wave inversion in posterior leads (within the RED rectangles in Figure-2) — is development of T wave peaking. The fact that T waves appear peaked and more-upright-than-expected at the end of the marked ST depression seen in leads V2 and V3 (as well as in other chest leads) — suggests that there may already have been some spontaneous reperfusion in ECG #1.
Final THOUGHTS on the Rhythm: Now that we’ve assessed the rest of 12-lead ECG (and now that we've diagnosed acute ongoing infero-postero MI with probable RV involvement) — we can return for a more detailed look at the rhythm. This is best done by means of a Laddergram:
- I’ve already highlighted features of the rhythm in ECG #1 that strongly suggest the Mobitz I ( = AV Wenckebach) form of 2nd-degree AV Block. These included — i) regular atrial rhythm; ii) group beating; iii) narrow QRS complex — and, iv) evidence of some conduction, in the form of similar PR intervals in front of several QRS complexes. The fact that we have now also have v) acute inferior STEMI (from acute RCA occlusion) — makes it all but certain that some form of AV Wenckebach is operative for the rhythm seen in ECG #1.
- The various possible forms of Mobitz I can be complex — and may involve multi-level AV block — AV nodal escape beats — and/or “concealed” conduction (that may alter the inherent escape pacemaker rate). Clearly, the brevity of the rhythm strip available in ECG #1 (which is further altered by slight angulation of the paper, therefore slight distortion of this tracing) makes definitive rhythm diagnosis impossible from assessment of this tracing alone. That said — I propose the mechanism that I've drawn in the laddergram shown below in Figure-3. Explanation of this laddergram appears in the legend to this Figure.
BOTTOM LINE Regarding Today’s Case: It's important to appreciate that precise determination of the rhythm in Figure-3 is not essential for initial clinical decision-making — as it will not alter initial management. Practically speaking — the following description of findings on ECG #1 should more than suffice for initial appropriate decision-making:
- There is sinus rhythm with 2nd-degree AV Block of the Mobitz I type, with intermittent AV dissociation and occasional junctional escape beats.
- Acute or at least recent infero-postero OMI (Occlusion-based MI) — with probable acute RV involvement (Posterior chest leads would be needed to confirm this).
- Some evolutionary changes — with development of inferior Q waves (in leads that still manifest ST elevation) — and, suggestion of at least partial coronary reperfusion, given taller-than-expected T wave peaking in anterior chest leads.
- Given the clinical presentation (ie, a man in his 50s with new-onset chest pain) — prompt cardiac catheterization is clearly indicated to better define the anatomy and current state of “culprit” artery opening (ie, it is likely that acute reperfusion could benefit this patient!).
Figure-3: Laddergram for the 6 beats we see in lead II of ECG #1. Colored arrows show regularity of the underlying sinus rhythm. The QRS complex is narrow and similar in morphology for all 6 beats.
- The PR interval preceding beat #3 is clearly too short to conduct. This tells us that beat #3 must be an AV nodal escape beat.
- The PR interval preceding beats #2 and 6 is the same — which suggests that both of these beats are conducted by the RED P waves that precede them.
- The PR interval preceding beats #1 and 5 is also the same, albeit slightly longer than the PR interval preceding beats #2 and 6. This suggests that beats #1 and 5 are also both conducted by the RED P waves that precede them (albeit with a slightly longer PR interval than for beats #2 and 6).
- The P waves highlighted by BLUE arrows are clearly not conducted. They all either occur during the refractory period — or, are isolated to a point in the middle of an R-R interval, and distant from any neighboring QRS complex.
- I was uncertain about the etiology of beat #4 (red Question Mark). Although theoretically possible for the PINK P wave preceding it to conduct — I suspected beat #4 was an AV nodal escape beat, because its PR interval is so much shorter than the PR interval for other beats on this tracing that we know are conducted.
- I selected PINK for those P waves in Figure-3 that I suspect would have conducted if not for “concealed” conduction from the 2 AV nodal escape beats.
- Alternatively — It could be that instead of a 2nd AV nodal escape beat, the BLUE P wave in the middle of the R-R interval of beats #3-to-4 might be conducting with a very long PR interval (which would still prevent conduction of the next sinus P wave by retrograde concealed conduction). Another (even less likely) theory — might be alternate conduction in dual AV nodal pathways that manifest different degrees of AV block.
- In Conclusion: While impossible to be certain of the precise mechanism for the rhythm in Figure-3 from this very short rhythm strip — it is virtually certain that some form of AV Wenckebach is present — since we see conducting P waves with dropped beats (in BLUE) — and, suggestion in at least the lower level of the AV node that PR intervals increase, punctuated by dropped beats.
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Acknowledgment:
- My appreciation to Antranik Ohanian (from Lebanon) for the case and this tracing.
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ADDITIONAL MATERIAL:
- For more on the Basics of AV Block — See my ECG Blog #186 —
- See ECG Blog #188 — for review on HOW to Read (and/or Draw) a Laddergram.
- For more on use of the Mirror Test to facilitate recognizing acute Posterior MI — See my ECG Blog #56 — and — My Comments at the bottom of the September 21, 2020 post and the February 16, 2019 post in Dr. Smith’s ECG Blog.
- David Richley offered the following alternative explanation to the laddergram I proposed above (Figure-4):
- A long rhythm strip would have been useful — but even without one, I think we can be confident that both beat #3 and beat #4 are NOT escape beats. For one thing, they are both preceded by very different RR intervals, and escape intervals should be constant.
- Secondly, if beat #3 were an escape beat — its preceding RR interval of 0.7 sec would be equivalent to an ‘escape’ rate of 86 bpm, in which case we would expect to see a prolonged accelerated junctional rhythm, perhaps interrupted by occasional capture beats.
- Instead, I think that beat #3 is a conducted sinus beat — but that the P wave that connects to it is the one on the T wave of beat #2.
- So — Is beat #4 the sole escape beat? I think it could be, but I suspect that it is another conducted beat, but with a shorter PR interval than the other conducted beats because of the relatively long preceding pause. This would be an example of RP/PR reciprocity — the longer the RP interval, the shorter the following PR interval.
- Figure-4 is the laddergram that I’ve drawn a to illustrate what I think is going on. The theory I have just outlined requires that there be 2 successive blocked P waves — which is certainly unusual in Wenckebach AV block, but I think I have seen it before. Of course, there may be better alternative explanations.
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| Figure-5: Final laddergram I propose as a potential mechanism for today's case ... |
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| Figure-6: Dr. Jerry Jones favors the laddergram from Figure-5. He labeled the 10 P waves for clarity (See explanation by Dr. Jones below). |
- P wave “a” conducted with a prolonged PR interval.
- P wave “b” did not conduct due to refractoriness because its RP interval was too short.
- P wave “c” conducted with a prolonged PR interval.
- P wave “d” conducted with a prolonged PR interval because its RP interval was sufficiently long to allow concudtion and there is no other way to explain the presence of R wave #3. A premature junctional beat would be essentially a deus ex machina.
- P wave “e” did not conduct because PR interval is too short.
- P wave “ f ” may or may not have conducted with a prolonged PR interval.
- P wave “g” did not conduct due to concealed conduction by the previous P wave and the likelihood of a significant 1 st degree AV block.
- P wave “h” conducted with a prolonged PR interval.
- P wave “ i ” did not conduct due to refractoriness because its RP interval was too short.
- P wave “ j ” conducted with a prolonged PR interval.
Dr. Jones added the following:
- Wenckebach conduction can be present without resulting in a dropped beat. I wouldn’t be influenced by the “normal” PR interval preceding R wave #4.
- We must assume that P wave “ f ” conducted because we HAD to assume that P wave “d” with a shorter RP interval conducted. I am not in favor of invoking sudden ectopic junctional beats to explain my way out of a difficult dysrhythmia.
- I don’t think P wave “g” could have conducted because: 1) I think there is a baseline significant 1 st degree AV block present; and, 2) since we must assume that P wave “f” conducted, it would have blocked P wave “g” due to concealed conduction. That does NOT rule out the possibility that P waves “f” and “g” both failed to conduct, resulting in a junctional escape beat (ie, beat #4). The PR interval involving P wave “f” may have simply taken too long and was usurped by a junctional escape focus.
- No P wave with an RP interval shorter than the RP of P wave “d” conducted. Certainly — a true rhythm strip could have clarified things immensely.
- The presence of a prolonged PR interval complicates the matter a bit. Some of the most challenging dysrhythmias I’ve ever encountered turned out to have nothing more than a 1st degree AV block as the basis.
- I teach my classes that you can recognize a 3rd degree AV block because there is no interruption of the escape rhythm and it is a very regular rhythm (unless interrupted by a PVC). Actually, that is not entirely true — the escape focus can develop a Mobitz I or II exit block, and result in an irregular rhythm, or allorhythm. That is very rare (unless you are an electrophysiologist). That said — I tried deciphering this as an accelerated junctional rhythm with an exit block, but I couldn’t get it to result in anything believable.
- I don’t think a multilevel AV block is applicable here because we are in sinus rhythm with a rate that looks like the low to mid 80’s. The P-P intervals shorten a bit at the end while the R-R intervals increase slightly.
- If any beat were an escape beat, it would have to be beat #4, because it ends the longest R-R interval.
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