2nd degree AV block: is this Mobitz I or II? And why the varying P-P intervals?

Written by Willy Frick

A middle aged man presented for elective outpatient surgery. The following ECG was obtained in the preoperative area.

What do you think?

The ECG shows sinus rhythm with a rate of about 78 and 2:1 AV conduction along with right bundle branch block and left anterior fascicular block. The PR interval on the conducted beats is prolonged, about 220 ms. Eagle eyed readers might notice PP interval variation.

One differential diagnosis would be blocked PACs, a common cause of pauses on ECGs. However, given that the P waves are all identical in morphology, the more likely explanation is the ventriculophasic response. The exact mechanism is subject to debate, but the characteristic finding is that PP intervals which contain a QRS complex are shorter than PP intervals which lack one. That is exactly what we see here. It can be seen in other forms of heart block as well (such as complete heart block). See Ken Grauer's comment below for more on this.

As this patient is scheduled for imminent elective surgery, it is important to determine whether this is Mobitz I (benign) or Mobitz II (requires pacing).

So...Which is it?

Answer: You cannot be certain from this ECG alone.

The usual way to discriminate between Mobitz I AV block and Mobitz II AV block is by comparing successive PR intervals. If there is PR prolongation from one to the next, this supports Mobitz I physiology which rarely benefits from pacing. Conversely, if the PR interval is constant, this supports Mobitz II physiology, which is an indication for pacing. 2:1 block is a special case, because the tracing lacks successive PR intervals. This pattern can be seen in both Mobitz I and Mobitz II physiology.

History is often helpful. If the patient is otherwise healthy and has a good reason to have high vagal tone (like nausea or somnolence), it is likely Mobitz I. On the other hand, history of syncope does not necessarily prove that it is Mobitz II. This is because high vagal tone can cause reflex syncope, as in this case.

You can also use bedside maneuvers to investigate further. Interventions which increase vagal tone tend to worsen Mobitz I block. Perhaps surprisingly, vagal maneuvers can actually improve conduction in Mobitz II block. This is because the slower sinus rate gives more time for the His-Purkinje system to recover. The opposite is true for maneuvers which reduce vagal tone (i.e., they improve conduction in Mobitz I and worsen it in Mobitz II).

So, for example: atropine and exercise should both improve conduction in Mobitz I block, but make it worse in Mobitz II. Conversely, carotid massage should worsen conduction in Mobitz I block, but make it better in Mobitz II.

In this case, you might suspect Mobitz II block since there is already infra-Hisian disease manifest with the bifascicular block. But this is only a guess. As it turns out, the patient had a repeat ECG obtained prior to evaluation by cardiology.

What do you think?

This is an extremely helpful ECG, because we now have two successive PR intervals to compare to each other (P-waves preceding QRS complexes 4 and 5). I have labeled the P waves below for ease of reference:

P waves 8 and 9 both conduct to the ventricles. You can probably tell just by eyeballing, but caliper measurement confirms that there is PR prolongation, thus confirming Mobitz I block.

So, should the patient go to surgery?

In order to test the hypothesis further, cardiology performed carotid massage while recording 12 leads of rhythm. This is shown below:

A few seconds into the strip you can see the carotid massage artifact (most pronounced in V1-2). Quite surprisingly, carotid massage slows the sinus rate slightly, and as a result instantly improves AV conduction to 1:1, supporting Mobitz II AV block!

The patient went for EP study and had prolonged HV interval which strongly supports placement of a pacemaker. He underwent dual chamber pacemaker implantation and did well.

Learning points:

• Mobitz I and Mobitz II can co-exist in the same patient at the same time

• Bedside maneuvers can help clarify the etiology of 2:1 AV block

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MY Comment, by KEN GRAUER, MD (11/12/2024):

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Questions often arise regarding the various forms of 2nd-degree AV block. Today's case proves insightful, not only by reviewing KEY concepts on this subject — but also by illustrating a case in which bedside maneuvers can help to distinguish between the types of 2nd-degree AV block — and, in which the patient "did not read the textbook".

• I focus my comment on some additional advanced concepts to those discussed in Dr. Frick's excellent review.

To Emphasize: For those in search of "the quick answer" — today's middle-aged man should not be approved for an outpatient elective surgical procedure without further evaluation. As I'll address momentarily — I thought the 2:1 AV block was subtle, and potentially easy to overlook if one was not systematic. But regardless of whether you identified the 2nd-degree block or not — the "quick answer" — is that this patient should not be approved for elective surgery without further evaluation.

• As per Dr. Frick — some history is needed, especially since some patients are at times less than forthcoming with a history of presyncope or syncope unless probing questions are asked.
• Finding a previous ECG from this patient for comparison would be tremendously helpful (Are the conduction defects new or old?).
• To Emphasize: This elective pre-op ECG is not normal. Even if the 2nd-degree AV block is not initially recognized — there are several significant ECG abnormalities (as highlighted by Dr. Frick) which include 1st-degree AV block (PR interval = 0.24 second) — and bifascicular block in the form of RBBB/LAHB. 
• More subtle, but equally important — is the question of when these ECG abnormalities may have occurred? The small-but-definitely-present initial q wave in lead V2 (within the dotted RED circle in Figure-1) is not a normal finding with this RBBB considering that there definitely is a typical triphasic (rsR' ) QRS complex in neighboring lead V1 (ie, So there has been loss of the initial r wave that was seen in lead V1 ).
• Further support that anterior infarction of unknown age may be the cause of the above noted conduction system abnormalities — is forthcoming from the ST segment flattening in multiple leads (BLUE arrows) that is not a typical finding with bifascicular block unless there is underlying heart disease. And although the inferior lead T wave inversion could simply be the result of the predominantly negative QRS complexes of the LAHB — ruling out recent MI seems advisable prior to approval for elective surgery.
• Finally — Regardless of whether the 2:1 AV block is seen — there is marked bradycardia (rate in the 40s), which of itself deserves investigation prior to approval for elective surgery. 
• 
  
• Therefore: The "quick" answer to today's case (obvious within seconds) — is that further evaluation (and potential pacemaker placement) is needed prior to approval for elective surgery.

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What follows is a "deep dive" into some of the intricacies of the 2nd-degree AV block for readers with an interest in advanced arrhythmia interpretation.

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Did YOU See the 2:1 AV Block?

Over the years — I've occasionally encountered tracings for which an unexpected 2:1 AV block makes me STOP for a moment to verify that the rhythm in front of me truly is 2:1 block (and not some masquerading T wave or U wave). This was the case for today's rhythm — for which the marked bradycardia made me suspect 2:1 conduction — but for which the deceptively flat T waves in multiple leads (See the BLUE arrows in leads V4,V5,V6 of Figure-1) made me initially question what was T wave vs U wave vs "extra" P wave vs some superposition of both? And, before cancelling a scheduled elective surgery (with the patient already prepped in the pre-op room) — I would want to be 100% certain that I was truly looking at 2:1 AV block.

• The timing of the potenial "extra deflection" is critical. Using calipers is the fastest and easiest way to check IF what appears to be an extra P wave deflection is real (and not just a look-alike T wave or prominent U wave). 
• As can be seen from the RED arrows in Figure-1 — the timing of these potential P wave deflections is consistent with the presence of an extra P wave.
• One needs to be aware of the phenomenon known as ventriculophasic sinus arrhythmia. It is common with both 2nd- and 3rd-degree AV block to see some variation in the P-P interval beyond that expected with a simple sinus arrhythmia. The proposed rationale for this "ventriculophasic" P-P interval variation — is that the P-P interval that contains a QRS complex "sandwiched" within it, tends to be slightly shorter than the P-P interval located away from the QRS — because coronary perfusion will be a little better immediately following ventricular contraction.
• As per the P-P intervals (in milliseconds) that I have meticulously measured in the lead V5 rhythm strip in Figure-1 — a subtle ventriculophasic sinus arrhythmia is seen in today's case (and it "fits" the typical model of slightly shorter P-P intervals when a QRS is contained within).
• PEARL: The real benefit of being aware of ventriculophasic sinus arrhythmia — is that because the variable P-P interval gently offsets the location of the non-conducted P wave — this allows greater certainty that the potential extra deflection is truly a P wave (ie, This is BEST appreciated in the long lead V1 rhythm strip in Figure-1). Whereas it might be difficult at first glance to distinguish the extra P wave from the T wave in leads II and V5 — Isn't it much easier to recognize the distinct biphasic P wave shape for each P wave in the long lead V1? A T wave would not produce this rounded, terminal negative deflection that so perfectly matches the terminal rounded negative deflection of the sinus P waves before each QRS — such that on seeing this picture in lead V1 — I knew that the rhythm was 2nd-degree AV block with 2 P waves for each QRS complex.

Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The 3 Types of 2nd-Degree AV Block:

Many textbooks still break down the 2nd-degree AV blocks into 2 categories: Mobitz I vs Mobitz II. Instead, I have always favored Marriott's approach for description of the 2nd-degree AV blocks. According to Marriott — there are 3 (not 2) Types of 2nd-degree AV block. These are:

• Mobitz I (which is the same thing as AV Wenckebach) — in which there is progressive PR interval prolongation until a beat is dropped.
• Mobitz II — in which the PR interval is constant, until one or more beats are dropped.
• 2:1 AV Block — in which it is impossible to be certain whether the type of 2nd-degree AV block is Mobitz I vs Mobitz II. As per Dr. Frick — the clinical importance of this distinction — is that Mobitz I is much more likely to be benign (dependent of course on clinical circumstances) — whereas Mobitz II is much more likely to need pacing (because of the disturbing tendency of Mobitz II to suddenly drop conduction of not one, but multiple successive complexes — potentially resulting in ventricular standstill).

How to Tell Mobitz I vs II when there is 2:1 AV Block?

The above said — most of the time we can with high accuracy distinguish between Mobitz I vs Mobitz II — simply by keeping the following clinical features in mind:

• Mobitz I is much more common than Mobitz II. While relative percentages of these 2 conduction disturbances may vary, depending on whether your practice is EP cardiology — outpatient medicine — or treating patients who present for acute care — Statistics strongly favor Mobitz I (ie, Over the 4+ decades that I've studied all AV blocks that have come my way — well over 90% turn out to be Mobitz I ). It's essential not to overlook the Mobitz II cases (because referral for pacing is needed) — but statistically, the overwhelming majority of cases non-EP-cardiologists will see will turn out to be Mobitz I.
• 
  
• The reason Mobitz I has a much better overall prognosis — is that this rhythm disturbance occurs at a higher level within the conduction system (usually within the AV Node). As a result — Mobitz I usually manifests a narrow QRS (unless there is underlying BBB) — Mobitz I is more likely to be influenced by increased vagal tone, and it tends to respond well to Atropine when given during the early hours of acute inferior MI (during which vagal tone is often temporarily increased) — with acute inferior MI probably being the most common clinical situation in which Mobitz I is seen. That said — there are occasions when even Mobitz I 2nd-degree AV block needs permanent pacing (ie, when Mobitz I is associated with marked bradycardia and/or the patient is clearly symptomatic).
• 
  
• In contrast — Mobitz II occurs lower down in the conduction system. As a result — Mobitz II is most often seen with acute anterior MI — there typically is QRS widening (with either BBB and/or hemiblock) — and atropine is unlikely to be effective.
• In general — the PR interval is more likely to be normal with Mobitz II. 
• In contrast — the PR interval is more likely to be prolonged with Mobitz I. This is because with those cases of acute inferior MI that develop AV block — there is often a sequential development of conduction disturbances. That is, there tends to be sequential progression from a normal PR interval — to 1st-degree AV block — to Mobitz I — and on occasion, to 3rd-degree block at the AV nodal level (ie, with a narrow QRS). And, when the AV conduction disturbance with these inferior MI patients resolves — it tends to do so in reverse progression (ie, regressing from 3rd-degree — to Mobitz I 2nd-degree — to 1st degree — until there finally is restoration of sinus rhythm with a normal PR interval).

Unique Features of Today's CASE:

• In general — it is uncommon (rare in my experience) — for a patient to go back-and-forth between Mobitz I and Mobitz II forms of 2nd-degree AV block. Therefore — if you see clear evidence of Mobitz I elsewhere on telemetry monitoring (ie, the 3:2 Mobitz I sequence highlighted by Dr. Frick on today's 2nd tracing) — this usually very strongly suggests that those periods of 2:1 AV block are also a manifestation of Mobitz I.
• KEY Point: Dr. Frick skillfully illustrates in today's case how this usually helpful indicator that the block is Mobitz I fails to hold true in today's case — because both Mobitz I and Mobitz II co-exist in today's patient (who I like to say — "failed to read the textbook" before coming to the hospital).
• Also in today's case — Statistics are wrong — because despite how much more common Mobitz I is than Mobitz II (and despite the prolonged PR interval that is so commonly seen with Mobitz I ) — today's patient also had Mobitz II.
• Then again — the bifascicular block (RBBB/LAHB) and suggestion of anterior MI at some point in time (the abnormal Q wave in V2 in association with multiple conduction disturbances and abnormal ST-T flattening in multiple leads) are factors in favor of Mobitz II.
• Finally — the ingenious use of bedside maneuvers (as described by Dr. Frick) provides a way to suspect in today's case that this patient may turn out to be one of the rare patients in whom Mobitz I and Mobitz II co-exist!

CASE Conclusion: While the need to defer elective surgery and refer today's patient for further evaluation should be obvious within seconds of seeing today's initial ECG — Close scrutiny of the details of today's case makes for a fascinating adventure in advanced arrhythmia interpretation with important lessons for clinical application. Our THANKS to Dr. Frick for sharing this case!

 

What does a final diagnosis of STEMI vs. NSTEMI depend upon?

Written by Pendell Meyers, few edits by Smith

A woman in her 70s was woken from sleep by midsternal chest pain radiating to left arm with nausea. EMS arrived and recorded this ECG:

What do you think?

Queen of hearts explainability image. Overall High confidence OMI. 

Smith: this is an "Active OMI".  The artery is occluded at this point in time.

The ECG shows sinus rhythm, normal QRS, and signs of inferoposterolateral OMI. The is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal TWI in aVL, and maximal STD in V2-V3 showing posterior OMI. The T waves in V5-6 are likely also hyperacute.

The ECG was transmitted to the Emergency Medicine physician who recognized inferior and posterior OMI findings, and confirmed that the patient has potential ACS symptoms. 

The cath lab was activated despite lack of STEMI criteria, around 2 am in the morning.

EMS gave aspirin and nitroglycerin, and the patient noted significant improvement on arrival to the Emergency Department.

Here is her ECG on arrival to the ED:

Improved, but still some signal of posterior OMI. Compared to prior, this suggests some improvement in TIMI flow of the culprit artery.

Queen of Hearts explainability image showing the diagnostic findings in V2.

She still gives an overall interpretation of OMI with High Confidence

Smith: Although it is improved, it still shows OMI findings.  The Queen of Hearts assesses each ECG by itself, without reference to the previous ECG.  And she also does not know that the symptoms are improved.  So she cannot say that there is evidence of reperfusion, whether partial or complete.

In the future, she will compare with serial ECGs and previous ECGs.  Just not yet.

We can say that this is at least a partially reperfused OMI.  33% of STEMI are reperfused by the time of angiography.  There are stubborn people on Twitter who think that since the artery is open at angiography, we should never have called it OMI and that the patient should not need to go for emergent angiogram.  They do not understand that OMI and STEMI are the same pathophysiology, and that 1/3 of either kind will open up spontaneously.  

We can't know at the time of presentation in which patients the artery will open and in  which it will not; therefore, they all need cath lab activation.  And they are still OMI at presentation even if the artery is open by the time of angiogram.  

It is hard for me to believe how often I need to spell this out to these skeptic.  Very frustrating.  They hold STEMI (-) OMI to a much higher standard than they hold STEMI (+) OMI.

Angiogram was done rapidly after arrival to the ED:

Culprit mid LCX 90% TIMI 3 flow, PCI performed with resultant TIMI 3 flow.

Pre-intervention
Exact TIMI-flow is uncertain.  TIMI-2 vs. TIMI-3

Post-intervention

First troponin T returned at 17 ng/mL (within normal limits using the cutoff of 20 ng/mL)

Subsequent troponins were:

1,051

2,316

3,437

(none further measured)

An MI with a Troponin T of 3473 is quite large, in spite of minimal ECG findings and at least partial spontaneous reperfusion.  This patient is very lucky to have had spontaneous reperfusion.

Echocardiogram:

EF 42%

Moderate hypokinesis of the mid anterolateral and apical lateral myocardium

Final diagnosis by the cardiologist was "STEMI" despite never meeting STEMI criteria. 

Smith: Pendell and I have data that shows that the final diagnosis of "STEMI" vs. "NSTEMI" does not depend on presence or absence of  ST Elevation, or Presence or absence of OMI.  

In fact, the final diagnosis depends on whether the patient gets a short or long door to balloon time.

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My Comment, by KEN GRAUER, MD (11/10/2024):

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Think of today's case as a check of your skill in recognizing when to activate the cath lab. Take another LOOK at the first 2 tracings in today's case — that I've reproduced in Figure-1. How would YOU answer the following questions?

• Knowing that today's patient was awakened by new-onset, severe CP (Chest Pain) — Did you recognize the need to activate the cath lab as soon as you saw today's initial ECG?
• Were you at all reluctant to activate the cath lab because STEMI criteria are not satisfied on this initial EMS ECG?
• Why do you think the repeat ECG looked better than ECG #1?
• Despite improvement in both the ECG and the patient's symptoms — Did you still feel prompt cath was needed after seeing ECG #2?

Figure-1: Comparison between the initial EMS ECG and the repeat ECG in the ED.

ANSWERS:

It literally took me no more than seconds to know that prompt cath was needed in today's case. 

• The history in today's case is classic for an acute cardiac event — as this older woman was awakened from sleep by chest pain radiating to her left arm with nausea.
• Given this history, and after recognizing that the rhythm in ECG #1 was sinus (upright P waves in lead II — with a constant and normal PR interval) — my "eye" was immediately drawn to lead III (the 1st lead within the RED rectangle in Figure-2). Given small size of the QRS complex in lead III — there is no way that the disproportionately "hypervoluminous" T wave in this lead could be normal.
• Confirmation that the T wave in lead III was indeed hyperacute — was immediately forthcoming from the finding in lead aVL of reciprocal ST-T wave depression (within the 2nd RED rectangle).
• My "eye" was next drawn to the other 2 inferior leads ( = leads II and aVF — within the 2 BLUE rectangles in Figure-2) — which, while not as flagrantly abnormal as the T wave in lead III — still show "bulkier"-than-they-should-be T waves, considering modest size of the QRS in these leads (BLUE arrows in leads II and aVF). In the context of the hyperacute T wave in lead III, in association with reciprocal ST depression in lead aVL — I interpreted the T waves in leads II and aVF as also hyperacute.
• Finally — Any doubt that could possibly have remained was immediately removed on seeing the QRST appearance of leads V2 and V3 in the chest leads (within the last 2 RED rectangles in Figure-2). These 2 chest leads show: i) Abrupt early transition to a surprisingly tall R wave already by lead V2; — and, ii) Shelf-like flat ST depression with terminal T wave positivity that clearly indicates posterior OMI (RED arrows in these leads).
• 
  
• IMPRESSION of ECG #1: In this older woman who presents with severe new CP — this ECG picture is absolutely diagnostic of acute infero-postero OMI (with need for prompt cath with PCI).

Did You Hesitate because STEMI Criteria are Not Met?

Fortunately — Neither the ED physician nor the cardiologist hesitated. The patient was promptly taken to the cath lab — where a "culprit" mid-LCx lesion was found and successfully stented.

• To Emphasize: There is nothing during the process of further evaluation that would have altered the decision to activate the cath lab. No matter what serial ECGs or Troponins might have shown — the need for prompt cath would have remained. So WHY wait?
• The still all-too-prevalent mindset of not performing acute cardiac catheterization unless ECG criteria for STEMI are met — needs to change. The clinical question that should be asked is not whether STEMI criteria are met — but rather whether the history and ECG suggest that an acute cardiac event is actively evolving (regardless of whether or not "enough" ST elevation is present to qualify as a stemi ).
• That the clinicians involved in today's case understood this KEY point — is evident from the fact that the cardiologist's final diagnosis was "STEMI", despite ECGs never meeting STEMI criteria.
• As per Drs. Meyers and Smith — whether the final diagnosis is "STEMI" vs "NSTEMI" primarily depends on whether the door-to-balloon time is long or short. The wisdom conveyed in this teaching message is powerful! (ie, IF the interventionist recognizes ECG findings of acute OMI before enough time has passed to allow ST elevation to develop — then successful PCI will mean that the "culprit" artery will be opened, and ST elevation will never develop).
• Waiting for ST elevation to develop when the diagnosis of acute OMI is secure — is waiting too long (as would have been the case had today's ED physician and cardiologist delayed cardiac catheterization).

Why did the Repeat ECG look Better than ECG #1?

The answer to this question becomes obvious when one correlates the clinical history to these first 2 ECGs.

• As emphasized by Dr. Smith in the November 8, 2024 post — as many as 1/3 of all acute STEMIs reperfuse spontaneously before treatment is implemented. Clinically we can usually tell when such spontaneous reperfusion occurs — because: i) The patient's CP resolves (or at least decreases); — and, ii) ST elevation resolves (or at least decreases) — and reperfusion T waves may be seen.
• In today's case — the patient felt better at the time ECG #2 was recorded. Side-by-side comparison between ECG #1 and ECG #2 in Figure-2 — clearly shows this improvement in patient symptoms corresponds to comparable improvement in the hyperacute inferior lead T waves and reciprocal changes in lead aVL. 
• In the chest leads — Note that the surprisingly tall R waves in leads V2,V3 are no longer present in the repeat ECG! (PEARL: Early transition with inappropriately tall anterior R waves is a "Q wave equivalent" sign when there is posterior OMI — such that I interpreted resolution of the tall R waves in V2,V3 as further indication of posterior wall reperfusion).
• 
  
• CONCLUSION: It is virtually certain that there has been some amount of spontaneous reperfusion at the time ECG #2 was recorded.

Is Prompt Cath with PCI Still Needed given Spontaneous Reperfusion?

The answer to this question is a definite YES — because: i) Although there has been some spontaneous reperfusion by the time the patient arrived in the ED — there rarely is complete spontaneous reperfusion (witness the 90% stenosis of the mid-LCx still present at the time of cath); — and, ii) Final "steady-state" of the acute coronary event is still in evolution — and, what spontaneously reopened — might just as easily (and at any time) spontaneously reclose.

• BOTTOM Line: By history, with correlation to serial ECGs (as well as to the elevated Troponin values) — We have diagnosed an acute infero-postero OMI. So while it is good that the patient feels better following ASA and nitroglycerin — as well as good that the acute ST-T wave changes seen in ECG #1 have improved in ECG #2 — the patient remains at high-risk of spontaneous reocclusion. Prompt cath with PCI is needed to prevent this (and to optimize outcome).

Figure-2: I've labeled the first 2 ECGs in today's case.

 

Baseline wander. But what else do you see?

Written by Magnus Nossen

The below ECG was obtained from a 65 year old man with ongoing chest pain. He has a history of hypertension and tobacco use. He is otherwise healthy. There is no prior ECG for comparison. What do you think?

ECG #1

Interpretation: The quality of the above ECG is not optimal. There is significant baseline wander that does make it more challenging to interpret ischemic changes. The ECG shows sinus rhythm at a rate of 90 bpm. There is a slightly wide QRS (just about 120ms) consistent with a nonspecific intraventricular conduction delay (IVCD). The PR interval is on the short side, but there are no clear delta waves.

Despite the baseline wander there is appreciable concordant ST segment elevation in lead III. There is likely some very slight concordant ST elevation also in lead aVF. The lateral leads I and aVL show reciprocal ST depression, with lead aVL showing concordant ST depression. The S-wave in lead V2 measures 17mm and the ST segment in lead V2 is isoelectric. With the slightly prolonged QRS and significant S-wave one would expect some discordant ST elevation in lead V2. In other words there is inappropriate isoelectric ST segment in V2.

Putting all the above findings together, the ECG is very concerning if not diagnostic for inferior and posterior OMI. These findings were not appreciated by providers. However, due to the nature of the symptoms, the patient was treated for ACS and admitted to the hospital. The below ECG was obtained 45 minutes after the first one with the patient being free of chest pain at the time of recording of ECG #2. 

What do you think now?

ECG #2

Again there is sinus rhythm, short PR and IVCD. The ECG now shows resolution of the concordant ST segments in the inferior leads. There is now a very slight ST elevation in V2, as one would expect appropriate discordant ST Elevation, discordant (in the opposite direction) from the preceeding majority negative QRS (S-wave). 

The artery has re-perfused. 

There was no comment by the providers on the dynamic ECG changes on the repeat ECG.

The patient in today's case was lucky to re-perfuse. He remained chest pain free and underwent coronary angiography the following day. The CAG showed a 99% thrombotic lesion of the proximal RCA, which was stented. Due to rapid spontaneous reperfusion, high sensitivity troponin I peaked at just under 5000 ng/L. 

This OMI went unrecognized and, had the artery not re-perfused by itself, the patient could have suffered a very large myocardial infarction. He was diagnosed with NSTEMI. 

What does the Queen of Hearts AI model say about the ECGs in today's case?

Below: Queen of Hearts interpretation ECG #1

Below: Queen of hearts interpretation ECG #2 

Discussion: OMI findings can be subtle. Whenever there is a wide QRS complex and baseline wander the interpretation is more difficult. The Queen of Hearts AI model confidently identifies the first ECG in today's case as occlusion myocardial infarction (OMI HIGH confidence). The repeat ECG, after reperfusion is equally confidently recognized as not OMI. 

The outcome in today's case was good but that was not due to expert ECG interpretation but rather a bit of luck. The OMI could have been recognized if the QoH had been used. 

Smith comment:

Approximately 33% of cases that everyone would call STEMI reperfuse spontaneously (TIMI-1, 2, 3 flow) before they undergo emergent angiogram (usually under 90 minute door to balloon time)  

20% have TIMI-3 flow.  

Of all OMI, approximately 43% present with diagnostic ST Elevation.  57% do not and are called "NSTEMI."   But many of these OMI will spontaneously reperfuse by the time of next day angiogram so that, at next day angiogram, 25% of NSTEMI have TIMI-0 flow and 34% have TIMI 0-1 flow without collateral flow. 

You don't know which will reperfuse at the time they present with OMI.  So all must be treated emergently.  Many subtle OMI do not get diagnosed until their next-day angiogram, at which time much myocardium is lost.  They have much higher mortality and worse LV function than the NSTEMI with open artery next day. 

Therefore, you must find a way to recognize these subtle OMI at arrival in order to get them rapid intervention.  Expert or AI ECG interpretation is the only way to do so.

A significant proportion of patients with OMI do not re-perfuse on their own and the use of the QoH can provide more timely treatment and a better outcome for these patients.  

Click here to sign up for Queen of Hearts Access.

Learning points: 

• With training one can learn to identify OMI despite baseline wander and a wide QRS complex. 
  
  
• The Queen of Hearts already does this very well and can improve the management of ACS patients 
  
  
• We need to better identify patients with ongoing coronary occlusion as we cannot count on patients being as lucky at the patient in today's case

• Whenever the ECG has poor quality obtaining a repeat tracing is advisable. Sometimes a poor quality tracing is all you have to make your decision.
  
  

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MY Comment, by KEN GRAUER, MD (11/8/2024):  

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Today’s case by Dr. Nossen brings out a series of important points:

• As per comments by Drs. Nossen and Smith — the initial ECG is absolutely diagnostic of acute infero-postero OMI.
• As per Dr. Nossen — the presence of both QRS widening and baseline wander + significant artifact make assessment of acute OMI more challenging. That said — this 65-year old man with risk factors (smoking, hypertension) — was admitted to the hospital for “ongoing CP” that apparently was severe enough, such that this chest pain (and not the initial ECG) was the reason that cardiac cath was ultimately performed (albeit cardiac cath was not done until the next day). The point is that today's patient was high-risk for having an acute event.

KEY Point: Although it is understandable that providers may have missed the subtle-but-real ST-T wave changes of acute OMI on the initial ECG — given the high-risk likelihood for an acute event — the technical concerns regarding the initial ECG should have immediately prompted repeating the ECG:

• Consider Figure-1 — in which I have labeled key findings in the limb leads. The question that arises is which of the 8 beats in the limb leads of the initial ECG accurately convey ST-T wave appearance?
• For example — IF the only 3 beats seen in the limb leads were beats #5,6,7 (within the dotted RED rectangles in Figure-1) — it would have been much clearer that there is hyperacute ST elevation in lead III, and to a lesser extent, also in lead aVF (RED arrows in these leads) — with reciprocal ST depression in lead aVL (PINK arrows).
• On the other hand — I would not have been at all certain about ST elevation in leads III and aVF (nor of reciprocal ST depression in lead aVL) — if the only beats seen in the limb leads looked like beats #3,4.
• And, as per Dr. Nossen — in the presence of acute inferior OMI — loss of the usual normal slight, gently upsloping ST elevation in lead V3 indicates associated posterior OMI (BLUE arrows in this lead showing slight J-point ST depression).

NOTE: It may help to recognize that the reason for so much artifact in the limb leads — is the result of some disturbance or movement (ie, tremor? fidgeting? scratching?) in the LA electrode.

• As per My Comment in the February 18, 2024 post in Dr. Smith’s ECG Blog — the LA (Left Arm) can be quickly identified as the “culprit” extremity because baseline artifact is maximal in leads I, III and aVL — present but less in leads aVR and aVF — and not present at all in lead II. 
• Being able to identify within seconds the “culprit” extremity responsible for the artifact may suggest a “quick fix” (ie, Asking the patient to stop scratching or moving the "culprit" extremity) — and then repeating the ECG to clarify the true nature of ST-T wave appearance.

Side NOTE: Did you notice how much narrower the QRS in lead V4 looks compared to other leads? This is because the subtle, terminal part of the QRS in V4 goes undetected because it almost entirely lies on the baseline (YELLOW arrows in this lead).

• This finding illustrates the importance of always using more than a single monitoring lead when assessing QRS width in a tachyarrhythmia (since you otherwise might mistake a wide tachycardia for an SVT — if part of the QRS lies on the baseline in the single lead of your 1-lead rhythm strip).

Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

How Not to Miss "Dynamic" ST-T Wave Changes:

Not only were the acute ST-T wave findings missed in ECG #1 — but the new limb lead ST-T wave changes in ECG #2 (compared to ECG #1) were also missed. Awareness of the following points can avoid overlooking these telltale "dynamic" ST-T wave changes:

• We need to be looking for "dynamic" ST-T wave changes in serial tracings — because when found (especially if the nature of these changes correlates with the clinical situation) — they are diagnostic of an acute event!
• In today's case — this patient with "ongoing CP" at the time of admission — no longer had CP 45 minutes later, at the time ECG #2 was obtained. We need to be aware that if ST elevation resolves in association with reduced (or relieved) CP, with replacement of ST elevation by reperfusion T waves (ST depression and/or T wave inversion) — that these "dynamic" ST-T wave changes tell us that the "culprit" artery has spontaneously reperfused!

PEARL: Unless serial ECGs are compared side-by-side — subtle-but-important ST-T wave changes will be missed. These ST-T wave changes between ECG #1 and ECG #2 were not seen in today's case.

• LOOK at Figure-2. 
• Isn't it much easier to recognize reperfusion ST-T wave changes now that I have placed the limb leads from ECG #1 and ECG #2 next to each other? (Comparison between RED/PINK vs BLUE arrows in Figure-2).
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• BOTTOM Line: Even if the acute findings in ECG #1 went unrecognized — the occurrence of reperfusion ST-T waves in association with resolution of CP at the time ECG #2 was obtained — would have confirmed acute OMI and the need for prompt cath (instead of cath being delayed until the next day).

Figure-2: Comparison of ST-T wave changes in the limb leads in ECG #1 vs ECG #2. (To improve visualization — I've digitized the original ECG using PMcardio).

 

Electrophysiological curiosity. Can you spot it?

        Written by Magnus Nossen (with comments and laddergram by Ken Grauer)

The patient in today’s case is a man in his 60s — who presented with palpitations and lightheadedness. He had no history of syncope. The patient had hypertension, but was otherwise healthy. Due to the reported symptoms, he was admitted for observation and put on telemetry monitoring. Below in Figure-1 is a tracing obtained from the in-house telemetry. 

• The rhythm strip in Figure-1 shows four ECG leads. (aVF, III, V1 and V5). The paper speed is 25mm/s. There is a bigeminal pattern with every other QRS complex being wide. Can you explain what is going on in this tracing? Do you notice anything unusual in this rhythm strip? 

Figure-1: The initial rhythm strip in today’s case.

Below in Figure-2 is another tracing from the same patient. Beat #9 is wide, and manifests a different QRS morphology than the other wide beats. What is the likely explanation for this?

Figure-2: A 2nd rhythm strip from today’s patient.

COMMENT:

Both rhythm strips show sinus rhythm with premature ventricular complexes (PVCs). Following most of these PVCs — there is retrograde conduction that begins from the ventricles, and then travels backward through the AV node and the atria (VA conduction). Because the atria are captured in retrograde fashion — the P waves are negative (with these retrograde P waves being partially hidden within the ST segments of the preceding PVC).

Of note is variation in the RP interval! (ie, the distance from the beginning of the PVC — until the retrograde P wave).

• There are 2 different RP intervals. This can be explained by having dual AV conduction pathways in the retrograde direction. One of these pathways conducts significantly slower than the other.
• When the retrograde impulse travels through the slower pathway — conduction time and RP interval is longer. 
• The opposite occurs when retrograde conduction is through the faster pathway (ie, faster retrograde conduction results in a shorter RP interval).

Because of added complexity in the 2nd tracing — I have labeled this 2nd rhythm strip in Figure-3:

• Green arrows point to sinus P waves in Figure-3 — with normal sinus conduction of beats #1,3,5,7 and 10.
• Beats #2,4,6 and 8 are PVCs with a similar (albeit not identical) QRS morphology. These PVCs most probably originate from the same ectopic site in the ventricles.
• The Orange arrow points to a retrograde P wave with a longer RP interval (295 msec.) — that is conducted from PVC beat #2.
• The Blue arrow points to a retrograde P wave with a shorter RP interval (170 msec.) — that is conducted from PVC beat #4.
• There is no retrograde conduction following the PVC beat #6.
• The Red arrow points to a retrograde P wave with a longer RP interval — that is conducted from the PVC beat #8. Note that this retrograde RP interval from beat #8 is slightly longer than the RP interval from beat #2 (330 msec. vs 295 msec.).

Figure-3: I’ve labeled Rhythm #2.

What about Beat #9?

• Note that beat #9 is wide — but with a different QRS morphology when compared to wide beats #2,4,6,8 (ie, Beat #9 manifests a predominantly negative QRS in all 4 monitoring leads).
• Beat #9 follows after the longest RP interval in this rhythm strip. The reason beat #9 looks different — is that beat #9 is a ventricular “echo” or reciprocal beat. The mechanism operative for this reciprocal beat in Figure-3 — is illustrated in Panel C of Figure-4.

Figure-4: Illustration of the mechanism for reciprocal (echo) beats. (Adapted from Strasberg et al — Am J Cardiol 48(4): 639-646, 1982 ).

KEY Clinical Point (Grauer):

The importance of Figure-4 — is that it shows the mechanism for initiation of many reentry SVT rhythms! (ie, See My Comment at the bottom of the page in the March 6, 2020 post in Dr. Smith's ECG Blog — in which I illustrate near the very end of my March 6, 2020 Comment the initiation of "fast-slow" form of AVNRT by what we see here in Panel B).

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Returning to the mechanism in Figure-3 of today's case:

Grauer: For clarity in Figure-5 — I've kept the same color coding, and illustrate Dr Nossen's above explanation of reciprocal beating in a Laddergram that concentrates on lead III from Figure-3.

• GREEN arrows and lines in the laddergram — show normal sinus-conducted beats.
• Beats #2,4,6 and 8 are PVCs (The PINK circles schematically show origin of these PVCs from the ventricle).
• The ORANGE dotted line — shows PVC beat #2 conducting backward to produce a retrograde P wave with an RP interval = 295 msec.
• The BLUE dotted line — shows PVC #4 conducting backward over the slower AV nodal pathway, to produce a retrograde P wave with an RP interval = 170 msec.
• PVC #6 — fails to make it all the way back to the atria.
• But — PVC #8 not only conducts backward, here over the slower AV nodal pathway to produce a retrograde P wave (the RED dotted line in the laddergram, leading to the RED arrow) — but because of its longer RP interval (330 msec.) — the faster AV nodal pathway has enough time to recover forward conduction properties — and therefore produces beat #9 (in PURPLE) — which is an "echo" beat that is conducted with rate-dependent aberrancy because beat #9 occurs so soon after beat #8.

Figure-5: My proposed Laddergram illustrating the mechanism of the "echo" beat in Figure-3.

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The CASE Continues:

The patient had many episodes of NSVT (Non-Sustained Ventricular Tachycardia) — like the one shown below in Figure-6. He experienced palpitations — both when having PVCs, as well as during his episodes of NSVT and VT. 

• Can YOU identify atrial activity in Figure-6?
•    Why does beat #3 prove that the wide beats are ventricular?

 

Figure-6: Subsequent 5-lead rhythm strip with an episode of NSVT.

Atrial Activity in Figure-6:

The rhythm in Figure-6 begins with a series of regular sinus P waves (GREEN arrows in Figure-7).

• It could be easy to overlook the 2nd and 3rd GREEN arrows — because they are partially hidden within the ST-T waves of beats #2 and 4. 
• The KEY is to recognize the 4th, 5th and 6th GREEN arrows — and to note that the P-P interval is fairly constant for these 3 P waves.
• Setting your calipers to approximately this P-P interval — should facilitate finding the 2nd and 3rd GREEN arrow P waves!
• Remember — Since the 1st beat in Figure-6 is sinus-conducted, It is logical for the underlying atrial rhythm to be regular, at least for the beginning of this tracing. So, we are looking for signs of an underlying regular atrial rhythm (with perhaps slight sinus arrhythmia) — and it is much easier to find this when you know what you are looking for! (and using calipers makes the partially-hidden P waves so easy to find! ).
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• We know beats #2 and #4 are PVCs — because these beats are wide, very different-looking from sinus-conducted beats, and these beats are not preceded by a premature P wave.
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• Isn't beat #3 intermediate in its QRS morphology? — compared to the morphology of sinus-conducted beat #1 and PVCs #2 and #4? The reason for this intermediate QRS morphology — is that beat #3 is a Fusion beat! ("F") — and this proves that all of the beats that look like #2 and #4 are also of ventricular etiology! (See "Lesson #3" in My Comment at the bottom of the page of the April 2, 2022 post for more on the diagnostic value of fusion beats).
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• Finally, knowing that today's patient shows a tendency for ventricular beats to conduct retrograde — I suspect that the YELLOW arrows in Figure-7 represent retrograde P waves following ventricular beats in the run of NSVT.

Figure-7: I've labeled Figure-6.

CASE Conclusion:

Today's patient had a structurally normal heart and a normal cardiac catheterization. A permanent pacemaker was placed and the patient was atrial paced at 60bpm. After pacemaker placement — a ß-blocker was initiated. The  hope was that the increased heart rate (from atrial pacing) combined with ß-blocker treatment would suppress most ventricular ectopic activity and the runs of NSVT. When these measures did not work — the patient underwent PVC ablation, which did achieve a good clinical result.

Learning points:

• Dual AV physiology in the retrograde direction does not necessarily mean there is dual AV conduction in the antegrade direction. 
• Dual AV physiology is necessary for AVNRT and reciprocal or "echo" beats. 
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• As shown above in Figure-4 — Echo beats provide a common mechanism for initiation of reentry SVT rhythms! (and — understanding the mechanism to produce "echo" beats provides insight for understanding how a run of NSVT may even produce a subsequent run of reentry SVT à la Panel C in Figure-4).