Is this OMI reperfused or active?

These ECGs were texted to me by one of our previous ultrasound fellows, Will Smoot

An elderly male arrived via EMS for acute substernal chest pain with radiation to left shoulder and arm that awakened him from sleep at 0030.  

He took two full strength aspirin prior to EMS arrival.  The pain was relieved by one prehospital NTG spray.  

He arrived at the ED just shy of two hours after onset, pain free.  

No prior similar symptoms or known CAD.  

PMHX significant for hypertension and BPH.  Family history significant for father with MI at age 56, lived to age 83.  No acute infectious prodrome, known pulmonary disease, or recent trauma.  

Here is the initial ED ECG:

Here that first ECG is cleaned up by PM Cardio app:

What do you think?

Smith: this ECG is diagnostic of inferior-posterior OMI.  There is subtle STE in III and aVF, with a domed T-wave and some terminal T-wave inversion.  There is precordial STD maximal in V2 and V3, diagnostic of posterior OMI.

The question is: is this Active OMI or is it Reperfused OMI?

I think the ECG is equivocal on this point.  The fact that the patient's pain is resolved is good evidence (but not fool-proof) that the artery is reperfused.

Before concluding that there is reperfusion, one should record another ECG to ascertain if there is evolution of reperfusion.

The Queen of Hearts Diagnosed "STEMI/STEMI equivalent" on that first ECG (she now uses "STEMI Equivalent" rather than OMI). This is the new version of the Queen.  The old version would diagnose "OMI" even if it was a reperfused OMI.  The fact that she states "STEMI-Equivalent" here means that she does not think it is reperfused, but she does not  know that the patient is pain free now.

And here is explainability:

Will Smoot: "Initial ECG upon arrival, high concern for OMI."   (Will ran the ECG through Queen of Hearts and received the "OMI" result.)

Bedside cardiac ultrasound (Will is an ultrasound fellowship trained EP) did not demonstrate severe LV systolic dysfunction, acute valvular abnormality, severe RV dilation, or pericardial effusion. 

Initial high sensitivity Troponin I:  36.5 (ng/L) -- slightly elevated.


Here is the repeat 12 Lead ECG approximately 20 minutes later (still pain free)

Now it shows definite reperfusion

More inferior T-wave inversion

Less STD in V2, V3.

Cleaned up:

 2 hr repeat troponin:  2820.4 ng/L (No further troponin obtained during hospitalization)

Will: "I discussed high suspicion for OMI with cardiology, and he recommended standard NSTEMI management and will plan to cath later that day.  Admitted to hospitalist service on heparin."  

Angiogram:

99% Circumflex occlusion (reperfused).  

TIMI flow is not specified, but presumably was adequate.

No peak troponin was measured.

TTE results:
Normal LV size.  LVEF 55-60%.  Mild hypokinesis of basal-mid inferolateral and inferior walls. 
Normal RV size and function. 

Learning Points:

1) Learn to recognize Subtle OMI

2) Before assuming an OMI is reperfused, verify it by obtaining more ECGs to see evolution of reperfusion.

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MY Comment, by KEN GRAUER, MD (11/19/2024):

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Today's initial ECG provides yet another example of a tracing with a "Quick" Answer — as well as a slower, more complete Answer.

• The "Quick" Answer — addresses how to approach this case assuming you are working in a busy ED (Emergency Department) in which 3 patients present at the same time with new CP (Chest Pain) — and YOU have just seconds to decide if the initial ECG does (or does not) represent acute OMI until proven otherwise?
• The slower more complete Answer — addresses one of the primary goals of Dr. Smith's ECG Blog, namely time-efficient assessment of KEY findings for the tracing in front of us, including more subtle changes that may be relevant to the case.

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First — the "Quick" Answer:

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For clarity in Figure-1 — I've reproduced those findings in the initial ECG that "jumped out to me", allowing me literally to know within 5 seconds that regardless of what follow-up ECGs and serial Troponins might show — this patient needs prompt cath!

• The History in today's case is very concerning! = a 72yo man awakened from sleep by severe CP radiating to his left arm and shoulder. This history immediately places this patient in a higher-risk category for having an acute cardiac event (ie, meaning we need to rule out an acute event, rather than the other way around). Therefore, even subtle ECG abnormalities need to be assumed acute until proven otherwise.
• PEARL #1: Given this history — my "eye" jumped to the ST-T waves in leads V2 and V3 (within the RED rectangle in Figure-1). As we often emphasize in Dr. Smith's ECG Blog — in a patient with new CP, the finding of ST depression maximal in leads V2, V3 and/or V4 = acute posterior OMI until proven otherwise.
• Knowing that additional support may be needed to convince a skeptical interventionist — my "eye" next jumped to the 2 leads within the light BLUE rectangles (ie, to inferior leads III and aVF). Each of these leads shows subtle-but-real ST segment coving with slight elevation.
• PEARL #2: The BEST way to confirm that potentially acute ST-T wave findings in lead III are "real" — is to engage the "magical" reciprocal ST-T wave relationship between lead III and lead aVL (which works because lead aVL lies almost directly opposite to lead III in the frontal axis plane). So my "eye" next jumped to lead aVL (within the PURPLE rectangle in Figure-1) — where I immediately saw reciprocal ST depression with terminal T wave positivity — thereby confirming probable acuity for the subtle inferior lead ST elevation.

My Impression (on seeing ECG #1 and learning the history): 

• Acute infero-postero OMI — until proven otherwise.
• Total time that I needed to appreciate the above KEY findings that appear within the colored rectangles in Figure-1 — literally less than 5 seconds.
• For any provider who might still be uncertain about their "quick" Answer interpretation of Figure-1 — Use of the QOH application would confirm your impression of acute OMI in need of prompt cath (as shown by the QOH interpretation, discussed above by Dr. Smith).
• BUT — simple appreciation of the importance of the clinical history and the 2 concepts reviewed in Pearl #1 and Pearl #2 (stated above) — allows you to confidently diagnose acute OMI with need for prompt cath either with (or without) assistance from QOH application.

Figure-1: The initial ECG in today's case. I've labeled KEY findings that give us the "Quick" Answer. (To improve visualization — I've digitized the original ECG using PMcardio).

==========================

Now — the Slower, More Complete Answer:

========================== 

I've labeled today's initial ECG more completely in Figure-2 — to include additional more subtle but relevant ECG findings.

• ST depression in lead V2 and lead V3 is not only deeper than in other chest leads — but the ST segments in these 2 leads are downsloping with terminal T wave positivity. This supports acute posterior OMI until proven otherwise.
• That said — the ST segment is straightened in the remaining chest leads ( = leads V4,V5,V6).
• ST segment straightening is also seen in lead I — and in lead II. 
• PEARL #3: While concern in today's case is greatest for ST-T wave changes suggestive of acute infero-postero OMI — ST segment straightening and/or depression is seen in no less than 8/12 leads (ie, in leads I,II,aVL; V2-thru-V6). The fact that this diffuse distribution of ST flattening/depression occurs in association with ST elevation in leads III,aVF and in lead aVR — suggests that this patient probably has underlying multi-vessel disease in addition to whatever acute abnormality may be ongoing (with features and clinical implications similar to Diffuse Subendocardial Ischemia and/or Aslanger Pattern).

The above leaves us with assessment of the ECG appearance of the QRST complex in lead V1. Potential clinically relevant implications of the lead V1 QRST appearance include the following:

• The rSr' morphology in lead V1 — is consistent with IRBBB (Incomplete Right Bundle Branch Block), given narrow terminal S waves in left-sided leads I and V6 — and QRS width that falls shy of 0.11 second.
• While possible that this rSr' morphology in lead V1 that we do not see in lead V2, is the result of too-high lead placement of the V1 chest electrode (which does show a negative P wave not seen in lead V2) — I interpreted this rSr' complex in lead V1 as most consistent with IRBBB given the lateral lead terminal S waves.
• Finally — Isn't the ST segment in lead V1 coved and slightly elevated? While difficult to appreciate because of small QRS amplitude in V1 — the BLUE arrow in this lead highlights a different ST-T wave appearance than the expected ST segment depression that should generally be seen in lead V1 with IRBBB.
• Confirmation that the ST segment in lead V1 is truly elevated and abnormal is forthcoming from: i) Comparison with the ST segment in neighboring lead V2 that is unmistakably depressed; — and, ii) The luxury we have of not just 2 beats — but 11 beats (ie, "looks") at the ST-T wave in the long lead V1 rhythm strip — all-11-of-which show similar ST segment coving with slight-but-real ST elevation (BLUE arrows in the long lead V1).

PEARL #4: What is the clinical relevance of this ST appearance in lead V1? In answer to this question — 2 considerations came to mind:

• In the setting of acute infero-postero OMI that we have in today's case — the ST elevation in lead V1 but not in neighboring leads V2,V3 — could reflect acute RV involvement. If this were true — this would localize the "culprit" artery to the proximal RCA, because the LCx does not supply the right ventricle.
• Alternatively — the ST coving and elevation that we see in lead V1 — in association with ST depression in 8/12 leads + ST elevation in leads III,aVR,aVF and V1 (with the most ST elevation being in lead aVR) — could simply be a reflection of DSI (Diffuse Subendocardial Ischemia) from altered collateral patterns and significant underlying multi-vessel coronary disease in addition to acute infero-postero OMI.

BOTTOM Line: It is disappointing that the consulting cardiologist in today's case delayed prompt cath because he/she misinterpreted the initial ECG as indicative of a "NSTEMI".

• Cardiac cath ultimately confirmed inf.-post OMI with significant multi-vessel coronary disease. 

Figure-2: The initial ECG showing the more complete Answer.

 

Acute chest pain and an abnormal ECG. Do precordial leads show benign T-wave inversion or ischemia?

Written by Willy Frick

A 51 year old man with hypertension presented with three hours of acute onset, severe midsternal chest pain associated with two episodes of nausea and vomiting.

ECG 1

What do you think?

Smith: Inferior leads have subtle ST Elevation with reciprocal STD in aVL.  The end of the T-wave in all of II, III, aVF has a rapid downturn, suggesting early T-wave inversion.  

In V3-V6, there are slightly upsloping ST segments with terminal T-wave inversion in V3-V6 which is classic for benign T-wave inversion.  This ST-T is associated with a tall R-wave and a small S-wave.  Benign T-wave inversion is most commonly seen in young African Americans, and less so over age 50, so one must be careful--they might be ischemic T-waves, but if they are ischemic they would most likely represent reperfusion T-waves.  Since the patient has active pain, that is less likely.  In any case, I would call this diagnostic of inferior OMI and it requires cath lab activation.  

Is this:

1) inferior OMI with benign T-wave inversion in precordial leads? or

2) Inferior and lateral OMI that is beginning to reperfuse, even though the patient still has chest pain?

• Benign T-wave Inversion -- Countless Examples (1)

The Queen of Hearts Active OMI model (aOMI) is shown below:

Willy: My initial impression looking at this ECG was that it was not ischemic. The morphology of the ST-T in leads V3 and V4 struck me as very similar to benign T wave inversion cases I have seen in the past.

I sent the ECG to Dr. Meyers and he said "might be a difficult BTWI, but I would have to figure out if there is inferior OMI immediately." He went on to point out that aVL is unusual for BTWI. In particular, there is STD and ischemic down-up T waves.

He concluded by saying that "History and concern should win regardless of EKG." He asked for any old recordings for comparison, but none were available at the time.

Even though this blog is devoted to understanding the nuances of EKG, we always need to remember that an EKG is only a single test. It is imperfect. Maybe the imperfections are entirely a function of fallible human readers (like me), and maybe some of it is inherent to the nature of the test. In this case, the context is a 51 year old man with risk factors presenting with acute onset substernal chest pain with nausea and vomiting. The pre-EKG probability for OMI could hardly be much higher! So an equivocal (or even normal) EKG is not enough. (It's the opposite of this case.)

Fortunately, the patient underwent immediate angiography. There was an 80% lesion in the mid to distal RCA with TIMI 3 flow (meaning normal flow). The operator performed intravascular ultrasound and visualized acute plaque rupture with thrombus formation and placed a stent. Repeat ECG the following morning is shown below:

ECG 2

This ECG shows clear biphasic reperfusion T waves in the inferior leads. To me, V4-6 show pretty convincing reperfusion T waves. But V3 is still hard to interpret, especially in the context of the presenting ECG. There is one final ECG 2 days after cath.

ECG 3

A few months later, I was finally able to track down a prior ECG, obtained during an office visit for hypertension management. This is shown below:

Prior baseline

For convenience, I have put leads from baseline, active OMI, and post PCI tracings side by side to help understand the differences.

Serial comparison makes the inferior leads quite obvious. Compared to baseline tracing, the ECG on presentation shows obviously new STE and HATW. The axis change makes serial comparison of aVL trickier. Still, it is a very bland looking lead in baseline, and therefore much more sinister when viewed through the lens of serial comparison.

The precordial leads are admittedly harder to make sense of. Here is my take:

• Baseline shows non-specific TWI.

• Post-PCI shows reperfusion TWI.

• Therefore, presentation ECG (obtained during active OMI) is the result of layering STE and HATW on top of non-specific TWI.

Smith: I agree with this.  There was reperfusion ischemia superimposed on benign T-wave inversion.

Fortunately, the patient had both spontaneous reperfusion and very rapid treatment. His high sensitivity troponin I peaked at 2974 ng/L (ref. <35). His echo showed ejection fraction > 70% with normal wall motion. He is very lucky that he spontaneously reperfused and was stented before he had the chance to re-occlude. He did well.

Learning points:

• In acute chest pain, STE in inferior leads with reciprocal STD in aVL is inferior OMI until proven otherwise.

• As always history is the most important diagnostic test.

• Serial ECG comparison remains undefeated.

• Benign looking features (precordial TWI from ECG 1) can co-exist with OMI findings

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MY Comment, by KEN GRAUER, MD (11/17/2024):

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The wonders of medicine keep us humble and honest. When I first saw today's initial ECG without knowing the history — I had the same impression as Dr. Frick, namely that the ECG was not ischemic. I thought so because:

• A fairly similar ST-T wave shape was present in multiple leads — and resembled that of certain repolarization variants.
• There is excellent R wave progression (with early transition showing abrupt transition to a predominant R wave already by lead V3).
• R waves are tall in V3,V4.
• The QTc appears to be relatively short.

The above said — I didn't feel so bad on learning that cardiac cath revealed an RCA "culprit" — because as emphasized by Drs. Frick and Meyers, "History and concern should win regardless of the ECG".

• When you do get fooled (as we all do at least some of the time) — GO BACK and review the tracing. Credit again to Dr. Meyers for his focus on the shape of the ST-T wave in lead aVL of ECG #1 — that simply does not look consistent with a repolarization variant.
• Considering the ST-T wave appearance of lead aVL — Lead I also demonstrates an uncharacteristically flat ST-T wave, that typically is not seen with repolarization variants.
• And — the History is that of a 51 yo man with 3 hours of new severe CP, associated with nausea and vomiting. So regardless of whatever your impression might have been on seeing today's initial ECG — prompt evaluation is indicated until a definitive answer is forthcoming.

Additional "Take-Home" Points from Today's CASE:

• We've reviewed ECG features of BTWI (Benign T Wave Inversion) on many occasions in Dr. Smith's ECG Blog. As per My Comment in the June 30, 2023 post (in which I review the 9 Criteria derived over the years by Drs. Wang and Smith as suggestive of BTWI) — Today's initial ECG deviates from these criteria because: i) J-point notching is absent, especially from leads V3,4,5,6 which are the chest leads with T wave inversion; — ii) Right-sided chest lead V2 shows ST segment straightening instead of a gently upsloping ST segment; — and, iii) Leads V3,V4 that manifest the most T wave inversion lack the usual amount of ST elevation that is typically seen with BTWI.
• When in need of a "Refresher" on what BTWI may look like — I suggest periodically checking out Dr. Meyers' March 22, 2022 post — in which he shows a series of cases illustrating BTWI in "all of its flavors".
• 
  
• Although telltale reperfusion T waves may be seen very soon after spontaneous or PCI reperfusion — it often takes a day or two for "the Answer" to become obvious (Witness comparison between ECG #1 vs ECG #3 done 2 days later).
• As per Dr. Frick — Confusion may result from the fact that some benign-looking features (that may be suggestive of BTWI) — may co-exist with subtle findings of acute OMI.

BOTTOM Line: The "good news" in today's case — is that this patient underwent immediate angiography, with identification of a mid-to-distal RCA "culprit" that was stented.

 

Prehospital Cath Lab Activation. What happened when the medics and patient arrived at this Academic ED?

This was texted to me by a paramedic while I was out running one day:

"54 yo male chest pain started at 1pm. History of diabetes type II and stent placement in 2018. I’m seeing hyperacute T waves III, aVF, down sloping depression I and aVL. Thoughts?"

What do you think?

I responded: "Definite inferior OMI.  And Right Ventricular.  Activated the Cath Lab."

He responded: "Copy that...Cath Lab activated. thank you"

Smith analysis: There is a massive hyperacute T-wave in lead III, and a massive reciprocally inverted hyperacute T-wave in aVL (and I).  There is minimal STE in III and reciprocal STD in aVL (and I).  There is some minimal STE in V1 (suggesting RV MI) and minimal STD in V2 (suggesting posterior OMI, and also mitigating the evidence of RV MI -- the posterior OMI pulls down the ST segment in V1 so there is less STE than there would otherwise be).  There are hyperacute T-waves in V3 and V4, further evidence of RV MI.  there is a bit of STD in V6 which is identical to "precordial swirl" which can be due to LAD OMI involving the septu, or to RV MI.

Let's see how the PMCardio Queen of Hearts AI Model performs:

"Acute Occlusive Myocardial Infarction"

She gave this a score of 1.0 (100% probability of acute OMI)

Here is the explainability map:

He arrived at the ER (this is a place with an Emergency Medicine Residency).

"We're in the ER now and they said 'the elevation is not convincing.'"  

They de-activated the cath lab.

This ECG is so obvious to me that it is hard to imagine that there are doctors who do not recognized it.  But it is true.  Many, if not most, doctors are so brainwashed by "1 mm of ST Elevation in 2 consecutive leads" that they cannot see OMI without it.

I contacted a doctor there whom I know to tell him about it and to get some follow up:

He wrote: "That is disappointing. Kudos to the medics."

"I found out that the interventionalist had just finished a case and came to the ED to see about the de-activated case. He saw the ECG and ordered an ED ECG."

Here it is:

Obvious inferior OMI, and now the STE in V1 is huge, with huge hyperacute T-waves of Right ventricular OMI

The cath lab was re-activated:

Angiogram:

100% occlusion mid-RCA occlusion (in-stent thrombosis). TIMI 0. Aspiration thrombectomy and DES x1. LVEDP 31.

The RV marginal branch must have a takeoff that is more distal than usual, as this is definitely an RV MI.

My friend also wrote this:

"Yeah. Apparently the intern also recognized it (he is an avid reader of the blog), but the staff overruled him." 

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My Comment, by KEN GRAUER, MD (11/14/2024):

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I share Dr. Smith's disappointment with regard to the failure to recognize the obvious acute OMI evident on today's initial ECG (that I've reproduced and labeled in Figure-1).

• The patient is a 54yo man with diabetes and a known history of coronary diseae (prior stent placement) — who presented with new CP (Chest Pain) — therefore very high likelihood for having an acute coronary event. This should mean that the initial ED physician should be looking for the slightest abnormalities — that need to be taken as acute until proven otherwise (and not the other way around).
• The initial ECG shows definite ST-T wave abnormalities in 11/12 leads — with marked hyperacute T waves in lead III (within the 1st RED rectangle in Figure-1). Given tiny size of the fragmented QRS complex in this lead (which I interpreted as a "Q-wave equivalent" given predominant negativity with notching on the S wave downslope) — this QRS complex could literally "swim" around within the huge ST-T wave in this lead (ie, that is clearly "hypervoluminous" ) .
• Confirmation of T wave hyperacuity in lead III is immediately forthcoming from mirror-image opposite ST-T wave depression in lead aVL (within the 2nd RED rectangle in Figure-1).
• In the context of these marked ST-T wave abnormalities in leads III and aVL — the T waves in leads II and aVF are also clearly hyperacute ("bulkier"-than-they-should-be given relative size of the QRS in these leads).
• 
  
• IMPRESSION: In this very high likelihood patient with new CP — the total time to diagnose acute inferior OMI with need for prompt cath should be no more than seconds, given the findings in these 4 limb leads. The paramedics on this case immediately recognized these findings. As per Dr. Smith — I also found it difficult to understand why the admitting ED physicians cancelled the cath lab activation.

QUESTION:

I've mentioned 4 specific leads (leads II,III,aVL,aVF) that show diagnostic changes of acute inferior OMI.

• Why did I say that 7 additional leads also show abnormal ST-T wave findings? 

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

ANSWER:

The following describes ST-T wave abnormalities in 7 additional leads:

• Lead I — also shows reciprocal ST-T wave depression. We have often emphasized the "magical" mirror-image opposite ST-T wave picture between leads III and aVL in the setting of acute inferior OMI. This is such a consistent finding — that we have to question whether inferior lead ST elevation truly indicates acute inferior OMI if we do not see this reciprocal relationship between leads III and aVL. Although usually not as marked as the ST-T wave depression that we see in lead aVL with acute inferior OMI — we will often also see indication of reciprocal ST depression in lead I (which together with aVL, is the other high-lateral lead).
• Lead V1 — shows ST segment coving of a broader-than-usual T wave for this lead, with slight-but-real ST elevation. In the setting of acute inferior OMI — seeing ST elevation in lead V1 suggests associated RV MI. This can be confirmed by obtaining right-sided chest leads (See the May 30, 2023 post in Dr. Smith's ECG Blog for more on the ECG diagnosis of RV MI).
• Lead V2 — shows ST segment flattening with ST depression. This is definitely abnormal — because leads V2 and V3 normally show a slight amount of gentle upsloping ST elevation — such that ST segment flattening with depression in association with acute inferior OMI is diagnostic of associated posterior OMI. Note that despite the marked hyperacute limb lead changes — the relative amount of ST depression in lead V2 is minimal. The reason for this is that what would have been much more ST depression from this posterior OMI — has been attenuated by the ST elevation produced in leads V1 and V2 (which correspond to right-sided leads V2 and V1).
• Leads V3,V4 and V5 — all show "bulkier"-than-they-should-be ST-T wave in these leads. They are also hyperacute T waves (ie, fatter-at-their-peak and wider-at-their-base than they should be given modest QRS amplitude in these leads). What is unusual about these hyperacute changes — is that usually this is seen with acute LAD OMI — though the "culprit" artery on cath was the RCA (mid-stent thrombosis). Since this patient has known coronary disease as well as diabetes — we can speculate that these changes in this anterior lead distribution may be the result of some compromise in collateral flow to the anterior wall. Regardless of its cause — the "answer" regarding these hyperacute changes in leads V3,V4,V5 is that it adds further support to the need for prompt cath.
• Lead V6 — shows abnormal ST segment "scooping" with slight depression — which I interpreted as an additional sign of diffuse, underlying coronary disease.

BOTTOM Line in Today's CASE: In a very high likelihood patient with new CP — the ECG changes in leads II,III,aVL and aVF (at the very least) — need to be promptly recognized (as they were by the paramedic on this case).

.

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):

===================================

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. 
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• 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.
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• 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).
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• 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!