Dueling OMI: does this 30 year old with chest pain have any signs of occlusion or reperfusion?

Written by Jesse McLaren, with edits from Smith

 

A 30 year old with a history of diabetes presented with two days of intermittent chest pain and diaphoresis, which recurred two hours prior to presentation. Below is ECG #1 at triage. Are there any signs of occlusion or reperfusion?

There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s mild inferior ST elevation in III that doesn’t meet STEMI criteria, but it’s associated with ST depression in aVL and V2 that makes it diagnostic of infero-posterior Occlusion MI (from either RCA or circumflex)– accompanied by inferior Q waves of unknown age. There are also subtle biphasic T waves in V3-4 of unclear significance (this can be seen in anterior or RV reperfusion, but this usually does not accompany infero-posterior occlusion).

Just so you know this ECG interpretation is not done by the retrospectoscope:

I sent it to Dr. Smith without any information, and he immediately responded: "Infero-postero-lateral OMI"

 

The ECG had a computer and final cardiology interpretation of “possible inferior infarct, age undetermined”, because of Q waves. It was signed off by an emergency physician as “STEMI negative” because it did not meet STEMI criteria. So the patient waited to be seen. First troponin I returned at 150 ng/L (<26 in males and <16 in females) and ECG #2 was performed, with the patient painfree. What do you think?  

 

 

Now the ST elevation in III with reciprocal change in aVL is resolving, and V2 shows normalization of ST segment and slightly bigger T wave – so there’s been infero-posterior reperfusion. And the biphasic T waves in V3-4 persist.

 

The patient was seen by an emergency physician 5 hours after arrival, reporting no symptoms, with repeat trop down to 125 ng/L and ECG #3. What do you think?

ST segment has risen again in III and there are bulkier inferior T waves, with reciprocal ST depression in aVL and ST depression in V2. But now there’s also been a loss of anterior R waves with new Q waves, and the previously biphasic T waves in V3-4 are now upright (pseudonormalization).  Moreover, T-waves in V3 and V4 are now bulky, suggesting they are hyperacute. So despite a declining initial troponin and resolution of symptoms, the ECG shows reocclusion with OMI affecting inferoposterior plus anterior walls. But it still doesn’t meet STEMI criteria, so the patient was referred to cardiology as ACS.

 

10 hours after arrival the patient was assessed by cardiology and had ECG #4:

 

The ST elevation and reciprocal ST depression in aVL has improved and T waves are no longer hyperacute. The transiently upright T waves in V3-4 have inverted again, and now there’s T wave inversion across the anterolateral wall. Now the main pattern is anterolateral reperfusion, most likely from proximal LAD

 

13 hours after arrival the patient complained chest pain and ECG #5 was obtained, and repeat troponin was 11,000 ng/L.

There’s further loss of precordial R waves (in fact, profound Q-waves), with increasing ST segment in V2 but ongoing reperfusion T wave inversion anterolateral. Recurring symptoms suggest reocclusion, with an ECG between reperfusion and reocclusion. The chest pain was refractory to nitro so the cath lab was activated: 100% proximal LAD and 99% mid circumflex occlusions.

 

Peak troponin was 15,000 ng/L, and echo found preserved EF but akinetic apex and hypokinesis of anterior and inferior walls. Next day ECG #6:

Evolution of LAD reperfusion with deeper T wave inversion anteriorly and aVL (with reciprocal taller T waves)

Discharge ECG #7 a few days later : 

Ongoing anterolateral reperfusion T wave inversion, with R wave recovery in V4-5 but not V2-3.

 

Dual OMI, and dueling OMI

 

STEMI is usually attributed to one infarct-related artery that becomes completely and irreversibly occluded, producing regional ST elevation that exceeds STEMI criteria. But this framework is proven to be unreliable, and the underlying pathology of Occlusion MI is much more complicated and dynamic: there can be little or no ST elevation but multiple other signs of OMI, and this dynamic state can fluctuate between spontaneous reperfusion and spontaneous reocclusion.

 

In addition, there are a number of other scenarios that complicate OMI and ECG interpretation:

·      the occlusion of one infarct-related artery can affect other territories based the site of occlusion. For example anterior and inferior ST elevation can be caused by proximal RCA or distal/wraparound LAD occlusion

·       the occlusion of one infarct-related artery can occlude collaterals that were serving another territory with chronic total occlusion

·       the occlusion of one infarct-related artery can induce subendocardial ischemia in another that had critical stenosis. For example, inferior OMI with concomitant critical stenosis produces a combined pattern (Aslanger’s pattern) with inferior STE and subendocardial ischemia 

·       occlusion of two infarct-related arteries simultaneously ("co-culprits")

 

In this case there were two infarct-related arteries. This complicated ECG interpretation because 1) there were two different patterns of Occlusion, 2) neither of which ever met STEMI criteria, 3) they were reperfusing/reoccluding at different times, and 4) had different effects on some of the same leads. For example aVL is a high lateral lead which is reciprocal to the inferior wall: inferior OMI can cause inferior ST elevation/hyperacute T with reciprocal ST depression in aVL (ECG #1/3), while lateral reperfusion can cause primary T wave inversion in aVL (ECG#4-7) with reciprocally tall inferior T wave. Similarly, the anterior lead V2 is reciprocal to the posterior wall: posterior OMI can cause reciprocal ST depression in V2, while anterior reperfusion can cause primary T wave inversion in V2.

 

In other words, there was not only dual OMI, but they were dueling – each going back and forth between occlusion and reperfusion, with clashing ECG patterns that sometimes favoured one and other times favoured the other:

·       ECG #1: circumflex OMI dominated, with subtle LAD reperfusion

·       ECG #2: reperfusion of circumflex, LAD still reperfused

·       ECG #3 reocclusion of circumflex and LAD

·       ECG #4-7: reperfusion of LCX and LAD, the latter of which dominated

 

Take away

1.     Young people can have acute coronary occlusion.

2.     Symptoms don’t always correlate with coronary artery occlusion/reperfusion: resolved symptoms but ongoing ECG signs of occlusion requires reperfusion.

3.     STEMI criteria is unreliable and leads to delayed reperfusion: neither of these occlusions ever meet STEMI criteria, but there were multiple other diagnostic signs of occlusion across the entire QRS-T complex – including loss of R waves and new Q waves, subtle ST elevation, reciprocal ST depression, pseudonormalization and hyperacute T waves.

4.     STEMI criteria also ignores spontaneous reperfusion at risk for reocclusion. The question is not whether the ECG meets STEMI criteria, but whether the patient has OMI, including reperfused OMI at risk for reocclusion.

5.     Troponin is a delayed marker of ischemia that is unreliable early in occlusion, or in spontaneous reperfusion at risk for reocclusion: here the first trop was only 150 and declined on repeat, only to rise to a peak of 15,000.

6.     The angiogram can highlight occlusions at the moment of the procedure, but it’s serial ECGs which tell the story of occlusion and reperfusion.

7.     OMI ECG changes can be complicated by site of occlusion, compromised collaterals to chronic total occlusions, concomitant critical stenoses, or co-culprits – resulting in combined ECG patterns with dynamic changes based on underlying reperfusion/reocclusion.

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My Comment by KEN GRAUER, MD (2/1/2023):

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Important post by Dr. McLaren, that underscores current problems with the outdated "STEMI Paradigm". In excellent fashion — Dr. McLaren traces the evolution of ECG findings over the course of the 7 serial tracings in today's case. Errors were made. 

• Errors in today's case resulted in a 13-hour delay. It wasn't until the 5th ECG was obtained (apparently done only because the patient's chest pain had returned) — that the by now markedly elevated Troponin and by now obvious ECG changes finally convinced providers of the need for cardiac cath. 
• Unfortunately, significant cardiac damage had already been done. This might have been minimized had the abnormalities been picked up earlier.

Even for providers who are still "stuck" in the old STEMI paradigm — Attention to the "Take-Aways" enumerated by Dr. McLaren should help to prevent the oversights in today's case. I focus my comment on how applying these Take-Aways at the time of the initial ECG could have prompted a much more rapid path to cardiac catheterization.

• The stuttering course of chest pain in today's case (ie, intermittent over 2 days — and then returning ~2 hours prior to ED arrival) — is relevant for optimal management of today's patient. 
• Even clinicians still "stuck" on the STEMI paradigm need to accept that acute coronary occlusion is often a dynamic evolving process, instead of a single "static" event. The "culprit" artery acutely occludes — but then it sometimes spontaneously reopens — and, occasionally continues for a period of time to spontaneously reopen and reclose a number of times, until eventually a permanent status is reached. The stuttering course of chest pain in today's case should have suggested this dynamic evolution — especially after seeing the initial ECG!

For clarity in Figure-1 — I've reproduced the initial ECG in today's case. The tracing shows sinus rhythm — normal intervals and axis — and no chamber enlargement. There are small and narrow q waves of uncertain significance in multiple leads. (Note that rather than a Q wave — there is an rSR' complex in lead III).

• Abnormal ST-T waves are actually present in 10/12 leads in ECG #1. While the ED physician was correct in saying that this initial ECG "did not meet STEMI criteria" — I feel there are ST-T wave changes in 3 leads that can not be ignored.

In the limb leads:

• I was not initially convinced that the subtle ST elevation in leads III and aVF was significant — until I saw the flat ("shelf-like") ST depression in lead aVL. While not necessarily acute — given the stuttering history of chest pain over the past 1-2 days, the ST-T wave appearance in lead aVL has to be interpreted as a reciprocal change from presumed recent infarction until proven otherwise.
• In the context of lead aVL — the other high-lateral lead ( = lead I) shows a lesser degree but-still-significant amount of flat ST depression.

In the chest leads:

• There is no way that the flat ("shelf-like") shape of ST depression in lead V2 is normal. Especially in association with an already surprisingly tall R wave in lead V2 — this (as per Dr. McLaren) is diagnostic of posterior OMI until proven otherwise. (Remember that normally — there is usually slight, upward sloping ST elevation in lead V2 — and virtually never ST depression).
• 
  
• In a patient with intermittent chest pain — the straightened ST segment take-off in lead V3, with terminal T wave inversion (RED arrow) is clearly of concern. This ST-T wave appearance is not expected with posterior OMI — but instead suggests the possibility of either Wellens' Syndrome (if chest pain has resolved) — or — reperfusion following recent LAD occlusion.
• In support of significance for the abnormal ST-T wave appearance in lead V3 — is the subtle-but-real terminal T wave inversion in neighboring leads V4 and V5.
• A final abnormal finding in the chest leads — is that the upright T wave in lead V1 is taller than the upright T wave in lead V6. Although this is a nonspecific finding — it is often associated with ischemia.

BOTTOM Line:

The history in today's case can not be ignored. While the patient is a younger that what we usually expect to see with acute infarction — the diabetes clearly increases risk.

• While millimeter criteria for a STEMI are not met in ECG #1 — and while ST-T wave changes in most leads in the initial ECG are not definitive — the ST-T wave appearance in 3 leads ( = leads aVL — V2 — V3) can not be ignored as indication that an acute event may have recently occurred.
• At the very least — the initial ECG should have been repeated within 10-20 minutes. Seeing even subtle ST-T waves changes (such as less ST depression in lead V2, with an increase in T wave positivity in this lead — as was eventually seen when the 2nd ECG in today's case was obtained) — would be evidence of dynamic change that confirms reperfusion from recent posterior OMI.
• The 1st troponin did come back elevated (150 ng/L). Given the worrisome history and the initial ECG — this result should have been enough to merit prompt cath.
• 
  
• To Emphasize: — I had no idea from the initial ECG that there were 2 "culprit" arteries in today's case. Had I known this — it would have explained some of the subtle contrasting ECG findings. But the point is that we do not need to know the anatomy in order to recognize that in a patient with new chest pain — the ST-T wave appearance in leads aVL, V2 and V3 of the initial ECG can not be ignored until we have actively ruled out a recent (or still ongoing) acute event.

Figure-1: I've labeled the 3 leads of most concern in the initial ECG from today's case.

QS-wave in V2: 2 cases, different paradigms lead to different treatment times (STEMI - NSTEMI vs. OMI - NOMI)

Submitted by anonymous, written by Pendell Meyers.  Additional case by Smith.

Case 1

A middle aged woman presented with acute chest pain and shortness of breath, unclear time since onset, and likely with episodic symptoms off and on throughout the day. Her vitals were within normal limits.

ED1 @1512

What do you think?

Meyers: Very clear and specific for acute LAD OMI, with hyperacute T waves in the LAD distribution including leads V2-V6, II, III and aVF. Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern. This ECG is pathognomonic, regardless of any information, prior ECG, etc available: it means the LAD territory is undergoing immediate and hyperacute full thickness infarction, with the most likely etiology being type 1 ACS. 

Prior ECG available on file from 2 months before:

We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Probably not the patient's "baseline" ECG, but it was the prior on file. Notice the normal precordial T waves.

That first ECG (the one at the top) was interpreted as "no evidence of ischemia."

A single high sensitivity troponin I was measured from triage (around 1500), which now returned elevated at 2,271 ng/L (upper limit of normal 12 for women, 20 for men).

(Amazingly, no further troponins were ever measured for this case)

ED2 @1559

Continued evolution of LAD OMI, with increasing STE and now likely meeting STEMI criteria to those who actually measure it.

With the elevated troponin and repeat ECG showing new STE, the patient was discussed with local PCI center, and the cath lab was activated. The patient was transferred.

Angiogram @ 1830 (3.3 hours after that first diagnostic ECG):

Mid-LAD culprit lesion, 99% stenosis, no pre-intervention TIMI flow available, but described as "severe subtotal lesion", which was stented with reported TIMI 3 flow resulting. Another lesion in the proximal LAD with 80% stenosis was stented as well. Other vessels had scattered 30-40% stenoses.

Post-cath ECG @1921

Significant evolution of MI including worsening precordial Q waves, notable absence of deflation of the T waves.  This is very concerning after reportedly "successful PCI" (successful in restoring flow in the epicardial coronary artery, but not necessarily to the downstream cells). Concerning for ongoing injury, concerning for the "No Reflow" phenomenon.

No peak troponin was measured. We do not know if the patient's symptoms resolved.

Next morning:

Slight evidence of reperfusion (or just completion) with terminal T wave inversion in many leads. QS waves from V2-V5 consistent with LV aneurysm morphology.

Echocardiogram:

EF 50%, akinesis of mid-apical anteroseptal, inferior, and inferoseptal myocardium. Normal RV, no valve stenosis or regurgitation.

The patient survived and was able to be discharged. 

2 weeks later:

Some slight R wave recovery in V4-V5, but overall still LV aneurysm morphology, and lingering T wave inversions which could be consistent with reperfusion or completed OMI.

Case 2.

Contrast the last case with this case, from a different institution, which operates by the OMI/NOMI paradigm:

70-something male presents through triage with 9 hours of chest pain.

Here is the triage ECG:

Sinus rhythm with Left Anterior Fascicular Block.

There is subtle STE in V2 - V4, I and aVL, diagnostic of proximal LAD OMI.  There is one hyperacute T-wave (in V3).  

There is a QS-waves in V2: is this "Old MI with persistent STE (otherwise known as LV aneurysm morphology)"?   The T-wave in V2 and V3 are too large for this: a T/QRS ratio ＞0.36 in one of leads V1-V4 is acute until proven otherwise.  

T/QRS ratio in V2 is 2.5/6.5 = 0.38.  In V3, it is even higher.

In this case, the MI is subacute, with symptoms of 9 hours duration.  QS-waves are typical of anterior OMI of this duration, as are the relatively flat T-waves (not hyperacute).  (When symptoms are present for more than 6 hours, the T/QRS ratio may be small due to subacute MI -- absence of hyperacute Ts).

It is difficult to say whether this ECG meets "STEMI criteria:" there is 2 mm of STE in V3.  But V2 does not have 2 mm and V4 is very close to 1 mm.  The computer did read "STEMI".

The cath lab was immediately activated.

Later, the initial hs troponin I returned very high.

Angiogram:

Primary PCI for Acute Antero-lateral STEMI.

Culprit is 100% stenosis in the Proximal LAD.

Culprit lesion was reduced to 0% and stented.

90% ostial LAD-D1 reduced to 35% with PTCA and stented.

Next day ECG:

There is now RBBB in addition to LAFB.

Some persistent STE in V2-V5 (with RBBB, there should be STD depression discordant to the positive R'-wave, so this is particularly worrisome)

Reperfusion T-waves in I, aVL, V2-V5,6

Echo

Normal left ventricular size and wall thickness with severely reduced systolic function.

The estimated left ventricular ejection fraction is 31%.

Akinesis in LAD territory:

- Basal to apical septum

- Mid to apical anterior wall

- Entire apex

The delay in patient presentation resulted in large irreversible infarction.

Learning Points:

Note that expert ECG interpretation diagnosed OMI at the time of arrival, STEMI criteria possibly at 45 minutes later, and the patient underwent cath at 3 hours after arrival, for a delay of approximately 3 hours since first medical contact. Better ECG interpretation would likely have led to more rapid reperfusion.

Understanding the entire OMI progression including hyperacute T waves is critical for diagnosing OMI.

The ECG is usually a better indicator of reperfusion than the angiogram.

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My Comment by KEN GRAUER, MD (1/28/2023):

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After reading about the course of case presented by Dr. Meyers — I have mixed emotions. I find it gratifying that so many of our readers have become highly competent interpreters, who are able to immediately recognize that the initial ECG in today's case is (as per Dr. Meyers) — "very clear and specific for acute LAD OMI".

• In this middle-aged woman who presented to the ED with new chest pain producing symptoms "on and off" throughout the day — the need for prompt cath lab activation with PCI is indisputable.
• 
  
• That said, on seeing the initial ECG for the 1st time — I shared Dr. Meyers' concern that this acute OMI might not be "understood" for the same reasons he expressed (ie, lack of millimeter criteria to be called a "STEMI" — and a "lack" of reciprocal changes).
• On reading what happened — I have to admit my frustration at learning that despite the incriminating history and diagnostic initial ECG in today's case — PCI was delayed for over 3 hours. 

I focus my comment on the case presented by Dr. Meyers — specifically regarding interpretation of the first 2 tracings in his case, which I consider at 2 LEVELS: i) The BASICS (ie, Why even less experienced interpreters should not misinterpret the diagnostic initial ECG); and, ii) PEARLS for the more advanced readers of Dr. Smith's ECG Blog (in which I'll point out some interesting subtleties in these first 2 tracings).

• For clarity in Figure-1 — I've reproduced and labeled these first 2 tracings in today's case.

Figure-1: I've reproduced and labeled the first 2 tracings in today's case.

My Initial Thoughts on Reading Today's CASE:

The aphorism, "Listen to the patient — he/she is telling you the diagnosis" — has been attributed to Dr. William Osler, the "Father" of Medicine. Ignoring this truism was the 1st oversight in today's case.

• Awareness that not only did the patient in today's case present to the ED with new chest pain — but that she indicated having this symptom "on and off" throughout the day. Knowing this history explains many of the ECG findings that were overlooked in the initial tracing.

The initial ECG shows sinus rhythm with a PAC ( = the early beat in leads V1,2,3). All intervals (PR, QRS, QTc) are normal. There is no chamber enlargement (On the contrary — overall QRS amplitude is decreased).

• The frontal plane axis in ECG #1 (Top tracing in Figure-1) — is markedly leftward, with a predominantly negative QRS in lead II. This suggests an axis of at least -45 degrees, and is consistent with LAHB (Left Anterior HemiBlock).
• 
  
• PEARL #1: It's often difficult to appreciate inferior infarction in association with LAHB (and vice versa). This is because the initial component of ventricular depolarization is oppositely directly with LAHB vs inferior infaction. The fact that there is a small-but-real initial q wave in lead II in this patient with LAHB (BLUE arrow in lead II) — consistent with a qrS complex in lead II, suggests inferior infarction has occurred at some point in time, in addition to the LAHB.
• In support of this premise that inferior MI has occurred at some point in time are: i) The QS in lead III (without any initial positive deflection at all); and, ii) The fragmentation we see in the tiny QS complex in lead aVF (this variable fragmention in lead III most probably produced by the beat-to-beat opposing orientation between the initial vectors from the LAHB and inferior MI).

Continuing my interpretation of ECG #1 — by assessing Q-R-S-T Changes:

• There are QS complexes in leads V1,V2,V3.
• We again see small initial q waves in leads V4,V5,V6.
• As a result of these QS complexes and the overall reduced voltage — there is poor R wave progression (with delayed transition, in that the R wave does not ever become taller than the S wave).
• 
  
• PEARL #2: Although small and narrow septal q waves may normally be seen in lateral chest leads — this is not what we see in ECG #1. Instead — the fact that following QS complexes in the first 3 chest leads — the initial negative deflection ( = q wave) that occurs before the tiny r in lead V4 is indicative of the extensive anterior infarction that has occurred at some point in time. 
• In support of this premise of extensive anterior MI — is continuation of the tiny R wave amplitude through to lead V6, with persistence of tiny q waves in V5,V6 (BLUE arrows in leads V4,5,6 in ECG #1).
• 
  
• PEARL #3: As we've pointed out on a number of occasions (ie, See My Comment at the bottom of the page in the November 12, 2020 post in Dr. Smith's ECG Blog) — the finding of low voltage in a patient with ongoing acute MI may be indication of cardiac "stunning" from extensive infarction.

The MOST Abnormal Lead in ECG #1:

The reason for my frustration in reading what happened in today's case — is a result of providers not realizing the abnormality in lead V4.

• PEARL #4: Changes of acute OMI may often be subtle in many leads. As a result — I find it most helpful to look for those 1 or 2 leads that you know are definitely abnormal. Once these definitely abnormal leads are identified — it becomes far easier to assess neighboring and reciprocal leads for changes that may not be as obvious. In ECG #1 — regardless of the experience of the interpreting clinician — there should be no doubt that in a patient who presents to the ED with new chest pain — that the ST-T wave lead V4 is disproportionately tall. Indication that this T wave in V4 is hyperacute is forthcoming from ST segment straightening of its upslope and its hypervoluminous T wave (clearly taller-than-it-should-be with a much wider base than should be present given tiny amplitude of the QRS).
• 
  
• I've added parallel RED lines in a number of other leads in ECG #1 — to highlight ST segment straight (and coving in lead V2) — that all provide support of the ongoing acute LAD occlusion.

WHY So Many Q Waves IF the MI is Acute?

The answer to this important question is forthcoming IF we remember Sir William Osler's famous quote: "Listen to the patient — he/she is telling you the diagnosis".

• Today's patient was having chest pain "on and off" throughout the day. As a result — there was more than ample time for infarction Q waves to develop — with resultant loss of QRS amplitude — and possibly some return-to-baseline of previously elevated ST-T waves.

Comparison with the Prior ECG:

As per Dr. Meyers — there is a significant difference between the 2 tracings in Figure-1. To emphasize — We do not know the circumstances under which the prior tracing was obtained — and this prior ECG #2 does show sinus tachycardia, PVCs and nonspecific ST segment flattening with slight depression in many leads.

• The above said — My frustration in this case is that IF any provider (at any level of clinical experience) made a lead-by-lead comparison between the initial tracing in today's case — and the prior tracing — it should be impossible not to notice the change in ST-T wave morphology.
• 
  
• PEARL #5: The EASY way to get good at comparing serial tracings — is to go lead-by-lead. Doing so (as I illustrate in Figure-1) — should reveal more left axis deviation in ECG #1 (new development of LAHB) — lack of inferior and lateral chest lead Q waves and small-but present initial R waves in leads V2,V3 (GREEN arrows in ECG #2). Most notable should be the change in ST-T wave morphology between the 2 tracings (shape of the RED lines I've drawn in ECGs #1 and #2 in Figure-1).

BOTTOM Line: The acute OMI in today's case should not have been missed, given the history and the appearance of the first 2 ECGs.

• There are simple things even less experienced providers can do to improve their ECG interpretation ability — so that oversights as described in today's case do not occur. 

What is this Rhythm?

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My Comment by KEN GRAUER, MD (1/26/2023):

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While reading ECGs — Dr. Smith came across the intriguing tracing shown in Figure-1. No history was available. However, the rhythm is indeed challenging — and illustrates a number of important principles in rhythm interpretation of interest to all emergency care providers.

• How would YOU interpret the ECG in Figure-1? 
• Can you come up with a definitive rhythm diagnosis?

Figure-1: 12-lead ECG and simultaneously-recorded 3-lead rhythm for today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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REVIEW: MY Approach to Rhythm Interpretation

• As always — I favor beginning my interpretation of 12-lead ECGs with a look at the cardiac rhythm. My systematic approach to rhythm interpretation entails assessment of the 5 KEY Parameters, which are easily recalled by use of the memory aid, "Watch your Ps, Qs and 3Rs". The questions to ask when assessing these 5 Parameters are:
• Are there P waves (or other sign of atrial activity)?
• Is the QRS wide?
• What is the Rate? (looking both at the atrial and ventricular rates IF these are different).
• Is the rhythm Regular? (and if not — Is the rhythm “irregularly irregular”, as in AFib — or is there a pattern of “regular" irregularity in the form of group beating?).
• If P waves are present — Are P waves Related to neighboring QRS complexes?
• 
  
• NOTE: It does not matter in what sequence you assess the above 5 Parameters — as long as you always assess all 5 of them. I generally look at whichever of the Parameters are easiest to recognize.
• CAUTION: In my experience over decades — Failure to systematically assess each of the above 5 Parameters will result in even the most “experienced” of clinicians missing the diagnosis of a number of non-sinus rhythms.
• To EMPHASIZE: Using the Ps, Qs, 3R system does not slow you down. On the contrary — it organizes my thinking, and allows me within seconds (!) to diagnose almost any arrhythmia.

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MY Approach to the Rhythm in Figure-1:

Using the Ps, Qs & 3R Approach:

• The QRS is narrow in all 12 leads of Figure-1 (So the rhythm is supraventricular!).
• The rhythm is not completely Regular. That said — Parts of the rhythm are regular (ie, Except for the 2 pauses between beats #4-5 and 10-11 — the R-R intervals between all other beats is essentially the same!).
• P waves are present!

PEARL #1: Overall — the best lead to look for P waves in, is lead II. In fact — sinus rhythm is defined by the presence of an upright P wave with fixed PR interval in lead II. 

• Remember that the 2nd-best lead to look for P waves in — is lead V1. 
• KEY Point: There are times when P waves will not be well seen in lead II — and may only be seen in lead V1. Such is the case in today’s tracing. We barely see P waves in the long lead II rhythm strip (and then, only before the 1st QRS complex that occurs at the end of each pause). However — regularly-occurring P waves at a Rate of ~80/minute are clearly seen throughout the entire long lead V1 rhythm strip (ie, RED arrows in Figure-2).

PEARL #2: The KEY for interpretation of complex AV block tracings — will often reside with the 5th Parameter = Whether or not P waves are Related to neighboring QRS complexes. 

• I look to see IF there are any PR intervals that repeat. The best place to look for this — is in front of the QRS complex that terminates a pause in the rhythm. In Figure-2 — Isn’t the PR interval before beats #5 and 11 equal? The fact that the same PR interval repeats before 2 or more beats is unlikely to be due to chance — and suggests that there probably is at least some conduction!

Figure-2: Regularly-occurring P waves are clearly seen in the long lead V1 rhythm strip (RED arrows).

Putting together what we’ve derived thus far:

• The rhythm in Figure-2 is supraventricular (narrow QRS). 
• Regular P waves at a rate of ~80/minute occur throughout the long lead V1 rhythm strip (RED arrows).
• Although the rhythm in Figure-2 is not completely regular — there are groups of beats with a constant R-R interval — that are separated by pauses of almost equal length (ie, The R-R interval between beats #4-5 and between #10-11 is virtually the same!).
• The PR intervals before the 2 beats that terminate the short pauses are equal (ie, the PR intervals before beats #5 and 11 in Figure-3). This tells us that at least 2 beats in this tracing are being conducted to the ventricles, albeit with a markedly prolonged PR interval ( = 0.54 second).

Figure-3: PR interval measurements for the beats just before the pause — and just after the pause.

PEARL #3: Our above description thus far of the 5 Parameters — should immediately suggest that of some form of AV Wenckebach (ie, 2nd-degree AV block of the Mobitz I type) is present in Figure-3. This is because:

• The QRS is narrow (The QRS is usually narrow with Mobitz I. The QRS is almost always wide with Mobitz II).
• There are regular P waves, as highlighted by the RED arrows in Figure-3 (The finding of a regular or at least almost regular atrial rhythm makes other causes of group beating such as PACs and sinus pauses far less likely).
• There is group beating — in which the R-R intervals of the 2 short pauses are approximately equal in duration (I always immediately suspect Wenckebach if the QRS is narrow and P waves are regular and there is group beating!).
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• The PR intervals before beats #5 and 11 are equal — which tells us that these beats are conducting to the ventricles. In contrast — the P waves that occur just after the QRS of beats #4 and 10 are not conducted — which in the setting of a regular atrial rhythm defines this tracing as some form of 2nd-Degree AV Block.
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• PEARL #4: Statistically — Mobitz I 2nd-degree AV block is much more common than Mobitz II (ie, In my experience — at least 90-95% of all 2nd-degree AV blocks I have seen over the years are Mobitz I. Mobitz II is distinctly uncommon).
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• PEARL #5: The finding of 1st-degree AV block (especially given the markedly prolonged PR interval in today's case) — further increases statistical likelihood of Mobitz I (There commonly occurs a progression from 1st-degree AV block — to Mobitz I 2nd-degree block).

PEARL #6: We are used to recognizing Mobitz I, 2nd-degree AV block by obvious progressive lengthening of the PR interval until a beat is dropped. The reason Mobitz I is difficult to recognize in today's tracing — is that we are presented with a long Wenckebach cycle, in which there is only minimal increase in the PR interval increment from one beat-to-the-next.

• In such cases — the EASY way to immediately recognize that the PR interval is in fact increasing — is to measure the PR interval just before the pause (ie, the PR intervals before beats #4 and 10 in Figure-3) — and to compare this to the PR interval before the first beat that ends each pause (ie, the PR intervals before beats #5 and 11 in Figure-3). Doing so confirms that the PR interval is ever-so-slowly increasing until a P wave is non-conducted.

Laddergram Illustration:

The laddergram in Figure-4 — illustrates the mechanism of today's rhythm. I've carefully measured each PR interval in milliseconds.

• NOTE: Many patients "don't read the textbook". There simply is not always a measurable beat-to-beat increase in the PR interval with all cases of Mobitz I, especially when there is a long Wenckebach cycle (as is seen from beat #5-to-#10 in Figure-4).
• That said — there should be no doubt that the PR interval before the first beat in this grouping ( = 540 msec. for the PR interval before beat #5) — is less than the last PR interval in this group ( = 640 msec. before beat #10).
• The next on-time P wave (ie, the YELLOW arrow that occurs just after beat #10) — is non-conducted. There follows a short pause (between beats #10-to-11) — after which the PR interval again shortens (to 540 msec. before beat #11) — as the next long Wenckebach cycle begins. This sequence of events confirms the diagnosis of a long Wenckebach cycle.

PEARL #7: We often think of 1st-degree AV block as a benign rhythm. This is because most patients with an isolated 1st-degree AV block remain asymptomatic without need for intervention. This is especially true when the severity of 1st-degree AV block is not great (ie, a PR interval less than 0.30 second).

• Once the PR interval extends much beyond 0.30 second — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. This may lead to a series of symptoms similar to “pacemaker syndrome” (ie, dizziness, fatigue, light-headedness, presyncope/syncope, dyspnea and/or chest pain).
• On occasion — implantation of a permanent pacemaker may be needed in a patient with a marked 1st-degree AV block (ie, PR interval significantly greater than 0.30 second) — IF the patient is symptomatic as a direct result of PR interval prolongation (For an example of this — See My Comment at the bottom of the page in the May 24, 2020 post in Dr. Smith's ECG Blog). 
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• Mobitz I, 2nd-degree AV block is also often a relatively benign rhythm — in that many patients with Mobitz I will not need a pacemaker. That said — the fact that the shortest PR interval in today's case for sinus-conducted beats is 0.54 msec. — suggests there is significant conduction system disease with high risk of symptoms similar to "pacemaker syndrome" (as described above for patients with a markedly prolonged 1st-degree block).

Final POINT in Today's CASE: To emphasize — that although the PR interval increment from one beat-to-the-next in today's rhythm is small (and not-at-all obvious) — Attention to the ECG findings highlighted above in Pearls #3-thru-6 allowed me to know that the rhythm was Mobitz I in less than 10 seconds.

Figure-4: Laddergram illustration of today's rhythm. The YELLOW arrows are on-time non-conducted P waves in each of the long Wenckebach cycles (See text).