A 50-something with chest pain. Is there OMI? And what is the rhythm?

Written by Willy Frick

A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chest pain and diaphoresis. His ECG is shown:

What do you think?

The history thus far is highly suggestive of OMI, so we must study the ECG very closely to see if we can confirm this. Looking at the rhythm strip, we see there is more going on than simple sinus rhythm, and in fact there are two different morphologies of QRS complexes. Take a closer look at the rhythm by itself and see if you can figure out what's going on before scrolling further.

If we set our calipers on the R waves and number them, we see that even though the PR interval shortens and the P wave disappears beneath the R wave, the R wave continues to occur at very regular intervals. That is, until the 7th R wave which comes a little bit sooner than expected.

I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. The Queen of Hearts does not care about rhythm analysis, she simply looks at the ECG and decides whether it represents OMI or not. 

Here is the Queen's verdict and her explanation:

She sees OMI but with low confidence. I sent this to Dr. Smith with no context and he said "Could very well be a septal OMI." He pointed out the precordial swirl sign.   He also pointed out that there is isorhythmic dissociation (see Ken Grauer's detail below)  As a reminder, precordial swirl occurs when the LAD is occluded at or proximal to the major septal perforators causing significant septal ischemia. This pulls the ST elevation vector rightward resulting in ST elevation most pronounced in the right precordial leads with reciprocal depression in the lateral precordial leads.

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Smith:

See a good example of RBBB with septal OMI here:

Chest Pain and RBBB. What do you think?

Here are more examples of septal OMI and at least one Mimic:

A 50-something with cocaine chest pain and ST Elevation in V1 - V3

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An aside on understanding the morphology of the escape complexes:

The QRS duration is very close to 120 ms which suggests it may be lower in the junction, perhaps even within the his-purkinje system (although the rate is a bit fast for ventricular escape). Inspecting the morphology can give us more information about the source of the escape rhythm. I have shown representative R waves from several leads below.

Step 1 is to inspect for right vs left bundle morpholoy, which depends on leads I and V1. Remember, we have to restrict our inspection to the QRS complexes that have the escape morphology (that is, R2 through R6). That leaves us with only R2 in lead I, which is negative in its terminal portion consistent with rightward depolarization (since I is oriented right to left). Lead V1 is positive in its terminal portion, also consistent with rightward depolarization (since V1 is oriented toward the right fourth intercostal space). This is consistent with RBBB morphology, which suggests that the impulse originates closer to the left bundle. (This may sound confusing, but if the impulse originates near the left bundle, then the right bundle must activate later. This is the exact same activation sequence as you would see in the case of right bundle change block.)

Step 2 is to inspect for fascicular morphology, which depends on the limb leads. We see marked right axis with rS complexes in I and aVL, and qR complexes in II, II, and aVF. (Strictly speaking, there is no visible Q wave in aVF but this is because of the buried P wave. Since II and III have Q waves, aVF must also have one.) This is left posterior fascicular block morphology, suggestive of left anterior fascicular origin. (This is the same logic as above, where right bundle branch morphology predicted left bundle branch origin.)

Back to the assessment of ischemia:

Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. The first beat in leads I and II, and both beats in V4-6 are sinus beats, and they all have ischemic appearing down-up T waves. We also see that aVL (with escape complexes only) has subtle ST depression which is inappropriately concordant to its predominantly negative QRS complex. Here the ECG is again:

Now that we see multiple areas with what appears to be reciprocal change, the final task is to find the primary vector of injury. Looking at V1, which has right bundle branch block morphology, there is concordant STE, which fits perfectly. Due to the precordial swirl Dr. Smith mentioned, the STD in the lateral leads is reciprocal to the STE in V1. And because swirl is a sign of LAD OMI, it is not surprising that there is reciprocal depression inferiorly in II.

Fortunately, the emergency physician evaluating the patient activated the cath lab immediately. (This is documented as a STEMI in the clinical notes and in the cath report, but certainly does not meet STEMI criteria and is therefore an NSTEMI by definition. For national registry purposes, this will be incorrectly classified as a STEMI.)

The first angiographic shot below is AP cranial, good for viewing the LAD and diagonal vessels.

(Right click the video and click "Loop" to see the video repeat endlessly.)

Below I have shown a still with arrows indicating the LAD, septal perforators, and a few diagonal vessels. At the tip of the red arrow, you can see a round filling defect which represents a thrombus and appears to involve the origin of the septal perforators (hence swirl sign).

This next angiographic shot is RAO caudal, best for viewing the LCx and its branches, the obtuse marginals. In this case, it also more clearly shows the subtotal occlusion of the septal perforator.

Below I have shown a still with arrows indicating the LAD, septal perforators, one diagonal vessel, LCx, and OM. The LAD thrombus is not as well visualized in this view, but the orange arrow points to the origin of the septal perforators which almost appears not to connect to LAD due to subtotal occlusion.

And finally, after placement of a stent in the LAD:

Before and after:

(Unfortunately, this resulted in the "jailing" of the septal branches behind the stent and probably some degree of plaque shift which is why they do not opacify well in the "after" shot. This was the cost of preventing infarction of the anterior wall.)

Despite very rapid presentation (presenting cTnI undetectable) and reperfusion, the patient still had peak cTnI 48.4 ng/mL (ref. < 0.049). 

Smith: this is a very high peak troponin.  Most STEMI have peak cTnI greater than 10.0.  Large STEMI are approximately 30-80.

Neverthelss, his anterior wall was saved and he had normal ejection fraction without heart failure.

Learning points:

• Precordial swirl can be seen in proximal LAD occlusion involving septal perforators, and you can miss it if you are depending on obvious anterior ST elevation.

• Ischemia can be disguised by a wide escape rhythm, which decreases the sensitivity of ECG.

• Right bundle branch escape morphology indicates left bundle branch origin, and left bundle branch morphology indicates right bundle branch origin.

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MY Comment, by KEN GRAUER, MD (3/22/2024):

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Superb and enlightening discussion of today's case by Dr. Willy Frick! His unique cath film demonstration removes all doubt about the anatomy — with the clearest illustration of acute septal perforator occlusion that I have seen!

• I always find it especially rewarding when the anatomy revealed in prompt cath findings matches our prediction from the initial ECG (ie, Dr. Smith's uncanny immediate impression that, "This ECG could very well represent a septal MI — given the Precordial Swirl Sign).

I focus my comment on 2 aspects of today's case: i) Offering another perspective on some of the findings in the initial ECG; — and, ii) Laddergram and a "deep dive" explanation of the initial rhythm.

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To amplify Dr. Frick's description of Precordial Swirl (taking from My Comment at the bottom of the page in the October 15, 2022 post of Dr. Smith's ECG Blog):

• In the setting of a very proximal site of LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia (as well as anterior wall and apical involvement) — the ECG will show ST elevation in leads V1 and aVR — and reciprocal ST depression in leads V5 and V6. This is precisely what we see in Figure-1, in which I've reproduced and labeled the initial tracing.
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• PEARL: Although assessment of ST-T wave changes in lead V1 for beats #5 and 6 is rendered more difficult (because of the RBBB morphology of beats #5,6 in lead V1) — the long lead rhythm strip in Figure-1 is recorded from Lead V1 — and, RED arrow P waves with a normal PR interval before the narrow and normal-appearing QRS complex of beats #1,7,8 reveal what the ST-T wave in sinus-conducted beats looks like! 
• Although the upright T wave with ST elevation is clearly abnormal for the RBBB morphology of beats #5 and 6 that we see in lead V1 — there can be no doubt that the straightened, hyperacute takeoff of the ST segment for sinus-conducted beats #1,7,8 in the long lead V1 represents (together with the ST elevation in lead aVR) — an even more convincing localized picture of acute septal OMI!
• The other PEARL for recognizing Precordial Swirl — is appreciation of a mirror-image opposite picture for the ST-T waves in leads V1 and V6 (that is not the result of LVH). Isn't it EASY to appreciate this mirror-image reciprocal ST-T wave picture between lead V1 and lead V6 by focusing on sinus-conducted beats #7 and 8 in lead V6 compared to the last 2 beats (just below lead V6) in the long lead V1 rhythm strip!

Figure-1: Details and my proposed laddergram for today's initial ECG (See text).

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I found the rhythm in today's initial tracing serves as a "treasure chest" of advanced arrhythmia concepts for readers who love deciphering intricate rhythms.

• NOTE: For readers who prefer "Just the basics" — Knowing there is sinus bradycardia with clearly abnormal ST-T wave morphology in both wide and narrow beats, that is consistent with the acute OMI proven on cath — is all that is needed for appropriate clinical management.
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• BUT — For Arrhythmia Lovers: Are YOU up for the challenge identifying the fascinating features included in this initial tracing?

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In Figure-1 — I've labeled the long lead V1 rhythm strip with arrows, interval measurements — and my proposed Laddergram.

• RED arrows highlight a fairly (but not completely) regular sinus rhythm, consistent with sinus bradycardia and arrhythmia (given this P-P interval irregularity — and an overall atrial rate below 60/minute).
• As noted by Dr. Frick — there are 2 principal QRS morphologies, which is why this rhythm is so intriguing. That said — We know that beats #1,7,8 are each sinus-conducted — because each of these beats is preceded by the same normal PR interval (of 0.18 second) — and each of these beats manifest a narrow and normal appearing rS morphology, as expected in a lead V1.
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• However — None of the other RED-arrow P waves on this tracing manifest normal sinus conduction (Not even the P waves preceding beats #2 and #6 — because the PR interval preceding these 2 beats is clearly less than the 0.18 second that sinus-conducted beats #1,7,8 tell us is needed for normal AV conduction).
• Instead — Beats #3,4,5 all appear to be arising from some type of lower level pacemaker — because the QRS complex of beats #3,4,5 is clearly wider than the QRS of pure sinus-conducted beats #1,7,8 — and — the R-R interval preceding beats #3,4,5 is identical ( = 1160 msec.).
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• KEY Point: The above 2 bullets tell us there is transient AV dissociation — because despite on-time sinus P waves (ie, the consistent RED arrows in Figure-1) — the P waves near beats #3,4,5 are clearly not conducting. 
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• Subtle-but-Important Point: Although the PR interval preceding beats #2 and 6 is shorter than the 0.18 second PR interval needed for normal sinus conduction — this PR interval is long enough to allow some penetration of these sinus P waves into the ventricles. And, the R wave of beats #2 and #6 is not quite as tall as the R wave of beats #3,4,5. I therefore believe that beat #2 (and probably also beat #6) are Fusion beats! (I've labeled beat #2 with an "F").
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• PEARL: The clinical importance of identifying fusion beats — is that this proves that a component of the QRS complex that we see for beats #2 and 6 is arising not from the AV node (which is a supraventricular structure) — but from the ventricles (ie, Fusion of QRS complexes does not occur from simultaneous depolarization of sinus and AV nodal beats). CLICK HERE — for more on fusion beats.
• That beats #2 and 6 are in part ventricular in origin, and arising from the same lower level escape pacemaker as are beats #3,4,5 — is supported by the similar QRS morphology and identical preceding R-R interval of these 5 beats (ie, Each of these 5 beats is preceded by an R-R interval of 1160 msecs.).
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• Dr. Frick has alluded to where the site of ventricular escape beats #2,3,4,5 and 6 is likely to arise. These QRS complexes are wider than normal, but not overly wide — and they manifest RBBB morphology (as seen by beats #5 and 6 in lead V1) and LPHB morphology (as seen by the rS complex with very deep S wave in lead I — and the predominant R waves in leads II,III) — which defines these ventricular escape beats as arising from a site in the fascicles.
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• PEARL: My easy way of deriving which of the 3 fascicles (the slender right bundle branch = RBB — and the left anterior and left posterior hemifascicle = LAH and LPH) is the site of the escape focus — is that the site is whichever of the 3 fascicles is not suggested on ECG.
• In simple words — Since escape beats in Figure-1 manifest RBBB/LPHB morphology — the site of ventricular escape must be in the LAH ( = Left Anterior Hemifascicle).
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• To Emphasize: Fascicular beats are ventricular beats — that are usually not as wide as other forms of ventricular escape rhythms that do not arise from a part of the conduction system. Given the R-R interval = 1160 msecs. between each of the fascicular escape beats in Figure-1 — the rate of this escape rhythm (ie, which is a bit faster than 50/minute) — is probably slightly accelerated, compared to a typical ventricular escape rate (which generally is between 20-40/minute) — suggesting that the Fascicular Rhythm that we see in today's tracing may be consistent with a form of AIVR (Accelerated IdioVentricular Rhythm) — which often appears a "reperfusion" arrhythmia following an acute OMI (For more on AIVR — See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's ECG Blog).

Finally — I always like to try to determine WHY an escape rhythm arises. Looking at the intervals that I carefully measured in Figure-1:

• The sinus rate is slower at the beginning of the long lead V1 rhythm strip (ie, P-P intervals of 1230, 1240 and 1220 msecs. for the first 3 beats in this tracing). This clearly provides a "space" for the slightly accelerated fascicular rhythm to emerge (ie, R-R intervals of 1160 msecs. preceding each of the fascicular beats — indicating a faster rate for the escape rhythm compared to the sinus bradycardia).
• This changes toward the end of the long lead rhythm strip, as the P-P interval drops below the 1160 msecs. R-R interval of the escape rhythm after beat #4 — allowing sinus "capture" for the last 2 beats on the tracing.
• NOTE: The above said — the rate of sinus bradycardia once again slows after beat #7 (P-P interval = 1210 msecs.) — so I would expect return of the fascicular escape rhythm IF monitoring would have been continued beyond beat #8.
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• As a last observation — the fluctuating intervals with nearly comparable P-P and R-R duration for sinus beats and fascicular escape in parts of today's tracing bears resemblance to the entity known as isorhythmic AV dissociation — in which the manner that these P-P and R-R intervals vary does not always follow the textbook — which may explain some of the difficulty predicting when the fascicular rhythm arises in today's tracing (For more on isorhythmic AV dissociation — Please see My Comment at the bottom of the page in the May 24, 2020 post in Dr. Smith's ECG Blog).