Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

I came across this post from 2015 while answering a question on Twitter, and decided to repost it:

http://hqmeded-ecg.blogspot.com/2015/12/syncope-shock-av-block-large-rv.html

Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

An elderly male had a syncopal episode.  911 was called.  When medics arrived, the patient was alert and following commands.  In the presence of the medics, he lost consciousness and became apneic and underwent 30 seconds of chest compressions, after which he started moaning and was again able to communicate and follow commands.   No shock was ever delivered.

A 12-lead was recorded:

Without a rhythm strip, this rhythm is difficult.  In any case, there is bradycardia.  There is either RBBB (see rSR' in V1) or there is a left sided escape rhythm that gives RBBB morphology.
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia.  There is no ST elevation.

The patient was moaning upon arrival to the ED, looked ashen, and had agonal respirations.  He was unresponsive to painful stimuli.

He was in profound shock.

He was intubated.

A bedside cardiac ultrasound was recorded:

If this video does not work, you can view it here: https://vimeo.com/148133345

Here is a still image of the echo:

The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber.
What do you think?

There is no pericardial fluid to account for shock.  The RV is huge.  This essentially rules out hypovolemia as the etiology (no GI bleed, no ruptured AAA, etc.).  It makes pulmonary embolism (PE) very likely.  It also makes large right ventricular infarct possible, but much less likely than PE.  The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure.  RV pressure appears to be high (large RV), so there is obstruction between the RV and LV (PE).

Alternatively, the RV is so ischemic as to be unable to generate high pressures (RVMI).  This is much less likely than PE.

Along with supportive cares, this first ED ECG was recorded:

What do you think?

Annotated with arrows:

The arrows show what I believe are P-waves.  So this is third degree AV block.  There is a wide QRS, so there is infra-HIS escape.  It is RBBB morphology (left bundle escape).
There is obvious ischemic ST elevation in V1-V3, maximal in V1.
There are slightly large T-waves inferior, with ST depression in aVL

What is going on?

First, what kind of arrest was this?  It was a PEA or bradyasystolic arrest, not a shockable rhythm.  There is 3rd degree heart block.  Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI.

Second: what does the ultrasound tell us about the condition? Is this an anterior (LV) MI?  No!          --The large RV and small LV on ultrasound make this a right ventricular process.  A standard anterior MI would have a large LV with poor function, not a small LV.  This LV is not filling.

Third: what does the ECG tell us about the left ventricle?  The STE is anterior, but is it anterior LV or anterior RV????   LV anterior STEMI does not give maximal ST elevation in V1.  So this ECG is typical of right ventricular (RV) STEMI.

Fourth:   RV STEMI is almost always accompanied by profound inferior STEMI.  Though there is some evidence of this in inferior leads, it is not convincing.

          Therefore, the ultrasound looks like PE, and the location of the ST elevation tells us that it is an RV STEMI (which manifests in "anterior" leads, as they overlie the anterior RV).  But it does not tell us whether this RV STEMI is due to type 1 MI (plaque rupture with thrombus) or due to type 2 MI (severe hypotension and increased RV pressure prevents RV perfusion)

Fifth: the ultrasound in RV MI can look identical to that of PE: there can be both McConnell's sign and "D" sign, as well as enlarged RV with poor function.

Sixth:  Severe shock (e.g., due to PE) may result in STEMI (and, if anterior, it can be from anterior LV or anterior RV ischemia, or both) from low coronary pressure and flow, simply due to the shock.  Here we have evidence of massive RV dysfunction.

Seventh: When the severe shock that is the etiology of STEMI is due to PE, the ST elevation likely reflects the RV, as there is both: 1) very low coronary flow in the RV marginal branch (due to BOTH low blood pressure AND due to high RV pressure), and high oxygen demand (increased volume increases wall stress and increased oxygen demand) leads to very low supply and high demand leads to subepicardial ischemia and ST Elevation.

Eighth: STEMI even if from low flow, not ACS, can cause ischemia of the conduction system and result in complete AV block, even infra-HIS AV block.

Ninth: Type II MI can be exacerbated by fixed coronary stenoses.  It may be that there is a stenosis of the proximal RCA, but it need not be thrombotic for this situation to cause extreme ischemia.  There need not be any stensosis at all.

All of this favors PE with resulting RV STEMI, but initiated by PE.

Summary:
1.  If this had been a shockable rhythm, STEMI would be most likely.  But it is bradyasystolic, so pulmonary embolism must be high on the differential.
2.  The echo shows that, if this is MI, it is most likely an RV MI.  It is not an (LV) anterior MI.
3.  The ECG also shows RV MI, not LV anterior MI
4.  So is this an isolated RV MI with shock?  Possible, but huge pulmonary embolism is more likely.

In a patient with such a differential diagnosis, and in profound shock, near death, the treatment is IV thrombolytics.  A 1/2 dose (50mg) of full dose (100 mg) bolus may be given when the patient is in extremis as this patient is.

Such isolated RV STEMI is rare, but pulmonary embolism is not.  Thus, this is most likely pulmonary embolism, not STEMI.  However, thrombolytics will treat both.  

Lytics are very effective early in the course of STEMI.  

Moreover, their use of lytics does not precluded subsequent angiography and PCI if this turns out to be RV STEMI.

Clinical course

The clinicians thought this was LV STEMI due to the "anterior" ST elevation.  The cath lab was activated.  In the cath lab, the coronaries were clean.  Pulmonary embolism was suspected a right side cath with pulmonary angiogram confirmed it.


Here is the left pulmonary artery

If this video does not work, you can view it here: https://vimeo.com/149178077

There is extensive clot in the main pulmonary artery

Here is the right pulmonary artery

If this video does not work, you can view it here: https://vimeo.com/149178152

Less thrombus here

Catheter-Based thrombectomy was undertaken.

Here is the post thrombectomy angiogram:

If this video does not work, you can view it here: https://vimeo.com/149178129

There is now good flow in both trunks.

Unfortunately, the patient was too ill to survive.

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MY Comment by KEN GRAUER, MD (9/25/2020):

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Brilliant explanation by Dr. Smith on this tremendously challenging case! I limit my comments to some advanced points regarding interpretation of the 2 ECGs shown in this case.

• For clarity — I’ve reproduced these 2 tracings in Figure-1.
• NOTE: Management of this case is not affected by the advanced points I make. My purpose is solely academic to highlight some additional observations in the hope of enhancing ECG interpretation.

Please Take ANOTHER LOOK at the 2 ECGs in this case.

• Is there evidence of atrial activity?
• Are there any sinus-conducted beats in either tracing?
• Does ECG #1 portend what happens in ECG #2?

Figure-1: The 2 ECGs in this case (See text).

I will again emphasize the brilliant problem-solving discussion of this case by Dr. Smith. As deduced by him (and confirmed by cath + pulmonary angiogram) — the primary event appears to have been a massive pulmonary embolism. The resultant severe shock led to RV MI with ischemic-induced conduction defects that proved too great for this elderly man to overcome.

The Rhythm in ECG #1: As per Dr. Smith — interpretation of the cardiac rhythm is ECG #1 is all but impossible in the absence of a simultaneously-recorded long lead rhythm strip. I fully acknowledge that I am in no way certain of the rhythm. Nevertheless, a number of observations can be made:

• There is atrial activity! The 4 RED arrows in lead I of Figure-2 identify similar-looking low amplitude, notched deflections at an almost-regular rate. I believe these are real — and identify atrial activity. These may not be P waves arising from the SA node, because the deflections we see in lead II are smaller than those highlighted by RED arrows in lead I.
• YELLOW arrows highlight what looks to be atrial activity in other leads — but amplitude is low and morphology inconsistent.
• The QRS complex is wide in ECG #1 — with morphology consistent with a RBBB pattern (rSR’ complex in lead V1 + wide terminal S waves in lateral leads I and V6). The overall ventricular rhythm is fairly regular at 60-65/minute.
• At the least — there appears to be high-grade 2nd-degree AV Block — as many of the deflections thought to be P waves are not conducted, and the PR interval preceding QRS complexes seems to be constantly changing.
• Two of the clues that I commonly look for when trying to distinguish between high-grade vs complete AV block are: i) Do any QRS complexes occur unexpectedly early? (which often indicates that such early beats are conducted); and, ii) Does QRS morphology change, with this change not being due to a premature beat? (ie,Such a change often signals that some beats are being conducted). None of the beats in ECG #1 occur unexpectedly early in ECG #1. The QRS complex of 2 of the beats in ECG #1 do look different (ie, beats #1 and 3) — but I’m hard pressed to know what (if anything) this means. Lead aVF makes one think beats #4 and 5 are conducted — but potential atrial deflections in other leads are not consistent with this.
• BOTTOM Line: I do not know what the rhythm in ECG #1 is. And, we lack a long lead rhythm strip. I think there is clearly some atrial activity — which is probably not conducting. I suspect at the least there is high-grade AV block with a fairly regular left bundle branch escape rhythm.

About ST-T Wave Changes in ECG #1: It is clearly more difficult to assess ST-T wave morphology for changes of ischemia when the QRS complex is wide. That said — since the escape focus in ECG #1 appears to be in the bundle branch system, we can often see ischemic ST-T wave changes.

• As I noted above — QRS morphology in ECG #1 is typical for RBBB (rSR’ complex in lead V1 + wide terminal S waves in lateral leads I and V6). What is not typical for simple RBBB — is the shape of the ST segment in each of the chest leads.
• With simple RBBB — one should not see ST segment coving — as highlighted by the curved RED lines in leads V1-thru-V5 of ECG #1.
• T wave inversion with simple RBBB is deepest in lead V1 — not in leads V2-thru-V4, as shown in ECG #1.
• Marked J-point depression (as is seen in leads V4, V5 and V6 in ECG #1) is not part of simple RBBB.
• The angled shape of the ST segment depression in lead V6 is clearly abnormal (RED lines in V6).
• Finally — with simple RBBB, the ST segment should be slightly depressed below the baseline in lead V1. The inverted T wave that we see in lead V1 of ECG #1 is an expected finding of RBBB — but the coved ST segment in lead V1 lies clearly higher than it should! Shortly thereafter, ECG #2 was obtained — and we now see the coved anterior ST segments from ECG #1 have evolved into marked ST elevation in leads V1-thru-V3.

Figure-2: I’ve labeled the 2 ECGs in this case — and added a laddergram for the 2nd tracing (See text).

The Rhythm in ECG #2: As per Dr. Smith — the long lead II rhythm strip in ECG #2 now shows consistent, regular deflections that clearly look like sinus P waves at ~48/minute (PURPLE arrows).

• There once again are regular, wide QRS complexes for the first 8 beats that manifest a very typical RBBB pattern.
• None of the P waves (PURPLE arrows) appear to be conducting during these first 8 beats in ECG #2.
• The R-R interval for ventricular beats is just under 6 large boxes in duration — which corresponds to a ventricular rate of ~52/minute. Given the typical RBBB pattern of these ventricular beats — the escape focus again seems to be in the left bundle branch.

Did YOU notice at the very end of the long lead II rhythm strip in ECG #2 that the QRS complex for the last beat ( = beat #9) looks different? IF you measure with calipers — beat #9 occurs ever-so-slightly EARLIER than the 8 different-looking QRS complexes that precede it.

• The reason beat #9 looks different and occurs slightly earlier compared to the R-R interval for the 8 beats that precede it — is that beat #9 is conducted! Note that the PR interval preceding beat #9 is different (shorter) than the PR interval preceding each of the 8 beats before it that were not conducted.
• Therefore — there is AV dissociation by “default” (ie, due to sinus bradycardia) — but the rhythm in ECG #2 is not complete AV block, because when a P wave does occur at the “right time”, it can conduct. How severe the AV conduction disturbance is can not be determined solely from the rhythm we see in ECG #2. Alas, the cause of this patient’s demise was not a result of his conduction disturbance.

Our THANKS again to Dr. Smith for his superb problem-solving analysis. Bradyasystolic arrest from massive pulmonary embolism portends an ominous prognosis. Unfortunately, nothing could save this patient.