Thursday, September 24, 2020

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:

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.



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

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

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

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); andii) 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.




Wednesday, September 23, 2020

A woman in her 60s with chest pain and prominent J waves

Case submitted by Dan Singer MD and Ryan Barnicle MD, Written by Pendell Meyers

A woman in her 60s with history of smoking presented to the ED with left sided chest pain radiating to the left arm and back, starting at about 1330. She described the pain as a "heaviness," without exacerbating or alleviating factors. Her pain at the time of arrival was 10/10.

Here is her triage ECG (no prior for comparison):

What do you think?







Findings:

 - Sinus rhythm at around 100 bpm

 - Grossly normal QRS complex

 - 1.0 mm STE in lead III, and just a hint of STE in aVF (both of which have to be measured just after significant J waves)

 - STD and T wave inversion in lead I and aVL

 - A suggestion of almost STD in V2, with negative T wave in V2


Interpretation:

Diagnostic of inferior (and likely also posterior) STEMI(-) OMI. Although J waves (J-point notching) are usually considered a morphologic feature that makes STE less likely to be due to OMI, we have many examples of OMI with J waves on this blog (just like every other ECG rule of thumb you've ever learned). If the inferior leads were viewed in isolation, I would be suspicious of the volume underneath the T waves especially in lead III, but I would not be 100% certain that they are hyperacute. However, lead aVL solves the case as usual, confirming inferior OMI: lead aVL has a narrow normal QRS complex followed by STD and large-volume T wave inversion. Lead aVL makes STE and T waves in lead III extremely likely to be due to OMI. The slight STD and T wave inversion in V2 support the diagnosis as these very likely represent posterior extension. Notice also that there is reciprocal STE in aVR (this is very slight and to some extent is due to baseline wander).

These findings were immediately recognized by Drs. Singer and Barnicle, and the cath lab was activated.

The cardiologists agreed with their concern and took the patient immediately to the lab (long before the first troponin T would return positive at 0.24 ng/mL). Despite the fact that it does not meet STEMI criteria, the cardiologists interestingly documented it as a STEMI (some people who have no other way to express the concept of OMI simply use the word "STEMI" incorrectly in place of the concept of OMI).

They found complete (TIMI 0) thrombotic occlusion of the OM1, opened successfully with one stent.

Before intervention: OM1 occlusion in center image 


Before intervention: occlusion annotated



After intervention: full course of the OM1 running from center screen to bottom right corner.



6 hours later the troponin peaked at 4.26 ng/mL.

Echo noted EF 50% with sever hypokinesis of the anterior, lateral, and apical walls.

Here are two ECGs taken soon after cath, then the next day:







Soon after intervention, showing almost complete resolution of inferior STE and reciprocal findings in aVL. Interestingly, there are no longer any J waves in this ECG except lead V6.


Next day, showing resolution of inferior and high lateral findings. The J waves have started to return in leads II, III, and aVF.




 
The patient did well.


Learning points:

No single rule of thumb can be trusted in isolation in ECG interpretation.

J waves are most commonly seen in the setting of normal variant STE, but can also be seen in OMI.

Lead aVL is invaluable for interpretation of inferior OMI.

Expert ECG interpretation leads to faster identification and reperfusion of OMI than STEMI criteria.




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

MY Comment by KEN GRAUER, MD (9/23/2020):

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

I thought this was a fascinating case for a number of Reasons!

  • Reason #1: Drs Singer, Barnicle and Meyers all diagnosed acute OMI primarily on the basis of the reciprocal ST-T depression in lead aVL — rather than by ST elevation in the inferior leads. Most often with OMIs, our attention is captured by that lead area that shows ST elevation rather than ST depression.
  • Reason #2: This case illustrates the concept of “inter-cardiologist variation in terminology”. As per Dr. Meyers — Despite not satisfying “millimeter-criteria” for a STEMI — the cardiology team documented this case in their notes for the record as a “STEMI”, perhaps because they promptly decided to take the patient for emergency catheterization. Although I am GLAD the cardiology team appropriately intervened with prompt cath and PCI (complete occlusion of the 1st-Obtuse Marginal branch of the LCx was found) — the optimal terminology (as per Dr. Meyers) should have been to call this an OMI ( = Occlusion-based MI, not clearly satisfying STEMI criteria). As we’ve shown many times on Dr. Smith’s ECG Blog — different cardiologists tend to define acute coronary syndromes using different terminology. The terminology that should count is being able to recognize acute occlusion of a major coronary artery — regardless of whether or not millimeter-criteria for a STEMI are met (SEE My Comment in the July 31, 2020 post on Dr. Smith’s ECG Blog).
  • Reason #3: The prominent J waves seen in multiple leads in the initial ECG for this case evolve over the course of the 3 serial ECGs that are presented. I would call these Osborn waves — and they provide a significant clue, not only to active ischemia — but also to potential risk of developing malignant ventricular arrhythmias! ( = another reason it was fortunate that this patient was catheterized and reperfused so promptly!).


For clarity and EASE of viewing — I have reproduced the 3 ECGs in this case in Figure-1.

  • WHAT changes do YOU see occurring over the course of these 3 tracings?


Figure-1: The 3 ECGs in today’s case (See text).




MY Thoughts on ECG #1: As per Dr. Meyers — the diagnosis of acute OMI in the initial ECG ( = ECG #1would have been equivocal based on the ST-T wave appearance in the inferior leads. That’s because there is only 1 mm of ST elevation in lead III — no more than a “hint” of ST elevation in lead aVF (when one discounts the J wave) — and no ST elevation at all in lead II.

  • Dr. Meyers highlights the abnormal appearance in ECG #1 of lead aVL (which shows ST depression and large-volume T wave inversion) as the KEY for strongly suggesting OMI.
  • While I completely agree with Dr. Meyers’ assessment — it’s helpful to remember that sometimes the T wave in lead aVL may be negative not due to ischemia, especially when the QRS complex is not predominantly positive (as seen here).
  • PEARL #1: I’d add that in addition to lead aVL — it is the ST-T wave appearance in lead I of ECG #1 that convinced me 100% that something acute was actively ongoing in this 60-something woman with new-onset chest pain. The straightening (flattening) of the depressed ST segment in lead I is unmistakable — and combines with the ST-T wave appearance in lead aVL to remove any doubt about the acute nature of what we see in the inferior leads.



Dr. Meyers also highlighted the presence of significant J waves in ECG #1.

  • Did YOU notice WHAT HAPPENS to these prominent J waves over the course of the next 2 ECGs that were done? (Figure-1).


OSBORN Waves: The Osborn wave has been described as a deflection with a dome or hump that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are exaggerated “J waves” or J-point waves. They’ve also been called the “camel-hump” sign.

  • First described in 1953 (by Dr. John Osborn) — these Osborn waves are most commonly associated with significant hypothermia (usually not seen until core temperature is below 90°F).
  • PEARL #2: It is important to appreciate that other conditions may also be associated with this prominent J-point deflection. Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI (SEE My Comment in the November 22, 2019 post on Dr. Smith’s Blog).
  • Rituparna et al describe an interesting case in which the most notable initial ECG change in a patient with acute coronary occlusion was development of localized and prominent J waves (Pacing Clin Electrophysiol 30[6] 817-819, 2007). They acknowledge the paucity of data in the literature regarding the occurrence of J waves as a result of acute ischemia — and they go on to propose development of a transmural voltage gradient during the early phases of ischemia as the mechanism for ischemic-induced J waves. With persistence of ischemia — J waves disappear and/or are integrated into the more typical acute infarction sign of ST elevation.
  • PEARL #3: Rituparna et al — as well as Chauhan and Brahma (Int. J. Crit. Illn. Inj. Sci 5[4] 268-270, 2015) both highlight a likely association between acute development of ischemic J waves — and high risk of developing malignant ventricular arrhythmias. Fortunately, the patient in today’s case was promptly catheterized and reperfused before malignant arrhythmias developed.


Figure-2: I've labeled J waves for the 3 ECGs in today's case (See text).






The Evolution of J Waves in Today’s Case:

To facilitate recognition of J waves in today’s case — I drew a vertical RED line up from where the most prominent J wave was seen in the initial ECG (See Figure-2). This identifies the precise location of J waves in the simultaneously-obtained long lead V1, that corresponds to the timing of J waves in other leads (as per the vertical BLUE lines that I drew for the other lead groupings).

  • The RED arrow in lead III of ECG #1 highlights the most prominent J wave in this initial ECG.
  • BLUE arrows in ECG #1 highlight other notable J-point deflections.
  • GREEN arrows in ECG #1 highlight negative notching that I thought looked unusual (ie, it looks like there is a 4-phase complex = rSr’s’ in lead V1 — and I don’t remember the last time I saw a qrs complex in lead aVL of the shape like the one we see in ECG #1).
  • NOTE: I would have loved to see a baseline tracing on today’s patient — to determine IF all J points (and if the other unusual notching) were new findings in today’s initial ECG.
  • KEY Point: Shortly after the cardiac catheterization (ie, shortly after reperfusion by PCI) — Note how 5 of the 6 leads that had manifested J waves in ECG #1 no longer do so in ECG #2! Note especially that despite virtually no change in QRS morphology or axis in the 6 limb leads — those overly prominent J waves that were seen in leads III and aVF in ECG #1 have disappeared.
  • As a “side note” — the extra negative terminal notch in lead V1 of ECG #2 has resolved (perhaps buried within the slurred S wave in V1). We still see that terminal negative notch in lead aVL (GREEN arrow in ECG #2).
  • Finally, in ECG #3 — those terminal negative notches in leads aVL and V1 are gone. There now is a J point in lead I — and hint of terminal QRS slurring (GREEN arrows in ECG #3) — but clearly, there is a notable reduction in J wave presence following acute reperfusion of the occluded coronary artery.


BOTTOM Line: Even without a baseline tracing on this patient — the fact that J wave prominence promptly diminished following acute reperfusion in this patient to me suggests that the prominent J waves in this case were an important manifestation of the acute ischemic process.

  • While clearly not common to see new development of prominent J waves as a manifestation of acute ischemia — it is good to be aware of this possibility. Appreciation of this potential relationship between new prominent J waves and OMI may sometimes serve as an important early marker of acute coronary occlusion.
  • As noted earlier — recognition of this unusual ECG finding takes on added importance given its predictive value for increased risk of impending malignant arrhythmias.



Monday, September 21, 2020

Interventionalist at the Receiving Hospital: "No STEMI, no cath. I do not accept the transfer."

Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? Yes. We don't know how many though.

I was texted these ECGs by a recent residency graduate after they had all been recorded, along with the following clinical information:

A 50-something with no cardiac history, but with h/o Diabetes, was doing physical work when he collapsed. He was found in ventricular fibrillation and defibrillated, then brought to a local ED which does not have a cath lab.

Here is the initial ED ECG:

This is pretty obviously and inferior posterior OMI, right?
There is slight inferior ST Elevation, with reciprocal ST depression in I & aVL, and an inverted T-wave.
There is deep ST depression in V2-V4, also with an inverted T-wave.
There is slight ST elevation in V5 and V6.
This is diagnostic of an infero-postero-lateral OMI

Some claim that posterior MI always has an upright T-wave (along with ST depression) in V2-V4;  THIS IS FALSE.  It may be inverted or upright or biphasic during the acute phase.

This right sided ECG was recorded about 30 minutes after the first:

V1R here = V2
V2R = V1
V3R is further right, etc.
There is no right sided STE
V1 and V2 have substantially less ST depression.  There may be some spontaneous reperfusion.
There is no STE in right sided leads -- no RV OMI


This ECG, in which V4-V6 are on the posterior thorax (V7, V8, V9) was recorded 2 hours later:

First, notice that the ST depression in V2 and V3 is almost all gone now.
So you would not expect there to be ST Elevation in V7-V9!!
For a posterior ECG to enlighten the standard ECG, they must be recorded at the same time.
Notice:
1) inferior leads no longer show OMI; there has been reperfusion
2) V2 and V3 have only minimal ST depression, further supporting reperfusion
3) The T-waves in V2, V3 are now upright and large.   This is what is to be expected when there is reperfusion of the posterior wall.  See discussion below of "posterior reperfusion T-waves"
4) V7-V9 have T-wave inversion, which further supports reperfusion of the posterior wall.

Case Continued

The emergency physician was worried about OMI. He called the interventionalist at the receiving institution.  This is the response he got:

Interventionist: "No STEMI, no cath.  I do not accept the transfer."

After stabilizing the patient and recording more ECGs, he tried again:

Interventionalist: "It isn't a STEMI."

Emergency physician: "I know. It is a STEMI equivalent.  He was occluded and now he has reperfused."

Interventionalist: "We don''t cath these patients. And we wouldn't do it tomorrow either."

The troponin I rose to 33 ng/mL, which is a typical level for STEMI/OMI.  He was treated medically for ACS and did not get an angiogram within 72 hours.  Then he did not awaken after 72 hours, so was put on comfort cares.  But until that point, no one could have known his neurologic outcome, and the stated reason for not accepting was not worry for neurologic outcome but that the ECG did not meet STEMI criteria.


Commentary

Pendell and I just did a study of the ECG in OMI, and submitted the manuscript to JACC.  I read over 4000 EKGs on 808 patients, many with OMI, many with Non-OMI, and many with MI ruled out (MIRO).

I read serial ECGs and, with each read, would decide "OMI" or "Not OMI" (both NOMI and MIRO were "Not OMI").  Many had serial ECGs; for each patient, after reading and interpreting ECG-1, and moving on to ECG-2, and -3, and -4, etc., I was unable to go back and change my read of each preceding ECG. I would also measure the ST segments and determine if it was a STEMI by millimeter criteria (as outlined in the 4th Universal Definition of MI), or OMI without STEMI.  The outcome measure was whether the patient ultimately had an OMI or not.  The details of the methods and results are of course complex, and you will see them when the paper is published, but suffice it to say that STEMI criteria were about 40% sensitive for OMI and my interpretation was about 90% sensitive (and equally specific), and I interpreted OMI a mean of 3 hours before the ECG which the treating clinicians determined was positive.  Pendell read about a third of the ECGs, and his results were the same.    

The cardiology reviewers said that "No one strictly follows STEMI criteria. The 4th universal definition mentions ST depression, posterior MI, and T-wave changes."  And the article was rejected.

There is no literature, to my knowledge, of how cardiologists and interventional cardiologists interpret the acute MI guidelines in the 4th Universal Definition of MI.  But anectotally, many follow the millimeter STEMI criteria strictly.   This blog is full of cases in which OMI that did not meet STEMI millimeter criteria were dismissed.

Posterior Reperfusion T-waves

Why do T-waves in V2 and V3 become large with reperfusion? Answer: Vectors.  1) The anterior wall has positive T-wave vectors (pointing anterior).  2) The posterior wall now has a negative T-wave vector (pointing posterior), which is the same as having a positive vector towards anterior leads.  So both vectors add up and result in abnormally large upright T-waves in V2 and V3!

I discovered this years back and call it "Posterior Reperfusion T-waves".  We studied it and wrote this paper: Driver BE. Shroff GR.  Smith SW. Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall.  

Here are a few examples of posterior reperfusion T-waves: 

A middle aged man with ST depression and a narrow window of opportunity



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MY Comment by KEN GRAUER, MD (9/21/2020):

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I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would begin reading Dr. Smith’s ECG Blog. IF they don’t — they will continue to overlook obvious OMIs that deserve to undergo prompt cardiac catheterization for optimal care.

  • The posterior wall of the LV is not directly viewed by any of the 12 leads on a standard ECG. Posterior leads (ie, leads V7, V8, V9) — have been suggested as a way to enhance ECG visualization of the posterior wall. With acute posterior MI — these posterior leads will sometimes manifest ST elevation not seen on the standard 12 leads.
  • CAVEAT: The amount of ST elevation you are likely to see with posterior leads in acute posterior MI is limited. As a result, the diagnostic utility of posterior leads is (in my experience) limited.


Suggested SOLUTION: Rather than taking the extra time to obtain another ECG with posterior leads (that at best — provides limited information) — GET GOOD at using the Mirror Test as an aid for recognizing acute posterior MI.

  • The Mirror Test is a simple visual aid: It helps the clinician recognize acute posterior infarction. It is based on the premise that the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the “mirror-image” of leads V1, V2, V3.
  • I’ve previously discussed clinical application of the Mirror Test on several occasions (SEE My Comment at the bottom of the page in both the September 13, 2020 post and the February 16, 2019 post in Dr. Smith’s ECG Blog).
  • As we will see momentarily — Use of the Mirror Test makes it difficult to understand HOW a cardiologist could look at the initial ECG in this case and fail to recognize acute OMI.


TODAY’s CASE: The patient in today’s case is a 50-something man who suddenly collapsed — and was found to be in VFib. The patient was defibrillated, and then taken to the nearest ED where ECG #1 was obtained (Figure-1).

  • As per Dr. Smith — there are obvious findings on this initial ECG that are diagnostic of acute OMI.


Figure-1: The initial ECG in the ED — as well as the 3rd tracing shown above, in which leads V4, V5 and V6 are replaced by posterior leads V7, V8 and V9. Mirror-image views of leads V1, V2 and V3 are shown to the right of each tracing (See text).



MY Thoughts on ECG #1: The rhythm is sinus tachycardia at 105-110/minute. The PR and QRS intervals are normal. The QTc looks somewhat prolonged — although this is difficult to assess given the increased rate. The frontal plane axis is normal at +70 degrees. There is no chamber enlargement. Regarding Q-R-S-T Changes for ECG #1:

  • There is a single small and narrow Q wave in lead III. This is of uncertain significance.
  • R wave progression shows normal transition, which occurs between leads V3-to-V4. Of note (and of significance) — the R wave becomes fairly tall (~7 mm) as early as in lead V2 (More on this in my discussion below).


Regarding ST-T Wave Changes:

  • The most remarkable finding in ECG #1 is the dramatic ST-T wave depression. This begins in lead V1 — and becomes marked in leads V2, V3 and V4.
  • Other ST-T wave changes in this tracing are more modest. There is slight ST elevation in lead III — reciprocal ST-T depression in leads I and aVL — and slight ST elevation in lead V6.


Using the Mirror Test in ECG #1:

  • To facilitate recognition of the clinical significance of the ST-T wave depression in leads V1-thru-V3 of ECG #1 — I’ve placed the mirror-image of these leads to the right of ECG #1 (Figure-1). Keep in mind that the mirror-image of these anterior leads gives us a picture of the electrical activity occurring in the posterior wall of the LV.
  • ISN’T the mirror-image view of these anterior leads for ECG #1 all but screaming out, “I’m having an acute posterior OMI” (ie, large Q waves with hyperacute and markedly elevated ST segments)?
  • Although I did not make a mirror-image of lead V4 from ECG #1 — it should be apparent that an inverted lead V4 would look virtually the same as inverted leads V2 and V3 do in the mirror-image view.
  • Returning to my comment above regarding R wave progression in ECG #1: — The rapid development of a surprisingly tall R wave as early as in lead V2 “becomes” a Q wave in the mirror-image view.
  • LEARNING Point: Maximal ST depression in leads V2-thru-V4 (especially when the ST-T waves are shaped as they are in ECG #1) in a patient with new chest pain (or sudden cardiac arrest, as in today’s case) — is diagnostic of acute Posterior OMI until proven otherwise!


Continuing with TODAY’s Case: The 1st tracing in this case to look at posterior leads was ECG #3, obtained 2 hours after ECG #1. As per Dr. Smith: For posterior leads to enlighten interpretation of the initial ECG — “they must be recorded at the same time”That said — several important points can still be made about ECG #3:

  • Note how small the amplitude of QRS complexes and ST-T waves in leads V8 and V9 of ECG #3 are. Even though this tracing was obtained 2 hours after ECG #1 — it would seem almost certain that the amplitude of ST-T wave changes in these posterior leads would not be nearly as large as we see for the amplitude of ST-T wave changes in the mirror-image of leads V1, V2, V3 for ECG #1. Posterior leads are not needed to make the diagnosis of acute posterior OMI in ECG #1.
  • Dr. Smith emphasized that the tall, upright T waves in leads V2, and especially in lead V3 of ECG #3 reflect reperfusion changes. AREN’T these reperfusion changes in ECG #3 much EASIER to visualize (and conceptualize) from the mirror-image view of leads V1, V2 and V3 seen to the right of ECG #3?
  • Dr. Smith also emphasized that the T wave inversion in leads V8 and V9 of ECG #3 provides another indication of acute reperfusion. Comparing the depth of the T wave inversion of leads V8 and V9 in ECG #3 — with the depth of the T wave inversion in the mirror-image view of leads V1, V2, V3 for ECG #3 — ISN’T it much EASIER to visualize (and conceptualize) these ECG changes of acute reperfusion from the mirror-image view? ST-T wave changes that are seen in posterior leads are generally much smaller in amplitude than ST-T wave changes seen in the mirror-image view for leads V1, V2 and V3.


BOTTOM Line from Today’s Case: It is hard to justify the decision by cardiology not to cath the patient in today's case because the ECG “did not show a STEMI”.






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