A woman in her 60s with 6 hours of chest pain, dyspnea, tachycardia, and hypoxemia

 Case submitted and written by Anonymous, with edits by Meyers and Smith

A female in her 60s presented with an ache in her chest that woke her from sleep six hours prior to arrival and was accompanied by dyspnea.
Her vitals on arrival to the ED were:
RR 26
BP 141/102
HR 120
SpO2 91

No prior ECGs were available. Here is her first ECG recorded (during ongoing pain and dyspnea):

What do you think?

With just a glance RBBB and LAFB are evident, a combination which can commonly represent acute LAD occlusion in the setting of ACS and a sick patient, even without obvious ST segment deviations.

Meyers side note:

The RCA usually supplies the SA and AV nodes, while the LAD usually supplies the bundle branches. When LAD occlusion results in ischemia to the bundle branches, the most common order of acute fascicle dysfunction is: right bundle branch block, left anterior fascicular block, and finally left posterior fascicular block (likely because the RBB and the LAF are located in the anterior septum, supplied by the LAD, for a longer course than the LPF which must exit more proximally and run along the upper lateral area of the LV). Thus, some of the most severe LAD occlusions present with acute RBBB and LAFB, and these findings carry the highest risk for acute ventricular fibrillation, acute cardiogenic shock, and highest in-hospital mortality when studied by Widimsky et al (in-hospital mortality was 18.8% for AMI with new RBBB alone, not to mention RBBB and LAFB). Additionally, the RBBB and LAFB make the recognition of the J point and STE more difficult and more likely to be misinterpreted. Upon successful and timely reperfusion, the patient may regain function of the previously ischemic or stunned fascicles.

As Dr. Meyers has emphasized on this blog, "When the QRS is wide, the J point will hide. So find it in any lead, then trace it down and copy it over." Here is the result, with the J point identified by the vertical blue thin lines:

Interpretation: sinus tachycardia with RBBB and LAFB. There is perhaps minimal STE in V2 and V3 and aVL. It certainly does not meet STEMI criteria. There is minimal reciprocal STD in inferior leads and V6. Recall that RBBB most commonly has slight discordant J point depression in V1-V2, so any amount of STE in those leads is concerning (and perhaps even isoelectric ST segments, assuming there is a pronounced R' as there is in this case). As previously identified, RBBB with LAFB is an ominous sign of LAD occlusion and mortality.

Smith comment: there are QR-waves in V1-V3 rather than typical rSR'. This is diagnostic of Q-wave infarct. This implies either old anterior MI or subacute anterior MI (which is consistent with 6 hours of chest pain). If old, the ECG in typical of LV aneurysm with RBBB. In any case, the Q-waves tell you that there is infarct here, though possibly old. The STE could be old also. The HISTORY is what tell you that this could be subacute. A history of previous anterior infarct would of course help, as would an old (previous) ECG recorded after that infarct. In a patient with new chest pain of 6 hours duration, and no proof of old anterior MI, the STE and Q waves are diagnostic of subacute MI requiring the cath lab.

These findings were recognized by the ED team, and the patient was diagnosed with likely OMI causing cardiogenic shock. Cardiology was summoned immediately summoned to the ED for emergent cath consult, but the lab was not directly activated (in this institution they require STEMI criteria for activation). 

Cardiology came to evaluate the patient, but disagreed with the ECG interpretation. They suggested heparin and cath the next day (despite the fact that it was currently 10 AM). 

In an effort to convince the cardiologists, the ED team performed the following bedside echo looking for wall motion abnormalities:

These echos show severe hypokinesis or akinesis of the anterior septum and apex, as well as part of the lateral wall. The high lateral wall in both views offers a perfectly contrasting example of both contraction and thickening, indicating no wall motion abnormality at that area (not supplied by the LAD, instead the LCX). A parasternal short view was not available.

These images were shown to cardiology, and yet the recommendations remained unchanged.

Aspirin was given, and heparin was started, but pain, dyspnea, and cardiogenic shock persisted. Yet the cardiologists refused to take her emergently to the cath lab (this is a violation of at least 2 separate indications for emergent cathetherization in the current ACC/AHA guidelines: ongoing ischemia persistent despite medical therapy, and ACS causing cardiogenic shock).

At the one hour mark from arrival, the initial contemporary troponin T returned at 1.84 ng/mL (already quite high, already in the range of STEMI peak troponins, most of which are in the 1-6 ng/mL range).

Smith comment: this very high initial troponin is diagnostic of subacute MI, and therefore perfectly consistent with the ECG (with Q-waves).  At this point, with chest pain and this troponin, one does not even need any ECG in order to activate the cath lab.  It is essential.

The lactic acid was 5.0 mmol/L, and the blood pressure began to decrease while the patient remained symptomatic.

Still the cardiologists refused to take her emergently to the cath lab.

At the 2.5 hour mark (roughly 12pm), the next troponin returned at 2.75 ng/mL. Cardiology was again informed that the patient has ongoing ischemia, rising troponins, and worsening cardiogenic shock. Finally they took the patient to cath at approximately 220 minutes after arrival.

They found a 100% thrombotic occlusion of the proximal LAD with TIMI 0 flow (left image), which was stented (right image):

The patient's symptoms did not seem to improve after reperfusion, and cardiogenic shock continued.

Troponin peaked at 34.2 ng/mL at 72 hours after arrival (Meyers comment: supermassive MI, to the point that I have never recorded a patient surviving the hospital stay at this level of peak troponin).

Here is her ECG after reperfusion of the LAD:

There is slightly more STE in V2-3 and aVL than the ECG on arrival, indicating some combination of the following: 1) the OMI has progressed beyond the point of significant reperfusion before the intervention, 2) there is a component of No-Reflow phenomenon, in which there is microvascular occlusion despite an open epicardial vessel.

The ultimate outcome is pending.  She remains intubated on multiple pressors after 9 days.

Meyers Discussion:

The management in this case is unfortunately common practice at many places around the world where we receive cases. Why would an interventionalist violate multiple recommendations from their own guidelines and watch at 10am while an LAD occlusion plays out in front of them? What could explain why some providers do not seem interested in the fact that LAD occlusion can be identified by something other than STEMI criteria? Or why the wall motion abnormality matching the distribution of concern is ignored? The only plausible explanation is that they have been taught that this is standard practice. Under the STEMI paradigm, providers believe things that their common sense would never support and they act in ways that their judgment would never allow otherwise.

Learning Points: 1. When the QRS is wide, the J point will hide. Find it where you can, then trace it down and copy it over.
2. RBBB and LAFB is a very ominous sign of LAD occlusion in the setting of a sick patient with ACS.  In the setting of LAD ACS, patients with RBBB + LAFB are extremely ill, most are either post cardiac arrest or in cardiogenic shock.
Here are several more cases of RBBB + LAFB.
3. Even in the outdated STEMI era guidelines, there are indications for emergent cath without STEMI criteria, including ongoing ischemia despite medial management, ACS causing cardiogenic shock, and ACS causing hemodynamic or electrical instability.
4. Use ultrasound in ACS to look for WMA.

References:

Widimsky PW, Rohác F, Stácek J, et al. Primary angioplasty in acute myocardial infarction with
right bundle branch block: should new onset right bundle branch block be added to future
guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86–95. 

https://pubmed.ncbi.nlm.nih.gov/21890488/

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MY Comment by KEN GRAUER, MD (8/24/2020):

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Sir William Osler (1849-1919) is often thought of as the Father of Modern Medicine. His best known quote is — “Listen to your patient; he is telling you the diagnosis”. Today’s case illustrates a similar principle that I’ve repeatedly found to be true during the decades that I’ve been studying ECGs, which is — Listen to your patient, and he/she will help you correlate what’s happening with his/her ECG.

• As Anonymous and Meyers have covered details of interpretation for this case in excellent fashion — I’ll limit my comments to the following thoughts.

Figure-1: The initial ECG in this case (See text).

Drs. Meyers, Smith and myself were all shown the initial ECG in today’s case before we learned the history. For clarity — I’ve reproduced this tracing in Figure-1.

• My eye was initially “caught” by the change in slope (RED arrows in leads III and aVF) — that I thought on initial glance represented the junction of the end of the S wave and beginning of the ST segment. IF true — then this meant there was significant reciprocal ST depression, which with ST elevation elsewhere would indicate acute coronary occlusion.
• Dr. Smith appropriately cautioned, “I don’t see this as necessarily acute. There is not much ST elevation (not even downsloping ST elevation) — and T waves are also down. Looks very much like LV aneurysm with RBBB in a sick patient with sinus tachycardia. I’m curious to know the presentation and outcome." As per Dr. Smith's comment (above) — there are Q waves in leads V1, V2, V3, which indicates infarction at some point in time (therefore potentially consistent with LV aneurysm given modest ST elevation).
• As I took another look (and drew the same horizontal BLUE lines that Anonymous and Meyers show above) — it became apparent that the change in slope that I highlight with RED arrows in leads III and aVF does not represent ST depression at all — but instead represents the terminal portion of the prolonged QRS complex.
• That said — my “relook” at this tracing still suggested to me that the shape of the ST-T wave in leads aVL, and V1, V2, V3 was not normal. I thought this shape suggested at least slight ST elevation in each of these leads (a bit more in V3). My IMPRESSION (that I wrote back) — The HISTORY would be everything, since IF this patient had new, cardiac-sounding chest pain (in the absence of a prior tracing for comparison) — I would not be certain from this tracing alone what was new vs old.
• PEARL #1 — As per Anonymous and Meyers, there is often slight discordant J-point depression in leads V1, V2 with RBBB. Take another careful look at the ST-T wave in leads V1 and V2 in Figure-1. This is not a normal shape for the ST-T wave with simple RBBB — because the abnormally coved ST segment “hugs” the baseline, whereas there should normally be at least slight ST depression.
• PEARL #2 — As alluded to by Dr. Smith (See above), sinus tachycardia may accentuate ST elevation that is not necessarily acute. That’s why he suggested (depending on the history) — that the lack of acute ST segment deviation in ECG #1 could reflect, “LV aneurysm with RBBB in a sick patient with sinus tachycardia”.

Returning to the KEY quote by Dr. Osler, “Listen to your patient; he/she is telling you the diagnosis”:

• The history in this case was that of a 60-something woman awakened from sleep 6 hours prior to the time ECG #1 was obtained. No prior tracing was available. The patient was acutely dyspneic, tachypneic, with ongoing chest pain at the time her initial ECG was recorded. Isn’t this patient essentially telling us, “I am in cardiogenic shock from my acute OMI with RBBB/LAHB?"
• Millimeter criteria for acute STEMI are clearly not satisfied in ECG #1. Isn’t this patient telling us? — “The reason I no longer have ST elevation is because my extensive STEMI has already evolved — because it began 6 hours ago! Look at my coved ST segments in leads aVL and V3, each now showing reperfusion T waves (T inversion). This is not what one sees in these leads with simple RBBB.” The reason for the abnormal ST coving without frank ST elevation in leads V1,V2 is that these ST segments are on their way down ...
• Bedside echo confirmed the above conclusions — as did elevated troponins and worsening cardiogenic shock. Finally (nearly 4 hours after arrival) — the patient was taken to cath.
• The Painful Lesson to Be Learned (especially by the cardiology team on this case) — A look at ECG #1 in today’s case without knowledge of the clinical setting can not tell you what is going on with the patient. This is often true for any single ECG. But clinical correlation with the history and physical exam of this patient clearly tells us that we have to assume extensive acute OMI that began 6 hours earlier is the cause of this patient’s worsening cardiogenic shock until proven otherwise. Cardiac cath should have been done much sooner in this patient.