Acute chest pain, right bundle branch block, no STEMI criteria, and negative initial troponin.

Written by Pendell Meyers

A man in his 40s called EMS for acute chest pain that awoke him from sleep, along with nausea and shortness of breath. His history included known heart failure with prior EF 18%, insulin dependent diabetes, and polysubstance abuse. Vitals were within normal limits except for tachypnea. 

Here are his EMS ECGs along with the Queen of Hearts interpretations below each one:

 EMS1 0650

EMS2 0707

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The ECGs show RBBB and LAFB, with small but important concordant STE in V2. In EMS2 ECG, the T waves in V5 is possibly hyperacute. Because the most severe LAD OMIs can cause ischemic failure of the RBB and LAF, any patient with ACS symptoms and new RBBB and LAFB with any concordant STE has LAD OMI until proven otherwise.

The paramedic called the EM physician ahead of arrival and discussed the case and ECGs, and both agreed upon activating "Code STEMI" (even though of course it is not STEMI by definition), so that the acute LAD occlusion could be treated as fast as possible. So the cath lab was activated.

Here is his ECG on arrival to the ED, still with active pain:

ED1 at 0727

A baseline ECG was available from 1 month ago:

First troponin was drawn before cath, which would soon return at 14 ng/L (within normal limits).

He was taken rapidly to the cath lab and here are some representative images before and after intervention:

Acute proximal LAD culprit with TIMI 0 flow, 100% stenosis, thrombotic occlusion, requiring thrombectomy and PCI.

Post cath 

EF was estimated at 15% with severe global hypokinesis, and akinesis of the apex.

Long term outcome is unavailable.

Learning Points:

Currently by definition, there is unfortunately no such thing as a formal diagnosis of STEMI or STEMI criteria in the setting of RBBB and LAFB. There is no recognition of STEMI equivalency in this setting in the USA guidelines currently. We recommend using the modified Sgarbossa criteria for all significantly wide QRS complexes.

This is an acute deadly proximal total LAD OMI in the setting of "NSTEMI". You must far exceed the guidelines and current world paradigm to deliver good care to these patients. As you can see above, AI can help.

Initial negative troponin is not uncommon even in the most dangerous OMI cases, when the time from occlusion to troponin is within the first few hours.

Smith: LAD OMI with RBBB/LAFB is not only subtle on the ECG, but most of these patients are extremely ill: most I have seen are post-ROSC, in cardiogenic shock, or arrested shortly after.  DO NOT MISS THESE!

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MY Comment, by KEN GRAUER, MD (9/13/2024):

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The KEY consideration in today's case is — How effectively can we diagnose acute OMI in a patient with RBBB? While fully acknowledging the challenge of recognizing OMI in such a patient, to the extent of being able to convince the On-Call interventionist of the need for prompt cath — today's case shows this can be accomplished in very time-efficient fashion.

• The "good news" in today's case — is that both the EMS team and the EM physician rapidly recognized strong suggestion of acute LAD occlusion on prehospital ECGs, thereby enabling activation of the cath lab even before the patient arrived in the ED.
• I focus my comment on the KEY ECG findings that led to this decision. For clarity in Figure-1 — I've labeled the 2 EMS ECGs and the baseline ECG recorded ~1 month earlier.

The Clinical Setting in Today's CASE:

Today's patient is a man in his 40s with underlying co-morbidities, including known heart failure with markedly reduced cardiac function (EF ~18%) — who was awakened from sleep with severe chest pain.

• Even before looking at the initial ECG — this patient is in a high prevalence group for having an acute event. Therefore — even subtle ECG abnormalities merit especially close scrutiny.

The Initial EMS ECG:

I've labeled key findings in ECG #1:

• The rhythm is sinus at ~90/minute. The PR interval is normal — but the QRS is wide with morphology consistent with RBBB (Right Bundle Branch Block) — in that the wide QRS is predominantly upright in lead V1 (with a QR pattern) — and there are terminal S waves in lateral leads I and V6. 
• There is fragmentation (especially of the S wave in inferior leads — and in the R wave irregularities in leads V3,V4,V5) — which is consistent with this patient's severe underlying heart disease.
• The predominantly negative QRS complex in each of the inferior leads indicates marked LAD (Left Axis Deviation) that is consistent with LAHB (Left Anterior HemiBlock) — with combined RBBB/LAHB indicating bifascicular block.
• Regarding chamber enlargement — biatrial abnormality is suggested by the tall, peaked P waves in the inferior leads (consistent with RAA) — and the deep negative component to the P wave in lead V1 (consistent with LAA).
• Assessment for LVH and RVH is difficult because: i) RBBB complicates such assessment; — and, ii) As is common with EMS tracings — QRS amplitude is truncated when R wave or S wave amplitude exceeds 10 mm (dotted PURPLE lines in Figure-1 that "cut off" the R in leads V3 and V4 — as well as the S in lead V6).
• More than just RBBB — there are deep and wide Q waves in leads V1 and V2 (BLUE arrows in these leads). When seen in association with RBBB — such Q waves suggest septal infarction has occurred at some point. 
• In addition — there are subtle-but-real ST-T wave abnormalities in leads V1-thru-V4 suggesting a recent acute event. The RED arrow highlights the most obvious of these — as the relative amount of ST-T wave depression with RBBB should decrease instead of increasing as one moves across the precordial leads. BLUE lines over these first 4 chest leads mark the subtle abnormal coving of the ST segment in leads V1-thru-V4, with a hint of ST elevation in leads V1,V2 (whereas with uncomplicated RBBB — the ST-T wave should be slightly depressed).
• 
  
• IMPRESSION: Given the history ( = this patient with known heart disease was awakened from sleep with severe CP) — this initial EMS ECG suggests acute LAD OMI until proven otherwise. Some findings are subtle — which may be the result of some "pseudonormalization" on the way to developing reperfusion T wave inversion (We do not know IF this patient's CP has lessened at this point in time) — and we do not yet have a previous ECG for comparison — but, as was recognized by today's EMS team — this may be acute!

Figure-1: To facilitate serial ECG comparison — I have placed ECGs #1 and #2 together, with the baseline tracing from ~1 month earlier.

The Repeat EMS ECG

17 minutes later — the diagnosis of acute LAD OMI is confirmed by a series of subtle-but-definitely-present ST-T wave changes in the chest leads (within the RED rectangle in ECG #2).

• Subtle ST-T wave changes on serial ECGs are BEST appreciated by lead-by-lead comparison when both tracings are placed side-by-side (as in Figure-1).
• RED dotted lines in ECG #2 that mark the ST segment baseline in lead V2, and leads V4,V5,V6 — document new ST elevation that was not present in ECG #1. That this finding is real — is supported by the increased ST coving in lead V4 and straightening of the ST segment takeoff in leads V5,V6 (Compare the light BLUE with the RED lines over the 1st QRST complex in leads V4,V5,V6 of ECGs #1 and 2).
• NOTE: While I fully acknowledge how subtle these changes in ST-T wave shape are — when they occur in multiple leads as they do here (in this patient with new severe CP) — these are real changes!

PEARL: Did YOU notice the Fusion Beat in ECG #2?

Although there is no long lead rhythm strip — there is a fusion beat (F) in ECG #2. Red arrows show on-time sinus P waves in lead aVF of this tracing — with the too-short-to-conduct PR interval before the 3rd complex indicating fusion of sinus conduction with a late-cycle ventricular beat.

• Realizing that the ST-T wave of this fusion beat is attenuated by the oppositely-directed ST-T wave contribution from partial sinus conduction — the shape of the ST-T wave in leads aVL and aVF of this fusion beat still looks "off", and supports chest lead ST-T wave findings that suggest an acute event.

And — the Baseline ECG!

The EMS team in today's case knew to activate the cath lab within the 17 minutes it took to record the first 2 ECGs. The EMS team did not need the baseline ECG to make this decision. That said — as soon as this baseline ECG was found, all doubt was removed.

• The prior tracing from ~1 month earlier shows sinus rhythm, LAHB, RAA and marked LVH (R ≥12 in aVL — and especially the very deep S waves in V2,V3 + ST-T wave changes of LV "strain" in multiple leads) — but no acute changes!
• Comparison of this baseline tracing with ECGs #1 and #2 confirms that the RBBB, septal Q waves and above described ST-T wave changes are all new — and consistent with the acute LAD occlusion found on cath.