Two patients with chest pain and RBBB: do either have occlusion MI?

Written by Jesse McLaren

 

Two patients in their 70s presented to the ED with chest pain and RBBB. Do either, both, or neither have occlusion MI?

Patient 1: a 75 year old called paramedics with one day of left shoulder pain which migrated to the central chest, which was worse with deep breaths. Past medical history included RBBB without other cardiac history, but old ECG was not available. Vitals were normal except for oxygen saturation of 94%. The prehospital and ED computer interpretation was inferior STEMI:

There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. As expected, the anterior leads with rsR’ have secondary, discordant and proportional ST depression and T wave inversion. The inferior leads have a positive deflection within the QRS, but if you measure the ST segment after the QRS there is no elevation. The inferior T waves are tall relative to the QRS but there’s no reciprocal changes in aVL, which makes inferior OMI highly unlikely.

Smith comment: before reading anything else, this case screamed pulmonary embolism to me.  First, the pain began in the shoulder; Second, it was pleuritic; Third, the oxygen saturation was 94%.  As for the ECG, it could represent OMI, but RBBB is also a clue that it may be PE.  On arrival, it is imperative to look for PE before activating the cath lab.  I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram.  

The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Comparing J-point between leads noted no significant ST elevation or depression, with QRS prolongation from RBBB.” The final cardiology interpretation was also RBBB without ischemic changes, but this was not available at the time. With both EMS and ED computer interpretations reading ‘STEMI’, the emergency physician activated the cath lab.

 

Coronaries were normal, as was serial troponin. Chest X-ray showed left lung base atelectasis vs consolidation suspicious for pneumonia, so the patient was discharged with antibiotics. Ten days later the patient returned with worsening pleuritic chest. CT chest showed left sided pulmonary embolism and a pulmonary infarct that had previously been mistaken for pneumonia.

 

 

Patient 2: a 70 year old called paramedics for 3 days of chest pain worse and shortness of breath over the past hour. Past medical history included diabetes and hypertension. Vitals were normal. The prehospital, ED computer, and final cardiology interpretation was STEMI negative.

There’s normal sinus rhythm, RBBB, normal axis and normal voltages. There’s some artifact in the limb leads and baseline wander in the precordial leads. But despite this there is clear concordant ST elevation in V1 and more subtle convex ST segment in V2-3, with reciprocal ST depression in V5-6 (precordial swirl):

 

 

Baseline ECG from a visit for hyperglycemia 10 days prior is below was normal:

So compared with baseline there is new RBBB + precordial swirl, diagnostic of proximal LAD occlusion. But with prehospital and ED ECGs being ‘STEMI negative’, the ECG was signed off and the patient waited to be seen. 

 

An hour later the first troponin returned at 1,500 ng/L (normal <16 in females and <26 in males), and the ECG was repeated:

Now there’s an acute Q wave in V2 and increasing ST elevation which now meets STEMI criteria in V1-2 but is still not labeled STEMI. The computer sees the lateral ST depression in V5-6 but not the ST elevation V1-2 to which it is reciprocal (precordial swirl).

 

The emergency physician asked for stat cardiology consult, bedside echo showed anterior akinesis, and the cath lab was activated – with door-to-cath time of 4 hours. There was 100% proximal LAD occlusion with TIMI 0 flow, and cardiac arrest in the cath lab. Peak troponin was a massive 500,000 ng/L, echo showed EF reduced to 20%, and follow up ECG showed LV aneurysm morphology with anterior Q wave and persisting ST elevation. The patient had a protracted hospitalization and did not survive.

The current STEMI paradigm is associated with false positive activations that are unnecessary and can miss other diagnoses, and delayed reperfusion and increased mortality for subtle occlusion. But advanced ECG interpretation, to identify false positives and negative STEMI, can be learned. I sent the initial ECG of both cases without any context to my colleague Mazen El-Baba, a senior EM resident with an interest in ECG interpretation, and he responded: “RBBB with first degree AV block” for the first (ie no acute coronary occlusion), and “RBBB and superimposed OMI” for the second. The paramedics of the first case identified it as false positive STEMI, and in this other case a cardiac tech identified RBBB plus subtle LAD occlusion.

 

Expert-trained AI can make these advances widely available, and Queen of Hearts could have made a difference in both cases. The ECG from patient 1 was identified as Not OMI with high confidence, which could have prevented unnecessary cath lab activation and caused a reconsideration of other concerning causes of chest pain. The ECG from patient 2 was identified as OMI with high confidence, which could have reduced reperfusion delay and saved myocardium. 

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Take away

1.        In a patient with acute chest pain/shortness of breath, RBBB could be old/unrelated, or new from acute PE or proximal LAD occlusion

2.        RBBB can be associated with false negative STEMI (eg subtle concordant STE from LAD occlusion) and false positive STEMI (eg mistaking the QRS for the ST segment)

3.        Precordial swirl (primary ischemic STE V1-2 with reciprocal STD V5-6) can help identify proximal LAD occlusion

4.        Reciprocal change in aVL is highly sensitive for inferior OMI, so inferior OMI is unlikely in the absence of reciprocal change in aVL

5.        Physicians need to consider paramedic input, which provides valuable clinical information including ECG interpretation

6.       Evidence-based advances in ECG interpretation can be learned across all levels of emergency providers

7.        The Queen of Hearts can identify subtle occlusions at risk of delayed reperfusion, and false positive STEMI at risk of unnecessary cath lab activation and missing other diagnoses

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MY Comment, by KEN GRAUER, MD (10/17/2024):

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On an increasing number of occasions, we have addressed the clinical question of — How effectively can we diagnose acute OMI in a patient with RBBB? (Among others — See My Comment at the bottom of the page in the September 13, 2024 post of Dr. Smith's ECG Blog). In today's case — Dr. McLaren adds a few "twists" to this clinical challenge.

• For clarity in Figure-1 — I've labeled the initial ECGs for both patients.

Patient #1: The "Tricky" Findings in the Initial ECG ...

The initial ECG for Patient #1 — shows sinus rhythm and RBBB (Right Bundle Branch Block).

• Dr. McLaren outlines with vertical lines the beginning and end of the QRS complex in each of the 12 leads — and he correctly emphasizes that there is no ST elevation. But I thought this was not easy to appreciate.

What is the ST Segment Baseline?

Having formally taught ECG interpretation for decades — I frequently encountered this seemingly simple clinical question from those I taught.

• I ultimately came to the conclusion that the answer is — It depends ...
• As I describe below in Figure-2 — there is no general consensus on what to use for the ST segment baseline, from which ST segment deviations (elevation or depression) are determined.
• Because there is no consensus — either the TP baseline or the PR segment baseline may be used. Although I generally favor using the PR segment baseline — that measurement will be faulty when there is PR segment depression, as there is in the initial ECG for Patient #1 (most marked in lead II).
• Not only is there fairly marked PR segment depression in a number of leads (leads I,II,III; aVF; V3,V4,V5,V6) — but the TP baseline is angled with a progressive decline.This makes it especially challenging to determine if there is (or is not) any ST elevation.
• To facilitate assessment — I've added horizontal dotted RED lines that start from the onset of the TP baseline in leads I,II,III; aVF and V6 — and these support Dr. McLaren's determination that there is no ST elevation in this Patient #1 ECG.
• 
  
• The above said — given the history of new chest pain — I thought the T waves in leads II, aVF and V6 were hyperacute (ie, disproportionately "bulky" with respect to amplitude of the QRS in these leads — as highlighted by the RED arrows).
• 
  
• BOTTOM Line: While I agree with Dr. McLaren that: i) There is no ST elevation in this Patient #1 ECG; and, ii) The lack of reciprocal ST depression in lead aVL weighs strongly against this being an acute OMI — there is no denying that there are hyperacute-looking T waves in this tracing.

My Speculation: 

Patient #1 was shown not to have an acute OMI. Instead, he was diagnosed with pneumonia — that turned out to be a left-sided pulmonary embolism that was initially missed.

• PR depression — has been shown to be a relatively common ECG sign associated with clinically silent PE (Kudo et al — JACC 39(12): 2000-2004, 2002). PR depression is marked and seen in multiple leads in this tracing.
• Although ECG signs of acute PE typically involve inferior and/or anterior lead ST depression/T wave inversion — on occasion, there can be ST elevation (Gheith et al — Cureus 14(9): e29249, 2022 — and — Siddiqa et al — Am J Case Reports 21: e927923-6, 2020).
• When seen — such ST elevation is typically seen in anterior leads. 
• Patient #1 in today's case does not manifest ST elevation on his initial ECG — but perhaps the hyperacute T waves in this tracing were also a manifestation of this patient's missed PE (in which case — I would expect resolution of these hyperacute T waves after treatment of the PE).

Figure-1: I've labeled the initial ECGs from the 2 patients in today's case.

Patient #2: RBBB and Acute OMI ...

The initial ECG for Patient #2 also shows RBBB. I'll highlight a few additional features.

• There is sinus tachycardia at ~100/minute. As often emphasized by Dr. Smith — sinus tachycardia is not a common finding with acute OMI unless something else is going on (ie, cardiogenic shock). In today's case — the sinus tachycardia may have been a harbinger of this patient's ultimate demise.
• As per Dr. McLaren — there is ST elevation in anterior leads V1,V2,V3 (within the RED rectangle). Normally there should be ST-T wave depression in anterior leads with RBBB — so in this patient with new CP, this is diagnostic of acute anteroseptal OMI (Precordial "Swirl", given ST depression in leads V5,V6 — as per Dr. McLaren). The RED arrow in lead V1 marks the end of the QRS and the beginning of the obviously elevated ST segment.
• Note the large infarction Q wave in lead V1, with smaller infarction Q wave in neighboring lead V2.
• Finally — Note that there is also T-QRS-D (Terminal QRS Distortion) in lead V3 (See My Comment in the November 14, 2019 post for review and illustration of T-QRS-D criteria). We don't often see T-QRS-D with RBBB — but it's presence in the Patient #2 ECG adds confirmation to the diagnosis of acute OMI.
• 
  
• P.S.: Assessment of the limb leads is difficult in this Patient #2 ECG — because of significant artifact and baseline wander. That said — BLUE arrows indicate what I believe indicates reciprocal ST depression, which is one more sign of proximal LAD occlusion in this Patient #2 ECG.

Figure-2: From Grauer K: ECG Pocket Brain-2014 ePub — regarding "My Take" on defining the ST segment baseline.