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.

Cath Lab occupied. Which patient should go now (or does only one need it? Or neither?)

This was sent to me by an undergraduate name Hans Helseth, who is an EKG tech, but who is an expert OMI ECG reader.  He wrote most of it and I (Smith) edited.

A prehospital “STEMI” activation was called on a 75 year old male (Patient 1) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. He arrived to the ED by helicopter at 1507, about three hours after the start of his chest pain while chopping wood around noon. 

While an EKG and labs were being obtained on Patient 1, a second announcement came through for another prehospital “STEMI” activation on a 58 year old male (Patient 2) with a history of some substance abuse. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chest pain around 1500 while eating. 

There was an active case in the hospital’s cath lab, and only room for one more patient.

EKGs were obtained in the ED right away for each patient:

Patient 1:

What do you think?

Patient 2, EKG 1:

What do you think?

Patient 1’s EKG was obtained first, so it was interpreted first. The EKG is diagnostic of acute inferior, posterior, and lateral OMI superimposed on “LV aneurysm” morphology. While a bit difficult to distinguish, the inferior T waves are hyperacute, especially within the context of the rest of the tracing; there is T wave inversion in aVL, downsloping ST depression with terminally upright T waves in V2-V4 indicating acute posterior OMI, and ST elevation with ST segment straightening in V6. 

There was a prehospital EKG for patient 1 available, taken in the helicopter:

OK.  This is obvious.

The findings in this prehospital EKG are more pronounced than they are in the one taken upon arrival to the ED, suggesting that the patient’s artery has opened. As expected, the patient reported total resolution of pain by the time he got to the ED. Additionally, his cardiac telemetry monitor showed runs of accelerated idioventricular rhythm, a benign arrhythmia often associated with coronary reperfusion.

Patient 2 was seen immediately after patient 1 by the same cardiologist. His EKG shows a variation of a distinct pattern which is often mistaken for OMI: Benign T wave inversion (BTWI). This pattern is most commonly seen in black men, and patient 2 was a black male. While patients with BTWI typically have higher voltage, there are a few features typical of BTWI on this EKG: There are J waves in aVL, V3 and V4, prominent U waves, and a relatively short QTC at 396 ms. The terminal portion of the T wave in lead V4 can be seen to dip just barely under the isoelectric line before coming back up above the isoelectric line and into the U wave.

A prehospital EKG was also available for Patient 2:

This EKG looks like the South Africa Flag Sign, indicating high lateral OMI. It should be treated as such unless there is more information such as old or serial EKGs that can confirm a benign diagnosis, as BTWI patterns can mimic the South Africa Flag Sign (Compare this EKG to case 4 here: https://hqmeded-ecg.blogspot.com/2022/05/quiz-post-which-of-these-if-any-are-omi.html). It is also important to recognize that BTWI patterns can be very dynamic. Two more EKGs were taken with identical lead placement on patient 2 only minutes apart:

Patient 2, EKG 2 at 1537:

Marquette 12 SL algorithm read: ACUTE MI/STEMI

Patient 2, EKG 3 at 1543:

Marquette 12 SL algorithm read: ACUTE MI/STEMI

One examining these serial EKGs may note the diminishing S wave depth in V3 and become worried about terminal QRS distortion. V3 has a J wave that becomes more prominent as the S wave becomes smaller, however. This is not consistent with TQRSD which cannot have an S wave or a J wave in V2 and/or V3.

Still, such dramatic changes cannot be overlooked. See this case, where a patient with BTWI morphology and dramatic EKG changes within minutes is diagnosed with myocarditis: https://hqmeded-ecg.blogspot.com/2019/07/what-does-this-ecg-with-significant-st.html

EKG 3 also has a saddleback morphology in V2, which is only rarely due to OMI.  

V2 has some features of type 2 Brugada phenocopy. The angle of the downslope of the saddleback-shaped T wave (beta angle) is greater than 35 degrees, consistent with type 2 Brugada morphology. Transient Brugada morphology has been observed in patients with fever, on sodium channel blocking drugs, or with hyperkalemia. The patient had none of these conditions.

Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. Additionally, a bedside echocardiogram showed no wall motion abnormality and normal LV function.

The two cases were considered:

Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He was given heparin and the decision was made to delay his catheterization until the next morning.

Patient 2 was diagnosed by the cardiologist with acute “STEMI” and he was taken emergently to the cath lab. Angiography revealed a 30% nonobstructive stenosis of the mid LAD. Serial high sensitivity troponin T (URL 15 ng/L) values were negative and stagnant.

Patient 1 remained in the hospital overnight. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia. He went to the cath lab at 0900 the next morning. There was a 70% culprit stenosis of the first obtuse marginal branch in a right dominant system. It was stented. His high sensitivity troponin T trended from 69 ng/L on ED arrival to 583 ng/L two hours later, and peaked at 5,258 ng/L overnight. This was a large OMI.  This is a good demonstration that when the artery reperfuses, it is at high risk of re-occlusion (in this case reoccluson/reperfusion/reocclusion/reperfusion).

A formal echocardiogram for patient 2 showed normal LV size, wall thickness, and global systolic function. He had another EKG taken the next morning:

The BTWI pattern is less prominent, but persists.

Patient 2 refused further workup and was discharged on day 2. The fluctuations of his BTWI pattern can be appreciated below:

A formal echocardiogram for patient 1 showed:

• Moderately increased LV size

• Reduced global systolic function with an estimated EF of 35-40%

• Mid and distal anterior wall, mid and distal anterior septum, entire apex, and mid septum segment wall motion abnormalities. Much of this is due to his prior LAD and Cx OMI.

An EKG for patient 1 was taken after catheterization:

The lateral T waves show terminal inversion, consistent with reperfusion.  There are well formed Q-waves in lateral precordial leads.

How did the Queen of Hearts perform?

Patient 1:

Prehospital EKG- OMI with high confidence

ED EKG- OMI with high confidence

Patient 2:

Prehospital EKG- OMI with high confidence

ED EKG 1- OMI with mid confidence

ED EKG 2- OMI with mid confidence

ED EKG 3- OMI with high confidence

A disappointing false positive by the Queen, but she did not miss the subtle OMI. 

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MY Comment, by KEN GRAUER, MD (10/15/2024):

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Outstanding step-by-step review by Dr. Smith of this "Tale of 2 Patients Who May Need the Cath Lab". More than simple assessment of each initial ECG — Dr. Smith's comprehensive discussion centers around having to chose which of these 2 patients was in more urgent need of immediate catheterization — because the cath lab only had room at that time for 1 of these 2 patients.

• I limit my comments to assessment of the initial ECGs from these 2 patients  that were recorded in the ED. For clarity in Figure-1 — I’ve labeled these 2 ED tracings.
• NOTE: Although clinical priorities in today’s case became clearer when prehospital ECGs were revealed — ED physicians must often make decisions without the benefit of prehospital tracings (that are not always immediately available to ED physicians). I therefore thought it worthwhile to review the decision-making process solely from the perspective of the initial ED tracings.

Patient #1: Assessment of the Initial ECG in the ED …

The History for Patient #1 — is clearly concerning for a higher-risk likelihood of having an acute event.

• The patient is a 75-year old man with known coronary disease, including prior LAD and LCx OMI.
• He presents with new-onset CP (Chest Pain) — brought on by activity, and persistent for 3 hours, being severe enough to prompt helicopter transport to the ED.

As is often the case in patients with previous LAD OMI — the distinction to be made is between ECG findings consistent with this patient's prior LAD OMI — vs — ECG findings of a new acute event superimposed on these prior ECG findings (See My Comment in the October 8, 2024 post — for another example of this).

• The initial ED ECG for Patient #1 (TOP tracing in Figure-1) — shows sinus rhythm — low voltage in the limb leads — normal intervals and axis — and no chamber enlargement.
• My "eye" was immediately drawn to lead III (within the RED rectangle). Considering the tiny amplitude of the QRS complex in this lead — I thought the upright T wave in this lead to clearly be more voluminous than-it-should-be, which in this patient with new and now persistent CP, qualifies as a hyperacute T wave.
• To emphasize that we clearly see evidence of prior infarction in this initial ED ECG from Patient #1 — as there are large, wide Q waves in multiple leads (ie, leads II,III,aVF; V5,V6) — with loss of r wave from lead V1-to-V2 + fragmented QS complexes in V3,V4. That this patient has severe underlying coronary disease is indisputable.
• BUT, in addition to the hyperacute T wave in lead III — the T waves in the other inferior leads are equally hyperacute (RED arrows within the BLUE rectangles).
• Note that the tiny QRS complex in lead aVL manifests T wave inversion (BLUE arrow in this lead) — consistent with reciprocal ST depression in response to an acute inferior OMI.
• Acute changes were also seen in the chest leads of this initial ED ECG from Patient #1 (within the PURPLE rectangles). Thus, the shelf-like ST depression (PURPLE arrows in leads V2,V3) — and the hyperacute-looking ST elevation in lead V6 (within the dotted PURPLE oval) strongly suggest associated acute postero-lateral OMI.
• 
  
• BOTTOM Line: Patient #1 demonstrates acute infero-postero-lateral OMI that is superimposed on severe underlying coronary disease with prior infarctions. Prompt cath with PCI is clearly needed for Patient #1 on the basis of this initial ED ECG.
• 
  
• P.S.: Without a prior tracing for comparison — it's impossible to know if the low voltage in the limb leads is an acute finding. This is relevant — because among the causes of new low voltage is myocardial "stunning" from a large acute MI, such that this ECG finding may serve as a harbinger of a reduction in LV function that may soon be occuring (See My Comment at the bottom of the page in the November 12, 2020 post of Dr. Smith's ECG Blog).

Figure-1: I've labeled the initial ED ECGs in today's case from Patient #1 and from Patient #2. (To improve visualization — I've digitized the original ECG using PMcardio).

Patient #2: Assessment of the Initial ECG in the ED …

While still of concern — I found the history for Patient #2 of a lower likelihood for an acute event. 

• This patient is a 58-year old black man. He had a history of substance abuse — but no prior history of coronary disease. His CP began shortly after eating. 
• To emphasize that the history for Patient #2 in no way rules out the possibility of an acute cardiac event — but it does sound less worrisome to me.

The initial ED ECG for Patient #2 (BOTTOM tracing in Figure-1) — shows sinus rhythm — normal intervals and axis — and no chamber enlargement.

• My "eye" was immediately drawn to lead V4 (within the RED rectangle). As per Dr. Smith — the shape of the QRST complex in lead V4 just "looks" like BTWI (Benign T Wave Inversion) — in that there is fairly tall R wave amplitude in a lateral chest lead, in which there is a J-point notch (PINK arrow) — slight ST elevation with terminal T wave inversion (RED arrow) — and a relatively short QTc interval (For more on BTWI — See the March 22, 2022 post, in which Dr. Meyers shows a series of BTWI cases "in all of its flavors" — with My Comment on BTWI at the bottom of the page).
• 
  
• Elsewhere on this initial ED ECG from Patient #2 are the following: i) Slight ST elevation in lead aVL, with terminal "slurring" of the QRS complex that is consistent with a repolarization variant (PINK arrow in this lead); and, ii) Benign-appearing small, rounded positive T waves in lateral leads V5,V6 — also consistent with a repolarization variant.
• There is T wave inversion in lead III — but this is not necessarily abnormal given the RSr' complex in this lead.
• The principal finding of concern relates to the leads with the question marks. The ST-T wave in lead V2 looks larger than I would expect given modest size of the QRS complex in this lead. Of even more concern — is the J-point ST elevation with straightening of the ST segment takeoff in lead V3. In this context — I could not rule out potential significance of the slightly elevated and straightened ST segment in lead V1 — and, I felt a need to "relook" at the ST elevation in lead V4.
• 
  
• BOTTOM Line: I did not feel comfortable ruling out the possibility of an acute cardiac event on the basis of this ED ECG from Patient #2. That said — I would not activate the cath lab on the sole basis of this tracing, but instead would get more history — repeat the ECG within 10-to-20 minutes — check serial Troponins — and do a bedside Echo during chest pain, looking for a wall motion abnormality.

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ADDENDUM: Availability of the prehospital ECGs on both patients proved enlightening. 

• The prehospital ECG of Patient #1 — showed an obvious acute STEMI. The PEARL to remember — is that by correlating the initial ED ECG with this patient's total resolution of CP at the time this ED ECG was recorded — we can establish that spontaneous reperfusion had occurred. This clinical correlation of patient symptoms to the timing of each ECG also establishes the need for prompt cath with PCI to prevent reocclusion (ie, A "culprit" vessel that spontaneously reopens — may just as easily spontaneously reclose if not promptly treated with PCI).
• 
  
• Patient #2 — had a series of insightful prehospital ECGs done, which showed marked change in ST-T wave appearance from one tracing to the next. As emphasized by Dr. Smith — the PEARL to remember is that "BTWI patterns can be very dynamic". As a result — great caution is needed so as not to misdiagnose the potential changing ECG pattern of a patient with BTWI as having dynamic ischemic changes. This can be tricky! — such that cardiac catheterization of Patient #2 in today's case was not at all inappropriate (albeit I thought Patient #1 merited priority for the cath room).