50 Year Old Male: Chest Pain, Hypotension, Pulmonary Edema (Conclusion)

This is the conclusion to Friday’s post. If you haven’t seen it, I suggest checking out the original patient presentation and ECG first. We have reproduced this case courtesy of Dr. Musa A. Sharkawi (@MusaSharkawi on Twitter).

A 50-year-old man presented with sudden-onset chest pain, respiratory distress, pulmonary edema, and hypotension. This was his ECG:

It shows:

  • Atrial fibrillation with rapid ventricular response: The rhythm is irregularly irregular at an increased rate with no discernible P-waves.
  • Probable fusion complex: QRS #7 looks like a fusion complex with a PVC—note the subtle change in morphology that QRS shows in aVR and V5. Since the initial depolarization is fairly normal and the terminal QRS is narrow, I suspect a PVC from the right ventricle.
    • The last two QRS complexes look a little funky too, but it’s much harder to make a case for fusion with such subtle changes.
  • Right bundle branch block: The QRS duration is approximately 170 ms with a typical RBBB morphology in V1 and V6.
  • Probable left anterior fascicular block: The initial QRS vector is tricky to calculate here. The RBBB delays depolarization in the right ventricle, producing a large, unopposed vector to the right and/or superiorly. That RV depolarization dominates the last 2/3 of the QRS and isn’t clinically useful. To work around that, we only measure the first 40-60 ms of the QRS since that’s when we can see the left ventricle depolarizing most clearly. With that in mind, I think there is left axis deviation. LAFB would also account for the short R-waves in the left precordial leads, and it fits with the rest of the ECG and clinical picture.
  • Marked ST-elevation in I, aVL, and V2: We will discuss this in a moment, but it’s indicative of myocardial injury.
  • Marked ST-depression in II, III, and aVF: We’ll cover these reciprocal changes as well.


While it’s correct to say that this pattern shows an “anterolateral” STEMI, we can go one step further:

This tracing is pathognomonic of acute left main coronary artery occlusion

It’s a STEMI of the left main coronary artery.

How am I so confident?

Well, it helps that I’ve seen dozens of similar cases. This pattern of massive anterolateral injury is associated with a proximal LAD or LMCA culprit and characterized by a constellation of findings:

  • Cardiogenic shock: Because of the large ischemic territory, these patients are often in cardiogenic shock and look sick. Many end up intubated and few are able to avoid vasoactive or mechanical circulatory support.
  • Bifascicular block: Probably the hallmark of this presentation, the ECG shows a (presumed) new-onset RBBB and LAFB. The septal branches of the LAD are typically the sole blood supply to the right bundle branch and left anterior fascicle, so an acute occlusion in the proximal LAD or LMCA can produce ischemia and dysfunction in those conduction pathways.
  • Tachycardia: These patients are often tachycardic secondary to cardiogenic shock, and it’s not uncommon for them to be in atrial fibrillation with RVR.
  • Maximal ST-elevation in aVL and V2: While other leads are often involved, this kind of STEMI usually shows the most elevation in aVL and V2. It seems counter-intuitive, but these two leads are contiguous because they examine similar areas of the myocardium (for more on this, check out my giant primer on my favorite lead, The 12 Leads of Christmas: V2).
    • You might have seen me discuss “mid-anterolateral STEMIs” that present with isolated, sometimes subtle ST-elevation in aVL and V2. That pattern is associated with diagonal, ramus intermedius, obtuse marginal, or left circumflex artery culprits, but does not present with cardiogenic shock or bifascicular block. The ST/T changes are typically less pronounced as well.

If you were paying close attention, you may have noticed a discrepancy in what I’ve written so far. I first boldly stated, “This tracing is pathognomonic of acute left main coronary artery occlusion,” then said, “This pattern of massive anterolateral injury is associated with a proximal LAD or LMCA culprit.” While I make plenty of mistakes in my writing, this is not one of them. Most of the time, it’s a toss-up between the proximal LAD and LMCA with this sort of tracing, but there is something particular to this ECG that singles out the LMCA as the culprit.

There is not enough ST-elevation in the precordial leads.

Allow me to lead you down a rabbit hole.

It’s difficult to identify the J-points on this tracing, so let’s use a trick that’s helpful in this scenario. First, we pick out the leads in which we can most clearly see the start and end of the QRS. V1–V3 will do nicely:

Next, we run a line straight down those arrows to make sure they align.

Nice! Since they line up, we’ve chosen the correct points and can extend those rulers into the rhythm strips below the 12-lead.

Since the QRS morphology is uniform across most of the rhythm, we can use the same start and end points in different complexes…

Then we extend those lines up to identify the beginning and end of the QRS in the trickier leads…

Now we can see where there is ST-elevation or depression:

There’s a lot of ST-elevation in I and aVL, with corresponding reciprocal ST-depression in II, but V2 is the only precordial lead with any significant ST-changes… and what we see there pretty unimpressive. What gives?

The answer gets into why this is one of my favorite STEMI patterns, and explains why the culprit here has to be the LMCA. There really is a massive anterior STEMI happening, we just can’t see it because the ST-elevation is being cancelled out by concomitant “posterior” ST-elevation.

(Not that I put “posterior” in quotes. What we consider the electrocardiographic posterior wall is really the lateral free wall of the heart. I have lots more on that in The 12 Leads of Christmas: V3.)

Recall that “posterior” STEMI presents with ST-depression in the right-precordial leads—the same leads that show ST-elevation during anterior STEMI. With left main coronary artery (LMCA) occlusion, those forces sometimes balance out because the LMCA splits into the left anterior descending artery (LAD), supplying the anteroseptal walls, and the left circumflex artery (LCx), which supplies the anterolateral (“posterior”) walls. The ST-elevation from the anterior injury clashes with the ST-depression from the posterior injury, leaving us with precordial leads that show neither ST-elevation or depression.

To better understand this, let’s look at a sagittal cross-section of the chest. I’ve labelled the right ventricular outflow tract (RVOT) and left ventricle (LV).

We can approximate this view of the heart with a short-axis cross-section (as seen in the parasternal short-axis echocardiographic window):

Now, let’s examine the territory of the left ventricle supplied by the LMCA in someone with right-dominant circulation (~85% of people).

During a STEMI, injury vectors are directed from the subendocardiun towards the subepicardial myocardium of the ischemic regions. This is just a fancy way of saying that the ST-elevation points outwards, towards the surface of the injured muscle.

When two vectors of the same magnitude point in opposite directions, they cancel each-other out. The septal and lateral wall injury negate one-another, so what we’re left with is a net injury vector that points straight upward.

When we put the heart back into the chest, notice that this injury vector points directly toward the patient’s head.

If it was pointed anteriorly, towards the patient’s chest, we would see ST-elevation in the precordial leads. If it was pointed posteriorly, towards the patient’s back, we would see ST-depression in the precordial leads (and ST-elevation in posterior leads V7–V9). Instead, the ST-vector doesn’t point towards either the chest or back, so even though there is a giant STEMI, we don’t see any ST-elevation or depression in the precordial leads.

Now let’s consider the limb leads, which look at the heart in the frontal (coronal) plane. First, we’ll take a coronal slice of the chest.

Next, we’ll isolate the left ventricle.

And then we’ll highlight the area of the LV fed by the LMCA.

Again, during a STEMI, the injury vectors point from the subendocardium to the subepicardium (in other words, from the inside-out).

This time, when we add up the small injury vectors, there’s no opposing force to cancel them out like we saw in the sagittal view. We again end up with an injury vector that points towards the patient’s head, but this time it’s also directed slightly towards his left shoulder. It’s also much stronger than the vector we found in the sagittal plane because fewer of the small vectors cancel out in this view.

It’s been a while since I’ve brought up the 360 Degree Heart. Hopefully you recall the hexaxial reference system from early in your ECG training.

Despite your best efforts to forget, it still exists, and it’s still sorta useful. We’re going to superimpose the frontal plan injury vector we just figured out over it.

For this case I’ll let you get rid of the negative (inverse) leads…

We’re left with an injury vector that points away  III, aVF, and II. Since that means the ST-elevation is pointing away from those inferior leads, we should see ST-depression in them. The ST-depression should be maximal in lead III since the injury vector is pointing directly away from it.

Likewise, the injury vector points towards aVL and lead I, so we expect to see ST-elevation in those leads. There will be more ST-elevation in aVL than lead I because it is closer to the direction the arrow is pointing.

aVR is perpendicular to the injury vector—the ST-elevation points neither towards or away from it. As a result, we expect an isoelectric J-point in that lead with no ST-elevation or depression.

When we map out the complexes from our 12-lead onto that diagram, it matches perfectly.

That, in a nutshell, is why these patients with giant STEMIs of their left main coronary artery can present with marked changes in the limb leads but almost no ST-deviations in the precordials.

The Conclusion of Our Case

Oh yeah! We were discussing a real patient. What happened there?

The patient was intubated for pulmonary edema complicating cardiogenic shock and taken immediately to the cath lab. Angiography of the right coronary artery was grossly normal, showing a dominant RCA.


When they shot the left coronary system, however, only a stump was visible due to a thrombotic 100% occlusion of the left main coronary artery.


Balloon angioplasty was performed…


…along with stenting.


Unfortunately I don’t know more about the patient’s outcome, but these cases are always difficult to manage and often end poorly even with optimal care. That’s all the more reason to know how to recognize this pattern and get the patient to definitive management as soon as possible.


I’d like to thank interventional cardiologist Dr. Musa A. Sharkawi yet again for allowing use to reproduce his case here.

For more on massive anterolateral STEMIs presenting with bifascicular block, check out my other posts on the topic:

To learn why diffuse ST-depression with ST-elevation in aVR is not cause by LMCA “occlusion” and not a STEM-equivalent, see:



50 Year Old Male: Chest Pain, Hypotension, Pulmonary Edema

Physician and cardiovascular fellow Dr. Musa A. Sharkawi shared this ECG on Twitter (@MusaSharkawi) and has graciously allowed us to reproduce it here.

A 50-year-old male presents with a chief complaint of abrupt-onset severe chest pain. He is pale, diaphoretic, and ill-appearing—in moderate respiratory distress with extensive biateral crackles and a low blood pressure. Further history is limited by the patient’s condition but listed below:

Onset – 30 min ago
Provocation/Palliation – None
Quality – Severe “crushing” pressure
Radiation – None
Severity – 10/10
Timing – Constant

Signs/Symptoms – The patient ate dinner approximately an hour ago and soon noted that he felt generally unwell. He sat on the couch to rest but then developed severe chest pressure followed by a single episode of vomiting. He currently feels like something is crushing his chest with severe shortness of breath and weakness.
Allergies – No known drug allergies
Medications – Metformin, lisinopril, aspirin, hydrochlorothiazide
Past Medical History – Type II diabetes, hypertension, chronic kidney disease (unknown stage)
Last Oral Intake – Dinner 1 hour ago
Events Preceding Presentation – See above

Temperature – 36.7 C (98.1 F)
Heart Rate – 100 bpm, irregular
Blood Pressure – 86/50 mmHg
Respiratory Rate – 30 /min, labored
SpO2 – 83% (room air)

General – Ill-appearing male in severe distress. Vomit noted on patient’s mouth and chest.
Skin – Pale, cool, and diaphoretic. No rashes seen.
Head/EENT – Unremarkable
Neck – JVD present
Respiratory – Moderate respiratory distress. Extensive bilateral rales with no wheezing or rhonchi.
Cardiovascular – S1/S2 present but difficult to hear. Radial pulse weak and irregular with occasional pulse deficit compared to apex.
Abdomen – Soft and non-tender with no distension or guarding.
Back – Not examined
Pelvis – Not examined
Extremities – Moves all four extremities. No lower extremity edema seen or felt. Calves non-tender to palpation and passive movement.
Neuro – Alert. Oriented to person, place, time, and events. Eyes open spontaneously. Answers all questions appropriately. Follows all commands. Speech clear.

The following 12-lead is performed on scene:

A simultaneous rhythm strip is also obtained:

What’s your next move?

What’s the most likely diagnosis?

Is this patient experiencing a STEMI? What is the rhythm?