Acute artery occlusion -- which one?

Written by Willy Frick with edits by Ken Grauer

A woman in her 70s with a history of hypertension presented with acute onset shortness of breath. She was out walking her dog when she developed sudden dizziness and light-headedness. When EMS found her, she was dyspneic and diaphoretic. Her ECG is shown below:

What do you think?

The conventional machine algorithm interpreted this ECG as STEMI. It shows sinus tachycardia with right bundle branch block. In addition, there is concordant STE in V1. New RBBB and concordant STE in V1 can be seen in LAD OMI. Additionally, with STE in V1 and STD in the lateral precordial leads, this may be precordial swirl pattern.

Alternatively, with STE in V1 and III, and STD in I and aVL, this ECG could represent proximal RCA OMI with right ventricular involvement.

Here is the Queen of Hearts interpretation with explainability!

Interesting to see the Queen of Hearts is not apparently troubled by V1, but does notice the concordant STE in III along with reciprocal concordant depression in I and aVL.

Taking a step back, remember that sinus tachycardia is less commonly seen in OMI (except in cases of impending cardiogenic shock). Additionally, there is borderline right axis deviation. There is also TWI in the right precordial leads and in lead III. In patients with narrow QRS (not this patient), this pattern is highly suggestive of acute pulmonary embolism.

Shown below are leads I and aVF showing borderline right axis:

Note that a terminal S wave is normal in RBBB. In this case, it is helpful to think about the QRS complex as broken up into a first half and a second half. This is shown below with a vertical dashed blue line.

Note that a wide terminal S wave is an expected finding in left-sided leads with RBBB (ie, because of the RBBB — the last component of ventricular depolarization is slow and directed away from the left ventricle). As a result — it may be helpful to think about the QRS complex in lead I as broken up into a first half and a second half. This is schematically shown below with a vertical dashed blue line.

The first part of the QRS (left of the blue line) represents that part of depolarization prior to impulse encountering the blocked right bundle branch (ie, consisting of left-to-right septal depolarization and then right-to-left depolarization of the unblocked LV). 

The second half of the QRS (right of the blue line but before the J point) represents depolarization of the myocardium supplied by the right bundle. Since the right bundle was blocked, this is the last to depolarize, and therefore represents the terminal QRS. Notice that even if we ignore the terminal QRS, there is still borderline right axis deviation. 

We also see leads V1 and III showing TWI (although this can be normal in RBBB)

In patients with wide QRS, it is important to determine the true duration in a lead where it is most apparent. Some leads may show a relatively isoelectric initial or terminal QRS, and this can lead to misunderstanding of the J point. For example, lead III might initially look to have massive STE with reciprocal depression in aVL. However, if we measure the QRS duration in V1 where it is easily appreciated:

Then apply this measurement to the other leads:

Now it becomes apparent that the STE/STD is modest.

What do you do clinically when the ECG looks like this? How do you emergently triage the patient to cath lab or possibly IR suite for thrombectomy? 

Answer: Bedside ultrasound!

The physicians taking care of the patient obtained the following parasternal short axis view.

Although it was technically difficult and the quality therefore leaves a lot to be desired, you can still make out RV dilation and septal flattening which is much more suggestive of pulmonary embolism than OMI. Taken together with the history of dyspnea and near syncope, this is extremely helpful in emergent triage. The patient subsequently had confirmed large, bilateral PE shown on CT below.

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Smith: RV infarct may also have this appearance on ultrasound.  So CT is required to find the diagnosis!  Of course it would also be nice to know about the patients oxygenation: in acute MI there is no hypoxia unless it results in pulmonary edema.  In PE, there is almost always some hypoxia without any pulmonary edema.  So hypoxia without B lines on lung ultrasound strongly weights toward PE.

See this post of RV MI with both McConnell sign and "D" sign: 

Inferior and Posterior STEMI. What else?

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Here are some representative stills with red arrows pointing to the emboli.

Thanks in part to rapid bedside diagnosis, the patient was able to avoid emergent coronary angiography. Instead, IR performed pulmonary thrombectomy and the patient did well. Repeat ECG was performed the following day:

Note resolution of the RBBB and leftward shift of the axis relative to the presenting ECG. Here is lead I from ECGs 1 and 2 shown side-by-side to highlight the change in axis from borderline right to completely normal.

Learning points:

• Acute PE and OMI can look similar on ECG

• Bedside ultrasound is often critical to tell them apart

• TWI in the right precordial leads and lead III is highly suggestive of PE in patients with narrow QRS

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MY Comment, by KEN GRAUER, MD (9/23/2024):

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Today's case provides an insightful example of why acute PE (Pulmonary Embolism) continues to be overlooked. Consider the following:

• We become attuned to looking for acute coronary occlusion in patients who present with acute symptoms to the ED (Emergency Department). But the History in today's case was acute shortness of breath with dizziness and lightheadedness — and, essentially without chest pain! As per Dr. Frick — this is a typical history for massive acute PE.
• Both the standard computerized interpretation and the QoH (Queen Of Hearts) interpretation said acute MI. Both were wrong.
• As per Dr. Frick — sinus tachycardia is usually not seen with acute OMI unless the patient is in cardiogenic shock.
• The ECG showed worrisome ST elevation in several leads — and what seemed to be equally worrisome reciprocal ST depression. BUT — the distribution of ST-T wave changes in the initial ECG (that I have reproduced and labeled in Figure-1) — is not truly suggestive of a single anatomic territory (only lead III of the inferior leads shows ST elevation — and isolated acute RV MI is uncommon in the absence of inferior OMI). While not completely ruling out acute coronary disease — another cause should be considered.
• In addition to sinus tachycardia (mentioned above) — there are other acute ECG findings potentially consistent with acute PE (See below).
• The clinical utility of stat bedside Echo for recognition of massive PE is not always immediately thought of ...

Figure-1: I've labeled the initial ECG in today's case.

ECG Findings of Acute PE in Today's Case:

We periodically highlight cases of acute PE (See the June 17, 2024 post in Dr. Smith's ECG Blog — that includes links to over 25 of these cases). I've excerpted the Table shown below in Figure-2 from My Comment in that June 17, 2024 post.

ECG findings in Figure-1 suggestive of a large acute PE include the following:

• Sinus tachycardia (here at ~110/minute).
• Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the dotted RED oval in Figure-1). In the context of a suggestive clinical history and other ECG signs — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain".
• S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-1) — is very helpful in today's case, given association with other ECG evidence pointing to a large acute PE. 
• Acute RV "Strain" — is suggested by inferior lead T wave inversion (in leads III,aVF) — and anterior lead T wave inversion (in leads V1,V2 — as per BLUE arrows).
• It is not generally appreciated that that anterior lead ST elevation can sometimes be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• In addition to lead V1 — other right-sided leads such as leads III and aVR — may face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads III, aVR and V1 in Figure-1).
• There is RBBB (predominantly positive, widened QRS in lead V1 — with a wide terminal S wave in lateral lead I ). 
• More than just RBBB — the qR pattern in lead V1 is an ECG indicator of pulmonary hypertension in today's case (See My Comment in the March 28, 2022 post in Dr. Smith's ECG Blog).

BOTTOM Line in Today's CASE: If thought of — the above noted ECG indicators strongly suggest massive acute PE. As per Dr. Frick — this diagnosis can be confirmed within minutes by Echo at the bedside!

Figure-2: ECG Findings associated with acute PE.
= = = = = = = =
The "Note" under the S1Q3T3 finding in Figure-2 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — which state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease.