Translated from the original Traditional Chinese post. Read the Chinese original →

ECG on arrival (Fig 1)

A case of out-of-hospital cardiac arrest — what was the cause?

76-year-old woman.

Arrived at an outside hospital in out-of-hospital cardiac arrest; after resuscitation, she got ROSC. She was transferred to our hospital, and the first ECG on arrival in our ED is shown above (at this point she was about to crash). Her heart stopped very soon after. After roughly another 10 minutes of CPR, she got ROSC again. We did another 12-lead ECG (Fig 2).

First ECG after resuscitation (Fig 2)

What do you think caused this?

First look at the ECG on arrival, right before she arrested. Long pause, RAD, RBBB, TWI over V1~V6, II, III.

Then look at Fig 2 → Rate: 90 bpm, SR, RAD, RBBB, TWI over V2~V4, II, III, aVF.

Here we need to think through and clarify a few questions!

  1. When there's TWI in V1~V4, what do you need to consider?
  2. Does the Precordial lead TWI here need to make us consider Wellens' syndrome?
  3. When the diagnosis comes down to Wellens' syndrome vs. PE, how do you make the differential diagnosis? What V2~V3 morphology leans toward RV strain?

When there's TWI in V1~V4, consider the following:

RBBB/ICRBBB appears → because the RBB runs along the septal wall next to the RV, and the RV wall isn't thick, RV strain causes RV wall ischemia, which in turn produces RBBB/ICRBBB

New Electrocardiographic Changes in Patients Diagnosed with Pulmonary Embolism

From Amal mattu

Does the Precordial lead TWI here need to make us consider Wellens' syndrome?

Yes, Wellens' syndrome does need to be considered

When the diagnosis comes down to Wellens' syndrome vs. PE, how do you make the differential diagnosis?

First, when the diagnosis comes down to Wellens vs. PE, it means we think this patient may have an AMI or a PE. So why do we think it's AMI (Wellens) or PE? Because we saw TWI in the R’t precordial leads, and that's what put the idea in our heads.

Here are some differentiating tips that can make our DDx more precise

First, we need to know that PE causes Pul.HTN, which in turn causes RV strain. So which ECG findings suggest there may be RV strain? (Four ECG signs of RV strain → note that PE, COPD, Acute Pul.HTN, and hypoxia from Pneumonia can all produce these changes: the ECG can't diagnose the underlying cause)

DDx for Tall R wave in V1

Here's a very important Paper conclusion: if the diagnosis is down to ACS vs. PE, when TWI is in the precordial leads and also in Lead III → Favor PE, not ACS (TWI in III and V1 is present in 1% of ACS and 88% of PE, so 99% specificity)²

After all that? How do you actually tell the TWI of PE from Wellens' T waves?

  1. Wellens' T waves appear in the pain-free period
  2. ACS, or especially reperfusion (Wellens), rarely has tachycardia
  3. Wellens' T waves and PE's T waves look different (sounds kind of mystical LOL)

PE’s T wave vs. Wellens’ T wave

Look closely: the top row is all different PE cases, and the bottom row is all different Wellens cases. Notice anything different?

What V2~V3 ECG morphology leans toward RV strain? (If RBBB is present, the criteria below don't apply)¹

PE's TWI is convex STE that then bends downward like a roller coaster; ACS-Wellens TWI drops steeply and is sharper

Back to the original Case~~~

This patient's ECG showed RAD, RBBB, TWI over V2~V4

We then did a Chest CTA, which showed the right upper pulmonary vessels completely occluded.

The patient went home to heaven that afternoon………

  1. Dr. Smith’s ECG Blog: A crashing patient with an abnormal ECG that you must recognize — link
  2. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves
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