A crashing patient with an abnormal ECG that you must recognize

Written by Pendell Meyers, with edits from Steve Smith


Let's consider this nearly pathognomonic ECG without the clinical context (because sometimes the clinical context will not be as easy as in this case).

What is the answer?

This ECG is diagnostic of hemodynamically significant acute right heart strain. Notice I did not say "pulmonary embolism," because any form of severe acute right heart strain may produce this ECG. This includes, but is not limited to, PE, asthma/COPD exacerbation, hypoxic vasoconstriction from pneumonia, acute pulmonary hypertension exacerbation.  It has even been seen anecdotally in acute cessation or discontinuation of continuous IV pulmonary vasodilator.

The findings include sinus tachycardia, characteristic QRS morphology most diagnostic in V3 with a small R wave followed by a very large S wave with a convex upward ST segment morphology, ST segment strain morphology in the inferior and anterior leads leading to deep symmetric T-wave inversion.

Why is it not Wellens??? (Wellens pattern is a term which refers to coronary reperfusion morphology in the anterior leads)

The best answer is because the entire gestalt of the ECG shows acute right heart strain instead, and just does not look like Wellens after you've seen Wellens hundreds of times. It is true that the morphology of the T-wave inversions can be very similar in anterior reperfusion syndrome (Wellens). It is also true that anterior and inferior T-wave inversion could be consistent with reperfusion of a type III wraparound LAD occlusion, despite the fact that Kosuge et al showed that T-wave inversion in lead III is much more likely to be PE than ACS if your differential contains nothing else.  However, in reperfusion (Wellens'), the symptoms are resolved at the time of the ECG.  Thus, it is critical to compare the ECG with the symptomatic state of the patient!  

Differences of Pulmonary Embolism T-waves from Wellens' T-waves:
1. Wellens' is a syndrome of a painless period following an anginal (chest pain) event.  Coronary reperfusion changes on ECG should be accompanied by significant reduction or resolution of symptoms. In this case we have a crashing patient while T-wave inversion is ongoing!

2. Acute coronary occlusion (especially during reperfusion) is very rarely accompanied by tachycardia.  When there is tachycardia, the patient is in cardiogenic shock with very poor LV function on bedside echo.

3. The T-waves simply look different in Wellens'.  Here is an example of Wellens'.  We hope you can see the difference:

See these cases for more examples: 

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

This is a great case:

Sudden Severe SOB and ST Segment Elevation: What is the Diagnosis and Treatment?

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

A 30-something with 8 hours of chest pain and an elevated troponin

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

Please notice in particular the morphology in V2-V3, as I believe this is particularly helpful to describe as evidence of acute right heart strain, including:

- Generally much bigger S-wave than R-wave
- Usually either isoelectric J-point or some small J-point elevation followed by convex upward ST segment elevation rollercoastering into T-wave inversion
- Usually some ST segment depression in the more lateral leads V4-V6 and the inferior leads, also with T-wave inversion
- Please note that these QRS characteristics will not apply in the not-uncommon scenario that the patient develops acute RBBB because of the strain on the RV

Here are the blown up images of V2-V3 from several of the cases on this blog with acute right heart strain (all but one of which was due to pulmonary embolism, and the other was due to acute severe asthma exacerbation)

Now that we've learned the lesson, let's watch this very interesting case play out:


A female in her 40s with history of HTN and obesity presented with progressively worsening dyspnea with mild exertion, and now with dyspnea at rest over the past 4 days. She also complained of generalized weakness, lightheadedness, diaphoresis, chest pain, and cough. On initial exam she appeared acutely ill, with initial vitals showing tachycardia, hypoxia, and borderline hypotension.

Here is her initial ECG, followed by her repeat ECG approximately 15 minutes later:

Bedside echo was done.  This one is from a previous case on this blog,  but is similar to this patient:



This shows impressively obvious right heart strain.  The LV is small (underfilled) with good function. 


She was appropriately anticoagulated immediately with heparin before going to CT scan.

There are filling defects in both main pulmonary arteries. The pulmonary artery trunk is dilated at 35mm per radiology report.

Filling defects are seen to extend to bilateral lobar, interloper, and segmental branches diffusely throughout both lungs. This is a very large clot burden. Radiology commented that the inter ventricular septum is bowed towards the left ventricle, suggestive of right heart strain.

Troponin T returned elevated at 0.12 ng/mL. NT pro BP returned at 10,676 pg/mL.

Despite heparin and supportive care, the patients mental status and blood pressure worsened. She was diagnosed with massive PE and given intravenous tPA with rapid improvement in hemodynamics and mental status.

She had an uneventful ICU course and improved steadily over the course of a week. She was discharged and did well.

Here is her ECG on day 2 after much improvement in hemodynamics and oxygenation:

Tachycardia has resolved. ST and T-wave abnormalities evolving appropriately.

Here is her ECG on day 4:

Almost entirely back to normal.

 Learning Points:

1) The history and exam will not always be this obvious, yet in cases this severe, the ECG findings often are obvious if you know what to look for.

2) The cells of the right ventricle do not know why they are having such a hard time when they report their acute strain on the ECG. Whether it's a PE or a severe asthma attack, the cellular physiology of these cells is acutely the same. Therefore the ECG is also indistinguishable between acute right heart strain etiologies.

3) Reperfusion T-wave inversion should be present in the pain free state. These T-wave inversions in the anterior and inferior leads during pain are likely to be due to acute right heart strain from PE.

Primer on the ECG in Pulmonary Embolism:

These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V₁ were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V₁ allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE.