Monday, March 12, 2018

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....

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 readingMarchik 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. 


  1. GREAT case with (as per the title) — an ECG pattern that MUST be recognized! I’d add the following comments regarding ECG signs suggestive of acute right heart strain (therefore acute PE given the clinical scenario here). First — I’d emphasize the thought that rather than any single ECG finding — RVH patterns (including acute RV “strain”) are what I call the “Detective Diagnosis” — in that there is no single ECG finding that is absolutely diagnostic — but instead, there is a series of clues, that like a good “detective story” when put together lead to strong suggestion of the clinical diagnosis. So, in addition to the sinus tachycardia with deep, symmetric T wave inversion in BOTH of the RV distributions (ie, both in inferior as well as anterior leads) — there is: i) RAA (tall, peaked and pointed P waves in each of the inferior leads); ii) an SI,SII,SIII pattern (one usually does not see S waves in all 3 standard leads); and iii) persistence of S waves all the way to V6 (lateral chest lead S waves are relatively uncommon). None of these additional findings that I mention is in any way diagnostic by itself — but ADDED to sinus tach and marked symmetric T wave inversion suggesting acute RV “strain” — these additional findings in the clinical context of acute dyspnea helps paint a highly suggestive picture. P.S. I suspect lead placement of lead V2 in the initial ECG is off — as it just doesn’t make physiologic sense to have deep T inversion in V1 and V3 but not in V2 … This is important to the overall initial picture, because acute RV strain should produce anterior T wave inversion (and lacking this in V2 just doesn’t “fit” unless that lead was malpositioned). Of interest, subsequent ECGs (during recovery) show variations in QRS morphology (probably due to this patients overweight body habitus, making it difficult to “standardize” lead placement …) — but the 2 later ECGs show resolution of those tall, peaked and pointed inferior lead P waves! (consistent with this finding’s utility for supporting our diagnosis of acute RV “strain”). THANKS for presenting this insightful case!

  2. Thanks to Dr.Smith and Dr.Pendell for the case and the well framed description and Dr.Ken for his additional points.. No questions left to ask. ☺️

  3. I can not understand it. In the right ventricular overload, there are high R waves and small S waves in V1. Here it says the opposite, big wave S in V3. I can not understand ... The big S wave in V3 I thought indicated hypertrophy VI

    1. The reason you're confused is that traditional ECG education has failed to differentiate acute from chronic right heart strain!

      I also remember being taught that acute right heart strain would cause large R waves in the right precordial leads. It's not true, it is an overconfident guess from instructors who have seen chronic right heart strain. Acute right heart strain presents as above, with actually small (I even believe diminished) R waves in the R precordial leads, with large S waves in V2-3, as above.

      In chronic right heart strain, the RV has had time to hypertrophy and creates a large narrow R wave in the right precordial leads. See these cases of RHV and compare them to the cases of acute R heart strain above:

      I'm sure this is already described, but here is the underlying principle to be learned here: Acute strain/injury/stunning/infarction to part of the myocardium generally causes diminished QRS forces in the overlying area, whereas chronic strain without death (therefore allowing hypertrophy) causes increased QRS forces due to increased muscle mass.

      This is supported by the fact that, in Dr. Smith's studies on 3 and 4-variable formulas to differentiate subtle LAD occlusion from early repolarization, the most important factor predicting LAD occlusion was decreased R-wave amplitude in V4. This is presumably because acutely injured myocardium does not conduct the action potential as well as healthy myocardium.

      Conversely, as you already know, LVH can produce massively increased R waves in the lateral leads.

    2. I’ll add to Pendell Meyers reply. In the average adult — the LV is about 3 times as thick, therefore in 3 dimensions there may be up to 10 times the mass in the adult LV compared to the RV. This is different than occurs in early childhood, in which the RV is much more comparable in mass to the LV. As a result of the fact that average LV mass so dramatically supercedes RV mass in the average adult — it takes a LOT of RVH to predominate to the point that a predominant R wave will be seen in lead V1. In fact, usually only with severe longstanding RVH or end-stage pulmonary disease with pulmonary hypertension will you see a predominant R wave in lead V1. In contrast — it is much more common to be able to see RVH marked by predominant R wave amplitude in V1 in congenital heart disease. So, as per my earlier comment — think of RVH as the “detective disease”, in which most of the time (unless RVH is severe/longstanding/accompanied by pulmonary hypertension) you won’t see a predominant R wave in lead V1 on the adult ECG — but instead, have to glean the diagnosis of RVH from a combination of other signs (ie, right or indeterminate axis; RAA; low voltage; RV strain; persistent precordial S waves in V5,V6). The case with acute RV strain applies these principles — in that most of the time duration of this “acute” RV strain is too recent for there have been adequate time for a predominant R wave to develop in lead V1 …


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