Submitted and written by Lucas Goss MD, edits by Meyers and Smith
A man in his 40’s with only past medical history of tobacco use presented with sharp RUQ abdominal pain that's worse with exertion and associated with nausea and diaphoresis. On arrival the provider noted him to be ill-appearing. His vitals are shown below, and on exam he had cool extremities and RUQ abdominal tenderness.
HR 108
RR 24
BP 106/85
SpO2 88%
Initial ECG:
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| What do you think? |
My interpretation:
Sinus tachycardia
Normal QRS
No HyperK
Normal QT
S1Q3T3
In V1-V4 (however most notable in V2 and V3) there are small R waves followed by large S waves with associated convex upward ST elevation followed by deep symmetric T wave inversions. Additionally there are symmetric T wave inversions in the inferior leads. These findings, in conjunction with tachycardia, hypoxemia, RUQ pain, and shortness of breath is quite specific for acute right heart strain, with the most common cause being acute PE.
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Smith comment: This ECG is all but pathognomonic for pulmonary embolism. The heart rate is 116: the easiest way to identify this ECG as “probably not ACS” is the tachycardia. ANY time I see tachycardia I doubt ACS as the etiology of the ST-T abnormalities (see abstract we wrote at the bottom). It is easy to recognize. This is a rule which is easy for even an ECG novice to apply, unlike T-wave morphology etc.
Neither 1. hypoxia nor 2. tachycardia occur in ACS UNLESS there is 1. pulmonary edema due to cardiogenic shock or 2. low stroke volume due to cardiogenic shock. Wellens syndrome does NOT cause cardiogenic shock since the artery is open. Bedside echo of course can tell you immediately about the stroke volume. Thus, Wellens' T-waves are not associated with tachycardia or hypoxia UNLESS there is a 2nd simultaneous pathology.
See our abstract on tachycardia in ACS at the bottom.
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His initial high sensitivity troponin I returned at 754 ng/L (URL for men 20 ng/L). The provider treating this patient was instead concerned for Wellens Syndrome (LAD reperfusion) and Cardiology was consulted. Other labs returned and showed mild elevation of AST and ALT along with an elevated BNP. When cardiology evaluated the patient he had significant RUQ tenderness and they were concerned for an intra-abdominal process somehow contributing to his increased troponin (as if by "demand ischemia"). Due to significant abdominal pain a CT of the abdomen and pelvis was performed. In the meantime a repeat troponin returned at 671 ng/L.
Repeat ECG:
As you can see, his ECG is essentially unchanged.
Why is the ECG and clinical picture not suggestive of reperfusion T waves in the anterior leads (Wellens Syndrome)?
When there are T wave inversions in the precordial leads, then T wave inversions in lead III are much more likely to be due to PE rather than ACS.
The patient’s symptoms are not resolved at the time of the ECG, rather they continue to get worse. In Wellens (LAD reperfusion), you'd expect the patient’s symptoms to be largely resolved or at least significantly improved.
Additionally he has mild hypoxia with clear lungs. This is not as typical for a large anterior MI in cardiogenic shock, where you’d expect pulmonary edema. Rather, this patient has a chest x-ray with clear lungs, symptoms of hepatic congestion/RV failure (RUQ pain, elevated liver enzymes), and tachycardia (usually not present in OMI unless cardiogenic shock is present) which all point towards acute RV failure.
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 APE (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."
Back to our case:
His CT of the abdomen and pelvis returned, and did not demonstrate any acute intra-abdominal process, however luckily did catch extensive bilateral pulmonary emboli.
A CTA of the chest was then performed.
6E648B51-D6CE-4383-BCCE-78DCAEE84363.mov from Lucas Robert on Vimeo.
CT Read: Large bilateral pulmonary emboli with elevated RV/LV ratio
A formal echo was also performed that demonstrated a severely dilated RV with hypokinesis of the free wall and preserved apical function (McConnell sign) consistent with acute right heart strain. He also was found to have a PFO with a right-left shunt.
Fortunately, the patient remained hemodynamically stable and was determined to have a severe-submassive PE. He was started on heparin and admitted to the ICU. Ultimately, he never required thrombolysis or other advanced therapies. He had a lower extremity ultrasound that demonstrated bilateral DVTs with portions of chronic thrombosis. He had an uneventful hospital course otherwise and was discharged home.
As you can see, it’s critical to apply these ECG findings to the right clinical context and use bedside echocardiography to aid in diagnosis.
It can sometimes be hard to tell the difference between anterior reperfusion T waves, anterior and inferior reperfusion T-waves in the case of a wrap-around LAD, and acute right heart strain as seen in this case. However, using the clinical picture, history of symptoms, and bedside echo can help differentiate the two. Additionally, remember that simultaneous TWI in III and anterior leads is more likely PE than ACS, as demonstrated in Kosuge et al.
More importantly, anterior reperfusion and PE simply look different on the ECG, in ways that I have a hard time describing in words, but just has to be visually memorized.
Below you can compare cases of acute right heart strain to cases of anterior reperfusion.
Here are some cases of PE with acute right heart strain:
Compare our patient’s ECG with these examples of anterior reperfusion:
You can see that in these examples of anterior reperfusion, the T waves are largely upright in leads III and aVF. Additionally, reperfusion T waves often extend into the lateral leads (depending on the area of the vessel that was previously occluded). This is compared to acute right heart strain where findings are often most maximal in the leads representing the RV (V2 and V3, sometimes out to V4).
Learning Points:
Tachycardia does not occur with Wellens and is unusual in ACS, unless the ACS is so severe that it results in cardiogenic shock, or unless there is another simultaneous pathology.
Hypoxia does not occur with Wellens and is unusual in ACS, unless the ACS is so severe that it results in cardiogenic shock with pulmonary edema (B-lines on ultrasound), or unless there is another simultaneous pathology.
All you have to do is memorize the shapes of these squiggly lines and you can instantly diagnose some of the most important PEs. You can avoid several hours delay to diagnosis, avoid the confusion of thinking this could be Wellens, etc. Sometimes the ECG is the more specific than the physical exam, sometimes not. If you can recognize when the ECG unlocks the understanding of the case, patients will benefit.
Although the ECG is not sensitive for any PE (especially those without right heart strain), the findings of symmetric t-wave inversions (most notably in V2 and V3) with associated T wave inversions in lead III and AVF, with the morphology shown above, can be specific for acute right heart strain.
Apply the ECG to the clinical context of the patient and use your bedside ultrasound if you are unable to distinguish this pattern from Wellens. The ultrasound is also very different between the two pathologies.
Wellens ECG findings are different from findings of acute right heart strain. In Wellens, there are usually no T-wave inversions in leads III and aVF and findings often extend out to the lateral leads. Again, this is in contrast to acute right heart strain where findings are often maximal in lead V2 and V3.
See Also:
A woman in her 50s with shortness of breath
A crashing patient with an abnormal ECG that you must recognize
A man in his 40s with a highly specific ECG
Chest pain, ST Elevation, and tachycardia in a 40-something woman
Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3
A young woman with altered mental status and hypotension
A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli
A 30-something with 8 hours of chest pain and an elevated troponin
Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....
Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis
Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?
Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis
Answer: pulmonary embolism. Now another, with ultrasound....
This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.
Chest Pain, SOB, anterior T-wave inversion, positive troponin
Anterior T wave inversion due to Pulmonary Embolism
Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")
Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma.
All cases with at least one elevated cTnI were adjudicated into specific MI type (or no MI) by two clinicians who reviewed all medical records. Patients were stratified according to presence or absence of type I MI, and of heart rate (HR) of less than 99 bpm, and less than 120 bpm on presenting ECG. All ECGs were coded by an expert clinician as having ST-elevation, ST-depression, T-wave inversion [ST/T abnormalities, (ST/T-A)], or none of the above.
In hemodynamically stable patients with chest pain, sinus tachycardia aids in the identification of patients unlikely to have type I MI, especially in those with HR greater than 120 bpm.
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MY Comment by KEN GRAUER, MD (4/28/2020):
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Insightful case presented by Drs. Goss and Meyers highlighting the importance of recognizing the ECG signs of acute PE. I focus my comments on further dissecting some of these "tell-tale" ECG features.
- The "theme" of today's case was "pattern recognition". Like the ECG diagnosis of RVH (Right Ventricular Hypertrophy) — ECG recognition of the "pattern" suggestive of acute PE is not made on the basis of any single ECG finding.
- Instead — in a patient with a History and Exam potentially consistent with the diagnosis — it is the constellation of ECG findings that when present, strongly suggests acute PE until proven otherwise.
As per Drs. Goss and Meyers — the ECG pattern of acute PE is one that we need to recognize within seconds of seeing it!
- For clarity — I've reproduced the initial ECG in today's case in Figure-1. I've added at the bottom of this Figure the Table that I showed in My Comment from the March 28, 2022 post of Dr. Smith's ECG Blog.
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| Figure-1: Assessment of the initial ECG in today's case for features suggestive of acute PE (See text). |
- Most patients do not "read the textbook" before they have their event. Today's patient was no exception — as clinical "context" was needed to interpret a number of the ECG findings that I highlighted with BLUE arrows.
- FIRST — Although today's patient did not complain of acute dyspnea — this "ill-appearing" 40-year old man was tachycardic (108/minute) — tachypneic (24/minute) and hypoxemic (SpO2 = 88%) — so his presentation was clearly "potentially consistent" with acute PE.
- Sinus Tachycardia: While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in today’s case is consistent with this at ~115/minute.
- RV (Right Ventricular) Strain: Recognition of the ECG picture of RV "strain" is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-too-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in the anterior leads (V1,V2,V3) — and/or in the inferior leads (II,III,aVF). In ECG #1 — the ST segment coving with deep, symmetric T wave inversion in anterior leads is perfectly consistent with the ECG picture of acute "RV strain". While inferior lead changes are not nearly as marked — the T wave is inverted in leads III and aVF, with a hint of inversion also in lead II.
- S1Q3T3: In my experience, it is rare (if ever) that the isolated finding of an S1Q3T3 pattern will make the diagnosis of a new significant PE. That said, this ECG sign may be extremely helpful IF seen in association with other ECG evidence of acute PE. NOTE: Technically — an S1Q3T3 sign is not present in ECG #1 — because there is a small-but-present initial positive deflection (r wave) in lead III. Clinical implications of an S1Q3T3 pattern have only been validated if all 3 components are present ( = an S wave in lead I — a Q wave in lead III — and T wave inversion in lead III).
- That said — despite the lack of a "true" S1Q3T3 sign — the deeper-than-expected S wave in lead I and the rSR' complex that we do see in lead III both add support to the ECG impression of acute RV "strain". The nearly isoelectric (if not slightly negative) QRS complex in lead I, in association with nearly isoelectric QRS complexes in most other limb leads result in an indeterminate frontal plane axis, that is one of the findings associated with acute RV "strain".
- Complete or incomplete RBBB is another ECG finding associated with acute PE. Lead III is a right-sided lead (with an electrical viewpoint of +120 degrees in the frontal plane). As a result — the finding of an rSR' complex in lead III (instead of in lead V1) serves as a surrogate form of incomplete RBBB, especially given the narrow S waves in lateral leads I and V6, and the terminal notch (instead of an R' complex) in lead V1.
- ECG findings in Figure-1 that are not present in today's tracing — include RAA, a predominant R wave in lead V1, ST elevation in lead aVR, and atrial fibrillation.
- The final ECG finding that is at least suggested — is persistence of precordial S waves through to lead V6 (albeit the s wave in lead V6 is small).
- Strengthening my impression of acute PE was the clinical presentation (ie, "ill-appearing patient", tachycardia, tachypnea, hypoxemia) — plus several more subtle additional ECG findings that "in context" further supported this diagnosis. These included — the deep S in lead I (with indeterminate frontal plane axis) — the suggestion of RV "strain" that is also present in the inferior leads — the surrogate IRBBB pattern in lead III — and persistence of S waves in the precordial leads (albeit the S wave in lead V6 was not overly deep).
- By the time you see significant hypoxemia, tachycardia and clear indication of acute RV "strain" on ECG (as in today's case) — you are almost certainly dealing with a hemodynamically significant PE in need of prompt diagnosis and treatment!
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