ECG Interpretation: ECG Blog #233 — Why Did the Patient Die?

The ECG shown in Figure-1 was obtained from a previously healthy 70-year old man, who presented to the ED (Emergency Department) with new-onset dyspnea.

Does the anterior T wave inversion represent acute ischemia from Wellens’ Syndrome?
If not — What is YOUR diagnosis?

Figure-1: ECG obtained from a previously healthy 70-year old man with new-onset dyspnea.

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NOTE #1: Some readers may prefer at this point to listen to the 7:40 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-49).

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Today’s ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).

NOTE #2: Among the topics discussed in this Audio Pearl are the ECG findings with acute PE (See Figure-3 and Figure-4 in the ADDENDUM below) — Wellens' Syndrome (reviewed in ECG Blog #209) — and — Giant T Wave Syndrome (reviewed in ECG Blog #59).

My THOUGHTS on the ECG in Figure-1:

The rhythm is sinus tachycardia at ~115/minute. The PR interval is normal. The QRS is not prolonged. The QTc appears to be no more than minimally prolonged (though this is difficult to assess given the tachycardia). The frontal plane axis is relatively vertical (almost +90 degrees) — but not quite rightward (since the S wave in lead I is not predominantly negative). There is no chamber enlargement.

Regarding Q-R-S-T Changes:

There is a Q wave in lead III — and perhaps a tiny q wave in lead aVF. There is a QS complex in lead V1.
Regarding R Wave Progression — a tiny initial r wave (positive deflection) is seen in lead V2 — with this R wave gradually increasing in size, until transition finally occurs between leads V5-to-V6.
ST segments are coved, with moderate symmetric T wave inversion in leads III, aVF and leads V1-thru-V4. A smaller effect on ST-T waves is seen in leads II, V5 and V6.

Additional ECG Findings Relevant to Today’s Case:

An S1Q3T3 pattern is present!
S waves persist across all chest leads (with a significant S wave still present in lateral lead V6).
Slight ST elevation is seen in lead aVR.

IMPRESSION:

The History is KEY in today’s case: This previously healthy 70-year old man presented with new-onset dyspnea. There is no mention of chest pain. As a result — acute coronary disease would seem to be much less likely. In contrast — acute PE (Pulmonary Embolism) is perfectly consistent with this history!

In association with the history in today’s case — several of the ECG findings noted above in Figure-1 place acute PE as the presumed diagnosis until proven otherwise.

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The ECG Diagnosis of Acute PE:

The ECG is far from optimal as an investigative tool for the diagnosis of acute PE. That said — there are times when the ECG, in conjunction with the clinical history — can be extremely helpful in suggesting the diagnosis even before additional testing can be accomplished. The ECG in Figure-1 provides an excellent example of this situation.

PEARL #1: The ECG is unlikely to identify patients with smaller PEs. Do not expect to see anything on the ECG of these patients (This may be a “blessing in disguise” — as longterm benefits of anticoagulating such patients are debatable). Sensitivity of the ECG for suggesting the possibility of acute PE is clearly better with large (especially submassive) PEs.

PEARL #2: One of the problems with using the ECG as a diagnostic tool for detecting acute PE — is that there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of several supportive ECG findings that occur in association with the “right” clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock, especially in a patient predisposed or with a prior history of venous thromboembolism).

We list the ECG findings to look for when considering the diagnosis of acute PE in Figure-2.
We expand upon these ECG findings in the Addendum below (See Figure-3 and Figure-4).

Figure-2: ECG findings associated with acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).

WHAT are the ECG Findings in Today's Case?

We list below positive and negative ECG findings from Figure-2 that are relevant to today's case:

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 Figure-1 is over 100/minute.
Acute RV “Strain” — Awareness of ECG evidence of RV (Right Ventricular) Strain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) — and/or — in inferior leads (II,III,aVF). Abnormal ST-T wave changes consistent with acute PE are seen in both of these lead areas in Figure-1.
S1Q3T3 — Whereas the diagnostic value of this pattern is minimal at best, when seen as an isolated finding — a definite S1Q3T3 pattern can be extremely helpful IF seen in association with other ECG evidence of acute PE. Such is the case here.
There is no RAA.
The frontal plane axis is relatively vertical — but not rightward.
Neither complete nor incomplete RBBB is present.
There is no tall R wave in lead V1.
Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
ST Elevation in Lead aVR — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Although subtle — there is ST elevation in lead aVR in Figure-1.
Atrial fibrillation is not present.

Putting It All Together: The one unifying diagosis that explains all of the ECG findings noted above in Figure-1, in this 70-year old man who presented to the ED with new-onset dyspnea (but no mention of chest discomfort) — is acute PE.

CASE FOLLOW-UP: A presumed diagnosis of acute PE was rapidly made by the treating clinicians. They promptly initiated thrombolytic therapy. Unfortunately, the patient’s condition deteriorated as treatment was being started. Resuscitation was unsuccessful. Although confirmatory testing was not completed (made impossible by the patient’s unstable and rapidly deteriorating condition) — I believe the circumstances of cardiac arrest within minutes of arrival in the ED, in association with the combination of ECG findings shown in Figure-1 is consistent with massive acute PE as by far the most likely etiology for explaining this patient's rapid demise.

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Acknowledgment: My appreciation to Ismail Mahmood (from Babil, Iraq) for making me aware of this case and allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case:

ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”.
ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
ECG Blog #59 — Reviews the causes of Giant T Wave Inversion.

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ADDENDUM (6/12/2021): I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus).