A man in his 30s with cardiac arrest and STE on the post-ROSC ECG

Written by Pendell Meyers and Peter Brooks MD

A man in his 30s with no known past medical history was reported to suddenly experience chest pain and shortness of breath at home in front of his family. He reportedly told his family "I think I'm having a heart attack", then they immediately drove him to the ED, and he was able to ambulate into the triage area before he collapsed and became unresponsive. CPR was initiated immediately.  It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation.

Initial ROSC was obtained, during which this ECG was obtained:

What do you think?

Meyers interpretation:

This is a complicated interpretation made even more so by the fact that it is immediately post ROSC. The rhythm is atrial fibrillation. The QRS complex is within normal limits. In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. 

Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia). There is also STD in V2-V4 (but maximal in V5-V6).  If this is ACS with Aslanger's pattern, the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral).  This counteracts the STE of II and aVF, without affecting lead III. (The inferior ST depression vector of subendocardial ischemia counteracts the inferior component of the STE vector in all inferior leads except lead III, hiding the OMI).

As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow).

In addition to all of the above, there are T wave inversions in III and aVF, as well as T wave inversions in V2-V4. The morphology of V2-V4 is very specific in my experience for acute right heart strain (which has many potential etiologies, but none more common and important in EM than acute pulmonary embolism).

I sent it to 2 of my ECG nerd colleagues with no clinical information whatsoever, who instantly said: 

"Looks like afib with subendocardial ischemia and right heart strain pattern."

"I was going to say the same thing."

__________

Smith comment: Almost all witnessed arrest from OMI or any ACS is due to ventricular fibrillation and only about 5% of arrest from pulmonary embolism is due to ventricular fibrillation.  When the ECG differential is between OMI on the one hand, and PE/type II OMI on the other, the absence of VT/VF strongly favors PE.

Pulseless electrical activity with witnessed arrest as a predictor of sudden death from massive pulmonary embolism in outpatients

Conclusions: outpatients with witnessed cardiac arrest and primary PEA carry a high probability of Massive Pulmonary Embolism

________________

Case Continued:

"Initial ROSC EKG showed what appeared to be in atrial fibrillation with inferior ST elevations, depressions in aVL, concerning for STEMI."

He had multiple cardiac arrests with ROSC regained each time. 

"Endotracheal tube re-intubation was confirmed multiple times, bilateral breath sounds, yet O2 saturation remained in the 50s and 60s. I was able to visualize the ETT on initial intubation pass through the cords however given his continued hypoxemia, I felt it best to replace the tube to ensure no cuff malfunction or iatrogenic cause of his low O2. I spoke with cardiology regarding his EKG findings, who did not feel as though patient was a cardiac catheterization candidate at that time."

Repeat ECG:

This is classic PE morphology, with T-wave inversions in V1-V4 and also in lead III

Limited ED US showed a dilated right ventricle and right lower extremity DVT.

"Decision was made to push tPA after approximately 25 minutes of CPR, and after approximately 25 minutes after tPA was given, O2 saturation increased to 97%, and the patient was no longer cyanotic, converted to normal sinus rhythm with anterior lateral T wave inversions with ST depressions."

"After approximately 1 hour of total intermittent CPR time, final ROSC achieved....Patient did have extremity movement during central line placement. On epinephrine and norepinephrine drips..."

CT angiogram showed extensive saddle pulmonary embolism.

He was transferred an interventional center where he was evaluated by the ECMO team, cardiology, vascular surgery, and CT surgery teams, who together decided against immediate ECMO and embolectomy given unclear neurologic prognosis. The next day, with worsening renal function, VA ECMO and continuous renal replacement therapy were initiated. 

Here are a few more ECGs during this time:

He was on ECMO for 5 days with improvement and decannulation, as well as discontinuation of CRRT. He spent almost 2 months in the hospital, and reportedly made a full neurologic recovery. Hypercoagulability workup was positive for lupus anticoagulant. He was prescribed apixaban.

See this relevant case;

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

See our other acute right heart strain cases:

A man in his 40s with RUQ abdominal pain

A woman in her 50s with shortness of breath

When the ECG is more revealing than the HPI

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

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

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

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

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")

Learning Points:

Sudden witnessed Cardiac Arrest due to ACS is almost always due to dysrhythmia.  If there is PEA, the suspect another etiology such as PE (and there are others of course)

You must learn the ECG pattern of acute right heart strain to take excellent care of dying PE patients. 

The ECG accurately reflects the physiologic state of the underlying myocardium, but there is always more than one possible etiology of that physiologic state. OMI findings on ECG (representing full thickness active infarction) are most commonly caused by acute coronary occlusion from type 1 ACS, but there are many other ways to achieve the same state of near-complete state of supply/demand mismatch to cause full thickness infarction. Perhaps the most common would be fixed CAD and post-cardiac arrest causing hypotension and low flow through the chronic lesion, resulting in true transmural injury but subsides when normal perfusion is returned.

Although it takes practice to learn the ECG differences between acute right heart strain and ACS such as reperfusion findings, it should not be hard to differentiate them clinically: When symptoms are acute and the inferior/anterior T waves are inverted, the PE patient is actively symptomatic and sick, with ultrasound findings of acute right heart strain; the reperfused LAD patient is better, usually the pain is gone, and ultrasound shows a normal RV and possible LAD region wall motion abnormality. Also, ACS does not cause hypoxemia out of proportion to hemodynamic compromise, as PE can.

If you use quantitative end-tidal CO2 monitoring, there is never any need to waste time making sure that the endotracheal tube is correctly placed. 

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MY Comment, by KEN GRAUER, MD (10/10/2022):

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Today’s case is a “Save”! This patient arrested shortly after hospital arrival. He was resuscitated — but subsequently had multiple cardiac arrest recurrences, with successful resuscitation each time. His course remained complicated — but amazingly, he was discharged from the hospital some 2 months later with intact neurologic status!

Drs. Brooks and Meyers highlight a number of important points brought out in the management of this complicated case. These include.

• Interpretation of a post-resuscitation ECG can be extremely challenging. This is because of how common it is to see ECG findings of diffuse subendocardial ischemia immediately after resuscitation (which is why many advise waiting a short period of time [ ~15 minutes] after ROSC, and then repeating the ECG to see if ischemic changes persist).
• Many (if not most) patients following successful resuscitation after cardiac arrest do not immediately regain consciousness. As a result — the history will often be limited to what was known prior to the arrest.
• Tachycardia, especially in association with rapid AFib — is notorious for producing transient ST elevation not due to acute infarction (that often resolves once heart rate slows). Tachycardia is of course, quite common in patients following cardiac arrest.
• The value of Stat Echo in the ED for confirming clinical and ECG suspicion of acute PE cannot be overstated! In today's case — distinction between OMI vs acute PE was made by the finding of a large, dilated right ventricle on Echo.

I focus my comment on Taking Another LOOK at the first 2 ECGs obtained in today's case. For clarity — I reproduce these 2 tracings in Figure-1.

Figure-1: The first 2 ECGs obtained in today's case.

MY Thoughts on the ECGs in Figure-1:

As per Drs. Brooks and Meyers — interpretation of ECG #1 is complicated by the fact that it was obtained immediately post-resuscitation.

• The rhythm is rapid AFib. As noted above — it is not uncommon to see transient ST elevation with rapid AFib that resolves once the rate slows. Whether this accounts for the ST elevation we see in lead III of ECG #1 is uncertain from this single tracing.
• QRS morphology for beats #5, 7, 8 and 9 is wider, variable, and quite different from QRS morphology of the other beats on this tracing. These beats are most likely supraventricular, conducted with different degrees of RBBB and/or LAHB aberration. From an ECG perspective — these wider and different-looking complexes limit the number of beats we have to assess ST-T wave appearance in leads aVL and aVF.
• Lead V2 looks "off" — because its isoelectric QRS complex and very shallowly inverted T wave looks nothing like QRST morphology in either of its neighboring leads (ie, leads V1 and V3). Given the importance we place on the first 3 anterior leads when looking for RV "strain" — malposition of lead V2 clearly hinders our ECG assessment.
• Otherwise (as noted by Drs. Brooks and Meyers) — there is ST depression in all lateral leads (I, aVL; V5,V6) — with ST elevation in lead aVR.
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• BOTTOM Line: ECG #1 shows rapid AFib — with the principal differential diagnosis being between acute RV strain (ie, presumably from massive acute PE in view of this patient's sudden cardiovascular collapse) — vs — Aslanger's Pattern (ie, inferior OMI with simultaneous subendocardial ischemia). How much of an effect the tachycardia and immediate post-resuscitation status of this patient may have on the shape and amount of ST-T wave deviation (elevation and depression) is unknown from this single tracing.

What About ECG #2?

As noted above — Echo showing a dilated right ventricle — Ultrasound suggesting lower extremity DVT — and markedly improved oxygenation with 25 minutes of administering TPA were the tests that indirectly confirmed acute massive PE as the diagnosis. That said, from an ECG assessment standpoint — I thought ECG #2 was much more supportive of this diagnosis of massive PE.

• ECG #2 shows restoration of sinus rhythm. The heart rate is still ~100/minute — but this is clearly slower than the rate of the rapid AFib that was seen in ECG #1.
• Although ST segment coving in lead III persists in ECG #2 — there is clearly less ST elevation at this slower rate. There is also less reciprocal ST depression in lead aVL. These ECG findings — in association with lack of OMI evolutionary changes in the other 2 inferior leads, dissuades me from Aslanger's Pattern with OMI.
• Lead V2 in ECG #2 now looks much more like it "fits" — in that the shape and relative amount of T wave inversion is now more consistent with that seen in its neighboring leads. In fact, given the clinical history — the overall ECG pattern of ST segment coving with symmetric T wave inversion in leads V1-thru-V4 are now diagnostic of acute RV "strain" until proven otherwise.
• Although ST-T wave changes of  RV "strain" on ECG are most commonly seen in anterior chest leads — they are also often seen in one or more of the inferior leads. In this context — the T wave inversion we see in lead III of ECG #2 is perfectly consistent with RV "strain".

Putting It All Together:

As stated — assessment of the ECGs in today's case is no simple matter. This patient underwent multiple resuscitations — which of itself may account for a series of ECG abnormalities. But the history of sudden cardiovascular collapse — in association with the findings in ECG #2 of sinus tachycardia — not quite S1Q3T3 (because there is a small initial positive deflection in lead III [ = "No Q, but an r wave in lead III]) — but an incomplete RBBB pattern (rSr' in lead V1 with narrow terminal s waves in leads I and V6) — and the classic ST-T wave appearance of RV "strain" in leads V1-thru-V4 says, "Large acute PE until proven otherwise!"

• NOTE: For more on the ECG diagnosis of acute RV "strain" (and acute PE) — Please check out My Comment at the bottom of the page in the March 28, 2022 post in Dr. Smith's ECG Blog.