Resuscitated from ventricular fibrillation. Should the cath lab be activated?

This patient was witnessed by bystanders to collapse.  They started CPR.  EMS arrived and found him in Ventricular Fibrillation (VF).  He was defibrillated into VT.  He then underwent dual sequential defibrillation into asystole.  After 1 mg of epinephrine they achieved ROSC.  Total prehospital meds were epinephrine 1 mg x 3, amiodarone 300 mg and 100 mL of 8.4% sodium bicarbonate.

The patient was brought to the ED and had this ECG recorded:

What do you think?  And what do you want to do?

The ECG shows severe ischemia, possibly posterior OMI.   But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia.  It takes time for that ischemia to resolve.  After cardiac arrest, I ALWAYS wait 15 minutes after an ECG like this and record another.  The ST depression usually resolves, or is clearly resolving (getting much better).

Just as important is pretest probability: did the patient report chest pain prior to collapse?  Then assume there is ACS.  In this case, the patient was 30 years old and there was reportedly some drug paraphernalia in the area.  This may or may not be true, but it should give you pause.  On the other hand, cardiac arrest from opiates is respiratory arrest followed by cardiac arrest, and the rhythm is usually brady-asystole, not ventricular fibrillation.  VF should make you think of ischemia, cardiomyopathy (especially scar from old MI), or one many other cardiac but non-ischemic etiologies.

In this case, the cath lab was activated and the patient had a normal angiogram.

See these related cases:

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

Cardiac arrest #3: ST depression, Is it STEMI? or is he an ACCESS Trial Candidate?

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MY Comment, by KEN GRAUER, MD (7/25/2024):

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Clinical ECG interpretation is a 2-Step process.

• For clarity in Figure-1 — I've reproduced today's ECG — obtained following successful resuscitation of out-of-hospital cardiac arrest.

Figure-1: The initial ECG in today's case.

   — The 2 Steps in ECG Interpretation —

STEP #1: Describe what you see ....

• The rhythm in Figure-1 is rapid and supraventricular (the QRS is narrow in all leads). The rate is ~130/minute. Although not immediately apparent (because it is hard to distinguish the limits of a P wave in lead II) — the rhythm is Sinus Tachycardia, as other leads correspond to the timing of what seems to be an upright deflection that is subtly notching the end of the T wave in lead II (and which almost certainly represents the sinus P wave). Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit (as the patient's condition improves) — allowing clearer definition between the T and P waves.
• Otherwise — there is early transition (predominant R wave already by lead V2) — and what appears to be generous voltage (that is probably not abnormal given the young adult age of today's patient).
• 
  
• The most remarkable finding is in Figure-1 — is the diffuse and marked ST depression (most prominent in the chest leads) — with ST elevation in lead aVR > V1.

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STEP #2: Clinically apply to the case at hand ....

• The ECG "picture" that we see in Figure-1 of a supraventricular rhythm with diffuse ST depression, except for ST elevation in lead aVR (and to a lesser extent in lead V1) — defines the important clinical entity known as DSI (Diffuse Subendocardial Ischemia).

As we have often emphasized on Dr. Smith's ECG Blog (See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease. Many patients with DSI do have severe coronary disease — but many do not. Therefore — recognition of DSI on ECG should prompt consideration of 2 Categories of diagnostic entities:

• Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• 
  
• Subendocardial Ischemia from some other Cause (ie, sustained tachycardia — sinus or from some other arrhythmia; shock/profound hypotension; GI bleeding; anemia, etc.) — or, potentially as occurred in today's case — Cardiac arrest secondary to respiratory arrest from a non-cardiac cause.

In Summary: Today's case serves as a reminder of the 2-Step process in clinical ECG interpretation. Rather than slowing the interpretation down — ECG assessment is actually sped up.

• Description of today's ECG findings (Sinus tachycardia with diffuse ST depression and ST elevation in aVR) — is diagnostic of DSI. 
• As demonstrated by Dr. Smith in his above discussion — Application of the ECG findings in Figure-1 to today's clinical scenario (ie, marked sinus tachycardia in this younger adult with drug overdose and respiratory arrest) — provides an immediate and much more likely explanation for DSI than trying to postulate ACS.