Wednesday, May 4, 2016

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

A reader (someone in training) sent me this ECG, and asked for my interpretation.

Clinical info:  "The patient was found down in cardiac arrest, defibrillated with ROSC in the field, was unconscious on arrival. Attached is the initial ED ECG."

"I will provide details and outcome to come after your impression." 

Here is the EKG: 

Here is my interpretation: Sinus at a rate of about 80, RBBB, LAFB, ST Elevation in aVL, reciprocal ST Depression in II, III, aVF.  No precordial ST Elevation, but STE often does not show in precordial leads when there is LAD occlusion with RBBB and LAFB.  Proximal LAD occlusion.

When confronted with RBBB and LAFB in a patient with cardiac arrest or typical chest pain or cardiogenic shock, one should assume acute LAD occlusion.  Any occlusion can fail to show in ECGs with normal conduction, with LBBB, and with RBBB.  But in my experience, huge myocardial infarctions are particularly difficult to discern in the presence of RBBB and LAFB.  This is not well described, but I have seen it very often.

See this paper by Widimsky et al., which shows the high association of RBBB, especially with LAFB, with LAD occlusion.  Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAFB) on the admission ECG.

How do you assess ST elevation on these ECGs?  First, find the lead which you believe most clearly manifests the end of the QRS.  I believe that in this ECG it is lead V4.  Then draw a line down to the lead II rhythm strip at the bottom.  Then, using the same point on the complex under leads (I, II, III), (aVR, aVL, aVF), (V1, V2, V3), you can draw a line up and see the end of the QRS in all leads.  In this way, one can see the subtle, downsloping ST elevation in aVL, with reciprocal ST depression in II, III, and aVF.

Here it is:

His response:


This was an interesting case, especially when you red the providers' interpretations of the ECGs.  After the 2nd ECG the diagnosis should be clear, but for some reason they call it "NSTEMI".   No cath done initially, and on day 3 they decided to avoid cath because they thought she was neurologically unrecoverable.

On autopsy on day seven, "99% LAD stenosis".

Here is more detail:

Old ECG on file:
Sinus.  Normal conduction (no BBB).  Baseline Q-waves in V2, V3. Nonspecific ST-T abnormalities.

ECG #2 at 19 minutes:
Smith: RBBB/LAFB persist, but the STEMI is quite obvious here

ECG #3 at 63 minutes
The right bundle branch block has resolved, suggesting that perhaps the artery has opened, but the ST elevation persists, especially in aVL.  [aVL II, III, aVF are diagnostic of high lateral STEMI with reciprocal ST depression. Note that there is NOT 1 mm STE in 2 consecutive leads, but in one lead only (aVL)]
There is some STE in V1-V3 and STD in V6 also.

ED Physician Assessment:
“Initially wide complex PEA. Responded best to bicarb and calcium. Had VT and VF and torsade in field as well…ECG shows wide complex rhythm in 80s. Suspected hyperK given wide complex and response to calcium and bicarb…On repeat ECG rate 77, sinus, now more of an incomplete LBBB pattern with STD in inferior leads and 2mm STE in aVL only. Concerning but technically does not meet STEMI criteria. Resident discussed with CCU fellow and cath lab. Not STEMI criteria.”

Initial potassium: 5.8 mmol/L

Smith comment: Although it is possible that such an ECG represents hyperkalemia, it is a very atypical ECG for hyperkalemia.  

More importantly, such an ECG would only be seen with a potassium greater than 7.0 mEq/L.


Here are some typical pseudoSTEMI patterns for hyperkalemia (multiple examples at this post):

Cardiac Arrest and ST Elevation: You Should Learn to Recognize This!

Here are some cases of RBBB and LAFB

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

don't miss this one!

Chest Pain and Right Bundle Branch Block


Clinical Course

Pt was admitted to MICU with cardiology following.

Troponin T (normal is less than 0.10 ng/mL): 1.19 ng/mL → 7.67 ng/mL → 19.53 ng/mL <0 .10="" 1.19="" 19.53.="" 7.67="" b="" nbsp="">(Smith comment: remember that, as far as one can correlate troponin levels with infarct size, troponin T levels are only 1/10th as high as troponin I levels.  So this may correspond to a troponin I level of about 200 ng/mL.)

ECG #4, next morning
There is some persistent STE in V1-V3 and aVL (and reciprocal STD), different from patient's baseline ECG.

Cardiology consult note on day 2:
“Inciting cause is unknown although there is evidence supporting coronary ischemia and metabolic derangements including hyperkalemia and acidosis.  Prognosis is tenuous and neurologic function cannot be assessed while the patient is sedated. The incremental benefits of an early invasive approach in management of this ACS may outweigh the risks as long as cognition improves and metabolic derangements are corrected. The clinical approach for ACS in ESRD is usually individualized; effectiveness data is limited and treatment related morbidity is not uncommon.”

“Assessment: “Cardiac arrest…..Non-ST elevation acute coronary syndrome”
“ECG 1: Sinus rhythm, rate 90, QRS duration ~190ms, left axis deviation with late terminal forces moving rightwards and anterior.
ECG 2: SR, rate 80; QRS 120ms with late terminal left/anterior, left axis deviation, ST elevation (~1mm in I, 1-1.5mm aVL)

ECG3: SR, rate ~75. ST elevation (1-2mm aVL, 1mm V2/3), ST depression (II, III, aVF, V4-6).”

Cardiology consult day 3:
“59 yo patient with ESRD on HD, DMII, who is currently in cardiogenic shock in the wake of cardiac arrest after NSTEMI. The pressing issue is whether this patient should undergo left heart catheterization today. I think this hinges on neurologic status, which at this time is largely unknown. Pt was reported to have 1 hour down time prior to being resuscitated. She has been without sedation for several hours and has no corneal or gag reflexes per the primary team. There is enough evidence to call into question her neurological viability at this time, thus a left heart catheterization would be of questionable utility.”

Autopsy, day 7:
Anoxic brain injury with total cerebral necrosis 99% stenosis of the proximal LAD, with acute transmural infarct of the anterior and anterolateral walls of the LV 75% stenosis LCx, 50% RCA, 25% LM


  1. Thanks for this case Dr. Smith. The most useful part to me was the teaching on how to find the ST-elevation in the first EKG. I saw the LAFB and RBBB at first but couldn't pin down ST-elevation/depressions.

    My question is on the decision making of the EP. With a initial K of 5.8, he/she states that the patient's responsiveness to bicarb and calcium is evidence of hyperkalemia. I thought that bicarb treatment for hyperK has not been found to be very effective?

    1. Correct. Bicarb not very effective, but somewhat. The ECG changed from "could be hyperK" (though it really could not be due to a K of 5.8) to "definitely STEMI".

  2. Great and instructive case as always.
    The main difficulties lie of course in the interpretation of the ED ECG and the subtle STE and STD; the way in assessing them is extraordinary and that was I've learned the most. Thank you Dr. Smith.

    I was surprised that the cath lab was not activated after the ECG#2 which does meet STEMI criteria unless I missed some important clinical informations (duration of resuscitation, significant comorbidities and so on). Indeed according to “Invasive coronary treatment strategies for out-of-hospital cardiac arrest: a consensus statement from the European Association for Percutaneous Cardiovascular Interventions (EAPCI/Stent for Life (SFL) groups” comatose survivors with ECG criteria for STEMI should go directly to cath lab.

    If I am correct there is also another ominous ECG sign: alternans of ECG RBBB+LAFB (ECG#1) and incomplete LBBB (ECG#3).

    Mario Parrinello

  3. So instructive
    Thank you Dr.Smith

    Can we say that a new RBBB in a patient who had recently VF should immediately put STEMI as the first diagnosis even if we could not find the subtle st/ t changes ?

    1. Bashar,
      I would say that is a fair assessment. Anyone with unexplained V Fib probably needs a cath soon anyway!

  4. GREAT case! What is most remarkable to me about this case is comparison of the initial ECG with ECG #2 taken 19 minutes later. In your experience Steve — is it just something about these large acute LAD occlusions involving the conduction system that produces disproportionate QRS widening of the terminal part of the QRS during the early minutes? Is this some kind of “peri-infarction block”? Is this worth writing up? THANKS for presenting!

    1. Ken,
      It is puzzling, and makes me think that the artery partly opened spontaneously in that interim, restoring conduction. All ACS is dynamic, and at cath 3 days later the artery had some flow (99%). Maybe it is worth writing up!


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

Recommended Resources