Tuesday, March 26, 2019

An 80 year old man in VF arrest

An elderly man suffered out of hospital cardiac arrest. He was found in V Fib by EMS. He was shocked out of VF multiple times and arrived in VF arrest. We administered the fourth shock on arrival and obtained ROSC.

His blood pressure was approximately 80/40, heart rate approximately 50 bpm.

Here is his ECG at that time:
What do you think? How does this affect your resuscitation?

The ECG shows a junctional bradycardia with diffuse ST depression (maximal in leads V4-V6 and lead II), with large reciprocal STE in aVR. This is consistent with diffuse severe subendocardial ischemia, but without any clear evidence of acute occlusion.

We have gone over the differential of this ECG many times on this blog. Diffuse nonfocal ischemia can be caused by any condition in which global myocyte perfusion is greatly diminished below the current demand. This can result from very high risk forms of ACS, such as left main ACS (but without complete occlusion), or from diminished cardiac output or blood pressure from any cause in the setting of preexisting (non-acute) left main or triple vessel disease. This patient could have any or all of the conditions above, including acute ACS, and/or simply very poor perfusion given his immediate post-ROSC state, as well as very low blood pressure and bradycardia (extremely low cardiac output). As the depth of ST depression (especially relative to QRS size) increases, the likelihood that the etiology is due to ACS increases (in other words, extremely severe ST deviations are more likely due to left main/triple vessel ACS than the common, mild global STD we see commonly in elderly patients with rapid atrial fibrillation).

Back to the case:

We activated the cath lab, but cardiology told us that they were approximately 30 minutes away from the lab. So we tried to stabilize the patient as much as possible while awaiting the cath lab team.

Despite epinephrine and norepinephrine drip, the heart rate started to fall. Atropine and calcium were also not effective. We attempted transcutaneous pacing, but could not obtain capture.

We placed a transvenous pacemaker, and as soon as we achieved capture with a paced rate of 90 bpm the blood pressure jumped to approximately 150/80, and pressor requirements were greatly reduced.

His ECG improved with this increased cardiac output, however there were still significant global STD with STE in aVR. (Sorry, I cannot find the ECGs with ventricular paced rhythm unfortunately)

He made it to cath which revealed severe three vessel disease, patent LIMA-LAD, and chronically occluded SVG (they were unable to identify which, if any of these stenoses were the culprit):

Left main: 90% stenosis
ostial LAD: 100% stenosis (chronic, with LIMA bypass to mid-LAD)
ostial Circumflex: 90% stenosis
ostial Ramus: 90% stenosis
proximal RCA: 75% stenosis

They attempted PCI of the ostial and proximal circumflex and which was unsuccessful as they were unable to cross the lesion with the balloon. They decided that further intervention could compromise current blood flow, and that further intervention would be indicated depending on neurologic outcome.

Troponin T rose from undetectable on arrival to 2.94 approximately 12 hours later.

He was admitted to the CCU. Eventually care was withdrawn and the patient expired.

Learning Points:

The likelihood of ACS as the cause of global STD with STE in aVR increases as the severity of the ECG findings increases.

Non-occlusive ACS of the left main and/or in the setting of triple vessel disease requires emergent invasive treatment (just as full Occlusion MI would) when the patient is hemodynamically or electrically unstable.

When there is a delay to the cath lab, thrombolytics should be considered, and every possible effort should be made to optimize hemodynamics and coronary perfusion until definitive reperfusion can be achieved.

Comment by KEN GRAUER, MD (3/27/2019):
As noted in the comment by Tom Fiero — this was an unfortunate but enlightening case. Key issues are covered in excellent fashion by Dr. Pendell Meyers. I limit my comments to the following additional points.
  • For clarity — I’ve labeled the tracing in Figure-1, and have added a laddergram at the bottom for illustrative purposes.
Figure-1: The initial post-resuscitation ECG in this case. Illustrative laddergram below (See text).
COMMENT: As per Dr. Meyers — Dr. Smith’s ECG Blog has covered the differential diagnosis of diffuse ST segment depression with ST elevation in lead aVR on numerous occasions. When this pattern is the result of diffuse subendocardial ischemia from severe coronary disease — one may not be able to distinguish between severe left main disease — vs proximal LAD stenosis — vs severe multi-vessel coronary disease — vs some combination of these.
  • In addition to the ST elevation seen in lead aVR with this pattern — there may also be ST elevation in lead V1. Usually, there is more ST elevation in lead aVR than in lead V1. The thought is that when the amount of ST elevation in lead V1 exceeds the amount in aVR — that severe proximal LAD disease is more likely than left main disease. The reverse is not necessarily true. That said, the point is that we should be accustomed to looking not only in lead aVR for ST elevation in this pattern — but also in lead V1.
  • The shape and amount of ST depression that is seen in no less than 8 leads in Figure-1 is remarkable. The amount of ST elevation in both leads aVR and V1 ( = 3mm! is equally remarkable — which as per Dr. Meyers’ first Learning Point — is clear indication of how severe this patient’s multi-vessel coronary disease was.
COMMENT on the Rhythm in ECG#1: From an academic standpoint — I thought the rhythm of the tracing in Figure-1 was highly interesting.
  • With the exception of beat #7 — the rhythm is almost (albeit not completely) regular at a rate of ~50/minute.
  • Normal sinus P waves are absent — because there is no upright P wave with constant PR interval in lead II.
  • Dr. Meyers correctly called this a junctional rhythm. That said, I initially thought this was a ventricular escape rhythm — because I did not initially see P waves, and I initially thought the QRS complex was wide. On further review — I agree with Dr. Meyers that this is a junctional rhythm — but thought it beneficial to illustrate why.
CONFESSION — I spent a good 20+ minutes staring at and contemplating the rhythm in Figure-1. Although there are some contradictory findings — my best effort at distinguishing between the biphasic (negative, then positive) P wave in lead II, and the narrow QRS is shown in Figure-1.
  • Using simultaneous vertical time lines — the BLUE line that I’ve drawn just before beat #2 indicates where I believe the initially negative junctional P wave in lead II begins.
  • The vertical RED line that follows indicates where I believe the QRS complex of beat #2 begins. Using this RED line defines the QRS as narrow, with supraventricular-like sharp deflections in most leads.
  • Taking the same point as indicated by the RED line as the beginning of the QRS complex in the long lead II — the vertical GREEN lines indicate where the QRS complex would begin in the other 9 leads.
  • I’ve added some RED arrows to illustrate regular occurrence of retrograde P waves (arising from this junctional escape rhythm) that appear just before the onset of the QRS complex.
  • Beat #7 is wide and manifests a very different QRS morphology than the junctional beats. Beat #7 is not preceded by any atrial activity — and it occurs slightly earlier-than-would-be-expected for the next junctional beat after beat #6. I therefore interpreted beat #7 as a late cycle (ie, end-diastolic) PVCNOTE: I believe the notch in the terminal part of the QRS of beat #7 (YELLOW arrow) is real, and indicates the on-time occurrence of the positive terminal portion of retrograde P waves — which if correct, supports our theory that the underlying rhythm is junctional with retrograde P waves that appear just before the QRS of junctional beats. The reason no junctional QRS is seen after beat #7 — is because this late-cycle PVC ( = beat #7) renders the ventricles refractory (See Laddergram in Figure-1).
  • P.S.: Finding a prior tracing on this patient would help to confirm QRS morphology during sinus rhythm ... (which presumably would look similar to QRS morphology in Figure-1 minus the P waves ... ).
  • SEMANTIC Point: There is “bradycardia” — because the heart rate is less than 60/minute. Technically, this is not a “junctional bradycardia” — because the normal AV nodal escape rate in adults is between 40-60/minute, and this rhythm is precisely within that range. Therefore, the rhythm is best described — as a junctional escape rhythm at an appropriate junctional escape rate of ~50/minute.
  • P.P.S.: Failure of the SA node to maintain a sinus mechanism, with resultant junctional escape at ~50/minute — is of course an abnormal rhythm in the clinical setting presented here. This provides yet one more manifestation of this patient's severe coronary disease + acute ischemia ...
Our THANKS to Dr. Meyers for his discussion of this case!


  1. thank you, Pendell. very unfortunate, but enlightening, case.

  2. I gotta bookmark this website it seems extremely helpful very useful. Thanks for sharing.

  3. Thank you very much for good case dr Pendell, unfortunate for patient. i want to ask one question, how do we differentiate STE in AvR and STD in other leads as ACS manifestation or prolonged severe hypotension or maybe severe aortic stenosis? Because I ever seen patient with STE in avR and STD in other leads has normal coronary and it was thought to be effect of prolonged severe hypotension

    i really love dr Ken explanation about STE in V1 > avR could predict Proximal LAD occlusion
    Thanks for the chance

    1. When the ECG manifests ischemia, it cannot tell us the etiology of the ischemia. Etiology (ACS vs. LVH/aortic stenosis or other) must be determined from the clinical presentation.


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