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.
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).|
- 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.
- 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.
- 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.
Our THANKS to Dr. Meyers for his discussion of this case!