A late middle aged male collapsed while walking and had immediate bystander CPR. He achieved ROSC at the door of the ED, 30 minutes after arrest.
The CPR provided had been so effective that the patient began to follow commands upon arrival. Why was it so effective? Because they used the inspiratory threshold device, ITD (ResQPod) and ResQPump.
Go here for the latest in CPR, a fast evolving field: Lecture by Keith Lurie that includes the latest on head-up CPR.
This was his initial ED 12-lead, with pH 7.09, pCO2 69, and bicarb 19. K was 2.8 (low K is common after resuscitation due to lots of exogenous epinephrine):
Is it LBBB?
No.
LBBB should have a slow upstroke ("intrinsicoid deflection") to the R-wave in lateral leads of at least 60 ms. This is a relatively rapid upstroke of about 40 ms (see red arrows below which show onset and peak of R-wave in lead V5).
Is this a wide QRS?
Yes, but I believe not nearly as wide as it first appears.
In the annotated version of the ECG (below), I put a short black line in V4 where I believe the QRS ends.
This a QRS that looks very wide because its terminal portion is obliterated by ST elevation.
This is "shark fin" ST elevation.
They have also been called "Giant R-waves": JE Madias.
Full text, with image: https://drive.google.com/open?id=1fCpHey_vILU9jNld6a4oBtxQbML8Z88k.
Here is an annotated version with lines and arrows:
Management decisions
We are enrolling patients in a study called "ACCESS" (ClinicalTrials.gov Identifier: NCT03119571). It is a randomized trial of early angiography/PCI for cardiac arrest victims who do not have "STEMI" or "STEMI equivalent." (The research question is: do patients with shockable rhythms who do not have STEMI need emergent cath lab activation?)
So the ECG interpretation is critical to whether this patient gets:
1) immediate angiography as if he is a STEMI patient or
2) randomized to early angiography vs. angiography later, as indicated by other data.
If you believe that:
A) This is a simple post arrest ECG with very wide QRS and no ST elevation or depression
Then the patient is randomized and not automatically studied with immediate angiography.
B) The QRS really is much shorter and only appears to be wide due to ST elevation and depression which obliterates the end of the QRS
Then, you activate the cath lab and do not enroll the patient in this randomized trial.
I was convinced that it was ST Elevation and Depression.
We activated the cath lab based on this ECG, with the knowledge that this subepicardial ischemia may simply be a result of cardiac arrest alone.
ECGs Immediately after Resuscitation from Cardiac Arrest
Any ECG recorded immediately after cardiac arrest can be wildly abnormal. During the 30 minutes of cardiac arrest, even if there is no acute MI, or even without any coronary disease, there can be severe ischemia from the low-flow state of cardiac arrest , as well as alterations from acidosis.(Cardiac output and blood pressure during CPR chest compressions is a fraction of normal.)
If there are fixed coronary lesions, the flow beyond that stenosis may be exceedingly poor, and the ischemia may be focal.
Thus, one should always record another ECG after the patient stabilizes. We recorded this one 25 minutes later:
What do you think?
Three Options:
1. The QRS really was very prolonged, and there is and was no focal ischemia
2. There was a thrombosis, probably of the LM or LAD, and it spontaneously reperfused (autolysis)
3. There is a fixed stenosis in the LM or LAD. During cardiac arrest, and shortly thereafter, there was profound ischemia in that territory, resulting in ST Elevation (a type 2 STEMI).
Further history came to light:
The patient had recently been experiencing exertional angina. He had a stress test a few days prior that was markedly positive, and was scheduled for an angiogram on the following day.
This suggests presence of a fixed stenosis.
What happened?
1. Maybe that stenotic plaque ruptured and thrombosed.
2. Maybe the stress of walking was enough to cause exertional ischemia and then ventricular fibrillation.
The patient went to the cath lab:
A 95% stenosis of the proximal LAD was found. The lesion did not appear to be acute (no ulcerated plaque and no thrombus). The lesion was reduced to 0% with intervention and stenting.
Peak Troponin I = 19 ng/mL (STEMI is greater than 10 ng/mL in about 70% of cases)
Formal Echo
Normal left ventricular size and thickness.
Mildly decreased left ventricular systolic function with an estimated EF
of 45%.
There is hypokinesis of the mid anterior wall.
It looks as though Option 3 was the correct one.
Conclusion
This is a type II STEMI due to fixed stenosis in the LAD which, in the setting of very low flow state of CPR resulted in severe hypoperfusion to the anterior wall, a wide QRS, and ST elevation and depression consistent with STEMI. The arrest was caused by exertional ischemia in the setting of a very tight fixed, non-thrombotic, LAD stenosis.
However, the discharge diagnosis was "NonSTEMI."
In retrospect, this patient could have been randomized in the ACCESS trial. He did not need immediate intervention, though he did get it.
Learning Points:
1. It is critical to find the end of the QRS before concluding that there is not STE or STD.
2. In the presence of a fixed stenosis, exertion can lead to ischemia and ventricular fibrillation. Stress tests are always done with resuscitative equipment available!
3. Low flow of cardiac arrest can lead to severe cardiac ischemia, especially in the presence of fixed coronary stenosis
4. The ECG immediately after cardiac arrest is often very abnormal. Wait 15 minutes after stabilization to record another one
5. We don't know if everyone who has cardiac arrest from a shockable rhythm needs emergent angiography. My bias is to send them, but the ACCESS trial's goal is to find out.
More on Type 2 STEMI:
The CPR provided had been so effective that the patient began to follow commands upon arrival. Why was it so effective? Because they used the inspiratory threshold device, ITD (ResQPod) and ResQPump.
Go here for the latest in CPR, a fast evolving field: Lecture by Keith Lurie that includes the latest on head-up CPR.
This was his initial ED 12-lead, with pH 7.09, pCO2 69, and bicarb 19. K was 2.8 (low K is common after resuscitation due to lots of exogenous epinephrine):
 |
| The computer diagnosed atrial fibrillation with left bundle branch block. I would have agreed with atrial fib except that the 3rd complex appears to be sinus (see double-peaked P-wave). So perhaps it is an accelerated idioventricular rhythm? |
Is it LBBB?
No.
LBBB should have a slow upstroke ("intrinsicoid deflection") to the R-wave in lateral leads of at least 60 ms. This is a relatively rapid upstroke of about 40 ms (see red arrows below which show onset and peak of R-wave in lead V5).
Is this a wide QRS?
Yes, but I believe not nearly as wide as it first appears.
In the annotated version of the ECG (below), I put a short black line in V4 where I believe the QRS ends.
This a QRS that looks very wide because its terminal portion is obliterated by ST elevation.
This is "shark fin" ST elevation.
They have also been called "Giant R-waves": JE Madias.
Full text, with image: https://drive.google.com/open?id=1fCpHey_vILU9jNld6a4oBtxQbML8Z88k.
Here is an annotated version with lines and arrows:
 |
| The red arrows show the onset and peak of the R-wave in lead V5 The short black line in V4 shows what I believe to be the end of the QRS. Thus, the QRS duration is about 140 ms. It would be easy to believe that it is 230 ms. --I then draw a long black line from that same point and extended it down to lead II. --I then draw that long black line from the corresponding points on other complexes of lead II, up to all other leads. Now, assuming my estimate of the end of the QRS is correct: 1. You can see concordant ST elevation in I, aVL, V3, V5, and V6. 2. You can see concordant reciprocal ST depression (STD) in II, III, aVF 3. There is also STD in V1 and V2. In any ventricular rhythm, including PVCs, concordant ST elevation implies subepicardial ischemia (STEMI) for another example of that downsloping ST elevation, see this case: Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation |
Management decisions
We are enrolling patients in a study called "ACCESS" (ClinicalTrials.gov Identifier: NCT03119571). It is a randomized trial of early angiography/PCI for cardiac arrest victims who do not have "STEMI" or "STEMI equivalent." (The research question is: do patients with shockable rhythms who do not have STEMI need emergent cath lab activation?)
So the ECG interpretation is critical to whether this patient gets:
1) immediate angiography as if he is a STEMI patient or
2) randomized to early angiography vs. angiography later, as indicated by other data.
If you believe that:
A) This is a simple post arrest ECG with very wide QRS and no ST elevation or depression
Then the patient is randomized and not automatically studied with immediate angiography.
B) The QRS really is much shorter and only appears to be wide due to ST elevation and depression which obliterates the end of the QRS
Then, you activate the cath lab and do not enroll the patient in this randomized trial.
I was convinced that it was ST Elevation and Depression.
We activated the cath lab based on this ECG, with the knowledge that this subepicardial ischemia may simply be a result of cardiac arrest alone.
ECGs Immediately after Resuscitation from Cardiac Arrest
Any ECG recorded immediately after cardiac arrest can be wildly abnormal. During the 30 minutes of cardiac arrest, even if there is no acute MI, or even without any coronary disease, there can be severe ischemia from the low-flow state of cardiac arrest , as well as alterations from acidosis.(Cardiac output and blood pressure during CPR chest compressions is a fraction of normal.)
If there are fixed coronary lesions, the flow beyond that stenosis may be exceedingly poor, and the ischemia may be focal.
Thus, one should always record another ECG after the patient stabilizes. We recorded this one 25 minutes later:
 |
| Sinus rhythm. Typical hypokalemia ECG. There is some residual STE in aVL and reciprocal STD in inferior leads |
What do you think?
Three Options:
1. The QRS really was very prolonged, and there is and was no focal ischemia
2. There was a thrombosis, probably of the LM or LAD, and it spontaneously reperfused (autolysis)
3. There is a fixed stenosis in the LM or LAD. During cardiac arrest, and shortly thereafter, there was profound ischemia in that territory, resulting in ST Elevation (a type 2 STEMI).
Further history came to light:
The patient had recently been experiencing exertional angina. He had a stress test a few days prior that was markedly positive, and was scheduled for an angiogram on the following day.
This suggests presence of a fixed stenosis.
What happened?
1. Maybe that stenotic plaque ruptured and thrombosed.
2. Maybe the stress of walking was enough to cause exertional ischemia and then ventricular fibrillation.
The patient went to the cath lab:
A 95% stenosis of the proximal LAD was found. The lesion did not appear to be acute (no ulcerated plaque and no thrombus). The lesion was reduced to 0% with intervention and stenting.
Peak Troponin I = 19 ng/mL (STEMI is greater than 10 ng/mL in about 70% of cases)
Formal Echo
Normal left ventricular size and thickness.
Mildly decreased left ventricular systolic function with an estimated EF
of 45%.
There is hypokinesis of the mid anterior wall.
It looks as though Option 3 was the correct one.
Conclusion
This is a type II STEMI due to fixed stenosis in the LAD which, in the setting of very low flow state of CPR resulted in severe hypoperfusion to the anterior wall, a wide QRS, and ST elevation and depression consistent with STEMI. The arrest was caused by exertional ischemia in the setting of a very tight fixed, non-thrombotic, LAD stenosis.
However, the discharge diagnosis was "NonSTEMI."
In retrospect, this patient could have been randomized in the ACCESS trial. He did not need immediate intervention, though he did get it.
Learning Points:
1. It is critical to find the end of the QRS before concluding that there is not STE or STD.
2. In the presence of a fixed stenosis, exertion can lead to ischemia and ventricular fibrillation. Stress tests are always done with resuscitative equipment available!
3. Low flow of cardiac arrest can lead to severe cardiac ischemia, especially in the presence of fixed coronary stenosis
4. The ECG immediately after cardiac arrest is often very abnormal. Wait 15 minutes after stabilization to record another one
5. We don't know if everyone who has cardiac arrest from a shockable rhythm needs emergent angiography. My bias is to send them, but the ACCESS trial's goal is to find out.
More on Type 2 STEMI:
Absolutely SUPERB case & discussion by Dr. Smith that highlights numerous points regarding ECG interpretation around the period of cardiac arrest. I would add 2 Comments to Learning Point #2, regarding Stress Testing (ETT). The KEY to optimizing safety when doing Stress Testing is to know when to STOP the test. The BEST time to stop (in my opinion), is the instant you (as the one performing the test) become able to decide what the next step in evaluation or management should now be. Usually, the decision is whether or not cardiac catheterization will be needed. Contemplating IN ADVANCE of doing the ETT precisely what result would lead you to refer for cath will greatly facilitate prompt cessation of the exercise test the moment this “End Point” is reached. For some patients, all that might be needed is minimal ST depression in association with symptoms at low level exercise. For practical purposes, this result would confirm significant coronary disease, and continuing the ETT until more ST depression is seen would not really alter management. Not recognizing the clinical “End Point” of when to stop the ETT on a patient such as the one in this case (who had a high-grade fixed obstruction in his LAD) could easily precipitate cardiac arrest during the test. Finally, I will play “Devil’s Advocate” — based on the history that this patient had recently been experiencing exertion angina, and had a markedly positive ETT “a few days prior” — and, was scheduled for cath “the next day” (which means he got to go home for a few days after his ETT …). Deciding which patients with symptoms and markedly positive out-patient ETTs can be allowed to go home for “a few days” before cath — vs which ones should be immediately admitted to the hospital to be prepped that night for cardiac cath done the next morning is indeed challenging … Hindsight is 100% in the “retrospectoscope” — but we should learn from this case how important such decision-making is! THANKS again to Dr. Smith for this highly insightful case!
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