A patient with unwitnessed arrest received a shock from the AED (presumably ventricular fibrillation). He underwent extensive resuscitation, was transported in full arrest, and arrived still in V Fib.
He was receiving chest compressions on the LUCAS device.
We placed a Transesophageal echo, as we do on all arrests.
Just after TEE was placed, he was shocked into an organized rhythm.
This is the TEE:
There is now an organized rhythm, at which time we stopped compressions and monitored cardiac activity continuously during the entire resuscitation.
Here I annotate the image to orient you:
|The white arrow is the left atrium; you can see that the probe in the esophagus is directly adjacent to the left atrium
The red arrow is the LV and it has reasonably good function.
The yellow arrow is the RV
A 12-lead ECG was recorded:
|This shows slow atrial fibrillation.
There is massive ST Depression in V2-V5.
There is ST Elevation in aVR.
Is it a Left Main Occlusion? (no, but it may be Left Main ACS)
Is it posterior MI?
Importantly, the ST depression is MAXIMAL in V3 and V4 (by ECG features alone, this is more likely to be posterior STEMI, NOT in V5 and V6, which would be more likely to be diffuse subendocardial ischemia).
However, in the setting of cardiac arrest, there is a higher pretest probability of diffuse subendocardial ischemia:
1. Cardiac arrest is more likely in the setting of LM, LAD, or 3-vessel ACS or CAD
2. The low flow state of cardiac arrest is likely to result in subendocardial ischemia regardless of the etiology of arrest.
We activated the cath lab.
There is an ongoing randomized clinical trial at our hospital called the ACCESS trial (ACCESS to the Cardiac Cath Lab in Patients Without STEMI Resuscitated From Out-of-hospital VT/VF Cardiac Arrest, ClinicalTrials.gov Identifier: NCT03119571)
In the ACCESS trial, patients with a shockable rhythm who do NOT have a STEMI are randomized to emergent cath vs. later angiography, as indicated.
Thus, we are only supposed to activate the lab for “True STEMI.” Others would get randomized.
However, if you read the ACCESS trial inclusion criteria closely, patients who have a “STEMI-Equivalent” are NOT supposed to be randomized; they are supposed to (appropriately) go to emergent angiography.
- Adult presumed or known to be 18-75 years old
- Resuscitated from OOHCA
- Initial cardiac arrest rhythm of pulseless VT/VF (including patients treated with an AED)
- No ST-segment elevation MI (No STEMI) (or STEMI-equivalent syndrome) on ED 12-lead ECG (as interpreted by a physician)
- Initial non-shockable out-of-hospital cardiac arrest rhythm (pulseless electrical activity or asystole)
- Valid do not resuscitate orders (DNR),
- Blunt, penetrating, or burn-related injury, drowning, electrocution or known overdose,
- Known prisoners
- Known pregnancy,
- ST-segment elevation on ED 12-lead ECG (as interpreted by a physician)
- Absolute contraindications to emergent coronary angiography including,
- known anaphylactic reaction to angiographic contrast media,
- active gastrointestinal or internal bleeding, or
- severe concomitant illness that drastically shortens life expectancy or increases risk of the procedure.
- Suspected or confirmed intracranial bleeding
- Refractory cardiac arrest (prior to randomization)
- Patients meeting ACCESS Trial eligibility criteria initially seen in an outside hospital and then transferred to an ACCESS Trial participating hospital
We recorded another ECG some 15-20 minutes later to determine if the ECG abnormalities were all due to post ROSC, as the low flow state of cardiac arrest can lead to severe ischemia and profound ECG abnormalities (see post on April 25, 2018):
|Still Atrial Fib. Still with profound ST depression.
Now you can also see some STE in lead III with reciprocal STD in aVL.
So this is likely to be infero-posterior MI, but still could be due to subendocardial ischemia (Diffuse STD with STE in aVR).
The patient went for angiography.
LMCA: The LM has a 70% stenosis in the mid portion of the vessel. This was a chronic stenosis.
LAD: Type III LAD is noted.
The LAD is a large caliber vessel.
The LAD has 70% disease in the ostial, proximal segment of the vessel. (This was also chronic, not an acute thrombotic event.)
The LADD 1 is a large caliber vessel.
LCx: Ostial-Proximal LCX has 100% disease. This is Chronic as it fills via a grade 3 RT to LT collaterals that fills the dominant LCX. OM1 fills via Lt to LT collaterals
RCA: RCA has Normal take off. Small non dominant. The Mid segment of the RCA has 100% disease between 2 RV marginal.
So the patient has profound 3-vessel disease, without apparent culprit. Thus, there was no intervention. The etiology of arrest is uncertain. The ECG findings are due to the ischemia of the low flow state.
If this is hemodynamically significant, it could lead to ischemia in a low flow state)
Here is a post cath ECG, after the effects of the low flow state have resolved:
|This shows Q-waves and reperfusion T-waves in inferior leads.
There are Large Precordial T-waves — Posterior Reperfusion T-waves
So this ECG supports an infero-posterior MI due to hypoperfusion (type II STEMI)
Diffuse ischemia from LM stenosis and low flow was likely contributory
Echocardiogram confirms infero-posterior MI:
Regional wall motion abnormality-lateral/inferolateral, akinesis.
Regional wall motion abnormality- basal inferior.
This was a primary ventricular fibrillation, not due to ACS, but (as with the case on April 24), causing severe ischemia due to low flow in the presence of severe coronary stenoses. The arrest might have been caused by demand ischemia (patient exerting himself in the setting of severe CAD with severe stenoses.)
The ST depression appears to have been transmural, subepicardial ischemia because the posterior wall requires collateral flow from the RCA for its perfusion, and the low flow in the RCA does not allow for enough perfusion.
So, again, this was not ACS. In retrospect, there was not a need for emergent angiogram as there was no culprit and no intervention.
But it would be impossible to know this prospectively.
1. STEMI-equivalents due to ACS (more appropriately called OMI — Occlusion Myocardial Infarction) should be brought emergently to the cath lab.
2. In the post arrest situation, it may be very difficult to ascertain whether a finding is due to OMI or due to the low flow state with fixed stenoses.
3. It is often only possible to make that determination after the emergent angiogram.
4. Use bedside transesophageal echo (TEE) for all cardiac arrest cases. It makes cardiac monitoring perfect and continuous.(1, 2)
We use TEE on all cardiac arrest cases and in cases of shock who are intubated. We will report our over 100 cases soon, but the preview is that it is incredibly helpful in managing these patients, and surprisingly easy to use.
1. Blaivas M. Transesophageal echocardiography during cardiopulmonary arrest in the emergency department. Resuscitation 78(2):135-40; August 2008.
Full text: https://pdfs.semanticscholar.org/d392/dccf6349f817c9a759d251ac4e876976c062.pdf
This article was commented on at REBEL EM: http://rebelem.com/the-role-of-tee-in-cardiac-arrest/