A middle-aged male had a V Fib arrest. He had not complained of any premonitory symptoms (which is very common). He had a history of CAD with CABG. Here was his initial ED ECG:
ST depression is common BOTH after resuscitation from cardiac arrest and during atrial fib with RVR.
The patient was cardioverted. Here is the post cardioversion ECG:
Does this patient have ACS? Should he necessarily go to the cath lab?
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion.
One must wait a short time (perhaps 15 minutes?), and repeat the ECG, to see if the apparent ischemia persists.
This was done. A third ECG was done about 25 minutes after the first:
The patient thus did not need immediate angiography.
An echocardiogram showed:
Left ventricular hypertrophy concentric .
The estimated left ventricular ejection fraction is 58 %
Aortic stenosis, mild, 9.0 mmHg mean gradient. 1.50 cm^2 valve area.
Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.
The patient underwent angiography later (the next day) and there was no culprit lesion. He did not have ACS.
He recovered and had an ICD implanted.
Learning Points:
1. Ventricular fibrillation is not only caused by acute coronary syndrome. There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. The remainder were due to other etiologies, (including NonSTEMI ACS). But approximately 50% were due to non-ACS etiologies.
2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.
3. One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.
4. Not all patients with ventricular fibrillation necessarily need emergent angiography. Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.
Reference:
Scott NL. Mulder M. Bart B. Smith SW. Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580). Academic Emergency Medicine 17(s1):S194; May 2010
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The patient was cardioverted. Here is the post cardioversion ECG:
 |
| ST depression, with ST elevation in aVR persists. |
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion.
One must wait a short time (perhaps 15 minutes?), and repeat the ECG, to see if the apparent ischemia persists.
This was done. A third ECG was done about 25 minutes after the first:
 |
| This shows resolution of all apparent ischemia. |
An echocardiogram showed:
Left ventricular hypertrophy concentric .
The estimated left ventricular ejection fraction is 58 %
Aortic stenosis, mild, 9.0 mmHg mean gradient. 1.50 cm^2 valve area.
Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.
The patient underwent angiography later (the next day) and there was no culprit lesion. He did not have ACS.
He recovered and had an ICD implanted.
Learning Points:
1. Ventricular fibrillation is not only caused by acute coronary syndrome. There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. The remainder were due to other etiologies, (including NonSTEMI ACS). But approximately 50% were due to non-ACS etiologies.
2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.
3. One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.
4. Not all patients with ventricular fibrillation necessarily need emergent angiography. Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.
Reference:
Scott NL. Mulder M. Bart B. Smith SW. Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580). Academic Emergency Medicine 17(s1):S194; May 2010
- Dr Steve is never tired: chapeau !
ReplyDelete- in 'prolonged' ACS this ECG would be correspond to a LMCA-stenosis (= insufficiency = subocclusion -- STE in aVR >
STE in V1): OK ?
- thanks for sharing
Al
But is equally often seen in 3 vessel disease with LAD stenosis. If there is widespread ST depression, with ST elevation in aVR, the best interpretation is that there is a high probability of need for CABG.
DeleteSee this post: http://hqmeded-ecg.blogspot.com/2014/08/the-difference-between-left-main.html
And this one: http://hqmeded-ecg.blogspot.com/2011/04/st-elevation-in-avr-with-widespread-st.html
The first ECG has STD that looks like DeWinter waves...is the depression extended too far laterally to qualify as DeWinter's? Or you just can't tell s/p arrest? Thanks!
ReplyDeleteMike,
ReplyDeleteI don't see any that look like de Winter's waves.
Here are de Winter's waves: http://hqmeded-ecg.blogspot.com/search/label/de%20Winter%27s%20T-waves
Steve Smith
I think I was seeing the ST depression in V2 and especially V3, and that looked like DeWinter waves, but I see now that there not a hyper-dynamic T wave. Is the primary distinguishing factor? Thanks!
ReplyDeleteI think I was seeing the ST depression in V2 and especially V3, and thinking that looked a lot like DeWinter waves. Looking at it again, it looks like there is no hyper-dynamic T wave as seen in true DeWinter's. Is this the distinguishing factor? Thanks!
ReplyDeleteThere are no hyperACUTE T-waves
DeleteThis comment has been removed by a blog administrator.
ReplyDeleteThis post is so informative and makes a very nice image on the topic in my mind. It is the first time I visit your blog, but I was extremely impressed.
ReplyDelete