A middle-aged male complained of chest pain and called 911. 3 prehospital ECGs were recorded.
Here is the time zero ECG:
|Just some non-diagnostic T-wave abnormalities
T-wave inversion in V2 is a bit abnormal, and frequently seen in posterior MI, but not diagnostic.
There is tiny bit of ST depression in V3 and V4 which is nonspecific and could be normal.
There is a large T-wave in lead II which is also nonspecific.
Here is the repeat at t = 9 minutes:
|Lots of artifact, but no apparent change
Here is the t = 25 minute ECG:
|Again, no significant change except that the ST segments in V3 and V4, which previously showed some minimal ST depression, are no longer depressed.
The patient arrived in the ED and, before another ECG could be recorded, he had a V Fib arrest.
He was defibrillated, then taken to the cath lab and had a 100% circumflex occlusion.
He did well.
MI in the setting of a normal or nondiagnostic ECG:
This is very common. Approximately 30% of MI have no diagnostic STE, STD, or T-wave inversion; in other words, they have no ECG findings specific for ischemia. It is also true that approximately 25-30% of complete occlusions do not have diagnostic ST elevation (but most have some evidence of ischemia!).
This is the reason we do not rely on the ECG to rule out MI! Over the years, I have shown you many ECGs that show evidence of MI that might not be seen by everyone, or evidence of coronary occlusion that might not be seen by everyone.
This one has no clear evidence of occlusion, and no reliable evidence of MI at all (occlusive or non-occlusive).
Learning Point: patients can have MI with a normal or nondiagnostic ECG, and they can even have complete occlusion!
That said, I showed it to Vince DeGiulio and he wrote back:
Going into this I figured the ECG showed ischemia since you shared it, but I’m being honest that I didn’t look at the outcome when I formulated my opinion (I sound like Ken). My thoughts were:
- My pretest probability of ischemia is high since Steve Smith sent this. I consider it similar to the patient coming in with a good story and positive Levine sign.
- There is slight ST-depression in V3 relative to the PR, but absolutely no ST-depression in V6. In my experience, when there is a decent pretest probability, that correlates highly with isolated posterior MI and is almost always due to LCx culprit. If the patient came in with belly pain I wouldn’t pay it might mind, but typical CP and this ECG has me thinking LCx until proven otherwise.
I wasn’t at all surprised to hear it was a 100% LCx.
The circumflex territory is the most “electrocardiographically silent” of the three epicardial arteries. 50% of circ occlusions do not show diagnostic ST elevation, but most do show some ST elevation less than 1 mm, or some ST depression.
Many circ occlusions result in only ST depression in leads V1-V4 [formerly known as isolated “posterior MI”, but now the echo and MRI societies want to call them all lateral or inferior — (a mistake if you ask me, but more on that later)]. If you do suspect occlusion but see no ST depression or elevation, try posterior leads V7-V9. Remember that the voltage of the QRS and of the ST segment and T-wave are diminished by the impedance of the lungs between the posterior wall and the posterior leads. Thus, data supports a cutoff of 0.5 mm of ST elevation (not 1 mm) when there is posterior ischemia. Like all other distributions, millimeter cutoffs have very imperfect sensitivity and specificity, and do not capture the changes of ACO that can be seen by a skilled interpreter.
Also, posterior leads are not sensitive enough to rule out posterior MI; frequently patients with right precordial ST depression from acute posterior MI do NOT have any posterior ST elevation. So if you make the diagnosis on the 12-lead, do not reverse your diagnosis based on absence of STE in posterior leads.
In any patient, if you strongly suspect ACS and the patient has continued, refractory pain, the European Society of Cardiology AND the ACC and AHA all recommend urgent (less than 2 hours) angiogram. However, this makes it very easy to have false positives, as we know that many patients have ongoing noncardiac chest pain. So this requires great clinical skills (or luck)! A positive troponin, or stat echocardiogram, or continued serial ECGs (or a cardiac arrest!) may help to identify these patients.
It should be rare that you activate the lab in the absence of all of these!