A male in his 60's with no previous cardiac history complained of substernal chest pain intermittently for 18 hours. It has more recently become constant. He was diaphoretic. He called 911 and had this prehospital ECG recorded:
We recorded this immediately:
BP was 140/80.
His pain continued and would be relieved from 8/10 to 6/10 with sublingual nitroglycerin. We gave aspirin and clopidogrel for high suspicion of ACS.
Had I looked for it (which, foolishly, I did not), I would have found this previous ECG from 9 months prior:
Had I seen this, I would have immediately diagnosed definite ACS and started high dose IV nitroglycerin.
As it was, we did give sublingual NTG, and sent a troponin and, while the pain continued, recorded this ECG 42 minutes later:
Not having seen the old one yet, and seeing no diagnostic evolution, I just kept a high index of suspicion. But I was pretty sure that, with the duration of pain, that if this chest discomfort was indeed due to ACS, that the first troponin would be at least slightly elevated.
The first troponin then returned at 0.20 ng/mL (normal up to 0.030 ng/mL). The diagnosis was clear. High dose nitro was started with no relief.
We activated "Pathway B", a system we have worked out which is intermittent between cath lab activation and no activation, and which covers patients with NonSTEMI but whom the emergency physician believes need to go to the cath lab immediately.
Patients with objective evidence of ongoing ischemia that is not relieved by anti-platelet, anti-thrombotic, and anti-ischemic therapy should go directly to the cath lab.
The cardiologist agreed, and the patient went straight up for angiogram:
Here is the post cath ECG:
Here is the next day ECG:
Next day echo showed Lateral and inferolateral wall motion abnormality.
Troponin I peaked at 28 ng/mL
Learning points:
1. Aggressively investigate suspicous ECG abnormalities in the context of typical chest discomfort and unrelieved symptoms
2. Compare with the old ECG!
3. Some NonSTEMI need the cath lab now! (objective evidence of ischemia and refractory symptoms)
4. Notice that, in ACUTE posterior infarction, there is not necessarily any increase in R-wave amplitude in V1-V3. In this case, there was a decrease.
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| I saw this when he arrived, and was worried about the slight ST depression in V2 and the size of the T-waves in V5 and V6, as well as the minimal terminal T-wave inversion in aVL and a bit of ST depression there. |
We recorded this immediately:
 |
| The same findings are here, without any evolution. |
BP was 140/80.
His pain continued and would be relieved from 8/10 to 6/10 with sublingual nitroglycerin. We gave aspirin and clopidogrel for high suspicion of ACS.
Had I looked for it (which, foolishly, I did not), I would have found this previous ECG from 9 months prior:
 |
| There are definite changes compared to this one |
Had I seen this, I would have immediately diagnosed definite ACS and started high dose IV nitroglycerin.
As it was, we did give sublingual NTG, and sent a troponin and, while the pain continued, recorded this ECG 42 minutes later:
 |
| The T-waves in V5 and V6 have less amplitude. This caught my eye. |
Not having seen the old one yet, and seeing no diagnostic evolution, I just kept a high index of suspicion. But I was pretty sure that, with the duration of pain, that if this chest discomfort was indeed due to ACS, that the first troponin would be at least slightly elevated.
The first troponin then returned at 0.20 ng/mL (normal up to 0.030 ng/mL). The diagnosis was clear. High dose nitro was started with no relief.
We activated "Pathway B", a system we have worked out which is intermittent between cath lab activation and no activation, and which covers patients with NonSTEMI but whom the emergency physician believes need to go to the cath lab immediately.
Patients with objective evidence of ongoing ischemia that is not relieved by anti-platelet, anti-thrombotic, and anti-ischemic therapy should go directly to the cath lab.
The cardiologist agreed, and the patient went straight up for angiogram:
 |
| The red arrow shows the very tight, hazy, acute thrombotic 95% stenosis of a very large Obtuse Marginal (this vessel is in the right position to either be a high takeoff OM, a high takeoff 1st diagonal, or a ramus intermedius, which is a vessel that is sometimes seen between the circumflex and the LAD). The black arrows point out its entire course, which now has TIMI III flow. |
Here is the post cath ECG:
 |
| The V2 ST depression is gone, and the V2 T-wave has much higher amplitude (posterior reperfusion T-wave). The T-waves in V5 and V6 are normalized. There is now T-wave inversion in aVL. There is much artifact in inferior leads. |
Here is the next day ECG:
 |
| There is deep T-wave inversion in I and aVL, with reciprocally large T-waves in III and aVF, and some terminal T-wave inversion in V5 and V6. |
Next day echo showed Lateral and inferolateral wall motion abnormality.
Troponin I peaked at 28 ng/mL
Learning points:
1. Aggressively investigate suspicous ECG abnormalities in the context of typical chest discomfort and unrelieved symptoms
2. Compare with the old ECG!
3. Some NonSTEMI need the cath lab now! (objective evidence of ischemia and refractory symptoms)
4. Notice that, in ACUTE posterior infarction, there is not necessarily any increase in R-wave amplitude in V1-V3. In this case, there was a decrease.
Nice, SUBTLE case with some great learning points. An interesting thing that I've been keeping an eye on lately is how reperfusion waves often involve significantly more leads than were initially apparent as showing injury during the ischemic phase. In this case leads I, V5, and V6 show clear signs of reperfusion even though they barely had any signs of involvement on the initial ECG (though V5 and V6 show super subtle T-wave enlargement and early takeoff). I've seen the same thing in a lot of LAD lesions that showed no inferior involvement during the STEMI phase but then show clear inferior terminal T-wave inversions following reperfusion (confirming a vessel that probably wraps around the apex, which we know isn't uncommon to find at cath but is less often suggested on the STEMI tracing).
ReplyDeleteSince terminal T-wave inversions are easier to spot than subtle signs of ischemia I think it shows that there can be a greater area of at-risk myocardium than the initial EKG may suggest.
I'm not sure if that information is useful for anything, just something I've been keeping in the back of my head for a while.
Vince,
DeleteI always teach that one way to know for certain if any subtle STE on the acute ECG is real if it evolves into T-wave inversion on the convalescent ECG. If there is none, then there was no infarction (negative trop). If the STE resolves without any T-wave inversion, beware unstable angina, with no troponin elevation, no infarction (with infarction, there is always some T inversion)
Steve
In very first ecg there is St depression in v2 & suspicious t wave in V5, V6 than why post leads v7, v8, v9 not recorded
ReplyDeleteIn my view, posterior leads only tell you what you already know. They are opposite the anterior leads. They cannot show anything but a 180 degree opposite view, but with even less voltage. They are really only useful if they are done when there is NO anterior ST depression as they will sometimes be more sensitive. It is possible that it would have increased diagnostic certainty. Every case I have ever seen where they were used, it only confirmed what was already known to me by looking at the 12 lead.
DeleteVery interesting and well handed.
ReplyDelete