A middle aged male presented with chest pain. EMS was called and an ECG was recorded which is virtually identical to the first ED ECG.
The cath lab was activated by the medics.
Here is that first ED ECG:
Where else is there evidence of STEMI?? (see below)?
There is absence of ST depression in lead V1. Given the profound ST depression (of posterior MI) in lead V2, there should also be ST depression in lead V1, but there is not. This suggests that something is "pulling up" the ST segment in lead V1. In other words, there is relative ST elevation in lead V1. As V1 sits directly over the right ventricle (RV), this suggests STEMI of the RV, which is caused by a proximal RCA occlusion, proximal to the RV marginal branch.
This patient did not have any of the hemodynamic characteristics of RVMI (hypotension, nitroglycerine sensitivity).
However, when I saw this I suspected RV MI and suggested to the treating physician that a right-sided ECG be recorded.
Here it is:
Does this matter? Won't the interventionalist just find the lesion and fix it?
Here is a case (in video form) in which the ST elevation in V1 was not noticed, a right-sided ECG was not recorded, and the angiogram showed occlusion of the mid-RCA, which was fixed. When I called the interventionalist to ask about the proximal RCA due to STE in V1, he went back to look at the angiogram: what he had not noticed was that this occlusion was an embolus from the ulcerated plaque in the Proximal RCA. He was thus able to go back and stent the actual culprit lesion.
Furthermore, it is good to know that the RV is involved in order to anticipate right sided heart failure with hypotension and nitroglycerine sensitivity.
How sensitive and specific is STE in V1 in the setting of RV MI, in cases with and without concomitant ST depression in lead V2?
We are just finishing a manuscript on this and cannot reveal our results. Suffice it to say that STE in V1 is pretty specific but not sensitive. Furthermore, that ST depression in lead I, though it does predict RCA occlusion, does not give any further information about whether that RCA occlusion is proximal (RVMI) or not.
In other words, all patients with inferior STEMI should have a right sided ECG recorded.
The cath lab was activated by the medics.
Here is that first ED ECG:
 |
| There is obvious inferior ST elevation, with reciprocal ST Depression in aVL (inferior STEMI). There is also ST Depression in lead I. This is good evidence that the inferior STEMI is caused by an RCA occlusion. There is ST depression maximal in lead V2. Thus, there is a posterior STEMI. There is also ST depression in V5 and V6. |
Where else is there evidence of STEMI?? (see below)?
There is absence of ST depression in lead V1. Given the profound ST depression (of posterior MI) in lead V2, there should also be ST depression in lead V1, but there is not. This suggests that something is "pulling up" the ST segment in lead V1. In other words, there is relative ST elevation in lead V1. As V1 sits directly over the right ventricle (RV), this suggests STEMI of the RV, which is caused by a proximal RCA occlusion, proximal to the RV marginal branch.
This patient did not have any of the hemodynamic characteristics of RVMI (hypotension, nitroglycerine sensitivity).
However, when I saw this I suspected RV MI and suggested to the treating physician that a right-sided ECG be recorded.
Here it is:
 |
| V1 should be labelled V1R, which is the same lead as V2 V2 should be labelled V2R, which is the same lead as V1 V3 is V3R V4 is V4R V5 is V5R V6 is V6R There is huge ST elevation across the right sided leads, diagnostic of RV STEMI. |
Does this matter? Won't the interventionalist just find the lesion and fix it?
Here is a case (in video form) in which the ST elevation in V1 was not noticed, a right-sided ECG was not recorded, and the angiogram showed occlusion of the mid-RCA, which was fixed. When I called the interventionalist to ask about the proximal RCA due to STE in V1, he went back to look at the angiogram: what he had not noticed was that this occlusion was an embolus from the ulcerated plaque in the Proximal RCA. He was thus able to go back and stent the actual culprit lesion.
Furthermore, it is good to know that the RV is involved in order to anticipate right sided heart failure with hypotension and nitroglycerine sensitivity.
How sensitive and specific is STE in V1 in the setting of RV MI, in cases with and without concomitant ST depression in lead V2?
We are just finishing a manuscript on this and cannot reveal our results. Suffice it to say that STE in V1 is pretty specific but not sensitive. Furthermore, that ST depression in lead I, though it does predict RCA occlusion, does not give any further information about whether that RCA occlusion is proximal (RVMI) or not.
In other words, all patients with inferior STEMI should have a right sided ECG recorded.
GREAT example of acute proximal RCA occlusion! What makes interpretation subtle in this case, is that there is really only one 1 QRS complex in lead V1 that we can adequately assess — because the 2nd complex in this lead is negatively scooped because of artifact, and the 3rd complex is a PVC. That said, there should be NO doubt (as per Dr. Smith) — that the ST segment for the 1st QRS complex in lead V1 is flat instead of depressed as we would anticipate, given the presence of acute posterior infarction. In further support of this premise, is the relatively modest amount of J-point ST depression in leads V2,V3 compared to a much more dramatic amount of inferior lead ST elevation (again, presumably because anterior ST depression is attenuated by opposing RV ST elevation). So this is an actual case in which the clinician should be able to diagnose acute proximal RCA occlusion within seconds, even before obtaining a right-sided ECG. Other findings of note is the early transition (R greater than S wave by V2) consistent with evolving posterior infarction — biatrial abnormality (tall, peaked P in lead II; prominent negative component to the P in V1) — and LVH (very tall R wave in lead V5) associated with lateral chest lead ST depression consistent with ischemia and/or LV strain. THANKS for posting this wonderful example of a 12-lead diagnostic of acute proximal RCA occlusion.
ReplyDeleteThanks as always, Ken!
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