A Middle-aged male had sudden onset severe substernal chest pain that woke him from sleep.
His BP was 238/118 on arrival.
Here is his first ED ECG:
What do you think?
There is ST depression maximal in V2-V4, which normally would be all but diagnostic for posterior MI. However, the extremely elevated BP makes it likely that this STD is really subendocardial ischemia from high oxygen demand. (There are also incidentally large U-waves -- the K was 4.1).
It is best to first manage the BP and then repeat the ECG.
So the physician did just that. He obtained a chest CT to rule out aortic dissection (which was negative).
He also gave nitroglycerine to bring the Systolic BP down to 180 mmHg, at which time the chest pain resolved. Then he recorded another ECG:
He gave aspirin, heparin and transferred to the nearest PCI center.
The initial troponin at that referral center was "negative", so they observed the patient. A later troponin returned at 0.346 ng/mL (unfortunately, I don't have the assay -- don't even know if TnI or TnT. In any case, that level is elevated and diagnostic of either type 1 or type 2 MI).
Shortly thereafter, the patient had sudden onset 10/10 pain again. Another ECG was recorded:
The ST depression is back!
He went for emergent angiogram and was found to have a 100% proximal circumflex occlusion with TIMI-0 flow.
Comment:
The physician was worried that he had made a mistake here.
I disagreed.
One must manage very abnormal vital signs first. There is no way to know whether the initial chest pain + EKG findings were not subendocardial ischemia due to high oxygen demand due to the extremely elevated BP.
The correct management is to manage the BP, then assess symptoms and a repeat ECG.
As it turned out, the ischemia was indeed due to ACS.
It is an unfortunate coincidence that the artery spontaneously opened (reperfused) at the same time that the BP was managed. The physician could not have known that.
It was only when the ischemia returned (both symptoms AND ECG findings, in this case) WITHOUT an elevated blood pressure that it could be ascertained that this was all due to coronary occlusion.
The ECG did indeed look more like posterior OMI than subendocardial ischemia
One certainly might strongly suspect that this is ischemia is due to posterior OMI rather than subendocardial ischemia, since posterior OMI usually has maximal STD in V2-V4, and subendocardial ischemia usually has STD in I, II, V4-V6, with reciprocal STE in aVR
See here for a case of LAD subendocardial ischemia that presented like a posterior OMI; it even had STE on posterior leads. Guess the culprit with ST Elevation in posterior leads
Summary: The physician was thrown a curveball, but he managed it very well. (That is a baseball metaphor, for those outside the U.S.!)
Extremely sorry for my question and this is mainly for those living outside US in your sentence:would be all but diagnostic for posterior MI..Doctor Smith what does the expression ALL BUT mean .. sorry one more time
ReplyDeleteSteve...
ReplyDeleteThis is a very unusual and instructive ECG and it also points out the problems with cancellation of forces.
Just as a proximal occlusion of a type 3 ("wrap around") LAD can cause a cancellation of forces in precordial and inferior leads, a proximal occlusion of the LCx - whether dominant or non-dominant - can present the same situation as it MAY have done in this ECG.
If the RCA is non-dominant, an occlusion will cause neither inferior nor posterior changes because you're not going to lose the PDA without losing the PL branch also. But that's NOT the case with the LCx in which the posterolateral branch leaves the LCx BEFORE the PDA. So, even though an occlusion of a non-dominant LCx cannot cause an inferior MI, it can still cause a posterolateral MI. And it will usually cause a change in Lead aVL even though the first diagonal usually covers that area also.
My question is "Why IS there no change in aVL?" Because either the first diagonal provided most of the circulation to the basolateral area (thus protecting it) or there was some cancellation of forces between the marginals and the more distal LCx circulation resulting in no net ST deviation in aVL.
As an aside, the branches of the LCx serving the basolateral and lateral areas of the left ventricle are called "marginal arteries (or branches)." There may be up to three marginal branches (usually). The title "Obtuse Marginal" can only belong to ONE of the marginal arteries - the largest of all of them. When you see the initials OM1, that is NOT referring to the "first" obtuse marginal artery. Those initials are telling you the the obtuse marginal is the first of the marginals that are present. It is in position 1. OM2 would imply that the obtuse marginal is the second marginal artery - NOT that there are two obtuse marginal arteries.
Thanks again for this really great post. And I agree that the ER doc handled this very well!
Jerry W. Jones, MD FACEP FAAEM
https://medicusofhouston.com
Jerry, that's a lot of analysis! All I can say is that it is not uncommon for a proximal circumflex occlusion to result in isolated ST depression in V1-V4. It is also not uncommon to have zero ST deviation. I have two examples on the blog of that, though can't find them at the moment. --Steve
DeleteHi, thanks for the case! What il the rythme in the first ECG? Junctional? There seems to be a P just after the qrs in AVL. Could it be due to ischemia?
ReplyDeleteOlivier, see answer below
DeleteHi,
ReplyDeleteThank you for the case! What is the rhythm at the begining of the the first ECG? Junctional? It seems to be a P just after the QRS in AVL. This could be ischemic?
See answer below
DeleteDr.Smith, Thank you once again for a wonderful post on subtle ECG features of culprit artery localisation (Friday, November 27th 2020 ). May I add a comment ?
ReplyDeleteThe first ED ECG is remarkable for prominant and concordantly POSITIVE U waves in many leads, more prominant in all precordial leads. And the next ECG done after controlling chest pain with medications shows almost complete subsidence of U waves, raising a possibility they may be related
to cardiac ischemia, hypokalemia being ruled out. Inverted U wave in association with ( LAD territory ) cardiac ischemia is well known, but positive U waves due to cardiac ischemia are not well recognised .
Mirror test of V2 in the first ED ECG is indeed suggestive of Posterior wall infarction. If so, can we also assume the Positive U waves to be reciprocal of infero-posterior infarct ? In this regard,
it is worth noting few old Japanese literature. Chikamora T et al ( ref 1) have demonstrated Positive U waves in right precordial leads ( and also left precordial and limb leads )during exercise induced ischemia due to LCX/RCA stenosis.
Angina induced Positive U waves in right precordial leads due to critical LCX/RCA stenosis (ref 2)
and transient Positive U waves as a marker of critical LCX stenosis and poster-inferior ischemia have also been reported ( ref 3 ).
1) Chikamora T et al
Am. J. Cardiol 1994; 74: 495-499
2) Hasegawa K et al
Heart. 1988; 20: 1033-1039
3) Hasegawa K et al
Heart 1988; 20: 269-275
with regards, Dr.R.Balasubramanian
Interesting case. What do you make of the P-wave axis in the first tracing. Initially, I thought this was a junctional rhythm, however, there are p-waves notable in V4-V6, though the PR interval seems to vary (in the only 2 beats I see them in). A rhythm strip at the bottom of this tracing would be helpful.
ReplyDeleteSee answer below!
DeleteGreat post! What is the rhythm in first ECG?
ReplyDeleteGood question. I'd need to take some time to closely analyze it, but don't have that time. Suffice it to say that I do not get too excited about rhythms like this because in a case like this they do not impact the management of the patient. It is a safe supraventricular rhythm that is neither too slow nor too fast, and the absence of a fixed relationship between the atria and ventricles is not affecting perfusion.
Delete