Also posted over at 12-Lead ECG Blog, go check out all the other great stuff there!
Here is the initial ECG and the subsequent 12-lead ECG. Sorry for the poor quality.
What do you see?
What do you want to know?
What do you want to do?
****Update****
His Vital Signs
HR correlates with monitor, pulse not palpable at radial.
Initial BP 78/60
AAOx3, normal mental status, just wants to make a bowel movement.
Skin - Pale, more pronounced and white from the waste down. Skin was relatively dry.
****Update 5/20/2010****
A new 12-lead ECG is captured during transport.
The patient's vital signs do not improve dramatically with IV fluids.
****Update 5/23/2010****
During transport the patient's condition declined rapidly. After the 12-lead ECG above was captured, the patient went in to a decorticate posture. As most of you know, this is indicative of some sort of neuro compromise. With his airway control, mental status, and respiratory rate all declining, brainstem herniation was at the top of the list of differentials.
The patient became pulseless and apneic just prior to arriving at the ER--according to my partners, just after he released the bowel movement. The patient was not revived.
So what happened here?
Me and the field training officer came up with a few possible solutions. First, there is ST-elevation in the inferolateral leads of the initial 12-lead ECG. With the hypotension, a RCA occlusion is a possibility. If the patient has a dominant RCA, there appears to be some ST-depression in the septal leads, but this is a RBBB pattern, so with the T-wave discordance, the ST-depression is not a good clinical indicator of posterior wall involvement.
First Possibility: Right-sided infarct with hemodynamic compromise leading to a syncopal episode. The syncope caused a secondary head injury which cerebrally herniated during transport. I would like to note that this is highly unlikely. Also, the patient did not improve with fluids, which would have happened with a traditional RV infarct.Second Possibility: It is much more likely that the patient had an atypical hemorrhagic stroke that presented with the first symptom of syncope. The changes on the 12-lead ECG could just be concurrent with cerebral ischemia. This is not completely understood, but theories involving nerve endings in the myocardium are abundant. The patient's ICP would have increased during transport with the final result being cardiac arrest.Third Possibility: Abdominal aortic aneurism with severe secondary cerebral ischemia due to hemodynamic instability. I'm not fond of this idea even though the AAA fit the picture in the beginning, it does not explain the decorticate posturing.
We also keep the huge possibility that we have no idea what happened on the list. Ok, so I wish I had more to give you, but an autopsy was not performed on this patient. It remains a mystery.
12 comments:
Can't get the full 3L up, but from the 12L it looks like ST w/ RBBB. I see inferiolateral changes as well. From what I can see on the 3L thumbnail it looks like ST w/ a run of VT.
There is concordant st elevation in V-5 and V-6--lateral wall MI.RBBB. Good thing lead I wasn't the only lead looked at. Another reason took check more than one lead. Iv O2 good hx Ntg and pain meds. Alert the cath lab. Kind of slow for VT. Would like to see another lead other than lead II with the rhythm change.
Good eye, Terry! Leads V5 and V6 do look troubling.
Strange presentation for acute STEMI though. The VT fits but I'd take a careful history, ask all the pertinent questions, and perform a physical exam including neuro exam.
What are you holding up your sleeve, Adam?
So this is a call that I was on. I diagnosed RBBB with inferolateral STEMI, leading me to believe that this guy had a dominant RCA that provided partial perfusion to the lateral wall. I know the changes are difficult to see on this readout, especially with the RBBB.
This was my partner's call and we had a trainee. So during transport, I was driving. I have the details though.
I will update as you ask the questions.
Side question that is relevant to this post.
When looking for ST-Elevation, do you compare to the PR-Segment or TP-Segment?
Why is that, Adam? The ST-segments appear to be slightly elevated above both the PR-segment and the TP-segment.
Remember the rule of proportionality!
The QRS complexes in leads V5 and V6 are both very small (less than 5 mm) so less ST-elevation is required in order to be significant.
Not to mention that the ST-elevation in lead V5 is, as Terry mentioned, concordant with the terminal deflection of the QRS complex (as is the T-wave).
So it's definitely abnormal.
What I'd like to see is some clinical correlation! The presentation doesn't exactly scream ACS.
Tom
How about a neuro exam?
Although.... :)
The J-points also seem to be elevated above the baseline in the inferior leads.
RBBB can be tricky, especially when it's tachy or borderline-tachy.
Remember this false-positive RBBB case?
That was one situation where PR-depression definitely confounded the computerized interpretive algorithm.
Tom
Tom,
Looks like you went through an evolution of thought there. The lateral leads have the clear ST-Elevation. It is the inferior leads I was speaking of, which it looks like you picked up on with your last comment. I am going to elaborate on this further at the end of the case presentation.
Neuro exam? You got straight A's in school didn't you?
At this time, there doesn't appear to be deficits. The atypical presentation was of concern to us as well, after further questioning the patient stated he did have minor pain in his chest. He was not a diabetic, and did not have previous ACS.
I have not heard of STE with cerebral events, but I have heard of ST-depression and deep T-wave inversion. Knowing that there are things that I don't know, I kept neuro problem on the list with this one.
There is more to come. Just waiting for more people to get a chance to join in.
Adam -
I've seen some CNS-related STEMI-mimics, and by STEMI mimic, I mean the ECG unambiguously showed acute STEMI.
Tom
Second 12-lead posted.
I'm not sure what rhythm the patient's in with the new 12-lead ECG but now it shows LBBB morphology in lead V1.
Odd that it's still isoelectric in lead I. Neither the RBBB nor the LBBB pattern is "typical".
We have discordant ST-elevation > 0.2 the QRS complex in lead V3 (ST/S ratio) and concordant ST-elevation in lead V4.
With a more compelling chief complaint and history of present illness this would be a slam dunk!
Tom
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