EKG

[Jabbed]

55 y/o black male with three days of transient positional and pleuritic chest pain.



No prior EKG or ECHO for comparison. Poor historian, but claims no hx of heart/lung disease. Troponin positive, but concomitant renal failure. Thoracic aneurysm on CT.

Thoughts:
1. ST elevation in right precordials and aVR with inferolateral depressions looks like LMA or proximal LAD lesion. Inferolateral ischemia with sinus tachycarida and P pulmonale also made me think of PE given the symptoms, although the CT was clean.
2. The marked P pulmonale and short PRI makes me wonder if the ST deviations are d/t atrial repolarization.

---

Members don't see this ad.

 

[Rendar5]

Dissecting aneurysm or regular aneurysm?
Ct or ct angio? Two different types of ct.

Inferior ischemia and stemis are associated with dissections because they hit the RCA once they reach the proximal aorta. This is due to their location along the greater radius of the aorta where shear forces are the greatest. You're not wrong about concerning features for pe being tachycardia and Rae.

I'm not sure what you're asking for though. Just ekg comments? If so don't worry about pr shortening here. It's either a clue to a subtle wpw or junctional rhythm or it's something to ignore (e.g. lgl syndrome or some other inconsequential feature)

 

[Rendar5]

btw the st changes are unrelated to atrial issues. They're all ischemic or strain related

 

[jdh71]

Is this homework?

 

[Jabbed]

Dissecting aneurysm or regular aneurysm?
Ct or ct angio? Two different types of ct.

Inferior ischemia and stemis are associated with dissections because they hit the RCA once they reach the proximal aorta. This is due to their location along the greater radius of the aorta where shear forces are the greatest. You're not wrong about concerning features for pe being tachycardia and Rae.

I'm not sure what you're asking for though. Just ekg comments? If so don't worry about pr shortening here. It's either a clue to a subtle wpw or junctional rhythm or it's something to ignore (e.g. lgl syndrome or some other inconsequential feature)

Plain CT aneurysm. He survived to discharge without intervention, so I think he's self-selected out of dissection criteria. The reason that I brought it up was because the decision was made to defer PCI as the STE/tachycardia resolved in the ED, so I don't have a cath report to validate my interpretation. PRI returned to normal as well, which I thought was interesting but I guess sub-clinical.

The history didn't seem c/w Prinzmetal's either, although I guess that's also a possibility.

Basically, I have no idea what's going on. Just looking for an interpretation that fits.

 

[Kahreek]

Carditis, perimiocarditis, pericarditis?

 

[Rendar5]

couple things to realize here. The ST elevations present are not ST elevations we typically refer to in terms of STEMI. aVL elevations typically refer to Left main disease, but usually in a chronic nature. You did correctly surmise that. V1 ST and T waes are also usually opposite everything else. So an elevation there can really be seen as a depression (posterior wall MI's have upright T-waves and ST depressions in V1). V2 appears to be a 1mm elevation, for STEMI's you're looking for 2mm in prechordials or 1mm in limb leads. and V3 looks like an elevation, but if you look for the j-point, it's honeslty <1mm elevated if at all. I agree with teh cardiologists not reading anything into the elevations.

If it was a non-con CT or a plain contrast CT, you won't see PE's, you'll sometimes catch dissections. If it's a CT Angio cath, you should hopefully catch the PE (though it is by no means a perfect test). timing of contrast bolus is usually different for dissection v. PE, though you hope for the best when you do it.

I agree with you that I'd be thinking PE. Pericarditis or pancarditis could be a possibility, I forget what stage III EKG changes looks like (you will usually only see either diffuse elevations or normal ekg. And that's honestly the only progression I saw on a case I saw lucky enough to see both times as an attending on the first visit and a repeat visit a week later on a pericarditis patient). It's either diffuse t-wave inversions or st depressions. If it's diffuse st depressions then sure it could feet. I would not be thinking dissection, as that would show up as tachycardia alone or a RCA STEMI if the coronory dissected off.

Lastly, a quesiton you might be able to answer. HOw did the troponins trend? If they stayed the same, then sure it could just be due to renal failure, people love to do that with trops. But if it rose and fell, that would indicate an MI of some sort.

 

[Jabbed]

couple things to realize here. The ST elevations present are not ST elevations we typically refer to in terms of STEMI. aVL elevations typically refer to Left main disease, but usually in a chronic nature. You did correctly surmise that. V1 ST and T waes are also usually opposite everything else. So an elevation there can really be seen as a depression (posterior wall MI's have upright T-waves and ST depressions in V1). V2 appears to be a 1mm elevation, for STEMI's you're looking for 2mm in prechordials or 1mm in limb leads. and V3 looks like an elevation, but if you look for the j-point, it's honeslty <1mm elevated if at all. I agree with teh cardiologists not reading anything into the elevations.

If it was a non-con CT or a plain contrast CT, you won't see PE's, you'll sometimes catch dissections. If it's a CT Angio cath, you should hopefully catch the PE (though it is by no means a perfect test). timing of contrast bolus is usually different for dissection v. PE, though you hope for the best when you do it.

I agree with you that I'd be thinking PE. Pericarditis or pancarditis could be a possibility, I forget what stage III EKG changes looks like (you will usually only see either diffuse elevations or normal ekg. And that's honestly the only progression I saw on a case I saw lucky enough to see both times as an attending on the first visit and a repeat visit a week later on a pericarditis patient). It's either diffuse t-wave inversions or st depressions. If it's diffuse st depressions then sure it could feet. I would not be thinking dissection, as that would show up as tachycardia alone or a RCA STEMI if the coronory dissected off.

Lastly, a quesiton you might be able to answer. HOw did the troponins trend? If they stayed the same, then sure it could just be due to renal failure, people love to do that with trops. But if it rose and fell, that would indicate an MI of some sort.

That was very informative, thank you. First troponin was 0.56, second one at the two hour mark was 0.60. I'll have to look up any later values as I only saw him in the ED.

Do you have an explanation as to why the ST elevations resolved so quickly in the ED? The combination of the atrial conduction defect, short PRI, and tachycardia made me wonder if it was caused by the atrial repolarization wave, which coincides with the resolution of the ST changes after the PRI and rate normalized. But I've never read about the atrial repolarization wave causing a pseudo-injury pattern before, so I'm not sure if I'm just making this up. The only information that I've found that almost corroborates this theory is one of Smith's ECG blog posts: http://hqmeded-ecg.blogspot.com/2011/11/atrial-repolarization-wave-mimicking-st.html. Even then, that pattern doesn't really fit with what I'm seeing here.

 

[loz95]

Hi could I just ask, is carditis a complication of rheumatic heart disease? Or would there be overlap as the definition of carditis is inflammation of the heart, which in itself is what rheumatic heart disease is? I'm a bit confused by it, as i'm doing a presentation on the complications of rheumatic heart disease.