Interesting ECG

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leviathan

leviathan

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28 y/o male c/o sharp, pleuritic-like chest pain during exercise and in supine position for the last year. Was asymptomatic when the ECG was taken. Seems pretty benign until we saw this, although the cardiologist interpretation was normal (besides possible LVH). Any thoughts?

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Ahhh, interesting. So I still suck at reading ECGs, but when I looked at it, I thought I saw ST elevation, maybe 1 or 2mm in the inferior leads. Mind you, this guy was asymptomatic, young, healthy so I didn't think he was infarcting, but I didn't know what to make of that elevation.

(There is also ST elevation in V2,V3 but I assume that is appropriate elevation for the voltage / deep S waves.)
 
I would normally expect a little deeper Q waves but looks a bit scary for HOCM particularly given the history.
 
leviathan said:
Ahhh, interesting. So I still suck at reading ECGs, but when I looked at it, I thought I saw ST elevation, maybe 1 or 2mm in the inferior leads. Mind you, this guy was asymptomatic, young, healthy so I didn't think he was infarcting, but I didn't know what to make of that elevation.

(There is also ST elevation in V2,V3 but I assume that is appropriate elevation for the voltage / deep S waves.)
Click to expand...

LVH can cause some ST elevation, though.... right?
 
Richspiders07 said:
LVH can cause some ST elevation, though.... right?
Click to expand...
That's true, but isn't it confined to the leads with the high voltage (like v2/v3)? This guy had about 1-2mm in the inferior leads if you look closely. Does anyone know if that is significant?

Gro2001: He wasn't an athlete.
 
So the ST segments when compared against the TP segment arent elevated in my opinion. Certainly not enough to make any opinion of. The reason that the segments look elevated is because the PR segment is slightly down but not diagnostic either.
 
EKG looks stone-cold normal. Nothing stands out for a guy his age.
 
Looks like pericarditis with some slight diffuse PR depression, and PR elevation in AVR (more specific for pericarditis) and some diffuse minimal STE, best seen in Inf leads. I bet the LVH stuff is due to a thin male with a thin chest wall and higher voltages. Weird history with symptoms for 1 yr.
 
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Hard to interpret the right side of the EKG due to the fuzziness. I'm not sure the possible LVH is anything but borderline. There is an early repolarization pattern and I don't see anything that looks like true ST elevation. I don't see any big Q waves (I think I see an appropriate upward deflection 1st in V1 through the fuzz). Maybe PRs look a little short, but no delta waves/wide QRSs. They're probably normal, but LGL is now considered a benign variant. I agree the PR depression/elevation pattern is weird, but pericarditis for a year would be a little odd. His CC does not sound all that scary either for cardiac chest pain. On a (very cursory) perusing on PR depression I found this: http://content.onlinejacc.org/cgi/content/full/39/12/2000. Interestingly, there was a subset of people with connective tissue disease had PR depression. Did this dude look skinny and tall? A lot of marfanoid people stand out, but those with Ehlers-Danlos have more subtle dysmorphology (maybe just a little tall and a mild pectus excavatum). The associated hypermobility with CTDs can cause MSK pain.
 
After you click the link, you can click "zoom in" to see it in full screen / full resolution. V1 does have an R wave. Guy was tall and thin but not necessarily Abe Lincolnish in appearance, if you know what I mean. This was in family practice btw, I think the preceptor was considering an echo but since the ECG and the history seem so benign, I'm not sure if she ordered one. I'll let you know when I find out more on Monday.

By the way, thanks for all the feedback so far, I obviously still have to learn a lot on EKGs. I've read through and 'mastered' Dubin's, but I think I'm going to pick up Garcia since that seems to be the book everyone recommends to get a deeper understanding.
 
Yeah def some PR depression, early repol. Would def get an ECHO as initial outpt wu. What did ya'll eventually decide to do?
 
Early Repol. Repeat EKG needed. And I think the majority of the PR depression is related to his/her resp rate.
 
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overall, I think we can all talk about wanting repeat ECG, Echo, etc etc...but the bottom line is that this ECG doesnt give any really important information and there is no clear pathology.


I think this thread is toasted.
 
I think the thread will be toasted once the OP gives a heads up as to what eventually played out. Def all academic at this point anyhow.
 
ThymeLess said:
overall, I think we can all talk about wanting repeat ECG, Echo, etc etc...but the bottom line is that this ECG doesnt give any really important information and there is no clear pathology...
Click to expand...

I agree. There's a clinical history that does not point to cardiac etiology and the abnormalities of the EGK (really only one-the PR stuff. I don't see LVH on the blown up image [thanks for the tip]) isn't very specific and, with the clinical history, is most likely an incidentaloma. It would seem that the only necessary follow up would be clinical monitoring with the PCP.

My caveat: I'm approaching this as a peds cardiology fellow reading this EKG/interpreting this clinical presentation. I would argue that, playing the odds, a 28 year old, if he had cardiac pathology, would likely have pathology routinely seen/handled by a pediatric cardiologist. But I am curious for the viewpoint of the emergency medicine folk here (moreso the ones that think follow up testing is necessary), what your thought process/worries are. I would also be curious to read the thoughts of any lurking IM/FM or IM-cardiology folk as well.
 
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So the patient has been booked for an appointment for echo. I'm in Canada, so this will be an interesting experiment to see what the wait times are like. I think the MD is just being cautious given the chest pain history.

Interestingly (but probably not relevant), when inquiring about family history, the patient's 1 year old nephew has MCAD deficiency and was recently found to have signs of HOCM on echo by his pediatric cardiologist. If it IS actually HOCM, that would be weird to me as I thought the etiology was mutations in myosin genes and never heard it being associated with metabolic diseases.
 
V2 kinda reminds me of the "saddle" shape of Brugada
 
Here's my crappy student interpretation: Looks like normal sinus rhythm @ ~75/min (although PR looks borderline long), normal axis with no hypertrophy. I think that looks like a bundle branch block in v1/v2 with the ST elevation so yeah, Brugada. The only thing is that if you want to call it a RBBB, it still looks like a narrow complex to me, and I don't see a slurred S wave in V6 or I. I don't know if those things 100% exclude it from being a block or not, or if you have to meet the criteria for a block to call it Brugada.
 
At the risk of jarring the momentum of the last few posts, but I don't think this looks like Brugada morphology based what I've seen Brugada to look like.

If anything, I'd say benign early repol
 
Tiger26 said:
At the risk of jarring the momentum of the last few posts, but I don't think this looks like Brugada morphology based what I've seen Brugada to look like.

If anything, I'd say benign early repol
Click to expand...

The EMRAP TV only describes type I.

I couldn't say it wasn't type II, and gave him cards f/u.
 
leviathan said:
Interestingly (but probably not relevant), when inquiring about family history, the patient's 1 year old nephew has MCAD deficiency and was recently found to have signs of HOCM on echo by his pediatric cardiologist. If it IS actually HOCM, that would be weird to me as I thought the etiology was mutations in myosin genes and never heard it being associated with metabolic diseases.
Click to expand...

There are multiple conditions that can cause a hypertrophic cardiomyopathy, with different underlying molecular etiologies. For example, infants of diabetic mothers can get what is usually a transient HCM (the septum is most affected). Those with Noonans syndrome can develop a HCM. Fatty oxidation defects, Beckwith-Weideman, and others. You were just thinking about familial HOCM/IHSS.
 
I'm just a 2nd year, but don't the T's look high, especially in v2 and v3? The T's in the rhythm strip look pretty symmetrical too. Check K levels?
 
devlyyn said:
I'm just a 2nd year, but don't the T's look high, especially in v2 and v3? The T's in the rhythm strip look pretty symmetrical too. Check K levels?
Click to expand...

They do look a little high to me, you're right. The electrolytes would be something to check, but realize that while tall, they may represent very little ultimately.
 
looks like a normal variant with j-point elevation. I wouldn't call it BER as it typically is associated with a notch in the ST-segment seem most often in lead V4.
 
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