Mr. Freeze

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Robbin's qbook, pg. 144, question 33.

I understand the hemodynamic part, but what in the fluff of the question is supposed to steer me toward restrictive cardiomyopathy instead of constrictive pericarditis, especially since it seems the difference between choices B and D are semantic? Except for the whole "longest answer that isn't A rationale".

For those that don't have it, it's a Prussian Blue showing hemochromatosis, in an afebrile 45 y/o pt. with 7 month hx of fatigue, exertional dyspnea, and episodic chest pain.

B. Reduced vent. compliance resulting in impaired ventricular filling during diastole, -or-
D. Lack of ventricular expansion during diastole.
 

Blesbok

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The only thing that makes me think B is that "lack of ventricular expansion during diastole" would indicate complete absence of ventricular expansion as opposed to just being impaired. Hemochromatosis wouldn't completely prevent it like sever constrictive pericarditis might. However, I don't think that is a very good question.
 
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Mr. Freeze

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I could see that. Lack would imply 0.0 compliance, as opposed to normal minus a little bit. It seems so simple after the fact. I hate that. :D

But I guess that also implies that you know hemochromatosis causes a REstrictive instead of a CONstrictive disorder. I think that's where i get mixed up, using terms more loosely than I should; much like my pre-lung phys conceptions of obstructive vs. restrictive.

What I'm finding is that restrictive comes from infiltrative conditions, and constrictive is an extrinsic (parietal sac) thickening. So they explain that D would result from constrictive, which I guess I could see if it were extensive enough.
 
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ROBINHO

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I think u answered the question yourself talking about Infiltration so not being Constrictive.

u can kill of the question with the history
past history of pericardial process vrs Infiltration

and I also imagine that a 7month history isn't probably a pericardial Process???(not sure), more probably an infiltration

At of curiosity were the physical exams presented??
cos a pericardial knock vrs S3 kills it off though
 
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Mr. Freeze

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Very little PE info given, and all "We Never Looked". Yeah, I was wanting heart sounds, etc. But I still would've been like, "Isn't that the same thing?" due to my not picking up the subtleties.

I found in my syllabus that pericarditis can look identical to restrictive cardiomyop., but edema, either pulm or system., is not a common feature.
 

ROBINHO

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Very little PE info given, and all "We Never Looked". Yeah, I was wanting heart sounds, etc. But I still would've been like, "Isn't that the same thing?" due to my not picking up the subtleties.

I found in my syllabus that pericarditis can look identical to restrictive cardiomyop., but edema, either pulm or system., is not a common feature.
It won't be the same thing. One comes with the pericardial knocks and the other with s3 sound during filling
 
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why does a restrictive cardiomyopathy cause S3? I thought S3 were created when there was like blood flowing into an already overfull ventricle (so like I get S3 in dilated cardiomyopathy)
 

vashka

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My understanding based on having done theta question and UWorld's cardio is: The picture provided tells you that it's iron deposition, which classically causes a restrictive cardiomyopathy.
In restrictive cardiomyopathy, the deposition of iron, amyloid, etc makes the tissue less compliant during all phases of the cardiac cycle.
Constrictive cardiomyopathy can occur after months of calcification around the heart(ex. due to TB) and restricts the expansion of the heart. Constrictive is different because it mostly disrupts the flow of blood into the heart during inspiration and diastole. Basically bc there's a wall around the heart, blood returning to the RA->RV cannot transfer the energy of that blood into the RV wall. So the IV septum bulges into the LV preventing LV filling during diastole. This means that there is less CO during systole in constrictive cardiomyopathy.
 
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