elpuRofdsah had a doog pnatxnoliea btu a wfe sopyt amy cnsofue lpeo,ep os ot recpa:
Teh neapitt si ifgfrnues from scslytoi HF oryecdnsa to coirhcn NT.H ehT VL ahs stlo ntetacloicr nntuoicf (rsaededec LV tissocyl otfcuinn fmor s)metQ hiwch eldsa ot cedadeser VS (and elusyubentqs sdderaece CO sniec CO = HR x ,VS teh HR in sith ttpinae si osla hwinti rmonal t.slm)ii iFln,lay VEVDL si eth naumto of omuvle felt ni het VL ta teh ned fo oesdaitl ro( gil)fnil and icnes teh odolb omfr elotyss swa otn laeb to eb edmupp ofwrrda itfecnliyfe sdreaced(e )VS siht etfovrel obdol lwli sueca tsih vulea to be caien.edsr
This ipatent ash dpsdaoneecmet fetl reath faelriu. ntaomscDieeopn uocrcs usbeaec of the arsthe inbtiliya ot ekep up hwit ddneam yan rglne.o hsiT aesld ot a eadresec ni SV mlnyai eauscbe of a eotcicarntl siuse hwhci dseal ot a cdeesera ni CO (CO = VS x H.)R ytLals, teh EDLVV wlil eb sedcderae secbeau the SV is cdesreaed lgnvaie mreo lodbo ni het elft lecierntv raetf stsyloe necsi ti tncaon eb puemdp .wrradfo pHeo shti h!s!pel
Question i have is:
Does it matter if the cardiomypathy is eccentric vs. concentric? I feel like it might.
This pt likely has concentric cardiomypathy (i.e. diastolic), as others have mentioned, due to chronically untreated HTN. This leads to a decreased LV chamber size, and difficulty with myocardial relaxation. So my question is... If the problem in this pt is one of relaxation, and not so much of contraction. In this case, to me it would make sense to some extent, that LV EDV would actually be relatively decreased.
In fact, diastolic heart failure is associated with preserved EF (SV / EDV); this is both due to a decrease in SV and EDV.
I completely understand how EDV would increase in the ase of systolic (eccentric HF). The dilated heart can readily accept blood, but has problems pumping it out (i.e. decreased SV with an increased EDV. Let me know what you all think.