VA Fualstsi tre-our lbood fmro eth ariralte yetssm to het vsoune sesy,tm sgianypb-s het esoelArrti = encIesar PL g;t---& ANSCEREI .VR lAl ni lla = srneIace O.C
rgAcnocdi ot oldU,Wr hte elerotasir aer a ajorm reuosc of nseacerist ... os siyabsngp het rtesrealoi lsertus in a rdeeseac ni ltoTa Plrerheapi aceRtssnei ... giuascn na acernsie ni eth atre dan oeulmv of dolbo rrntnuieg to eth tre.ah I ma erpytt suer htere si orem to hte hiolyypsgo nhbdei htis, tbu I hepo stih eiaxldpne a letitl.
I don't feel like any of these comments have fully addressed why the patient currently has increased resting CO and NOT decreased SV. Here is how a friend of mine explained it:
MAP (at resting HR) = 2/3 DBP + 1/3 SBP = 77 mmHg in this patient, which is lower than normal (93 mmHg if you use 120/80). So MAP is decreased and the kidneys/other organs aren't getting the perfusion they need, leading to RAAS activation and SOB/edema. MAP = CO × TPR, so this could be due to low CO relative to TPR (what we usually expect) or low TPR relative to CO. This patient's large AV fistula has dropped her TPR very low, which means her CO must have been very high for the past 15 years to compensate (high output heart failure. She has only 5 days of symptoms, which means she is early on in her HF. Since she had such a high CO to begin with, her drop in SV this early on would still leave here with an INCREASED SV compared to a normal patient. Unless her pulse is super high, her heart must be pumping a massive stroke volume to maintain a normal systolic blood pressure with such a low TPR (MAP = SV x HR x TPR). Eventually, her SV may decrease to be below normal, but not so early on.
For completeness: Not decreased arterial O2 sat because blood is flowing from artery to vein, not the other way around. Not decreased mixed venous O2 sat because arterial blood is flooding the subclavian vein right before mixed O2 sat would be measured. Not increased SVR because of the large AV fistula.
But shre'e my bmrpeol iwth this o:utsiqen it yssa atth ehs ash a 5 dya ihystor fo SOB dna ellwnos l.egs So yubvlisoo teh ahret is nlagif.i I dkcpie dceaesDre oStrke omVelu orf ahtt seraon.
CO is rnedicase wthi 1 ) sedeaercd aorfeta2 )dl icdesrane 3p)d loaer Incderaes ttcatliroinyc
nA oarsoueievtn ltsuifa ertcsae an vteaieatnrl outer for atirla lodbo itno the neuvos norclaticui w/o ggnio taps eht atoersreil eht( jamor ausce of .serei)u,nt aTshsc yb dongi os teh TRP rtdolaaf)e( ecadseers dna het CO si .esecidran
V'sFA = snireaecd caradci TotUt.uupB isth i'stn wen ofr this ?resnpo I ivew hsti sa a earht ttha hsa aylfnil gnbeu to lfia -- drseeacde veieefcft aoitulccyrr vuelom t&;-g- riacedsne S.RV
uBt i gsseu uyo tac'n ahev B efrboe A -- atewhrve -\-
oyAnne aehv an aeid wyh the edeaercds rearaitl O2 uaiotsnrta si tceicornr? nsAgsium ehs hsa uplm edmea cneis seh has EL eem,da nodu'wlt a elwro O2 sat be dcpeexet oto?
rHtae lefruai: hsTi is eth mtso ssruoei noictpolamci fo aerlg vurtooeiasenr sautifsl. nceSi uoyr odolb sowfl remo ycuqlki tgohhru an ruavtieoerson ltfiusa than ti uwldo fi oyru loodb owfdel thhruog a malnor uerosc fo e,rsetair alreiscpail adn vs,eni ruoy retah usmpp ehdrar to eacpetnmso orf hte rpdo in dloob persures lc(leda tpguithoh-u ehtra r.iaelf)u vOer ,tiem the eceirnasd tninsieyt of yruo tshea'r gpmipun cna kaenew uryo thaer lcu,sme lgnedai ot aetrh rafe.uil