NBME 21 Increased resting cardiac output (NBME Answers)

NBME 21 Answers

nbme21/Block 3/Question#35 (reveal difficulty score)
A 63-year-old woman comes to the physician ...
Increased resting cardiac output 🔍 / 📺 / 🌳
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+29
submitted by ∗drdoom(1113),

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+20
submitted by ∗cellgamesgojan(42),

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AV Fsitusla otr-eru odblo mfor the latareri myesst ot eth sneovu y,setms sniysgabp- teh otAreirels = aecIsrne PL --gt-&; ECAENIRS RV. llA in lla = rcsIenea .CO

odirgcAnc ot WUdr,ol eth rreoeailst are a ojrma rescuo fo cariseetsn ... os painsgbys het otirlsaeer stsurle in a erescead ni ltoaT lprarheiPe aenseiRstc ... uiscgan na inrcesea ni het rate and emvulo of dloob ueirgntrn ot eth erhta. I am yttper esur htree is orem ot eth olgyhspoiy ndhebi s,hit ubt I peho tshi eapxlndie a .leiltt

big92 "Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554) There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH). +31

hungrybox Jesus big92 you went in on the research lmao u must be MSTP +6

temmy big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +4

kevin what is "increase PL" +5

jhan17 According to wiki "When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance because it by pass arteriole (where major BP is formed) . This lowered peripheral resistance causes the heart to increase resting cardiac output to maintain proper blood flow to all tissues." +

+5
submitted by ∗azibird(227),

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I otd'n efel like ayn fo ehtes tesmoncm evha yfllu reseadsdd hwy teh taeintp ulryenrtc has seniaercd sgiertn OC dan OTN ecserdaed V.S rHee is how a frndie of inem inxeldape t:i

AMP (ta gtirnes )HR = 32/ PDB + 31/ PSB = 77 mHmg ni ihts nieap,tt cwihh is lrweo tnah loarnm (39 mgmH if yuo esu /.02108) So APM is sdeecdrae adn eht kt/dyneesiorh ognsar ert'na tigtneg het rfeuniops tyhe ,eden igdenla ot RSAA icvitontaa nda m.edSeB/aO APM = CO × ,TPR os sith ucldo be eud ot wol OC reteilav to RPT (ahwt ew ayllusu exep)ct ro olw RTP eritvela ot C.O This ieastnt'p eagrl VA iatlfus sah doeppdr reh PRT vrey o,lw chhiw snmea rhe CO stmu have been yrev high rof the aspt 15 arsey to eopacentsm (ihhg oputtu heart .euafirl Seh sah yonl 5 yasd of ostmsm,py hciwh emsna esh si lyrea no in ehr .HF eScni hes dha cuhs a hhgi CO to nebgi ,ithw her ordp ni VS itsh ryael on dluwo llist eelva here with an DNICEAESR VS admrpceo to a namlor atnip.te sUesln ehr elusp si pesru ighh, erh etarh stum be ppuingm a veasmsi tokres uomvle ot nmaiinta a rnloma sloyscit obdol useesrpr ithw husc a low TPR P(AM = SV x HR x R.TP) tlavunyleE, reh SV yma aecersed to eb boewl ,olrnma tub not so yaler .on

orF clmes tepNtne:oso eeddcersa ilaertar 2O tas aubscee ldobo si olfniwg ofrm yrreta to e,ivn tno eht ohert wya odaNourtn. eedadsrce xeimd oevnsu O2 sta eeuasbc teiralra oldob si ofogldni eht banvcilasu ienv trhig efreob ixdme 2O ast dwulo be tuN. aeemdrso erceadnis SRV aucbsee fo eht garle VA faiut.ls

+2
submitted by ∗the260guy(18),

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tuB res'he ym lrombpe ihwt tish eutnso:qi ti ayss atht seh hsa a 5 yad isotrhy of OBS and leonwsl eg.ls oS looyvsbiu eht ehtar is a.nligif I ecpkid adsDreeec torkeS mueoVl for ahtt r.oeans

nwinkelmann AV fistulas are one cause of high-output cardiac failure. This person presents with heart failure, but it is due to chronically increased resting CO. +2

lukin4answer @nwinkelmann yes thats right, he has failing heart. but question is asking what is the finding of this patient, I understand the cause is Fistula causing high output failure, but they didn't ask the reason of his HF, they are asking the finding. I choose decrease Stroke VOlume :/ +

happyhib_ This was my logic and got to decreased stroke volume as well; they arent asking what caused his HF or anything it says what is the most likley finding in this patient. If his heart is failing due to LVH from consistent increased CO wouldnt he AT THIS VERY MOMENT WITH his heart failing have decreased stroke volume?.. +

+2
submitted by ∗usmleuser007(444),

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CO si cnedraies hitw 1) erasdcede teola dfar)2 eseidcnra adol )p3er eaescIndr ntrccliotatiy

nA toasireevuon tfusali scaetre na laeritantev truoe rof artail oldbo tion eth uenovs ulniccoirat wo/ ggino stpa het earoirsetl e(th omarj ecsua of ) hausrsee,ntc.Tsi by nigod os the RTP la(oft)erda eacsesder dan het OC is irs.neadce

+1
submitted by ∗uslme123(83),

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sAVF' = eeascrind iacdrca oBttpuT.U u htsi si'nt wne rof this npreo?s I ivwe isht as a teahr ttha ahs failnyl nbegu to ialf -- edeasderc etefiefvc icryolcurta vuoelm --;gt& ecrdiasen V.RS

uBt i guess yuo cnt'a vhae B fbeeor A -- awvrehet --\

happyhib_ his bp was something like 130/50; with diastolic around 50 I figured he couldnt have increased SVR because his diastolic would be higher? +1

trazobone I had this same reasoning I completely glossed over the BP 🤦🏻‍♀️ +

+1
submitted by nuts4med(7),

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ynoenA vhae na iead hwy het eesardecd eliraatr 2O snaortiatu si nc?ctieorr iugsnAsm seh ash mlup edmae esicn hes hsa EL adeem, wont'uld a wroel 2O tsa eb eetdpexc to?o

haliburton I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average. +7

hungrybox ty both of you for this, was wondering the same thing +

coxsack O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would). +5

hungrybox just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol) +2

chandlerbas ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter +

+0
submitted by ∗step1soon(47),

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reatH fuelar:i This si the tmos oisuser opocimnctlai fo ealgr vaoeutorrneis ulsast.if neSic oruy oobdl ofswl moer cqkyuil hruhtog na steruioaveron staflui athn it wdlou fi yoru boldo feolwd hghotur a nolamr scoreu of srtear,ie asielplriac and evnsi, yruo thera muspp ahrrde to moetnscpae ofr eth rpdo in dolbo susrrpee cld(lae -tuoptguihh rheta ulr.)iafe veOr ei,mt eht criesaned esntiinyt fo ruoy 'harste gmnpuip nac ekenwa uryo hreta emulc,s gladien to tarhe .fraulie