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NBME 21 Answers

nbme21/Block 3/Question#35 (52.5 difficulty score)
A 63-year-old woman comes to the physician ...
Increased resting cardiac output🔍
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 +17 
submitted by cellgamesgojan(38),
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VA tssiaulF o-eurrt bdolo mrfo eht talirrae smytse ot het vunsoe ,ytsems gnab-ispsy the sitAorerel = creIaesn PL g;-t-&- EICRAESN V.R llA ni all = enaIserc .OC

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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). +15  
hungrybox  Jesus big92 you went in on the research lmao u must be MSTP +5  
temmy  big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts. +3  
kevin  what is "increase PL" +1  



 +1 
submitted by the260guy(6),
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tuB heser' my pobrlme thwi shit nuesot:iq ti asys atth hse hsa a 5 day rythiso of BOS dan lolsnew esl.g So boylviuso teh trahe is filinga. I dkepci eaecDsder kotreS elouVm for atht .rosena

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?.. +  



 +1 
submitted by nuts4med(6),
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nyneAo vhea an aide why eht rddeeacse arrailet O2 siuratoatn si nriteo?crc nmAsgusi ehs ash mpul admee necis esh sah EL m,deae tolw'dnu a olerw O2 sat be exdcpeet oto?

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. +6  
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). +4  
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 +  



 +1 
submitted by usmleuser007(335),
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OC is aseendcir iwht 1) seceadedr ea2tfdoal )r dsniecrae dl 3eopr)a ecanderIs rcitynilotact

nA avroenutosei aiuftsl eeacrts na etetraivlan rteou fro laiatr lobod into het ovsenu intcucaiolr /ow ongig apst teh erroeaistl ht(e raomj auecs of shnsT).ts,ereaicu by doign os teh PTR a)t(dalofer acedssere and hte CO is rnsead.cie




 +0 
submitted by uslme123(51),
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AsVF' = eanidrcse raiccad upto .BTUut sthi stn'i wen fro tsih opsn?re I eivw thsi sa a teahr that has nafliyl neugb ot liaf -- eaedescdr iecteffev rltcryaoicu lmuvoe -;t-g& rneeaisdc S.RV

uBt i gssue you cnta' ahev B erobef A -- ehaevwtr -\-

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? +  



 +0 
submitted by azibird(92),

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.




 +0 
submitted by step1soon(43),

Heart failure: This is the most serious complication of large arteriovenous fistulas. Since your blood flows more quickly through an arteriovenous fistula than it would if your blood flowed through a normal course of arteries, capillaries and veins, your heart pumps harder to compensate for the drop in blood pressure (called high-output heart failure). Over time, the increased intensity of your heart's pumping can weaken your heart muscle, leading to heart failure.