NBME 21 Answers : Block 3 : #35 = A 63-year-old woman comes to the physician because ...

NBME 21 Answers

nbme21/Block 3/Question#35

A 63-year-old woman comes to the physician because ...

Increased resting cardiac output

+7 upvote downvote
submitted by cellgamesgojan(17),

AV Fistulas re-rout blood from the arterial system to the venous system, by-passing the Arterioles = Increase PL ---> INCREASE VR. All in all = Increase CO.

According to UWorld, the arterioles are a major source of resistance ... so bypassing the arterioles results in a decrease in Total Peripheral Resistance ... causing an increase in the rate and volume of blood returning to the heart. I am pretty sure there is more to the physiology behind this, but I hope this explained a little.

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). +3

hungrybox Jesus big92 you went in on the research lmao u must be MSTP +1

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

+1 upvote downvote
submitted by nuts4med(3),

Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?

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. +1

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). +1

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) +1

+1 upvote downvote
submitted by usmleuser007(113),

CO is increased with 1) decreased afterload 2) increased preload 3) Increased contractility

An ateriovenous fistula creates an alternative route for atrial blood into the venous circulation w/o going past the arterioles (the major cause of resistance). Thus, by doing so the TPR (afterload) decreases and the CO is increased.

+0 upvote downvote
submitted by uslme123(9),

AVF's = increased cardiac output. BUT this isn't new for this person? I view this as a heart that has finally begun to fail -- decreased effective circulatory volume --> increased SVR.

But i guess you can't have B before A -- whatever --\

+0 upvote downvote
submitted by the260guy(0),

But here's my problem with this question: it says that she has a 5 day history of SOB and swollen legs. So obviously the heart is failing. I picked Decreased Stroke Volume for that reason.

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. +

+0 upvote downvote
submitted by step1soon(8),

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.