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 ร 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 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.
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.
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 --\
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?
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.
submitted by โcellgamesgojan(43)
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.