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