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Cardiac Physiology II-c, Cardiac Physiology II-c Coronary Blood Flow Fed by L/R cor. aa. 20% humans-L dominant 50%-R dominant->Post. IV a. 30%-balanced Venous flow L vent->cor. sinus R vent->ant. cardiac vv. some thru Thebesian channels -directly to ventricles, Cardiac Physiology II-c Cardiac Performance Venous return curves ΔP=MSFP-RAP (pressure to drive venous return) -curve as fcn of RAP mean systemic filling P~7mmHg (fullness of vasculature) shift curve up by ⇑MSFP -venoconstriction, transfusion shift down w/ blood loss return greater w/ lower TPR, Cardiac Physiology II-c Special Circulations Splanchnic, Splanchnic ???? Liver sinusoids very permeable ->low P needed~5mmHg aa'oles autoregulate P- hepatic not portal can store excess blood -due to ⇑RAP, Cardiac Physiology II-c Coronary Blood Flow Heart faliure compensated HF-part. recovered decomp'd HF-no renal fnc, fluid balance -need to get certain CO for fluid balance digitalis->increase contratility diuretic->prevent edema, Cardiac Physiology II-c Coronary Blood Flow Neural Influence-myocardial needs dominate Parasympa-w/ high BP, chemo direct->slight vasodil (NO) indirect->⇓HR, contractility, O2 use, =>cor. blood flow ⇓ SNS-cold pressor, exercise, low BP direct->α1 receptor-vasoconstrict indirect->HR, contractility, O2 use ⇑ more time in systole ⇓ flow but =>cor. blood flow ⇑⇑, Cardiac Physiology II-c Cardiac Performance Cardiac Output curves vs Atrial P, viewed as 1 pump shift up w/ SNS down w/ Ca channel, β1 blockers, MI cardiac reserve-CO above normal 300-400% of normal, Cardiac Output curves vs Atrial P, viewed as 1 pump shift up w/ SNS down w/ Ca channel, β1 blockers, MI cardiac reserve-CO above normal 300-400% of normal Measurement Fick Principle CO=O2 consumed/AV O2 diff but venous sample from rt. atrium, Cardiac Physiology II-c Coronary Blood Flow Autoregulated from 60-180mmHg -due to metabolic activity, O2 usage Tension-time index-for myocard O2 -estimate w/ MAP*HR, Cardiac Physiology II-c Coronary Blood Flow Myocardial infarction -lose O2, could die -dead cells->no tension ->systolic stretch-bulge out ->reduce Stroke Volume anastomoses to save cells -coronary steal-healthy tissue steals blood from collaterals ->vasodilators not used for MI -but nitroglycerine ⇑ flow to large cor. aa.