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Phys2 Det Myocar Per

Cardiac output (CO) volume of BL pumped by each ventricle (Volume/min). Normally 5L/min. **CO = HR X SV
Stroke Volume (SV) Volume of BL ejected (Volume/beat). **SV = EDV - ESV
What is Ejection Fraction (EF) and what should it be in a healthy person? It is a measure of contractility. In a healthy person it should be greater than 55%. **EF = SV / EDV.
Preload Amount of volume at the end of diastole (affects the EDV)
Afterload the resistance the ventricle must overcome to empty its contents (affects ESV). **Inversely proportional to wall thickness (Hypertrophy). **Directly proportional to ventricular radius
What causes an increase in AFTERLOAD? 1.Hypertension (higher aortic pressure that the LV must overcome). 2.Dilated ventricle (increased ventricular radius).
What causes a decrease in AFTERLOAD? 1.Hypertrophy (inc wall thickness)
What 2 things change the ESV? 1.Afterload. 2.Ionotropy.
What 3 things change the Preload (and thus EDV)? 1.Compliance (Directly proportional). 2.HR: Diastolic filling time (Inversely proportional). 3.Increased Inflow Resistance/Stenosis (Inversely proptional).
Frank Starling Law of the heart Increase LENGTH (via inc Preload->EDV->SV->CO) increases the force of contraction. **Due to Inc sensativity of Troponin C to Ca2+ and Inc Ca2+ release.
What happens to the Passive tension curve (diastole) on a Vol/Press graph if compliance is decreased? The line is not as flat b/c a change in volume has a greater change in pressure than normal.
Volume/Pressure Graph: Point D (or C) ESV
Volume/Pressure Graph: Point A (or B) EDV
Volume/Pressure Graph: Line A-B Isovolumetric contraction (raising from 15-100 with both valves closed).
Volume/Pressure Graph: Line B-C SV. Since A is EDV and D ESV
Volume/Pressure Graph: Mitral valve closing Point A (LV pressure is higher than atria, initiates isovolumetric contraction phase 2)
Volume/Pressure Graph: Aortic Semilunar valve Opening Point B (when pressure in the LV is greater than MAP, initiates Rapid Ejection phase 3)
Volume/Pressure Graph: Aortic Semilunar valve Closing Point C (MAP is greater than LV, initiates isovolumetric relaxation phase 4)
Volume/Pressure Graph: Mitral valve opening Point D (LV pressure matches L atrial pressure, initiates rapid filling & diastole phase 1a)
How would increasing preload by Increasing venous pressure (EDP) effect CO? what are some ways of increasing it? It would increase the EDV (shifting point A further Right), increasing SV (more Ca+ and affinity), increasing CO. **Done by increasing EDP via: exercise, elevating legs, Inc BL volume.
How would decreasing preload by decreasing venous pressure (EDP) effect CO? what are some ways of decreasing it? It would decrease the EDV (shifting point A further Left), decreasing SV & CO. **Decrease EDP via: Dilation on veins, DVT, Hemorrhage.
How would increasing afterload by increasing mean arterial pressure (MAP) effect CO? It would increase the required Pre-ejection pressure needed in the LV to open the aortic semilunar valve, which means that less BL will escape before the valve closes, Inc ESV, thus Dec SV and CO
How would decreasing afterload by decreasing mean arterial pressure (MAP) effect CO? It would decrease the pressure needed to be generated from the isovolumetric contraction which would allow the semilunar valve to stay open longer and more BL to be ejected, Dec ESV, thus Inc SV & CO
How would Increasing inotropy (contractility) effect CO? Inc inotropy (greater velocity of shortening for a given load) will increase the amt of BL ejected from the LV during systole, Dec ESV, thus Inc SV and CO. **shifts systolic curve up & Left
How would Decreasing inotropy (contractility) effect CO? Dec inotropy (less velocity of shortening for a given load) will decrease the amt of BL ejected during systole, Inc ESV, thus Dec SV & CO. **shifts systolic curve down and right
How would decreasing preload by decreasing ventricular compliance effect CO? Dec compliance (causing pressure to build rapidly with less volume change) would dec EDV (b/c the mitral valve will close with less filling due to inc pressure), thus dec SV & CO
How would increasing preload by increasing ventricular compliance effect CO? Inc compliance (less pressure change with inc vol change) would inc EDV (allowing more BL to fill before pressure closes mitral valve), thus Inc SV & CO **Inc compliance also Inc length (Frank Starling)
Force-velocity curve applied to Afterload and cardiac muscle As Afterload (Force needed to generate the pressure to open semilunar valve) increases, the velocity decreases. **For a given afterlong, the longer the cardiac muscle cell length, the greater it's velocity of shortening.
What do positive inotropes do? INCREASE contractility: 1.Open Ca+ channels (DHPR for longer). 2.Inhibit Na/Ca exchanger. 3.Inhibit Ca ATPase. 4.Activate SERCA pumps. **All of these Inc [Ca+] in the cell and SR.
How do B1 adrenergic receptors work in the ventricles? POSITIVE INOTROPES. NE binds to B1 which then activates Galpha, activating adenylyl cyclase, activating cAMP, phosphorlyating PKA: 1.Open more DHPR, opening more RYRs. 2.Inc SERCA pump activity.
How does digitalis work? what type of inotrope is it? POSITIVE INOTROPE. **Directly inhibits the Na+/K+ ATPase which will indirectly inhibit the Na/Ca exchanger
What two Ions can increase inotropy? 1.Inc Extracellular Ca2+. 2.Decreased extracellular Na+
How can Increased HR increase inotropy and decrease ESV (increasing SV and CO) Staircase phenomenon: leads to inc in SR [Ca2+], Ca2+ release from SR, and Ca2+ entry through DHPR.
Negative inotropes 1.Ca2+ channel blockers. 2.Low extracellular Ca+. 3.High extracellular Na+
What are the 3 ways to change HR? 1.Phase 4 Diastolic depolarization rate in the SA node. 2.Diastolic Em. 3.Threshold.
Parasympathetic effects on HR? 1.Dec diastolic dep at SA node via dec I(f) channels. 2.Opens GIRK (inward rectifier K+), dec Em. 3.Decrease Ca+ channels which raises threshold & elongates phase 4 slope.
Sympathetic effects on HR? 1.Inc I(f) at SA node, increasing diastolic depolarization. 2.Inc Ca+ channels lowering the threshold.
Created by: WeeG



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