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13 Cards in this Set
- Front
- Back
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Preload
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- forces on venous side affecting contractility
inc venous return = more blood in ventricles = intraventricular pressure rises = inc vent stretching = inc force of contraction (Frank Starling law) (increased stroke volume) |
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Preload in CHF
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preload elevated by blood volume and venous tone
**Venodilator drugs reduce preload by redistributing blood from heart to peripheral veins inc symp and RAS activity inc venous return (inc bv and venous tone) |
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Afterload
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amount of blood left in ventricles after pump
arterial resistance against the heart pumps determined by aortic impedence and vascular resistance |
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Afterload in CHF
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afterload is increased in CHF
symp and RAS activity elevate peripheral resistance via arterial constriction **Arteriodilator drugs reduce afterload by dilating arteries to decrease periph vascular resistance |
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Myocardial contractility in CHF
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contractility is reduced b/c muscle fibers stretched past elastic limit and ventricles become dilated
- CHF - muscles can't contract well **contractility is increased by ionotropic drugs and decreased by BB |
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Heart rate in CHF
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reflex tachycardia results from increased HR from symp overactivity and BR activation from decreased cardiac output
**BB reduce cardiac work by slowing HR |
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Goals of drug treatment in CHF:
high preload |
high preload due to high blood volume and high venous tone
goal: reduce preload drug: diuretic or venodilator |
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Goals of drug treatment in CHF:
high afterload |
high afterload due to increased aortic impedance and increased arterial constriction
goal: reduce after load drug: arteriodilator |
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Goals of drug treatment in CHF:
low contractility |
low contractility due to ventricular dilation which reduces pumping force
goal: increase contractility drug: inotropic drug |
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Goals of drug treatment in CHF:
increased heart rate |
increased HR due to reflex tachycardia caused by sympathetic hyperactivity
goal: reduce energy expenditure drug: BB |
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Inotropic agents (3 classes)
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For CHF
1. Digitalis - Digoxin 2. Phosphodiesterase inhibitors - Inamrinone - Milrinone 3. Sympathomimetics - Dobutamine - Dopamine |
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Mechanism of action of Digitalis
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CHF
inhibition of membrane Na/K ATPase - increased intracellular Na --> decreased expulsion of intracellular Ca --> increased intracellular Ca = decreased intracellular K |
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K and digitalis interaction (CHF)
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- both inhibit binding to Na/K ATPase receptor so K counteracts digitalis toxicity
- K reduces abnormal cardiac automaticity Ca enhances digitalis toxicity **digitalis toxicity w/ K...NOT Ca |
