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Cardiac glycosides
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increase myocardial contractility and efficiency, improve systemic circulation, improve renal perfusion, and reduce edema.
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Cardiac glycosides
increase myocardial contractility and efficiency, improve systemic circulation, improve renal perfusion, and reduce edema.
Cardiac glycosides
when given in therapeutic doses, produce inotropic effects by inhibiting membrane-bound Na+/K+-activatedATPase.
Effects of Cardiac Glycosides:
increase the rate of tension development, the contractility, and the rate of relaxation of cardiac muscle.
Effects include: a.
a. increase in intracellular sodium concentration
Effects include: b.
b. reduction in calcium transport from the cell by the sodium-calcium exchanger
Effects include: c.
c. facilitation of calcium entry via voltage-gated membrane channels
Effects include: d.
d. increased release of calcium from sarcoplasmic reticulum
Therapeutic doses of cardiac glycosides also causes: a.
a. a negative chronotropic effect from increased vagal tone of the sinoatrial(SA) node
Therapeutic doses of cardiac glycosides also causes: b.
b. diminished central nervous system (CNS) sympathetic ouflow from increased carotid sinus baroreceptor sensitivity
Therapeutic doses of cardiac glycosides also causes: c.
c. systemic arteriolar and venous constriction, which increases venous return and, thus, increases cardiac output
Amrinone and milrinone
produce positive inotropic effects and vasodilation via selective inhibition of type lll phosphodiesterase (PDE) isozyme, leading to an increase in cyclic adenosine monophosphate (cAMP) in cardiac and smooth muscle.
Inhibition of type lll PDE produces: a.
a. Vasodilation and fall in vascular resistance
Inhibition of type lll PDE produces: b.
b. increased force of cardiac contraction
Inhibition of type lll PDE produces: c.
c. increased velocity of cardiac relaxation
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