| Term | Definition |
|---|
| 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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