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Flashcards in Iontrophic Agent Deck (49):
1

how does Digoxin differs from Digitoxin

-Digoxin has a quicker onset via oral and IV
-Has a quicker peak effect oral and IV
-has less intestinal absorption bc more water soluble; less protein binding
-greater volume of distribution
-shorter half life
-eliminated vai renal (not hepatic)
-requires a small therapeutic [ ]

2

MOA of digitalis glycosides

reversible inhibition of Na/K ATPase

3

digitalis glycosides has a higher affinity for what conformation

E2

4

Na and Mg change the conformation to

E2, phosphorylates

5

K+ changes the conformation to

E1, dephosphorylates

6

digitalis glycosides have what 2 major concurrent actions on the heart

1. mechanical
2 electrical (direct and indirect)

7

function of mechanical action of DG

increase myocardial contractility

8

what are the direct electrical effects of DG

depolarize membrane potential

9

what are the indirect effect of DG

increased vagal tone at SA & AV node

10

what are the mechanical effects of Digoxin

1) increase in Tension development - less time in mechanical systole
2) improvement in cardiac function - greater stroke work at each L ventricular end-diastolic pressure

11

what is the eqn of efficiency

cardiac work/cardiac O2 consumption
-this occurs by increase Ca++ availability

12

what are the direct electrical effects of digoxin

1) increased automaticity
2) decreased conduction velocity
3) shorter duration of the AP

13

what are the indirect electrical effects of digoxin

1) increase vagal (PSN) effects - central vagal nuclei are stimulated, Ach effects are facilitated, increased baroreceptor responsiveness
2) electrophysiological implications
-vagus innervates atrial muscles and nodes
-atrial muscle decreases automaticity
-SA node stimulation --> bradycardia
-AV node stimulation --> heart block

14

what is the therapeutic window of Digoxin

narrow therapeutic window

15

digoxin toxicity

-altered serum electrolytes ( hypokalemia/hyperkalemia, hypercalcemia, hypomagnesemia)
-acidosis inhibits Na/K pump
-altered thyroid status
-renal disease impairs elimination
-increased sympathetic tone
-respiratory disease & hypoxia

16

digoxin decreases absorption of what drug

cholestyramine, bran, etc.

17

digoxin increases plasma levels of what drugs

Quinidine, propafenone, verapamil, amidoarone, etc.

18

digoxin increases absorption of what drug

antibiotic treatments

19

digoxin increase automaticity due to electrolyte alteration of what drugs

furosemide, chlorothiazide, etc

20

digoxin exacerbate A-V node inhibition of what drugs

verapamil, dilitazem

21

what are the neurological and GI symptoms of Digoxin Toxicity

- malaise, dizziness, confusion, delerium
-anorexia, nausea, vomiting, abdominal pain
-disturbed color vision

22

what are the early cardiac signs of digoxin toxicity

-sinus bradycardia
-first degree AV block
-AV pacemaker or ectopic impulses originating from the AV node

23

what are the serious cardiac signs of digoxin toxicity

-marked sinus bradycardia
-SA node arrest
-2nd or 3rd AV block

24

how do you treat serious cardiac digoxin toxicity

give atropine, consider giving K+ and possibly pacing

25

what is the most serious cardiac sign of digoxin toxicity

any of the previous signs PLUS premature ventricular arrhythmias (PVC's)

26

how do you treat the most serious digoxin toxicity

DIGIBIND (Fab immunoglobulin against digoxin)

27

MOA of Digoxin

-inhibition of Na/K ATPase results in increased intracellular Ca++
-enhances vagal tone

28

clinical uses of Digoxin

-CHF
-AV nodal reentrant arrhythmias
-atrial fib

29

pharmacokinetics of Digoxin

-oral admin
-primary renal ecretion
-half-life of 36 hrs

30

Adverse Effects of Digoxin

neurological and GI symptoms

31

early cardiac signs of Digoxin toxicity

-sinus bradycardia and/or 1st degree heart block

32

serious cardiac signs of Digoxin toxicity

-SA node arrest and/or complete heart block
-PVCs & ventricular arrhythmias

33

positive inotrophic effect in ventricular m. leads to what clinical/ECF effect

improved cardiac function

34

lengthens AP duration in nodes leads to what clinical/ECF effect

bradycardia & prolonged PR

35

shortens AP duration in cardiac m leads to what clinical/ECF effect

shortened QT interval

36

increases automaticity in ventricular m leads to what clinical/ECF effect

increased change of PVC's

37

MOA of Dopamine

stimulates B-1 adrenergic and dopamine receptors

38

pharmacodynamics of dopamine

-positive inotrophic effect
-at low doses, causes dilation of renal vessels via D1 receptors

39

AE of dopamine

-tachycardia
-proarrhythmogenic

40

MOA of dobutamine

stimulates B1&B2 -adrenergic receptors

41

pharmacodynamics of dobutamine

-positive inotrophic effect (B-1)
-vasodilation of the vasculature (B-2)

42

AE of dobutamine

-tachycardia (but less than Dopamine)
proarrhythmogenic (but less than Dopamine)
-tolerance after several days

43

MOA of inamrione

phosphodiesterase inhibitor: selective for isozye III, found in cardiac and vascular smooth m, which causes increased cAMP levels in the cells

44

pharmacodynamics of Inamrione

-positive inotropic effect
-vasodilaion

45

AE of inamrione

-proarrhythmogenic w/ prolonged use (a few days)
-thrombocytopenia & liver damage

46

Heart Failure Diuretic drugs

Loops, thiazides, & Spironolactone

47

Heart Failure Vasodilator Drugs

ACE Inhibitors (Enalapril, Lisinopril, Ramipril)
A-II receptor blockers (Losartan, Valsartan, Candesartan)
Hydralazine/Isosorbide dinitrate combination

48

Heart Failure Beta Blocker Drugs

Carvedilol, Metoprolol

49

Heart Failure Inotrope Drugs

Digoxin, Dopamine, Dobutamine, Inamrinone