Iontrophic Agent Flashcards
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 [ ]
MOA of digitalis glycosides
reversible inhibition of Na/K ATPase
digitalis glycosides has a higher affinity for what conformation
E2
Na and Mg change the conformation to
E2, phosphorylates
K+ changes the conformation to
E1, dephosphorylates
digitalis glycosides have what 2 major concurrent actions on the heart
1. mechanical 2 electrical (direct and indirect)
function of mechanical action of DG
increase myocardial contractility
what are the direct electrical effects of DG
depolarize membrane potential
what are the indirect effect of DG
increased vagal tone at SA & AV node
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
what is the eqn of efficiency
cardiac work/cardiac O2 consumption
-this occurs by increase Ca++ availability
what are the direct electrical effects of digoxin
1) increased automaticity
2) decreased conduction velocity
3) shorter duration of the AP
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
what is the therapeutic window of Digoxin
narrow therapeutic window
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
digoxin decreases absorption of what drug
cholestyramine, bran, etc.
digoxin increases plasma levels of what drugs
Quinidine, propafenone, verapamil, amidoarone, etc.
digoxin increases absorption of what drug
antibiotic treatments
digoxin increase automaticity due to electrolyte alteration of what drugs
furosemide, chlorothiazide, etc
digoxin exacerbate A-V node inhibition of what drugs
verapamil, dilitazem
what are the neurological and GI symptoms of Digoxin Toxicity
- malaise, dizziness, confusion, delerium
- anorexia, nausea, vomiting, abdominal pain
- disturbed color vision
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
what are the serious cardiac signs of digoxin toxicity
- marked sinus bradycardia
- SA node arrest
- 2nd or 3rd AV block
how do you treat serious cardiac digoxin toxicity
give atropine, consider giving K+ and possibly pacing
what is the most serious cardiac sign of digoxin toxicity
any of the previous signs PLUS premature ventricular arrhythmias (PVC’s)
how do you treat the most serious digoxin toxicity
DIGIBIND (Fab immunoglobulin against digoxin)
MOA of Digoxin
- inhibition of Na/K ATPase results in increased intracellular Ca++
- enhances vagal tone
clinical uses of Digoxin
- CHF
- AV nodal reentrant arrhythmias
- atrial fib
pharmacokinetics of Digoxin
- oral admin
- primary renal ecretion
- half-life of 36 hrs
Adverse Effects of Digoxin
neurological and GI symptoms
early cardiac signs of Digoxin toxicity
-sinus bradycardia and/or 1st degree heart block
serious cardiac signs of Digoxin toxicity
- SA node arrest and/or complete heart block
- PVCs & ventricular arrhythmias
positive inotrophic effect in ventricular m. leads to what clinical/ECF effect
improved cardiac function
lengthens AP duration in nodes leads to what clinical/ECF effect
bradycardia & prolonged PR
shortens AP duration in cardiac m leads to what clinical/ECF effect
shortened QT interval
increases automaticity in ventricular m leads to what clinical/ECF effect
increased change of PVC’s
MOA of Dopamine
stimulates B-1 adrenergic and dopamine receptors
pharmacodynamics of dopamine
- positive inotrophic effect
- at low doses, causes dilation of renal vessels via D1 receptors
AE of dopamine
- tachycardia
- proarrhythmogenic
MOA of dobutamine
stimulates B1&B2 -adrenergic receptors
pharmacodynamics of dobutamine
- positive inotrophic effect (B-1)
- vasodilation of the vasculature (B-2)
AE of dobutamine
-tachycardia (but less than Dopamine)
proarrhythmogenic (but less than Dopamine)
-tolerance after several days
MOA of inamrione
phosphodiesterase inhibitor: selective for isozye III, found in cardiac and vascular smooth m, which causes increased cAMP levels in the cells
pharmacodynamics of Inamrione
- positive inotropic effect
- vasodilaion
AE of inamrione
- proarrhythmogenic w/ prolonged use (a few days)
- thrombocytopenia & liver damage
Heart Failure Diuretic drugs
Loops, thiazides, & Spironolactone
Heart Failure Vasodilator Drugs
ACE Inhibitors (Enalapril, Lisinopril, Ramipril)
A-II receptor blockers (Losartan, Valsartan, Candesartan)
Hydralazine/Isosorbide dinitrate combination
Heart Failure Beta Blocker Drugs
Carvedilol, Metoprolol
Heart Failure Inotrope Drugs
Digoxin, Dopamine, Dobutamine, Inamrinone
