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46 Cards in this Set

  • Front
  • Back
what are the inotropic drugs
digoxin (lanoxin)
Inamrinone
dobutamine
dopamine
what are the ACE inhibitors
captopril
enalapril
angiotensin II receptor inhibitors
losartan
B-blockers
Bisprolol
carvedilol
metaprolol
digitalis antibody
digoxin immune fab
what are the sources of Digitalis (cardiac glycosides)
foxglove or digitalis plants
what is the mech of action for digoxin
inhibits the Na+/K+ ATPase pump
what are the mechanical effects of digoxin
positive inotropic effects

inc contractility
dec in HR
Inc CO
what is the structure of digoxin/glycosides
aglycone (genin)
3 sugar rings: tri-digitoxose
what does the inhibition of the Na+/K+ pump by digoxin do to the intracellular conditions
Inc Na+ conc
dec K+ conc
Inc Ca++ concentration via retention
inc actin/myosin interactions
inc contractility
how do K+ and digoxin interact with each other
the are competitive inhibitors of each other
they both compete for the Na+/K+ ATPase
what increases the effect of digoxin and should never be added to the body while taking digoxin
Ca++
what dec digoxin toxicity
Mg++
how does digoxin reduce the HR in a normal heart
parasympathtic like effects by
-stimulation of vagal nuclei
-inc SA sensitivity to Ach

also, Inc baroreceptor sensitivity causing vasoconstriction. which is why CO is not inc in pts with normal hearts
how does digoxin reduce the heart rate in a failing heart
the inc in contractility causes a dec in baroreceptor response in an already massively vasoconstrictive periphery. the dec baroreceptor reflex causes vasodilation and vagal stimulation which slows the HR
what are the renal effects of digoxin
inc diuresis (because of hemodynamic improvement
what type of effects does digoxin have on the GI tract
direct irritation: anorexia, diarrhea
stimulation of a chemoreceptor zone: vomiting
mesenteric arteriolar constriction: abdominal pain
what are the pharmokinetic properties of digoxin
good oral absorption
40 hr half life
>80% renal elimination*
why do all digitalis drugs have a narrow margin of safety
because the Theraputic dose is 50% - 60% of the Toxic dose
howmany pts have to discontinue digoxin due to the toxic side effects
5-25%
what are the earliest signs of digoxin toxicity
GI sympt
what are the most common and most dangerous effects of digoxin toxicity
cardiac toxicity
what are the effects of cardiac toxicity by digioxin
bradycardia
ectopic ventricular beats
AV block
bigeminy
what are the CNS side effects of digoxin
headache, fatigue, malaise, drowsiness, trigeminal neuralgia
disorientation and hallucinations
color and visual disturbances occur occasionally in the elderly
how do you treat digitalis toxicity
discontinue
give K+*
digitalis immune fab*
lidocaine, phenytoin, propranolol*
what are the effects of the interaction between digoxin and quinidine
quinidine displaces digoxin from its tissue binding sites and dec renal clearance.
thus inc plasma conc and inc digoxins toxicity
digoxin + dirrhea or diuretics =
hypokalemia
digoxin+ B-antagonists +
dec SA and AV nodeactivity

bradycardia
digoxin + erythromycin =
inc absorption
digoxin + catecholamines (NE releasing agents) =
arrhythmias
what reduces digoxin absorption and toxicity*
cholestryamine
what type of arrhythmia is digoxin contraindicated with
wolf-parkinson-white
what are the phosphodiesterase inhibitors
inamrinone
Milrinone
what are inamrinonoe and milrinone reffered to as?
inodilators
what is the mode of action for inamrinonoe and milrinone
the inhibit cAMP PDE
this improves diastoic fxn and contractility
when should you use inamrinonoe and milrinone
as a last ditch effort in patients that you can monitor closely
what is a major side effect of this drug
doesnt consistently relieve sympt and actually results in a higher mortality and hospitalization rate
what are the sympathetomimetic drugs
dobutamine
dopamine
effects of dopamine
increases CO and renal blood flow in severe refractory CHF
dobutamine=
B1 selective agonist

inc contractility c less tachy
inc O2 demand
IV
nesiritide=
BNP mimic (recombinant)
vasodilator effect
used in decompensated CHF to reduce PCWP (norm= 8-10mmHg)
body does not develop a tolerance to it like it does with NTG
Poss hypotension (must monitor pt)
what is the fxn of ACE linhibitors
to block the conversion of angiotensin I to angiotensin II

Angiotensin Converting Enzyme
B-blockers and heart disease
Dangerous in sever heart disease

useful in cardiomyopathies or diastolic dysfxn (w/out severe CHF)
redeced HR and arrhythmias
reduced mortality
effect of sodium nitroprusside
arterial and venus vasodilator

adverse: hypotension
effect of NTG and isosorbid dinitrate
venodilation more than arteriodilation

tolerance develops quickly
effect of hydralazine
peripherial, arteriolar vasodilation
ANS response: inc HR, CO, EF

slow development of tolerance