Pharm Chf Drugs Winter 2009

Front 1

Digoxin
Lanoxin

Back 1

digitalis glycoside - CHF
1. Directly increases intrinsic myocardial contraction by inhibiting Na/K ATPase which increases intracellular Ca = increases myocardial contractility
2. decrease HR vagally and extravagally
OD/SE: virtually all systems -- Gi, arrythimias, "digitalis delirium," blurred vision, halos
Renal excretion

Front 2

Digoxin Imuune Fab
Digibind

Back 2

to treat digoxin OD; antibody fragments that bind to digoxin and complexes are then excreted in urine

Front 3

Dobutamine

Back 3

synthetic beta 1 adrenergic agonist/non glycoside inotrope
-Treats severe refractory CHF
IV only in ICU
1. increase CO by increasing ventricular beta one receptor action
SE: tolerance possible

Front 4

Dopamine

Back 4

synthetic beta 1 adrenergic agonist/non glycoside inotrope
-Treats severe refractory CHF
IV only in ICU
**Increases HR MORE than dobutamine
1. increase CO by increasing ventricular beta one receptor action
SE: tolerance possible

Front 5

Inamrinone

Back 5

nonglycoside inotropic agent
-Treats severe refractory CHF or after tolerance develops to dobutamine/dopamine
1. phosphodiesterase inhibition; increase cAMP --> increased free Ca availability to contractile proteins during systole.
2. improves diastolic relaxation by increasing SR Ca uptake
SE: thrombocytopenia, increased myocardial oxygen requirements
*Not dependent on adequate # of beta receptors
*No tolerance

Front 6

Milrinone
Primacor

Back 6

nonglycoside inotropic agent
-Treats severe refractory CHF or after tolerance develops to dobutamine/dopamine
1. phosphodiesterase inhibition; increase cAMP --> increased free Ca availability to contractile proteins during systole.
2. improves diastolic relaxation by increasing SR Ca uptake
SE: increased myocardial oxygen requirements
*Not dependent on adequate # of beta receptors
*No tolerance

Front 7

Captopril
Capoten

Back 7

ACE inhibitor
-decrease vasoconstriction and decrease aldosterone levels
1. decreases angiontensin II, decreases preload, afterload, and increases CO, exercise capacity.
2. decreases pulmonary and peripheral congestion
SE: non-productive cough (due to increase in bradykinin levels)
CI: pts w/bilateral renovascular HTN
**Most predictable bc does not need to be activated in liver

Front 8

Enalapril
Vasotec

Back 8

ACE inhibitor; prodrug -- must be activated in liver
-decrease vasoconstriction and decrease aldosterone levels
1. decreases angiontensin II, decreases preload, afterload, and increases CO, exercise capacity.
2. decreases pulmonary and peripheral congestion
SE: non-productive cough (due to increase in bradykinin levels)
CI: pts w/bilateral renovascular HTN

Front 9

Fosinopril
Monopril

Back 9

ACE inhibitor; prodrug - must be activated in liver
-decrease vasoconstriction and decrease aldosterone levels
1. decreases angiontensin II, decreases preload, afterload, and increases CO, exercise capacity.
2. decreases pulmonary and peripheral congestion
SE: non-productive cough (due to increase in bradykinin levels)
CI: pts w/bilateral renovascular HTN

Front 10

Quinapril
Accupril

Back 10

ACE inhibitor
-decrease vasoconstriction and decrease aldosterone levels
1. decreases angiontensin II, decreases preload, afterload, and increases CO, exercise capacity.
2. decreases pulmonary and peripheral congestion
SE: non-productive cough (due to increase in bradykinin levels)
CI: pts w/bilateral renovascular HTN

Front 11

Losartan
Cozaar

Back 11

ARB
24 hr. control
-decrease vasoconstriction and aldosterone levels
1. competitive antagonist of A-II at level of A-II receptor subtype 1
*No cough
*ACE escape phenomenon: in heart, local production of A-II is both ACE dependent and independent so ARBS may more effectively contribute to A-II inhibition in cardiac hypertrophy

Front 12

Valsartan
Diovan

Back 12

ARB
-decrease vasoconstriction and aldosterone levels
1. competitive antagonist of A-II at level of A-II receptor subtype 1
*No cough
*ACE escape phenomenon: in heart, local production of A-II is both ACE dependent and independent so ARBS may more effectively contribute to A-II inhibition in cardiac hypertrophy

Front 13

Candesartan
Atacand

Back 13

ARB
-decrease vasoconstriction and aldosterone levels
1. competitive antagonist of A-II at level of A-II receptor subtype 1
*No cough
*ACE escape phenomenon: in heart, local production of A-II is both ACE dependent and independent so ARBS may more effectively contribute to A-II inhibition in cardiac hypertrophy

Front 14

Hydrochlorothiazide
Microzide

Back 14

Thiazide diuretic
-reduces extracellular fluid volume; decreases preload, pulmonary congestion, and peripheral edema
-distal convoluted tubule
inhibits Na/Cl symport
decreases Ca excretion
*Use if GFR > 30
SE: hypokalemia

Front 15

Furosemide
Lasix

Back 15

Loop diuretic
-reduces extracellular fluid volume; decreases preload, pulmonary congestion, and peripheral edema
-thick ascending limb
blocks Na/K/2Cl
Increases Ca excretion
*use if GFR < 30 or non responsive to thiazides
SE: hypochloremic met. acidosis

Front 16

Spironolactone
Aldactone

Back 16

K+ sparing diuretic; aldosterone antagonist
-reduces extracellular fluid volume; decreases preload, pulmonary congestion, and peripheral edema
-prevent aldosterone induced gene transcription
- dual benefits in CHF pts -- decrease stiffness in fibrosis pts
SE: life-threatening hyperkalemia

Front 17

Epleronone
Inspra

Back 17

K+ sparing diuretic; aldosterone antagonist
-reduces extracellular fluid volume; decreases preload, pulmonary congestion, and peripheral edema
-prevent aldosterone induced gene transcription
- dual benefits in CHF pts -- decrease stiffness in fibrosis pts
SE: life-threatening hyperkalemia

Front 18

Hydralazine

Back 18

direct vasodilator
severe CHF refractory to other txs
for pts after MI with pre-existing chronic CHF
-Primarily reduces afterload
-increases survival chronically but not as much as ACE inhibitors

Front 19

Nitroprusside
Nitropress

Back 19

direct vasodilator
severe CHF refractory to other txs
for pts after MI with pre-existing chronic CHF
-Preload AND afterload reduction
-IV only in ICU -- monitor hemodynamics closely

Front 20

Nitroglycerin
Minitran

Back 20

direct vasodilator
severe CHF refractory to other txs
for pts after MI with pre-existing chronic CHF
-Primarily reduces pre-load
-long term use can lead to tolerance

Front 21

Isosorbide Dinitrate
Icosordil

Back 21

direct vasodilator
severe CHF refractory to other txs
for pts after MI with pre-existing chronic CHF
-Primarily reduces pre-load
-long term use can lead to tolerance

Front 22

Nesiritide
Natrecor

Back 22

direct vasodilator
severe CHF refractory to other txs
for pts after MI with pre-existing chronic CHF
-vasodilator AND diuretic
-IV only in ICU -- monitor hemodynamics closely

Front 23

Bisoprolol
Zebeta

Back 23

Beta blocker
prevent down regulation of beta adrenergic receptor #s, prevent excessive tachycardia and arrhtyhmias
may inhibit overexpression of RAAS

Front 24

Carvedilol
Coreg

Back 24

Beta blocker
prevent down regulation of beta adrenergic receptor #s, prevent excessive tachycardia and arrhtyhmias
may inhibit overexpression of RAAS
**antioxidant and alpha blocker too!

Front 25

Metoprolol
Troprol-XL

Back 25

Beta blocker
prevent down regulation of beta adrenergic receptor #s, prevent excessive tachycardia and arrhtyhmias
may inhibit overexpression of RAAS