KG - Pharm 2 Exam 2, Drugs for CHF Flashcards
drug class used to reduce preload
diuretic or venodilator
drug class used to reduce afterload
arteriodilator
drug class used to increase contractility
inotropic drugs
drug class used to reduce energy expenditure
Beta-adrenergic antagonist
digoxin - mechanism of action
- inhibition Na/K/ATPase
leads to: increased Ca2+ stores, increased contractility, increased intracellular Na+
digoxin - cardiac effects
- HR reduced/slowed
- as digitalis increases myocardial contractility, sympathetic tone will be reduced
digoxin - pharmacokinetics
- oral
- 80% excreted by kidneys (best of glycosides)
digoxin - adverse effects
- toxic (like all glycosides)
- narrow safety margin
- earliest signs toxicity = GI (N/V, diarrhea, etc)
- CNS
- ARRHYTHMIAS (bradycardia, vent beats, AV block, bigeminy)
digoxin - what should you do if intoxication occurs?
- discontinue
- oral/IV K+
- lidocaine/phenytoin/propranolol
- digitalis immune fab (in overdose cases)
- NO CARDIOVERSION (except v fib)
digoxin - enhanced toxicity by…
- decr renal clearance
- QUINIDINE displaces digoxin from tissue binding sites
- incr GI absorption
digoxin - what causes reduced toxicity?
decr GI absorption (ie: cholestyramine)
digoxin - what happens w/ hypokalemia?
more digitalis action
ie: w/ thiazides, loops, diarrhea
digoxin - what happens w/ further decr SA/AV node activity?
incr digoxin activity
ie: with Beta blockers
digoxin - what happens w/ myocardium?
myocardial sensitization to digoxin
NE releasing agents
what class of drugs are INAMRINONE & MILRINONE?
positive inotropic drugs, INODILATORS
inamrinone, milrinone - mech of action
- inhibit cAMP phosphodiesterase
- incr cAMP
- incr Ca2+ influx (like B1 stim)
inamrinone, milrinone - indications/therapeutic effects
- acute heart failure
incr CO
inamrinone, milrinone - contraindications
long term effect = decreased survival & ARRHYTHMIAS!!!
dopamine - low dose effects/location?
renal vasodilation @ D1 receptors in kidney
dopamine - mod dose effects/location?
inotropic effect @ B1 receptors in heart
dopamine - high dose effects/location?
vasoconstriction @ alpha receptors in vessels
When to use dopamine?
SEVERE, REFRACTORY CHF
dopamine - pharmacokinetics
IV
dobutamine - mech of action
selective B1 agonist
dobutamine - indications
- positive inotropic, less tachycardia
- decr filling pressure, incr O2 consumption
dobutamine - pharmacokinetics
IV
diuretics - indications
- decr salt, H20 retention
- decr venous pressure (decr edema, decr cardiac size)
spironolactone, eplerenone - why do these drugs have additional benefits over other diuretics for CHF?
- inhibit Aldo receptors
- REDUCED MORTALITY RATE
which drugs reduce CHF mortality?
- Aldo antagonists
- beta blockers (beg only)
- ARBs
- ACE inhibitors
what three things does angiotensin II cause that you do NOT want in CHF? (or ever..)
- increased after load
- increased preload
- increased remodeling
ACE inhibitors - mech of action
inhibits angiotensin converting enzyme (ACE), will not make ATII
which drugs are ACE inhibitors?
-pril
ARBs - mech of action
block angiotensin II from binding to the ATI receptor
which drugs are ARBs?
-sartan
which drugs are the backbone of CHF treatment?
ACE INHIBITORS
therapy w/ ACE INHIBITORS will diminish cardiac workload by:
- decr afterload (decr vasoconstriction)
- decr preload (decr aldo release)
RAS inhibitors - adverse effects & why
dry cough bc reduction in bradykinin metabolism
beta blockers (ie: Carvedilol, Metoprolol) - indications
- DECR MORTALITY
- decr renin secretion
- decr HR
- decr remodeling
- up regulate B receptors
when are beta blockers effective in CHF?
early stages only - dangerous in end stage bc of neg inotropic effects
list of vasodilators?
- sodium nitroprusside
- isosorbide dinitrate
- hydralazine
vasodilators - how are they effective?
reduce:
- preload (venodilation)
- afterload (arteriolar dilation)
- or both!
also reduces damaging remodeling of heart
