Drugs Used in Heart Failure I Flashcards Preview

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Flashcards in Drugs Used in Heart Failure I Deck (40):
1

heart failure

CO inadequate to proved O2 needed by body

CAD, MI, HTN, damaged valves, external pressure around heart, Vit B deficiency, cardiac muscle disease

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decreased mortality in HF

ACE, ARBs, aldosterone antagonists, beta-blockers

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Tx for symptoms of HF

volume overload - diuretics

myocardial dysfunction - positive inotropes

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most efficacious for reducing volume overload

loop diuretics

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loop diuretics

forusemide
bumetadine
ethacrynic acid (no sulfa)
torsemide

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furosemide

loop diuretic
-inhibit Na, K, 2Cl cotransporter in thick ascending limb of loop of henle

decreased reabsorption of Ca and Mg

improve symptoms, NOT mortality

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ethacrynic acid

loop diuretic - no sulfa allergy

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adverse of loops

hypokalemia
alkalosis
hypocalcemia
hypomagnesemia
hyperuricemia

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hypercalcemic state

loop diuretic

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nagging cough and swollen tongue

ACE inhibitor

angioedema

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combination with furosemide to control BP and edema in CHF patient

losartan

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ACE and ARBs

reduce mortality for CHF***

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ANG II

blocked by ACE and ARB

vasoconstrictor
Na/water retention
increased aldosterone
catecholamine release
arrhythmias
hypertrophy of cardiac
myocyte death

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HF drug - symptoms first worse and then better

beta blocker

3-6 months

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beta blocker

reduce symptoms AND improve mortality in HF patients

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beta blockers in HF

increased CO initially
-dowregulation of beta receptors
-reduced responsive myocardium

low dose beta blockers***
-increased EF, slow HR, reduce symptoms and mortality

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spironolactone

aldosterone antagonist

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eplerone

aldosterone antagonist

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hydralazine and nitrate

reduce mortality
-improves quality of life

in HF patients

useful, especially in AA patients who have persistance symptoms regardless of ACE and beta blocker therapy

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aldosterone antagonists

reduce mortality with CHF

monitor for normal plasma K levels

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drug that may cause paroxysmal atrial tachycardia with block at high concentrations

digoxin

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digoxin

cardiac glycoside

inhibit Na/K ATPase and increase myocardial contractility

narrow therapeutic index

NO effect on mortality for HF
-only reduces symptoms

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mechanism of digoxin

block Na/K ATPase
-decreased Na/Ca exchange
-results in more Ca intracellular
-stronger contraction

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effects of therapeutic digoxin

prolongation of AP with AP shortening
-increased intracellular calcium

-increased cardiac contractility

increased PS tone, decreased S tone

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effects of toxic digoxin

shortened AP with depolarizing afterpotentials**

-results in premature ectopic beats
-tachycardia may deteriorate into fibrillation

-toxic levels - sympathetic outflow increased

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digoxin at SA node

decreased rate

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digoxin on EKG

therapeutic - increased PR interval, decreased QT interval

toxic - tachycardia, fib, arrest at very high doses

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increased PR interval

seen with digoxin

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digoxin at AV node

decreased conduction velocity and increased refractory period

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potentiate toxic effects of digoxin

furosemide
-due to potassium levels

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hyperkalemia

can reduce effects of digoxin - especially the toxic effects

binds to competing site of Na/K ATPase

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hypokalemia

can potentiate toxic effects of digoxin***

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hypercalcemia and hypomagnesemia

increase risk of digoxin induced arrhythmia


hypercalcemia - accelerates overloading of intracellular Ca stores

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increase force of heart contraction and produce vasodilation

bipyridines

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inamrinone

bipyridine

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milrinone

bipyridine

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bipyridine

selective inhibition of PDE3 phosphodiesterase

PDE3 degrades cAMP

increases concentrations of cAMP in heart - stimulate myocardial contractility and accelerate relaxation

balance arterial and venous dilation

38

PDE3 phosphodiesterase

inhibited by bipyridines

39

short term support of circulation in advanced HF

bipyridines

40

cAMP in cardiac vs. smooth muscle cells

smooth m - increased vascular smooth m contraction