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25 Cards in this Set

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  • Back

what are the major actions of drugs used to treat heart failure?

preservation or recovery of cardiac function and reduction of symptomatic edema



what does the heart do during heart failure that makes it selfish?

suppress requests of periphery, augment heart function, reverse fluid retention

how do you determine right heart failure?




left heart failure?

right- systemic edema




left- pulmonary edema

what are the four effects of cardiovascular adaptation during heart failure?




what are the negative effects of each?

increase preload, arterial constriction, tachycardia and inotropy, ventricular hypertrophy


preload- pulmonary and systemic edema, increased myocardial o2 consumption


constriction- increased after load, decrease stroke volume, increase mv02


tachy ino- short filling, increased mv02, down regulation of b receptors


hypertrophy- diastolic and systolic dysfunctin, risk of cell death and arrythmia

what part of the above dose digoxin work?

on tachycardia and inotropy

how does hypertrophy effect look if you have systolic failure?




dystiolic failure?

systolic- thin chambers




dystolic- thick chambers



MOA of thiazide diuretic?




MOA of loop diurectic?

inhibit the sodium chloride symporter in the DVT




loop- na,k,cl symporter in ascending loop of henele



how do diuretics reduce symptoms of heart failure?

reduce preload which results in reduced capillary overload and ventricular wall stress (prevents remodeling)

why are loops perferred over thiazides?

more efficacious in fluid reduction

MOA of aldosterone antagonist?




effects on electolytes?

inhibits the sodium reabsorption in the collecting duct by preventing synthesis of sodium channels




decrease na increase k and mg

what do the aldosterone antagonist directly effect on the heart? why is this good to prevent?

prevents myocardial fibrosis and fibroblast formation, these increase risk of arrythmia since conduction becomes blocked



main benefit of the aldonsterone antagonsits?

improve survival

what are the detrimental effects of angiotensin 2?

vascular hypertrophy, arteriolar constriction, peripheral NE release, catecholamine release from adrenal medulla, sodium reasorption, aldosterone release, adh release

MOA of hydralazine?




does it increase venous capcitance? what does this mean?

direct arteriolar vasodilator which reduces afterload




does not increase venous capcitance so combine with isosrbide dinitrate to prevent more edema

why are beta adrenergic agonists bad during heart failure?




what did the beta antagonists show?

contributing to viscious cycle, more stimulation is toxic to the myocardium




reversal of myocardial damage, improved ejection fraction



how long does it take to see benefit of beta blockers in heart failure

at least 3 months

what is digoxin dosed on? why?

lean body mass, does not go into fat

describe the MOA of cardiac glycoside like digoxin? start with normal phsiology

action potential stimulates na entry


this stimulates calcium entry via L type channel in the transverse tubule


this activates the ryanodine receptor to release more ca


this causes contraction


reversed by removal of ca into sr or by na/ca exchanger which uses atp


digoxin inhibits the na/k atpase pump to prevent sodium leaving, decreasing electrochemical gradient


this decreases the function of the na/ca exchanger and ca remains in the cell


this extra ca is pumped into sr and greater ca release leading to inotropy

what do the cardiac glycosides to contractility of the atrium and ventricle?




AV and SA node?




on conductivity?




on refractory period?

increase both




no effect on either




c- decrease both




r- increase both

why do cardiac glycoside have no effect on av and sa node?

the nodes are sensitized to vagal nerve and depend on stimulation form there

what can cardiac glycosides do at therapetuic levels?




toxic levels?

decrease SNS




increase SNS

where is digoxin abosrbed? what does it depend on?




how is eliminated?

intestine, P-gp activity




renally

where are the p-gp transporters found?




generally what does inhibiting it cause?

renal, liver, gi




blocking it prevents removal of things, and things remain in the body longer

what drugs result in digoxin toxcity?




what are each of there effects?

quinidine tox, verapamil tox, rifampin lower levels, loop and thiazide diuretics or anything that deplets potassium tox

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