Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove Ads
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards




share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

NURS 572 Pharm Ch 47

Pharm Ch 47 Heart failure

QuestionAnswer
2 major causes of HF CAD---HTN
HF compensations result in long-term cardiac remodeling bwo 2 systems SNS---RAAS contribute to remodeling that result in fibrous, non-contractile scar tissue
How does heart compensate to HF ventricles dilate and hypertrophy--> become shperical in an attempt to compensate for decreased CO. Only works short term, then leads to viscous cycle
what is viscous cycle in HF compensatory SNS/RAAS ---inc HR/venous pressure/arterial pressure ---remodeling occurs---heart continues with compensatory mechs but heart can no longer respond
S/S CHF dec exercise tol---fatigue--tachy---tachypnea/sob/doe/pnd/orthopenea----peripheral edema---venous JVD/HJR, HSM---cardiomegaly/tachy/LVH strain
class of drugs used to tx HF - 4 diuretics---ACEIs----BB---Inotropic agents (subclasses sympathomimetics and glycosides-digoxin)
Most common diuretics are thiazides ---if RF, then loop diuretics. MOA in HF MOA to decrease preload---decrease peripheral/pulmonary edema----cardiac dilation
what are the thiazide diuretics again? hydrochlorothiazide---chlorothiazide---chlorothalidone---metolazone
what are the loop diuretics again furosemide---bumetadine---torsemide
what are benefits to selecting K-sparing diuretics spironolactone or eplerenone (if you can afford it!) benefit is that this class inhibits aldosterone effect in RAAS that contributes to both cardiac remodeling ----and SNS activation ---and baroreceptor dysfunction
ACEIs are used to tx HF, MOA is block Angio-2 which minimizes remodeling ---vasoDIL arteries and veins so DECREASES pre/after loads---aldosterone decreases intravascular volume/remodeling
ACEIs are prils, but let's review their ADRs cough---angioedema---first dose effect---category D
There are ONLY 3 BBs approved for HF. MOA in HF is counterintuitive MOA - expect they would slow heart down, which is what we're treating for. HOWEVER for some reason they work at very precise doses - start low, go slow - so just go with it
what are the 3 BBs approved for HF caverdilol---bisoprolol---metoprolol------- ONLY IN SUSTAINED RELEASE FOR METOPROLOL
ADRs of BBs if dose too high ADRs of brady---heart block---dec bp---fluid retention---fatigue
Inotropic agents - sympathomimetics - their use only used temporary, IV ---last line/Stage D drugs due to SEs
Name 2 sympathomimetics for ST/IV only use dopamine---dobutamine (both B-1 agonists, remember dopa steps up the stairs in terms of what receptors it hits)
Now, in cardiac glycosides class we have digoxin is in this class
Effects of digoxin in terms of inotropy positive inotrophy---inc contractility/force---inc CO---DECREASED sympathetic tone which dec tachy, pre/after load----increased urine production leads to decreased Na/H20 retention
MOA digoxin poisons Na/K/ATP pump which re-sets the cell after depol/repol as it tries to restore Na in ECF and K ICF---REMEMBER---Ca goes wherever Na goes (see next slide)
MOA digoxin as affects Ca like I was saying, if pump is poisoned, then Na/Ca can't leave cell as fast---when Ca in cell longer, heart has longer contraction time--->positive inotrophy!
what state of serum K predisposes to cardiac toxicity HYPOkalemia----digoxin competes with K ---if K is low, then more digoxin can bind to render its effects. too much of a good thing
what types of cardiac ADR for digoxin ALMOST ANY!!! dysrhythmia, so monitor closely
what are non-cardiac ADRs digoxin a/n/v---crosses BBB so CNS distrurbances
what is effect of K-WASTING diuretics such as loop or thiazides hypokalemia possible, which may lead to digoxin toxicity
what is effect of K-SPARING diuretics hyperkalemia ---now too much K competing with digoxin---could decrease efficacy
In a 3 drug regiment, what drugs to we use - in order of adding them sequentially Stage A = ACEIs-----Stage B = ACEI+ BB----Stage 3 = ACEI +BB + diuretic
so when do we add digoxin? Digoxin is only considered if first 3 drug lines not effected then you ADD digoxin----as in add it to ACEI+BB+diuretic
What other drug classes MIGHT be considered at time digoxin is considered (stage C if first 3 not effective) may consider ARB+ACEI combo or spiractolone
Created by: lorrelaws