Heart Failure Flashcards
overall broad goals of using drugs to treat HF
- increase contraction (b/c heart has an inability to pump)
2. decrease HR (decrease O2 demands of heart, so doesn’t have to work as hard)
what are the 3 go to drugs for treating HF?
- diuretics
- drugs that inhibit RAAS
- Beta Blockers / HCN Channel Blockers
what is our 1st line therapy for volume overload?
diuretics
MOA of diuretics
decrease blood volume = decreases preload
what are the 3 types of diuretics for HF?
- loop
- thiazide
- K+ sparing
what drug class would be given for acute pulmonary edema from HF?
diuretics (Loop = furosemide)
which drug class will still be effective even with low GFR?
loop diuretics
MOA of loop diuretics
inhibit reabsorption of Na and Cl @ LOOP of henle
prototype for loop diuretics
furosemide (Lasix)
onset of furosemide:
PO:
IV:
PO: 1 hour
IV: 5 mins (GET BEDPAN READY!!)
SE of furosemide
- electrolyte imbalances (hypokalemia esp. concerning)
- hypotension
- risk of digoxin toxicity + lithium toxicity
- gout exacerbation
- ototoxicity (too quick or too high dose)
onset of HCTZ + how long does it last?
2 hrs –> lasts 12 hrs
SE of HCTZ
- electrolyte imbalance
- hypotension
- hyperglycemia
- gout exacerbation
- risk of lithium + digoxin toxicity
which diuretic is contraindicated with sulfa allergies? (ex: TMP/SMX)
thiazide
MOA of spironolactone
blocks aldosterone in distal tubule –> H2O loss but K+ remains
SE of spironolactone
- hyperkalemia
- gynecomastia
important teaching for pts on K+ sparing diuretics
don’t consume salt substitutes (often contain K+)
which diuretic is contraindicated in renal patients?
potassium sparing (spironolactone)
can preggos have lasix?
NOPE
for HF, what are the 4 types of RAAS drugs?
- ACE inhibitors
- ARBs
- ARNIs
- Aldosterone antagonists
blocking angiotensin leads to __________
vasodilation + decreased Na/H2O retention
blocks angie + al
blocking aldosterone leads to what?
preventing Na and H2O retention
which drugs improve functional status and prolongs life in HF?
ACE inhibitors
re: preload and afterload, ACE inhibitors are working on which?
BOTH!! decreases how hard the heart has to work
what can cause angioedema and cough with ACE inhibitor use?
increased bradykinin - inflammation (body/lungs)
potential SE with all RAAS drugs
electrolyte imbalances
SE of lisinopril
- dry cough
- angioedema
- hypotension
- hyperkalemia
which RAAS drugs can we use in pregnancy?
trick question…. NONE!
hello
you’re doing great :)
hi you!
you’re gonna rock this test :) keep it positive!
will we still give someone ACE inhibitors if they have hypotension?
yes b/c they’re so helpful; but in SMALL doses
between ACE inhibitors + ARBs, which one decreases cardiac remodeling?
ACE inhibitors GoLd StaR
prototype for ARB used for HF
valsartan (Diovan)
SE of valsartan
- cough
- angioedema
- hyperkalemia
- all much less of a problem compared to ACEs*
what is neprolysin
enzyme that blocks breakdown of natriuretic peptide - they tell your body to get rid of fluid
“body’s internal/natural diuretic”
MOA of angiotensin receptor neprilysin inhibitor (ARNI)
inhibiting neprilysin –> increases natriuretic peptides –> tells body to get rid of fluid
+ ARB action
prototype of ARNI
sacubitril/valsartan (Entresto)
SE of sacubitril/valsartan
- angioedema
- cough
- dizziness
- renal failure
since contains “sartan,” SE are similar
what is the important thing to know re: ARNIs + ACEs?
MUST be off ACE inhibitor for 36 hours before starting ARNI (“wash out” period)
what is the prototype for the aldosterone receptor blockers (for HF)?
spironolactone (blocking aldosterone)
SE of spironolactone
- hyperkalemia
- gynecomastia
what are the two classes of beta blockers?
cardio selective (B1) non-selective (B1 + B2)
MOA of beta blockers
- decrease HR
- decrease conduction
- decrease contractility
=decreases work on heart
is it OK to use BB on HF patients? why or why not?
research has shown it’s OK if done properly - SNS effect on heart is reduced, but that is a chance it could make it worse. use with caution.
what are the 3 BB approved for HF?
- carvedilol
- metoprolol XL (succinate)
- bisoprolol
what combo drug therapy is common for HF patients?
BB low dose + ACE + diuretic
HF = BAD!!!!
what will we see regarding dosing with BB and HF patients?
BABY DOSES (1/10 or 1/20) + double q2 weeks until normal
SE of metoprolol XL
- bradycardia
- decreased CO (watch for worsening HF)
- AV heart block
- fatigue, drowsy, dizzy, depression (slooowwwwed down)
if Beta Blocker stopped suddenly what could happen?
rebound cardiac excitation
–> MI or angina risk
major patient teaching re: beta blockers + patients with DM
can mask s+s of hypoglycemia; monitor BG closely
prototype of HCN Channel blockers
ivabradine
brady = bradine
MOA of ivabradine
slows HR (reduces conduction)
with HF patients, what is HR goal?
50-60bpm
HCN channel blockers may be used with HF patients if HR is ______
> 70bpm
SE of ivabradine
- bradycardia
- HTN
- afib
- luminous phenomena (enhanced brightness)
patient teaching for ivabradine
- visual changes - transient + will disappear
2. how to check radial pulse - report brady or irregular
prototype for cardiac glycosides
digoxin (Lanoxin)
MOA of digoxin
- decrease HR
- increase force of contraction (positive ionotrope)
what is the therapeutic range of digoxin? KNOW THIS
(0.5-0.8ng/ml)
NARROW therapeutic range
describe digitalization
half life is 1.5 days, so we will give pt loading doses to get to therapeutic quicker, then move to routine dosing
what is routine digoxin dosing?
0.125-0.25mg
what can increase the risk of digoxin toxicity?
HYPOkalemia (K+ competes with digoxin at pump)
AE of digoxin
fatigue, drowsiness, dizziness, dysrhythmias, AV block, bradycardia
(b/c slowing down HR)
what is 1st sign of digoxin toxicity?
GI (nausea, vomiting, anorexia, fatigue)
will make the toxicity worse b/c dehydration
what is late sign of digoxin toxicity?
visual disturbances (yellow-green halos, blurring)
antidote for digoxin toxicity
digoxin immune fab (Digibind)
EXPENSIVE!!!
What drug-drug and drug-food interactions exist with digoxin?
fiber, antacids, CCB + BB - increase risk of AV heart block
diuretics b/c of hypokalemia –> dig tox
if patient can’t take ACE or ARB, what might they be prescribed?
direct vasodilator (we wouldn’t go for ARNI b/c it has an ARB in it)
prototype for direct vasodilator (for HF) (combo)
- isosorbide dinitrate + hydralazine
re: direct vasodilators, what is the MOA of isosorbide dinitrate?
relaxation of VENOUS smooth muscle
re: direct vasodilators, what is the MOA of hydralazine?
dilation of ARTERIOLES
SE of isosorbide dinitrate + hydralazine
- orthostatic hypotension
- reflex tachycardia (compensation)
- SLE syndrome (b/c of hydralazine)
