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Pharm 323 Spring 22 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

overall broad goals of using drugs to treat HF

A
  1. 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)

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2
Q

what are the 3 go to drugs for treating HF?

A
  1. diuretics
  2. drugs that inhibit RAAS
  3. Beta Blockers / HCN Channel Blockers
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3
Q

what is our 1st line therapy for volume overload?

A

diuretics

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4
Q

MOA of diuretics

A

decrease blood volume = decreases preload

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5
Q

what are the 3 types of diuretics for HF?

A
  1. loop
  2. thiazide
  3. K+ sparing
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6
Q

what drug class would be given for acute pulmonary edema from HF?

A

diuretics (Loop = furosemide)

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7
Q

which drug class will still be effective even with low GFR?

A

loop diuretics

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8
Q

MOA of loop diuretics

A

inhibit reabsorption of Na and Cl @ LOOP of henle

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9
Q

prototype for loop diuretics

A

furosemide (Lasix)

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10
Q

onset of furosemide:
PO:
IV:

A

PO: 1 hour
IV: 5 mins (GET BEDPAN READY!!)

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11
Q

SE of furosemide

A
  • electrolyte imbalances (hypokalemia esp. concerning)
  • hypotension
  • risk of digoxin toxicity + lithium toxicity
  • gout exacerbation
  • ototoxicity (too quick or too high dose)
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12
Q

onset of HCTZ + how long does it last?

A

2 hrs –> lasts 12 hrs

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13
Q

SE of HCTZ

A
  • electrolyte imbalance
  • hypotension
  • hyperglycemia
  • gout exacerbation
  • risk of lithium + digoxin toxicity
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14
Q

which diuretic is contraindicated with sulfa allergies? (ex: TMP/SMX)

A

thiazide

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15
Q

MOA of spironolactone

A

blocks aldosterone in distal tubule –> H2O loss but K+ remains

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16
Q

SE of spironolactone

A
  • hyperkalemia

- gynecomastia

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17
Q

important teaching for pts on K+ sparing diuretics

A

don’t consume salt substitutes (often contain K+)

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18
Q

which diuretic is contraindicated in renal patients?

A

potassium sparing (spironolactone)

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19
Q

can preggos have lasix?

A

NOPE

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20
Q

for HF, what are the 4 types of RAAS drugs?

A
  1. ACE inhibitors
  2. ARBs
  3. ARNIs
  4. Aldosterone antagonists
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21
Q

blocking angiotensin leads to __________

A

vasodilation + decreased Na/H2O retention

blocks angie + al

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22
Q

blocking aldosterone leads to what?

A

preventing Na and H2O retention

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23
Q

which drugs improve functional status and prolongs life in HF?

A

ACE inhibitors

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24
Q

re: preload and afterload, ACE inhibitors are working on which?

A

BOTH!! decreases how hard the heart has to work

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25
what can cause angioedema and cough with ACE inhibitor use?
increased bradykinin - inflammation (body/lungs)
26
potential SE with all RAAS drugs
electrolyte imbalances
27
SE of lisinopril
- dry cough - angioedema - hypotension - hyperkalemia
28
which RAAS drugs can we use in pregnancy?
*trick question*.... NONE!
29
hello
you're doing great :)
30
hi you!
you're gonna rock this test :) keep it positive!
31
will we still give someone ACE inhibitors if they have hypotension?
yes b/c they're so helpful; but in SMALL doses
32
between ACE inhibitors + ARBs, which one decreases cardiac remodeling?
ACE inhibitors *GoLd StaR*
33
prototype for ARB used for HF
valsartan (Diovan)
34
SE of valsartan
- cough - angioedema - hyperkalemia * all much less of a problem compared to ACEs*
35
what is neprolysin
enzyme that blocks breakdown of natriuretic peptide - they tell your body to get rid of fluid "body's internal/natural diuretic"
36
MOA of angiotensin receptor neprilysin inhibitor (ARNI)
inhibiting neprilysin --> increases natriuretic peptides --> tells body to get rid of fluid + ARB action
37
prototype of ARNI
sacubitril/valsartan (Entresto)
38
SE of sacubitril/valsartan
- angioedema - cough - dizziness - renal failure *since contains "sartan," SE are similar*
39
what is the important thing to know re: ARNIs + ACEs?
MUST be off ACE inhibitor for 36 hours before starting ARNI ("wash out" period)
40
what is the prototype for the aldosterone receptor blockers (for HF)?
spironolactone (blocking aldosterone)
41
SE of spironolactone
- hyperkalemia | - gynecomastia
42
what are the two classes of beta blockers?
``` cardio selective (B1) non-selective (B1 + B2) ```
43
MOA of beta blockers
1. decrease HR 2. decrease conduction 3. decrease contractility =decreases work on heart
44
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.
45
what are the 3 BB approved for HF?
1. carvedilol 2. metoprolol XL (succinate) 3. bisoprolol
46
what combo drug therapy is common for HF patients?
BB low dose + ACE + diuretic HF = BAD!!!!
47
what will we see regarding dosing with BB and HF patients?
BABY DOSES (1/10 or 1/20) + double q2 weeks until normal
48
SE of metoprolol XL
- bradycardia - decreased CO (watch for worsening HF) - AV heart block - fatigue, drowsy, dizzy, depression (slooowwwwed down)
49
if Beta Blocker stopped suddenly what could happen?
rebound cardiac excitation | --> MI or angina risk
50
major patient teaching re: beta blockers + patients with DM
can mask s+s of hypoglycemia; monitor BG closely
51
prototype of HCN Channel blockers
ivabradine | brady = bradine
52
MOA of ivabradine
slows HR (reduces conduction)
53
with HF patients, what is HR goal?
50-60bpm
54
HCN channel blockers may be used with HF patients if HR is ______
>70bpm
55
SE of ivabradine
- bradycardia - HTN - afib - luminous phenomena (enhanced brightness)
56
patient teaching for ivabradine
1. visual changes - transient + will disappear | 2. how to check radial pulse - report brady or irregular
57
prototype for cardiac glycosides
digoxin (Lanoxin)
58
MOA of digoxin
- decrease HR | - increase force of contraction (positive ionotrope)
59
what is the therapeutic range of digoxin? ***KNOW THIS***
(0.5-0.8ng/ml) NARROW therapeutic range
60
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
61
what is routine digoxin dosing?
0.125-0.25mg
62
what can increase the risk of digoxin toxicity?
HYPOkalemia (K+ competes with digoxin at pump)
63
AE of digoxin
fatigue, drowsiness, dizziness, dysrhythmias, AV block, bradycardia (b/c slowing down HR)
64
what is 1st sign of digoxin toxicity?
GI (nausea, vomiting, anorexia, fatigue) *will make the toxicity worse b/c dehydration*
65
what is late sign of digoxin toxicity?
visual disturbances (yellow-green halos, blurring)
66
antidote for digoxin toxicity
digoxin immune fab (Digibind) *EXPENSIVE!!!*
67
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
68
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)
69
prototype for direct vasodilator (for HF) (combo)
1. isosorbide dinitrate + hydralazine
70
re: direct vasodilators, what is the MOA of isosorbide dinitrate?
relaxation of VENOUS smooth muscle
71
re: direct vasodilators, what is the MOA of hydralazine?
dilation of ARTERIOLES
72
SE of isosorbide dinitrate + hydralazine
- orthostatic hypotension - reflex tachycardia (compensation) - SLE syndrome (b/c of hydralazine)

Pharm 323 Spring 22 (18 decks)

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