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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
Q

what can cause angioedema and cough with ACE inhibitor use?

A

increased bradykinin - inflammation (body/lungs)

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26
Q

potential SE with all RAAS drugs

A

electrolyte imbalances

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27
Q

SE of lisinopril

A
  • dry cough
  • angioedema
  • hypotension
  • hyperkalemia
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28
Q

which RAAS drugs can we use in pregnancy?

A

trick question…. NONE!

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29
Q

hello

A

you’re doing great :)

30
Q

hi you!

A

you’re gonna rock this test :) keep it positive!

31
Q

will we still give someone ACE inhibitors if they have hypotension?

A

yes b/c they’re so helpful; but in SMALL doses

32
Q

between ACE inhibitors + ARBs, which one decreases cardiac remodeling?

A

ACE inhibitors GoLd StaR

33
Q

prototype for ARB used for HF

A

valsartan (Diovan)

34
Q

SE of valsartan

A
  • cough
  • angioedema
  • hyperkalemia
  • all much less of a problem compared to ACEs*
35
Q

what is neprolysin

A

enzyme that blocks breakdown of natriuretic peptide - they tell your body to get rid of fluid

“body’s internal/natural diuretic”

36
Q

MOA of angiotensin receptor neprilysin inhibitor (ARNI)

A

inhibiting neprilysin –> increases natriuretic peptides –> tells body to get rid of fluid

+ ARB action

37
Q

prototype of ARNI

A

sacubitril/valsartan (Entresto)

38
Q

SE of sacubitril/valsartan

A
  • angioedema
  • cough
  • dizziness
  • renal failure

since contains “sartan,” SE are similar

39
Q

what is the important thing to know re: ARNIs + ACEs?

A

MUST be off ACE inhibitor for 36 hours before starting ARNI (“wash out” period)

40
Q

what is the prototype for the aldosterone receptor blockers (for HF)?

A

spironolactone (blocking aldosterone)

41
Q

SE of spironolactone

A
  • hyperkalemia

- gynecomastia

42
Q

what are the two classes of beta blockers?

A 
cardio selective (B1)
non-selective (B1 + B2)
43
Q

MOA of beta blockers

A
  1. decrease HR
  2. decrease conduction
  3. decrease contractility

=decreases work on heart

44
Q

is it OK to use BB on HF patients? why or why not?

A

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
Q

what are the 3 BB approved for HF?

A
  1. carvedilol
  2. metoprolol XL (succinate)
  3. bisoprolol
46
Q

what combo drug therapy is common for HF patients?

A

BB low dose + ACE + diuretic

HF = BAD!!!!

47
Q

what will we see regarding dosing with BB and HF patients?

A

BABY DOSES (1/10 or 1/20) + double q2 weeks until normal

48
Q

SE of metoprolol XL

A
  • bradycardia
  • decreased CO (watch for worsening HF)
  • AV heart block
  • fatigue, drowsy, dizzy, depression (slooowwwwed down)
49
Q

if Beta Blocker stopped suddenly what could happen?

A

rebound cardiac excitation

–> MI or angina risk

50
Q

major patient teaching re: beta blockers + patients with DM

A

can mask s+s of hypoglycemia; monitor BG closely

51
Q

prototype of HCN Channel blockers

A

ivabradine

brady = bradine

52
Q

MOA of ivabradine

A

slows HR (reduces conduction)

53
Q

with HF patients, what is HR goal?

A

50-60bpm

54
Q

HCN channel blockers may be used with HF patients if HR is ______

A

> 70bpm

55
Q

SE of ivabradine

A
  • bradycardia
  • HTN
  • afib
  • luminous phenomena (enhanced brightness)
56
Q

patient teaching for ivabradine

A
  1. visual changes - transient + will disappear

2. how to check radial pulse - report brady or irregular

57
Q

prototype for cardiac glycosides

A

digoxin (Lanoxin)

58
Q

MOA of digoxin

A
  • decrease HR

- increase force of contraction (positive ionotrope)

59
Q

what is the therapeutic range of digoxin? KNOW THIS

A

(0.5-0.8ng/ml)

NARROW therapeutic range

60
Q

describe digitalization

A

half life is 1.5 days, so we will give pt loading doses to get to therapeutic quicker, then move to routine dosing

61
Q

what is routine digoxin dosing?

A

0.125-0.25mg

62
Q

what can increase the risk of digoxin toxicity?

A

HYPOkalemia (K+ competes with digoxin at pump)

63
Q

AE of digoxin

A

fatigue, drowsiness, dizziness, dysrhythmias, AV block, bradycardia

(b/c slowing down HR)

64
Q

what is 1st sign of digoxin toxicity?

A

GI (nausea, vomiting, anorexia, fatigue)

will make the toxicity worse b/c dehydration

65
Q

what is late sign of digoxin toxicity?

A

visual disturbances (yellow-green halos, blurring)

66
Q

antidote for digoxin toxicity

A

digoxin immune fab (Digibind)

EXPENSIVE!!!

67
Q

What drug-drug and drug-food interactions exist with digoxin?

A

fiber, antacids, CCB + BB - increase risk of AV heart block

diuretics b/c of hypokalemia –> dig tox

68
Q

if patient can’t take ACE or ARB, what might they be prescribed?

A

direct vasodilator (we wouldn’t go for ARNI b/c it has an ARB in it)

69
Q

prototype for direct vasodilator (for HF) (combo)

A
  1. isosorbide dinitrate + hydralazine
70
Q

re: direct vasodilators, what is the MOA of isosorbide dinitrate?

A

relaxation of VENOUS smooth muscle

71
Q

re: direct vasodilators, what is the MOA of hydralazine?

A

dilation of ARTERIOLES

72
Q

SE of isosorbide dinitrate + hydralazine

A
  • orthostatic hypotension
  • reflex tachycardia (compensation)
  • SLE syndrome (b/c of hydralazine)

Pharm 323 Spring 22 (18 decks)

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