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PHRM 845 > HF pt3 > Flashcards

HF pt3 Flashcards

1
Q

What is elevated in HF?

A

Aldosterone

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2
Q

What does an elevation in aldosterone cause?

A
  • Continued sympathetic activation
  • Parasympathetic inhibition
  • Cardiac and vascular remodeling
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3
Q

What are the aldosterone receptor antagonists (MRA)?

A
  • Spironolactone
  • Eplerenone
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4
Q

What is the general MOA of aldosterone receptor antagonists?

A

Block aldosterone effects independent of the effects of ACEi and ARBs

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5
Q

What are the effects of spironolactone and eplerenone?

A
  • Decrease K and Mg losses: may protect against arrhythmias
  • Decrease Na retention: decrease fluid retention
  • Decreases sympathetic simulation
  • Blocks direct fibrotic action on myocardium
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6
Q

Which MRA is the nonselective agent?

A

Spironolactone

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7
Q

What is the MOA of spironolactone?

A

Inhibits effects of dihydrotestosterone at receptor site and increases peripheral conversion of test into estradiol

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8
Q

What are the AEs of spironolactone?

A
  • Gynecomastia (about 10%)
  • Impotence
  • Menstrual irregularities
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9
Q

Which MRA is the selective agent?

A

Eplerenone

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10
Q

What is the MOA of eplerenone?

A

Selective agent w a 100- to 1000- lower affinity for androgen, glucocorticoid, and progesterone receptors than spironolactone

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11
Q

What is the benefit to eplerenone over spironolactone?

A

No antiandrogenic effects

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12
Q

What is a possible downside to eplerenone?

A

Substrate of CYP3A4 (not a problem most of the time)

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13
Q

What is the administration of MRAs?

A

Should be added to ACEi/ARB/ARNI and BB therapy

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14
Q

When should MRAs be avoided?

A
  • SCr >2.5 in males or >2 in females OR CrCl <30 and serum K >5
  • Hx of severe hyperkalemia or recent worsening renal fx
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15
Q

Use of what other therapies must be avoided w MRAs?

A
  • Concomitant use of K sparing diuretics or supps (unless hypokalemia of serum K <4)
  • Avoid NSAIDs and caution in high dose ACEi/ARB
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16
Q

What are the benefits of SGLT2i in HF?

A
  • Decreased arterial pressure and stiffness
  • Preload and afterload reduction and associated reduction in hypertrophy and fibrosis (reduced myocardial remodeling)
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17
Q

What is the indication of SLGT2i?

A

Reduce risk of CV death or hospitalizations for HFrEF pts w NYHA class 2-4

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18
Q

What are the drugs in the SGLT2i class?

A

Dapagliflozin and empagliflozin

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19
Q

What is the dosing of dapa and empa?

A

Both 10 mg once daily

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20
Q

What eGFR must pts have to be on dapa?

A

eGFR >= 30

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21
Q

What eGFR must pts have to be on empa?

A

eGFR >= 20

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22
Q

What are the AEs of SGLT2i?

A
  • Volume depletion
  • Ketoacidosis in DM
  • Hypoglycemia
  • Infection risk
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23
Q

What are the titration strategies after 42 days?

A
  • Maintenance or additional titration of four foundational therapies
  • Consideration of EP device therapies or transcatheter mitral valve repair
  • Consideration of add on meds or advanced therapies, if refractory
  • Manage comobidities
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24
Q

What brand name drug is ISDN/hydralazine?

A

BiDil

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25
Q

What is ISDN/hydralazine known for?

A

The first drug combo w reduction in mortality

26
Q

What is BiDil indicated for?

A

For tx of HF in black pts as an adjunct to standard therapy

27
Q

What are the AEs of ISDN/hydralazine?

A
  • HA, nausea, flushing, dizziness, tachycardia, lupus like syndrome
  • Hypotension, increased HR, myocardial ischemia, fluid retention
28
Q

What is the principal site of action of hydralazine?

A

Arteriolar VD

29
Q

What is the initial dose of hydralazine?

A

25 mg TID/QD

30
Q

What is the target dose of hydralazine?

31
Q

What is the max dose of hydralazine?

A

100 mg TID

32
Q

What is the principal dose of ISDN?

33
Q

What is the initial dose of ISDN?

A

20 mg TID/QD

34
Q

What is the target of ISDN?

35
Q

What is the max dose of ISND?

36
Q

What is initial dose of BiDil?

A

20/37.5 mg TID

37
Q

What target and max dose of BiDil?

A

40/75 mg TID

38
Q

What is the indication of ivabradine?

A

Reduce the risk of hospitalization (worsening HF) for sx HF, EF <= 35% in normal sinus rhythm w resting HR >= 70 in max tolerated BB or w BB CI

39
Q

What is the dosing of ivabradine?

A

2.5-5 mg BID, adjust q2 wks based on HR

40
Q

What is the max dose of ivabradine?

A
  • 7.5 mg BID
  • 2.5 mg BID if conduction defects or when bradycardia is a concern
41
Q

What are the dosing adjustments of ivabradine?

A
  • HR >60: increase dose by 2.5 (given BID) up to a max dose of 7.5 mg BID
  • HR 50-60: Maintain dose
  • HR <50 or s/sx of bradycardia: decrease dose by 2.5 mg (given BID); if current dose is 2.5 mg BID, d/c therapy
42
Q

What are the AEs of ivabradine?

A
  • Fetal toxicity
  • Afib
  • Bradycardia and conduction disturbances
43
Q

What is the MOA of digoxin?

A

Inhibits the Na/K ATPase altering excitation-contraction couping:
- Increases intracellular Ca, enhancing force of contraction
- relatively mild + inotrope

44
Q

What are the benefits of neurohormonal modulation effects of digoxin?

A
  • Increases parasympathetic activity
  • Vagolytic effects at AV and SA nodes which reduces HR at rest and slows AVN conduction (afib tx)
  • Re-sensitization of baroreceptors
45
Q

What is the place of digoxin in HF tx?

A

Efficacy of digoxin in HF w afib is well established

46
Q

What is the dose of digoxin?

A

0.125-0.25 mg daily

47
Q

What is the goal serum digoxin conc?

A

0.5-0.9 ng/mL

48
Q

When do you lower doses in digoxin?

A

Age >70, impaired renal fx, low weight

49
Q

What does amiodarone do to digoxin conc?

A

Doubles dig conc

50
Q

What does quinidine and verapamil do to digoxin conc?

A

70% increase in dig conc

51
Q

What does itra/ktz do to digoxin conc?

A

50-100% increase in dig conc

52
Q

What are the noncardiac AEs of dig?

A

Mainly affects CNS:
- Anorexia, nausea, vomiting, abdominal pain
- Visual disturbances: halos, photophobia, altered color perception
- Fatigue, weakness, dizziness, HA, neuralgias, confusion, delirium, psychosis

53
Q

What are the cardiac AEs of dig?

A
  • Ventricular: PVCs, bigeminy, trigeminy, VT, VF
  • AV block: first, second, and third degree
  • AV junctional escape rhythms, junctional tachycardia
  • Atrial arrhythmias w slowed AV conduction or AV block
  • Sinus bradycardia
54
Q

What drug class is vericiguat?

A

Soluble guanylate cyclase stimulator

55
Q

What are the clinical effects of vericiguat?

A

Reduces CV death and hospitalizations

56
Q

What are the safety hazards of vericiguat?

A
  • CI in pregnancy
  • Hypotensions and anemia most common AEs
57
Q

Where can a pt get omega 3 polyunsaturated fatty acids?

58
Q

What did several studies suggest about the use of omega 3 polyunsaturated FAs?

A

Reduce the risk in HF (2-4) pts

59
Q

What is the use of antiplatelets in HF?

A

Long term therapy w ASA 75-81 mg/day is recommended in pts w HF AND IHD/CAD/ASCVD

60
Q

What is the use of anticoags in HF?

A
  • Recommended in HF if afib w one additional r/f
  • Pts w other indications (hx of systemic or pulmonary embolism)
  • Otherwise, routine anticoag is not recommended
61
Q

What is the use of CCBs in HF?

A
  • Diltiazem, verapamil, and nifedipine should not be used
  • Felodipine and amlodipine may be useful in managing angina/HTN if not effectively managed w HF therapies

PHRM 845 (48 decks)

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