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Therapeutics III > Sowinski Heart Failure Part 3 > Flashcards

Sowinski Heart Failure Part 3 Flashcards

1
Q

What does elevated aldosterone lead to in HF?

A

-Continued sympathetic activation
-Parasympathetic inhibition
-Cardiac and vascular remodeling

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2
Q

Beneficial effects of aldosterone receptor antagonists

A

-Decrease K and Mg losses: May protect against arrhythmias
-Decrease Na retention: Decrease fluid retention
-Decreases sympathetic stimulation: numerous effects
-Blocks direct fibrotic action on myocardium

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3
Q

Spironolactone mechanism of action

A

-Non-selective agent, structurally similar to progesterone
-Inhibits the effects of dihydrotestosterone at the receptor site and increases peripheral conversion of testosterone into estradiol

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4
Q

Spironolactone adverse effects

A

-Gynecomastia
-Impotence
-Menstrual irregularities

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5
Q

Eplerenone mechanism of action

A

-Selective agent with 100- to 1000-fold lower affinity for androgen, glucocorticoid, and progesterone receptors than spironolactone
-No antiandrogenic effects
-Substrate of CYP3A4

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6
Q

Initial dosing for eplerenone when eCrCl is 50 or more

A

25 mg once daily

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7
Q

Initial dosing for eplerenone when eCrCl is 30-49

A

25 mg every other day

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8
Q

Initial dosing for spironolactone when eCrCl is 50 or more

A

12.5-25 mg once daily

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9
Q

Initial dosing for spironolactone when eCrCl is 30-49

A

12.5 mg every other day

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10
Q

Maintenance dosing for eplerenone when eCrCl is 50 or more

A

50 mg once daily

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11
Q

Maintenance dosing for eplerenone when eCrCl is 30-49

A

25 mg once daily

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12
Q

Maintenance dosing for spironolactone when eCrCl is 50 or more

A

25 mg once daily

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13
Q

Maintenance dosing for spironolactone when eCrCl is 30-49

A

12.5-25 mg once daily

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14
Q

When should aldosterone antagonists be avoided?

A

-SeCr >2.5 for men and >2.0 for women (or CrCl <30)
-SeK >5
-History of severe hyperkalemia or recent worsening renal function

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15
Q

What should be avoided when taking aldosterone antagonists?

A

-Concomitant use of potassium sparing diuretics or potassium supplements (unless hypokalemic with SeK <4)
-NSAIDS
-Caution when using with high dose ARNI/ARB

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16
Q

Aldosterone antagonist monitoring

A

-Renal function and potassium within 3 days-1 week after change or addition
-Diseases or acute illnesses that may influence potassium concentrations
-Monitor every month for 3 months then every 3-4 months
-Monitor with increased ACEI or ARB restart

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17
Q

What should patients taking aldosterone antagonists be counseled on?

A

-Avoidance of salt substitutes
-Close questioning for all other sources of potassium

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18
Q

Stage B recommendations for aldosterone antagonist use

A

Not recommended

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19
Q

Stage C recommendations for aldosterone antagonist use

A

-Should be used in all patients with NYHA II-IV and HFrEF, and eGFR >30 and K <5
-Careful monitoring of K, renal function, and diuretic dosing is essential
-Patients taking aldosterone antagonists in which potassium can not be maintained below 5.5 should be discontinued to avoid life threatening hyperkalemia

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20
Q

SGLT2 inhibitors benefits in HFrEF patients

A

-Unclear benefits in heart failure
-Osmotic diuresis and natriuresis
-Decreased arterial pressure and stiffness
-Preload and afterload reduction and associated reduction in hypertrophy and fibrosis
-Reduced myocardial remodeling

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21
Q

SGLT2I indication

A

Reduce the risk of CV death or hospitalization for HFrEF patients with NYHA class II-IV

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22
Q

Dapagliflozin dosing

A

10 mg once daily

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23
Q

Empagliflozin dosing

A

10 mg once daily

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24
Q

At what eGFR can dapagliflozin be used?

A

30 or more

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25
Q

At what eGFR can empagliflozin be used?

A

20 or more

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26
Q

Adverse effects of SGLT2 inhibitors

A

-Volume depletion
-KTA in DM
-Hypoglycemia
-Infection risk (UTI/PN, NFP, Mycotic)

27
Q

When are SGLT2 inhibitors recommended?

A

Patients with symptomatic chronic HFrEF with or without DM to reduce hospitalizations and CV mortality

28
Q

ISDN/Hydralazine mechanism of action

A

Combination produces VD effects, causing reductions in both preload and afterload

29
Q

When is ISDN/Hydralazine indicated?

A

For the treatment of HF in black patients as an adjunct to standard therapy

30
Q

Adverse effects of ISDN/Hydralazine

A

-Headache
-Nausea
-Flushing
-Dizziness
-Tachycardia
-Lupus-like syndrome
-Hypotension
-Increased heart rate
-Myocardial ischemia
-Fluid retention
-AEs are a significant problem and a major limiting factor in clinical trials

31
Q

Initial hydralazine dose

A

25 mg TID/QD

32
Q

Target hydralazine dose

A

75 mg TID

33
Q

Maximal hydralazine dose

A

100 mg TID

34
Q

Initial ISDN dose

A

20 mg TID/QD

35
Q

Target ISDN dose

A

40 mg TID

36
Q

Maximal ISDN dose

A

80 mg TID

37
Q

Initial ISDN/Hydralazine dose

A

20/37.5 mg TID

38
Q

Target/maximal ISDN/Hydralazine dose

A

40/75 mg TID

39
Q

Stage B recommendations for ISDN/Hydralazine

A

No recommendations

40
Q

Stage C recommendations for ISDN/Hydralazine

A

-Black patients with NYHA III-IV, receiving optimal medical therapy, to improve symptoms and reduce M/M
-Patients with symptoms, who can not receive ARNI, ACE or ARB might be considered

41
Q

Ivabradine indication

A

Reduce the risk of hospitalization for symptomatic HF, EF <35% in NSR with rHR 70 or more in max tolerated beta-blocker or with CI

42
Q

Maintenance dosing for ivabradine

A

-2.5-5 mg BID
-Adjust every 2 weeks based on HR

43
Q

Max dose for ivabradine

A

7.5 mg BID

44
Q

How should ivabradine be adjusted when HR is greater than 60?

A

Increase dose by 2.5 mg (given BID) up to a maximum dose of 7.5 mg BID

45
Q

How should ivabradine be adjusted when HR is 50-60?

A

Maintain dose

46
Q

How should ivabradine be adjusted if HR is less than 50 or signs/symptoms of bradycardia?

A

Decrease dose by 2.5 mg (given BID); if current dose is 2.5 mg BID, discontinue therapy

47
Q

Adverse effects of ivabradine

A

-Fetal toxicity
-Atrial fibrillation
-Bradycardia and conduction disturbances
-Cost: >$6000/year

48
Q

Ivabradine contraindications

A

-KTZ CI
-Avoid diltiazem, verapamil, GFJ

49
Q

Digoxin benefits

A

-Benefits are due to neurohormonal modulation effects
-Increases parasympathetic activity
-Vagolytic effects at the AV and SA nods]es . . . reduces HR at rest and slows AVN conduction
-Re-sensitization of baroreceptors
-Inhibits the Na+/K+ ATPase altering excitation- contraction-coupling
-Increases intracellular Ca2+, enhancing the force of contraction
-Relatively mild positive inotrope

50
Q

When to consider digoxin for treatment of HF

A

Consider in patients with symptomatic HFrEF despite (optimized) GDMT, or who can not tolerate GDMT to decrease hospitalization for HF

51
Q

Digoxin dosing

A

-Most of the time digoxin is dosed empirically
-0.125-0.25 mg daily
-0.125 mg used in the majority of patients with 0.5-0.9 ng/mL being the goal serum digoxin concentration
-Lower doses in >70 years, impaired renal function, low weight

52
Q

Digoxin drug interactions

A

-Amiodarone (doubles concentration)
-Quinidine
-Verapamil
-Itra/KTZ

53
Q

Noncardiac adverse effects of digoxin

A

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

54
Q

Cardiac adverse effects of digoxin

A

-Ventricular: PVCs, bigeminy, trigeminy, VT, VF
-AV block: First, second and third degree
-AV junctional escape rhythms, junctional tachycardia
-Atrial arrhythmias with slowed AV conduction or AV block
-Sinus bradycardia

55
Q

Vericiguat mechanism of action

A

Soluble guanylate cyclase stimulator

56
Q

Vericiguat contraindication

A

Pregnancy

57
Q

Vericiguat adverse effects

A

-Hypotension
-Anemia

58
Q

When to consider vericiguat in HF treatment

A

Consider in selected high-risk patients with recent worsening with symptomatic HFrEF despite (optimized) GDMT, to decrease hospitalization for HF and CV death

59
Q

When are omega-3 polyunsaturated fatty acids recommended in the treatment of HF?

A

Reasonable as adjunctive therapy

60
Q

When are antiplatelets recommended in the treatment of HF?

A

-Long term therapy with aspirin (75-81 mg/day) is recommended in patients with HF and IHD/CAD/ASCVD
-Otherwise aspirin is not recommended for routine use
-If contraindicated/not tolerated, consider alternatives

61
Q

When are anticoagulants recommended in the treatment of HF?

A

-Recommended in HF if atrial fib with one additional risk factor
-Reasonable if no additional risk factors
-Patients with other indications such as history of systemic or pulmonary embolism
-Routine anticoagulation is not recommended

62
Q

When are calcium channel antagonists recommended in the treatment of HF?

A

-Diltiazem, verapamil and nifedipine should not be routinely used
-Felodipine and amlodipine may be useful in managing angina/HTN if not effectively managed with HF therapies

63
Q

Non-pharmacologic therapies for HF

A

-Implantation of ICD
-Cardiac resynchronization therapy

64
Q

Treatment of HFpEF

A

-SBP/DBP should be controlled in patients with HFpEF based on current practice
-Diuretics should be used for relief of symptoms due to volume overload in patients with HFpEF, no mortality benefits
-Management of AF according to published clinical practice guidelines in patients with HFpEF can improve symptomatic HF
-SGLT2i may reduce hospitalizations and CV mortality
-The use of ARBs, ARNIs, MRAs, and ACEIs may be considered to decrease hospitalizations for selected patients with HFpEF, especially at the lower end of LVEF
-ACEIs and ARBS have not been shown to reduce mortality (ACEIs improve exercise tolerance and reduce hospitalizations) (ARBs may reduce hospitalizations)
-MRAs may improve diastolic function and reduce remodeling (less convincing than HFrEF)
-Digoxin has no affect on mortality or hospitalizations
-Nitrates should be limited to use in patients with HFpEF who may need treatment for symptomatic CAD
-CCBs may be useful to treat other conditions such as HTN

Therapeutics III (42 decks)

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