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PCM Exam 2 > Drugs Used In Heart Failure > Flashcards

Drugs Used In Heart Failure Flashcards

1
Q

Risk factors for HF:

A
  • HTN
  • coronary artery disease
  • MI
  • diabetes
  • family history of cardiomyopathy
  • use of cardiotoxins
  • obesity
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2
Q

HF with preserved ejection fraction is ______ heart failure

A

Diastolic

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3
Q

What can you do to reduce systolic HF?

A

↓ afterload and ↓ preload

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4
Q

What is the effect of the ↑ angiotensin II in the compensatory physiological response to HF?

A
  • ↑ preload
  • ↑ afterload
  • remodeling
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5
Q

What is the definition of preload?

A

The force stretching the ventricles; ↑ length of stretching of myocardial cells → ↑ force of contraction

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6
Q

Why would ↓’ing preload in CHF patients ↑ the contractility

A

In CHF patients there is so much volume overload that the preload is too high and that results in poor contractility

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7
Q

What is afterload?

A

The force against which ventricles must act: vascular resistance (aortic BP)

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8
Q

How is calcium removed from cardiac muscle cells?

A
  • Na/Ca exchange

- storage in sarcoplasmic reticulum

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9
Q

What should patients with chronic heart failure NOT take?

A
  • NSAIDS
  • alcohol
  • calcium channel blockers
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10
Q

What drugs are used to treat HFrEF (systolic HF)

A

HFrEF = heart failure with reduced ejection fraction

  • diuretics
  • spironolactone
  • ACEI’s and ARB’s
  • direct vasodilators (hydralazine and nitrates)
  • β blockers
  • ionotropic agents
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11
Q

What drugs are used to treat HFpEF (diastolic HF)

A
  • diuretics (careful not to ↓ preload too much because that can ↓ filling)
  • ACEI/ARB’s
  • β blockers
  • calcium channel blockers
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12
Q

Calcium channel blockers is a class of drugs uses to treat only _________ type of HF

A

Diastolic HF; helps with relaxation of ventricles to aid in filling

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13
Q

Can you give β blockers to treat systolic HF?

A

Yes; β blockers is prescribed for BOTH types of HF

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14
Q

What are the 4 different AHA stage classifications of HF?

A

Stage A: high risk fo developing HF
Stage B: asymptomatic HF
Stage C: symptomatic HF
Stage D: refractory end stage HF

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15
Q

Describe the 4 classes of the NYHA HF symptom classification

A

Class I: no symptom limitation with ordinary physical activity

Class II: ordinary activity somewhat limited by dyspnea (long distance walking, climbing 2 sets of stairs)

Class III: exercise limited by dyspnea with moderate workload (short distance walking, one flight of stairs)

Class IV: dyspnea at rest with very little exertion

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16
Q

What is the 1st line treatment for people with stage C CHF?

A

Diuretics, ACEI, and β blockers

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17
Q

In addition to β blockers and diuretics, what else would you give in symptomatic patients with CHF? ACEI or ARB?

A

ACEI

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18
Q

What is the effect of diuretics on preload and afterload?

A

↓ preload: ↓ plasma volume and thus ↓ venous return to the heart and thus ↓ cardiac workload and oxygen demand

↓ afterload: ↓ plasma volume causes a ↓ in BP

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19
Q

What are some of the effects of ACEI in patients with CHF?

A

↓ preload: ↓ Na and water retention
↓ afterload: ↓ vascular resistance and BP
Both above will ↑ CO

Can also undo some of the remodeling of the heart

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20
Q

What drugs are ACEI’s?

A
  • captopril
  • lisinopril
  • enalapril
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21
Q

What patients are recommended to take ACEI’s?

A
  • symptomatic HF
  • asymptomatic HF patients with ↓ LVEF or history of MI
  • patients at high risk for developing HF due to : atherosclerotic disease, obesity, DM or HTN
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22
Q

Patient who is asymptomatic but has a history of MI, what kind of drug would you recommend?

A

ACEI

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23
Q

Contraindications of ACEI?

A
  • pregnant women
  • patients with bilateral renal artery stenosis
  • previous history of angioedema

CANT GIVE ARB’S TO pregnant patients or those with bilateral renal artery stenosis

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24
Q

Candesartan and valsartan are what kind of drugs?

A

ARB’s

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25
Q

When would you give someone an ARB?

A

When you cant give an ACEI such as for patients who have severe cough or angioedema

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26
Q

What drugs are ARB’s?

A

Candesartan and valsartan

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27
Q

Direct vasodilators are given in combination of:

A
  • Hydralazine (arterial dilation which ↓ afterload)
  • isosorbid dinitrate (venous dilation will ↓ preload)

Produces same effect of ↓ preload AND afterload like with ACEI

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28
Q

When would prescribe concurrent use of hydralazine and isosorbide dinitrate?

A
  • patients who cant tolerate ACEI or ARB’s

- African American patients with advanced HF as an adjunct to standard therapy

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29
Q

What medication therapy would you give to a pregnant patient with CHF?

A
  • hydralazine + isosorbide dinitrate because ACEI’s and ARB’s are teratogenic
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30
Q

An African American patient is currently taking ACEI, β blocker and a loop diuretic to treat his CHF but he still has symptoms. What would be the next step in therapy?

A

Direct vasodilators: concurrent use of hydralazine and isosorbide dinitrate

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31
Q

Lupus like syndrome is an adverse effect seen with __________

A

Hydralazine

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32
Q

Contraindications with direct vasodilators

A

Can’t give sildenafil

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33
Q

AE of hydralazine:

A
  • tachycardia
  • peripheral neuritis
  • lupus like syndrome
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34
Q

Which β blockers are given to treat CHF?

A
  • carvedilol and metoprolol

- studies should they reverse cardiac remodeling and reduce morality and hospitalization

35
Q

How do β blockers help treat CHF when they ↓ chronotropy and ↓ ionotropy?

A

They act on the β1 receptors in the kidneys which are responsible for activating the RAAS pathway → ↓ preload and ↓ afterload

36
Q

Patient is given a drug to treat their CHF. They come back to the physician complaining to them that their symptoms are getting worse instead of better. Doctor tells them their symptoms will improve after a few weeks. What kind of drug did he prescribe?

A

A β blocker (↓ in HR and contractility but acts on the β1 receptors in the kidneys to inhibit release of renin)

37
Q

β blockers should be used very cautiously in patients with _______ HF

A

Decompensated HF; these patients may not be able to cope with the initial reduction in CO

38
Q

Use of β blockers is contraindicated in _________

A

Cardiogenic shock because these patients can not handle the initial ↓ in CO

39
Q

Spironolactone is a ________ antagonist

A

Aldosterone; prevents Na region, myocardial hypertrophy and hypokalemia

40
Q

_________ is used as a second line drug in addition to the standard first line therapy for CHF for NON African Americans

A
  • spironolactone

When spironolactone is given WITH ACEI’s will see ↓ in morbidity and mortality in patients with HF

African Americans are given direct vasodilators

41
Q

What are some AE’s of spironolactone

A
  • hyperkalemia
  • GI disturbances such as gastritis and peptic ulcers
  • CNS effects: lethargy and confusion
  • endocrine abnormalities: gynecomastia, ↓ libido, menstrual irregularities
42
Q

What kind of drug is digoxin?

A

Inotropic agent that is a cardiac glycoside widely used in HF

43
Q

Does digoxin ↑ a patient’s survival?

A

NO; it helps ↓ symptoms of HF, ↑ exercise tolerance and ↓ rate of hospitalization

44
Q

5 disadvantages of digoxin

A
  • narrow therapeutic margin
  • complicated pharmacokinetics
  • drug sensitivity varies between patients
  • drug sensitivity can change during therapy
  • severe and potentially lethal adverse effects
45
Q

MOA of digoxin?

A
  • positively inotropic: ↑ contractility

- negatively chronotropic: ↓ HR

46
Q

Digoxin ______ contractility of heart and _______ heart rate

A

↑ contractility and ↓ HR

47
Q

What population of patients is digoxin prescribed to treat CHF?

A

Patients who have tachyarrhythmias and CHF (digoxin ↓ HR and ↑ contractility and thus treats both problems)

48
Q

Digoxin will ____ CO

A

↑

49
Q

How does digoxin ↓ myocardial O2 demand?

A
  • enhances vagal tone → ↓ HR
  • ↓ sympathetic activity
  • ↓ peripheral resistance
50
Q

How does digoxin ↑ cytoplasmic calcium in the myocytes?

A

Inhibits the Na/K exchange in Na/K ATPase which then inhibits the ability of the cell to push calcium out of the cell via the Na/Ca exchanger

Na/K ATPase provides the high extracellular Na that powers the cell to push out the cytoplasmic calcium in exchange for sodium

* inhibits the exist of calicum*

51
Q

Digoxin inhibits _______________ on the cardiac muscle membrane and results in:

A

Na/K ATPase;
↑ intracellular calcium and sodium
↑ extracellular potassium → hyperkalemia

52
Q

What is the adverse effect if the Na/K ATPase is extensively inhabited by digoxin?

A

Dysrhythmias (and consistent contractility)

53
Q

Digoxin ↓ chronotropic action by:

A
  • ↓ in degree of activation of sympathetic AND RAAS
54
Q

Digoxin ↓ conduction velocity through the ____ node

A

AV;

Negative dromotropic agent

55
Q

Main use of digoxin is in _______

A

HF with atrial fibrillation

56
Q

Digoxin as a very large Vd and thus accumulates in _______. What should you be careful because of this?

A

Muscle; if you give another drug with a large Vd then it’ll compete and displace it and will see high levels in the plasma

57
Q

What are some AE effects of digoxin toxicity?

A
  • arrhythmias (slowing of AV conduction)
  • GI effects: anorexia, nausea and vomiting
  • CNS effects: headache, fatigue, confusion, blurred vision, alteration of color perception in which everything has a yellow/green hue, and halos on dark objects
58
Q

A patient complains of nausea and vomiting and a recent blurry vision and complains about things have a yellow-green hue. This is mostly likely an adverse effect of what drug?

A

Digoxin

59
Q

What is the biggest risk factor for developing digoxin toxicity?

A

HYPOkalemia because the less K, then the more digoxin can bind to the Na/K ATPase (think of digoxin and K competing for the same binding site )

60
Q

Cause of digoxin toxicity is __________

A

Hypokalemia

61
Q

The result of digoxin toxicity is ________

A

Hyperkalemia

62
Q

______kalemia reduces digoxin activity

A

Hyperkalemia

63
Q

Calcium accelerates overloading fo calcium scores ant thus facilitates toxic actions of digoxin, but ______ antagonizes the effects of calcium

A

Magnesium

64
Q

Factors predisposing to digoxin toxicity:

A
  • K depleting diuretics
  • corticosteroids
  • hypothyroidism
  • hypoxia
  • renal failure
  • myocarditis
65
Q

_______, ______, and _______ can cause digoxin toxicity by displacing it from the tissue protein binding sites

A

Quinidine, verapamil, and amiodarone

66
Q

What are the DOC to treat ventricular tachyarrhythmia due to digoxin?

A
  • lidocaine or magnesium
67
Q

digitalis antibodies are used to treat _________

A

Severe digoxin intoxication

68
Q

What are some situations where digoxin is contraindicated?

A
  • if they have a diastolic HF or right sided HF
  • presence of uncontrolled HTN
  • presence of bradyarhythmias
  • in non responders or intolerant patients
69
Q

Calcium channel blockers are prescribed in ______ HF Beulah’s they improve _____ and ________

A

Diastolic; improve ventricular relaxation and reduce heart rate

70
Q

Hyper/hypomagnesemia can precipitate digoxin toxicity

A

Hypomagnesemia

71
Q

Hypo/hypercalcemia can precipitate digoxin toxicity

A

Hypercalcemia

72
Q

For persistently symptomatic African American patients with HF, you want to add ____________ to the regular regiment of ACEI + β blocker

A

Hydralazine + isosorbide dinitrate

73
Q

For patients with HF and have renal failure (creatinine > 30ml/min and K <5.0 mEq/dL) what else would you add to their regular regiment of ACEI + β blocker?

A

Spironolactone

74
Q

Which ionotropic agents are used in the treatment of ACUTE heart failure?

A
  • phosphodiesterase III inhibitors: inamrionone, milrinone

- dopamine

75
Q

What drugs are inamrinone and milrinone?

What is their MOA?

A

phosphodiesterase III inhibitors; inhibit myocardial cAMP phosphodiesterase activity → ↑ cAMP → POSITIVE ionotropic effect and ↑ CO

76
Q

What is the effect of PDE III inhibitors on preload and afterload?

A

↓ preload and ↓ afterload → ↑ CO

77
Q

Low doses of dopamine mainly has _________ effect

A

Dopaminergic stimulating = renal and mesenteric vasodilation

78
Q

What are the effects of administering high dose dopamine?

A

Both dopaminergic AND β1 stimulating (produce cardiac stimulation and renal vasodilation)

79
Q

LARGE doses of dopamine stimulates _____ receptors

A

Stimulates α receptors → vasoconstriction

80
Q

Dopamine also promotes __________ and thus is why it is useful in treating shock that has persisted after adequate fluid volume replacement

A

Diuresis

81
Q

At therapeutic levels of dobutamine, stimulation of _____ receptors predominate

A

β1 → -potent ionotropic effect with little change in HR

Vasodilation due to β2

82
Q

Glucagon has positive _________ and _____ effects

A

Ionotropic and chronotropic

83
Q

When would you want to give glucagon?

A

In cases of β blocker OD because glucagon does not need to bind to the β receptors to ↑ cAMP

84
Q

Patient accidentally took too much propranolol. What drug is the best to give treat their severe bradycardia?

A

GLUCAGON

PCM Exam 2 (32 decks)

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