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Drugs for Heart Failure Flashcards

1
Q

•impaired ability of the ventricle to fill with or eject blood

A

HEART FAILURE

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2
Q

•inability of the heart to pump blood to meet the metabolic demands of the body

A

HEART FAILURE

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3
Q

•formerly called CHF

A

HEART FAILURE

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4
Q

HEART FAILURE

•common cause:

A

–Left systolic dysfunction secondary to CAD (~70%)

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5
Q

•primary manifestations: HF

A

–dyspnea
–fatigue
–fluid retention

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6
Q

–pulmonary congestion

A

•Left Ventricular Failure

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7
Q

–pulmonary edema

A

•Left Ventricular Failure

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8
Q

–dyspnea, orthopnea

A

•Left Ventricular Failure

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9
Q

–systemic congestion

A

•Right Ventricular Failure

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10
Q

–peripheral edema

A

•Right Ventricular Failure

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11
Q

–jugular venous distention

A

•Right Ventricular Failure

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12
Q

–due to NE → increased HR (can only increase O2 demand)

A

•tachycardia & increased contractility

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13
Q

–increased preload → increased SV (leads to congestion)

A

•Frank-Starling mechanism

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14
Q

–to redistribute blood flow (increases afterload)

A

•vasoconstriction

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15
Q

–changes in cardiac muscle mass, size, shape, structure, function

A

•ventricular hypertrophy & remodelling

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16
Q

GOALS OF PHARMACOLOGIC INTERVENTION

A

•To alleviate symptoms, slow disease progression, and improve survival

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17
Q

•6 classes of drugs:

A
  • 1) inhibitors of the renin-angiotensin system
  • 2) ß-adrenoreceptor blockers
  • 3) diuretics
  • 4) direct vasodilators
  • 5) inotropic agents
  • 6) aldosterone antagonists
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18
Q

BENEFICIAL EFFECTS OF DRUGS FOR HF

A
  • Reduction of the load on the myocardium
  • Decreased extracellular fluid volume
  • Improved cardiac contractility
  • Slowing the rate of cardiac remodeling
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19
Q

•Agents of choice in HF

A

ACE INHIBITORS

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20
Q

•Block ACE (conversion of angiotensin I to II)

A

ACE INHIBITORS

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21
Q

•Diminish the rate of bradykinin inactivation

A

ACE INHIBITORS

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22
Q

•Decrease vascular resistance, venous tone, BP

A

ACE INHIBITORS

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23
Q

•Reduce preload and afterload -> increased cardiac output

A

ACE INHIBITORS

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24
Q

•Indicated in patients with all stages of left ventricular failure

A

ACE INHIBITORS

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25
Q

•Should be taken on an empty stomach

A

ACE INHIBITORS

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26
Q

•Pro-drugs that require activation by hydrolysis via hepatic enzymes (except ______)

A

ACE INHIBITORS

Captopril

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27
Q

• are adequately but incompletely absorbed following oral administration

A

ACE INHIBITORS

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28
Q

•Monopeptide, orally active compounds that are extremely potent competitive antagonists of the AT1 receptor

A

ARBs

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29
Q

•Advantage of more complete blockade of angiotensin action

A

ARBs

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30
Q

•Do not affect bradykinin levels

A

ARBs

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31
Q

•Similar actions with ACEIs but not therapeutically identical

A

ARBs

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32
Q

•Alternative to the ACEIs

A

ARBs

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33
Q

•All require only once-daily dosing

A

ARBs

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34
Q

only ARB that undergoes extensive first-pass effect, along with conversion to its active metabolite

A

Losartan:

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35
Q

•All are highly protein-bound

A

ARBs

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36
Q

•All have large Vd (except ______)

A

candesartan

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37
Q

•Ability to prevent the myocardial changes because of the chronic inactivation of the sympathetic nervous system –decreasing HR and inhibiting the release of renin

A

BETA-BLOCKERS

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38
Q

•Prevent direct deleterious effects of NE on the cardiac muscle fibers -> decreasing remodeling, hypertrophy, and cell death

A

BETA-BLOCKERS

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39
Q

is recommended for all patients with heart disease except those who are at high risk but have no symptoms and those who are in acute HF

A

BETA-BLOCKERS

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40
Q

nonselective ß-adrenoreceptor antagonist that also blocks alpha-adrenoreceptors

A

•Carvedilol:

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41
Q

long-acting ß1-selective antagonist

A

•Metoprolol:

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42
Q

•Reduce morbidity and mortality associated with HF

A

Carvedilol and Metoprolol

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43
Q

•Treatment should be started at low doses and gradually titrated to effective doses based on patient tolerance

A

Carvedilol and Metoprolol

44
Q

•Additional benefit of antihypertensive action

A

Carvedilol and Metoprolol

45
Q

•Relieve pulmonary congestion and peripheral edema

46
Q

•Useful in reducing the symptoms of volume overload (e.g., orthopnea, PND)

47
Q

•Decrease plasma volume -> decreased venous return to the heart (preload) -> decreased cardiac workload and oxygen demand

48
Q

•Decrease afterload by reducing plasma volume decreased BP

49
Q

relatively mild diuretics and lose efficacy if patient creatinine clearance is less than 50 mL/min

A

•Thiazide diuretics:

50
Q

used for patients who require extensive diuresis and those with renal insufficiency; most commonly used diuretics in HF

A

•Loop diuretics:

51
Q

–Overdoses can lead to profound hypovolemia

52
Q

•Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing the venous capacitance

A

DIRECT VASODILATORS

53
Q

reduce systemic arteriolar resistance and decrease afterload

A

•Arterial dilators

54
Q

commonly used venous dilators for patients with congestive HF

A

•Nitrates:

55
Q

if the patient is intolerant of ACEIs or ß-blockers, or if additional vasodilator response is required

A

•Hydralazine+ ISDN:

56
Q

enhance cardiac muscle contractility -> increased cardiac output

A

INOTROPIC DRUGS

•Positive inotropic agents

57
Q

–Result of an increased cytoplasmic Ca concentration that enhances the contractility of cardiac muscle

A

INOTROPIC DRUGS

•Positive inotropic agents

58
Q

•Digitalis or digitalis glycosides (digitalis/foxglove plant)

A

I. DIGITALIS GLYCOSIDES

59
Q

•Group of chemically similar compounds that can increase the contractility of the heart muscle

A

I. DIGITALIS GLYCOSIDES

60
Q

•Influence Na and Ca ion flows in the cardiac muscle -> increased contraction of AV myocardium (positive inotropic action)

A

I. DIGITALIS GLYCOSIDES

61
Q

•Narrow therapeutic index

A

I. DIGITALIS GLYCOSIDES

62
Q

most widely used agent digitalis glycoside

A

•Digoxin:

63
Q

•Digoxin (Lanoxin®)

A

DIGITALIS GLYCOSIDES

64
Q

•Digitalis purpurea, Digitalis lanata

A

DIGITALIS GLYCOSIDES

65
Q

•inhibit Na+/K+ - ATPase pump

A

DIGITALIS GLYCOSIDES

66
Q

•Increases the force of cardiac contraction -> decreased EDV -> increased efficiency of contraction (EF) -> improved circulation -> reduced sympathetic activity -> reduced peripheral resistance -> decreased HR

67
Q

•Increased vaga ltone -> decreased HR -> diminished myocardial oxygen demand

68
Q

•Slows down AV conduction velocity (use in AF)

69
Q

•Severe LVSD after initiation of ACEI and diuretic therapy

70
Q

•HF with atrial fibrillation

71
Q

•Only digitalis glycoside available in the US

72
Q

•Very potent, with a narrow margin of safety

73
Q

•Long half-life of ~36 hours

74
Q

•Mainly eliminated intact by the kidney, requiring dose adjustment based on CrCl

75
Q

•Large Vd: accumulates in muscle

76
Q

•Dosage based on lean BW

77
Q

•Loading dose regimen is used when acute digitalization is needed

78
Q

•Cardiac: arrhythmia (slowing of AV conduction associated with atrial arrhythmias)

79
Q

GI: anorexia, N/V

80
Q

•CNS: headache, fatigue, confusion, blurred vision, alteration of color perception, halos on dark objects

81
Q

PREDISPOSING FACTORS OF DIGOXIN TOXICITY

A
  • Hypothyroidism
  • Hypoxia
  • Renal failure
  • Myocarditis
82
Q

MANAGEMENT OF DIGOXIN TOXICITY

A
  • Discontinuation of cardiac glycoside therapy
  • Determination of serum K levels
  • Oral K supplementation (if indicated)
  • Close monitoring of digoxin levels in renal insufficiency -> dose adjustments
  • Administration of antiarrhythmic drugs
  • Digoxin immune Fab
83
Q

•Dobutamine and dopamine

A

II. BETA-ADRENERGIC AGONISTS

84
Q

•Intravenous inotropic agent administered at the hospital

A

II. BETA-ADRENERGIC AGONISTS

–250 mg/20 mL vial
–250 mg/250 mL pre-mix (1:1)
–500 mg/250 mL pre-mix (2:1)
•Dobutamine and dopamine

85
Q

•Positive inotropic effect and vasodilation

A

II. BETA-ADRENERGIC AGONISTS

•Dobutamine and dopamine

86
Q

•Treatment of acute HF

A

II. BETA-ADRENERGIC AGONISTS

•Dobutamine and dopamine

87
Q

III. PHOSPHODIESTERASE INHIBITORS

A

II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone

88
Q

•Long-term treatment = higher risk of mortality

A

II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone

89
Q

•Short-term IV milrinone: not associated with increased risk of mortality; symptomatic benefit in refractory HF

A

II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone

90
Q

•Direct antagonist of aldosterone -> prevents salt retention, myocardial hypertrophy, hypokalemia

A

ALDOSTERONE ANTAGONISTS (Spironolactone)

91
Q

•Reserved for the most advanced cases of HF

A

ALDOSTERONE ANTAGONISTS (Spironolactone)

92
Q

•AEs: GI disturbances (e.g., gastritis, peptic ulcer); CNS effects (lethargy, confusion); endocrine abnormalities (e.g., gynecomastia, decreased libido, menstrual irregularities)

A

ALDOSTERONE ANTAGONISTS (Spironolactone)

93
Q

•Competitive antagonist of aldosterone at mineralocorticoid receptors

A

ALDOSTERONE ANTAGONISTS (Eplerenone)

94
Q

•Lower incidence of endocrine-related SE due to reduced affinity for glucocorticoid, androgen, and progesterone receptors

A

ALDOSTERONE ANTAGONISTS (Eplerenone)

95
Q

•Reduces mortality in patients with LVSD and HF after acute MI

A

ALDOSTERONE ANTAGONISTS (Eplerenone)

96
Q

At risk for developingHF. No identified structural or functional abnormality; no signs and symptoms.

97
Q

Developed structural heart diseasethat is strongly associated with the development of HF, but without signs and symptoms.

98
Q

SymptomaticHF associated with underlying structural heart disease

99
Q

Advanced structural heart disease and markedsymptoms of HF at rest despite maximal medical therapy

100
Q

No limitation of physical activity. Ordinary physicalactivity does not cause undue fatigue, palpitation, or dyspnea

101
Q

Slight limitation of physical activity. Comfortableat rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea

102
Q

Marked limitation of physicalactivity. Comfortable at rest, but less than ordinary activity results in fatigue, palpitation, or dyspnea

103
Q

Unable to carry on anyphysical activity without discomfort. Symptoms at rest. If any physical activity is undertaken, discomfort is increased.

104
Q

Stageof heart failurebased on structure and damage to heart muscle

A

ACC/AHAStages of Heart Failure

105
Q

Severity based on symptoms and physical activity

A

NYHA Functional Classification

Pharmacology (12 decks)

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