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Pharmacology > Module 3.2.2: Drugs Used in Heart Failure > Flashcards

Module 3.2.2: Drugs Used in Heart Failure Flashcards

1
Q

 Occurs when cardiac output is inadequate to provide oxygen needed by the body.

 It is a progressive disease that is characterize by a gradual reduction in cardiac performance, punctuated in many cases by episodes of acute decompensation

 Most common cause: coronary artery disease.

A

Heart failure

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2
Q

o reduced cardiac output.

o reduced ejection rate fraction (

A

Systolic failure

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3
Q

o A result of hypertrophy and stiffening and loss of adequate relaxation of the myocardium.
o Cardiac output is reduced.
o Ejection fraction may be normal.
o Does not usually respond optimally to positive inotropic drugs.
o Proportion of patients increase with age.
o Stroke volume is significantly decreased.

A

Diastolic failure

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4
Q

o Result from hyperthyroidism, beriberi, anemia, and arteriovenous shunts.
o Treated by correcting the underlying cause.

Manifestations:
o Heart failure tachycardia
o Decreased exercise tolerance
o Shortness of breath
o Peripheral and pulmonary edema
o Cardiomegaly
o Rare form of heart failure.
o Demands of the body are so great that even an increase in cardiac output is insufficient.
A

High-output failure

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5
Q

______ helpful mainly in acute systolic failure and also reduces symptoms in chronic systolic heart failure.

A

Positive inotropic drugs

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6
Q

o A sodium pump and the site of action of cardiac glycosides.
o The major determinant of sodium oncentration in the cell.
o The primary target of Digoxin and other cardiac glycosides.

A

Na+/K+-ATPase

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7
Q

o A sodium-calcium exchanger.
o Uses the sodium gradient to move calcium against its concentration gradient from the cytoplasm to the extra-cellular space.

A

NCX

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8
Q

o A voltage-gated, L-type calcium channel.

A

Cav-L

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9
Q

o A calcium transporter ATPase that pumps calcium into the sarcoplasmic reticulum (SR).
o Maintains free cytoplasmic calcium at very low levels during diastole by pumping calcium into the SR.

A

SERCA (sarcoplasmic endoplasmic reticulum Ca2+ -ATPase)

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10
Q

SERCA is inhibited by _______; phosphorylation of _______ by protein kinase A (eg, by βagonists) removes this inhibition.

A

phospholamban

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11
Q

A calcium bound to calsequestrin, a high-capacity Ca2+-binding protein.

A

CalS

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12
Q

A calcium-activated calcium channel in the membrane of the SR that is triggered to release stored calcium.

A

RyR (ryanodine RyR2 receptor)

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13
Q

Acts at the actin-troponin-tropomyosin complex where activator calcium brings about the contractile interaction of actin and myosin.

A

Calcium sensitizers

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14
Q

_____ increases calcium sensitivity, inhibits phosphodiesterase, and reduces symptoms of heart failure.

A

Levosimedan

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15
Q

Neurohumoral or extrinsic compensation involves two major mechanisms:

A

o Sympathetic Nervous System

o Renin-Angiotensin-Aldosterone Hormonal Response

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16
Q

The most important intrinsic compensatory mechanism is ______.

A

myocardial hypertrophy

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17
Q

the term applied to dilation (other than that due to passive stretch) and other slow structural changes that occur in the stressed myocardium. It may include proliferation of connective tissue cells as well as abnormal myocardial cells with some bio-chemical characteristics of fetal myocytes.

A

Remodeling

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18
Q

o Failure is associated with no limitations on ordinary activities
o Symptomatic only with greater than ordinary activity (severe exercise.

A

HEART FAILURE: Class I

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19
Q

o Slight limitation of ordinary activities

o Fatigue and palpitations with ordinary physical activity.

A

HEART FAILURE: Class II

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20
Q

o Failure results in no symptoms at rest.

o Fatigue, shortness of breath, and tachycardia occur with less than ordinary physical activity.

A

HEART FAILURE: Class III

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21
Q

o Associated with symptoms even when the patient is at rest.

A

HEART FAILURE: Class IV

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22
Q

______ patients are at high risk because of other disease but have no signs or symptoms of heart failure.

Treatment of patients at high risk should be focused on control of hypertension, hyperlipidemia, and diabetes, if present.

A

Stage A

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23
Q

______ patients have evidence of structural heart disease but no symptoms of heart failure.

Treatment of patients at high risk should be focused on control of hypertension, hyperlipidemia, and diabetes, if present.

A

Stage B

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24
Q

______ patients have structural heart disease and symptoms of failure, and symptoms are responsive to ordinary therapy.

Active treatment must be initiated.

A

Stage C

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25
Q

______ patients have heart failure refractory to ordinary therapy, and special interventions (resynchronization therapy, transplant) are required.

A

Stage D

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26
Q

Cardiac performance is a function of four primary factors:

A
  1. Preload
  2. Afterload
  3. Contractility
  4. Heart rate
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27
Q

Digitalis that inhibit the Na+/K+-ATPase pump

A

cardiac glycosides

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28
Q

… are steroids proposed to have endogenous digitalis-like properties.

A

Ouabain or marinobufagenin

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29
Q

 Obtained from Digitalis lanata (white foxglove)

 MOA: inhibits Na+/K+ ATPase (sodium pump)

A

Digoxin

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30
Q

cardiac glycosides increase contraction of the cardiac sarcomere by increasing the free calcium concentration in the vicinity of the contractile proteins during systole.

A

Mechanical effects of Digoxin

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31
Q

A mixture of direct and autonomic actions. Direct actions on the membranes of cardiac cells follow a well-defined progression: an early, brief prolongation of the action potential, followed by shortening (plateau phase).

A

Electrical Effects of Digoxin

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32
Q

At low dose:

cardiac _______ effects predominate; account for early electrical effects of digitalis.

A

parasympathomimetic

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33
Q

At toxic levels: ______ outflow is increased; sensitizes the myocardium and exaggerates all the toxic effects of the drug.

A

sympathetic

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34
Q

GI tract – most common extra cardiac site of digitalis toxicity, which are ….

A

Anorexia, nausea, vomiting, and diarrhea

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35
Q

______ reduces the enzyme-inhibiting actions of cardiac glycosides, whereas ______ facilitates these actions.

A

Hyperkalemia

hypokalemia

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36
Q

Abnormal automaticity is inhibited by ________: Moderately increased extracellular K+ reduces the effects of digitalis, especially the toxic effects.

A

hyperkalemia

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37
Q

_____ facilitates the toxic actions of cardiac glycosides by accelerating the overloading of intracellular calcium stores.

A

Ca2+

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38
Q

______ increases the risk of a digitalis induced arrhythmia.

A

Hypercalcemia

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39
Q

In severe intoxication, serum K+ is already elevated, automaticity is depressed, and anti-arrhythmic agents administered in this setting may lead to cardiac arrest.

A

Digoxin Toxicity

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40
Q

Digoxin Toxicity Treatment: prompt insertion of a ______ and administration of _________ (digoxin immune fab)

A

pacemaker

digitalis antibodies

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41
Q

… is an investigational steroid derivative that increases contractility by inhibiting Na+/K+ -ATPase (like cardiac glycosides) but in addition facilitates sequestration of Ca2+ by the SR.

A

Istaroxime

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42
Q

MOA:

 inhibit phosphodiesterases

 Inhibition of phosphodiesterase increases cAMP and increases contractility and vasodilation.

 increase myocardial contractility by increasing inward calcium flux in the heart during the action potential.

 Although they have positive inotropic effects, most of their benefits derive from vasodilation

A

Bipyridines

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43
Q

– used only intravenously and only for acute heart failure or severe exacerbation of chronic heart failure.

A

Inamrinone and Milrinone

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44
Q

Inamrinone toxic effects include:

A

o nausea and vomiting
o arrhythmias
o thrombocytopenia
o liver enzyme changes

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45
Q

______ appears less likely to cause bone marrow and liver toxicity

A

Milrinone

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46
Q

(selective β1 agonist), a parenteral drug

A

Dobutamine

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47
Q

 It increases cardiac output with a decrease in ventricular filling pressure.

 Tachycardia may occur use with caution in patients with CAD or arrhythmia.

 Tachyphylaxis may be seen

A

β-Stimulants/ Beta-adrenoceptor Agonists

48
Q

– also used in acute heart failure and may be particularly helpful if there is a need to raise blood pressure.

A

Dopamine

49
Q

 Have no direct effect on cardiac contractility.

 Reduces venous pressure and ventricular preload&raquo_space; Reduction of edema and cardiac size&raquo_space; Improvement of pump efficiency.

A

Diuretics

50
Q

Aldosterone antagonists that decrease morbidity and mortality in patients with severe heart failure.

A

Spironolactone and Eplerenone,

51
Q

These drugs reduce the long-term remodeling of the heart and vessels, an effect that may be responsible for the observed reduction in mortality and morbidity.

A

ACE inhibitors and ARBs

52
Q

In cases of patients intolerant of ACE inhibitors due to incessant cough, add ______ (an Angiotensin receptor blocker) with the ACE inhibitor to have beneficial effects.

A

candesartan

53
Q

______ a renin inhibitor, appears to have efficacy similar to that of ACE inhibitors.

A

Aliskiren

54
Q

 Effective in acute heart failure.

 Reduce preload (venodilation), or afterload (arteriolar dilation), or both.

 Most common adverse effect: Excessive hypotension.

A

Vasodilators

55
Q

Long-term use of these vasodilators can also reduce damaging remodeling of the heart.

A

Hydralazine and Isosorbide dinitrate

56
Q

inhibitors of endothelin, approved in pulmonary hypotension.

A

Bosentan and Tezosentan

57
Q

…has significant teratogenic and hepatotoxic effects.

A

Bosentan

58
Q

______, approved for use in acute cardiac failure, increases cGMP in smooth muscle cells and reduces venous and arteriolar tone in experimental preparations. It also causes diuresis.

A

Nesiritide

59
Q

MOA:

o Attenuation of the adverse effects of high concentrations of catecholamines (including apoptosis)

o Up-regulation of β-receptors

o Decreased heart rate

o Reduced remodeling through inhibition of the mitogenic activity of catecholamines

A

β-Blockes/ Beta-adrenoceptor blockers

60
Q

first-line therapy for heart failure

A

Diuretics

61
Q

______ is reserved for patients who do not respond adequately to diuretics, ace inhibitors and β-blockers.

A

Digitalis

62
Q

Give ______ if systolic dysfunction with 3rd heart sound or atrial fibrillation is present.

A

digitalis

63
Q

Give ______ to patients with stable class II-IV heart failure.

A

β-blockers

64
Q

In mild failure, start with a ______, switching to ______ as required.

A

Thiazide diuretic

Furosemide

65
Q

…. should be considered in all patients with moderate or severe heart failure.

A

Spironolactone or eplerenone

66
Q

______ should be monitored in patients receiving any of these HF drugs

A

Serum potassium

67
Q

 In patients with left ventricular dysfunction but no edema, ______ should be used first.

 ______ are superior to vasodilators and must be considered, along with diuretics, as first-line therapy for chronic failure.

 ______ are nonselective arteriolar and venous dilators.

A

ACE inhibitors

68
Q

….should only be used in patients who are intolerant of ACE inhibitors (usually because of cough).

A

ARBs (losartan, candesartan)

69
Q

… is useful in atrial arrhythmias due to its cardioselective parasympathomimetic effects

A

Digitalis

70
Q

Contraindicated in patients with Wolff-Parkinson-White syndrome and atrial fibrillation.

(increases the conduction of atrial arrhythmia through the aberrant pathway)

A

Digitalis

71
Q

A common cause of acute failure is ….

A

MI

72
Q

Acute MI patients can be characterized on the basis of three hemodynamic measurements:

A

arterial pressure,
left ventricular filling pressure,
and cardiac index.

73
Q

A new V1a and V2 receptor antagonist, ______, has recently been approved for the parenteral treatment of euvomic hyponatremia.

A

conivaptan

74
Q

Studies suggest that ______ is effective in both systolic and diastolic failure.

A

Nebivolol

75
Q

MOA:

Loop diuretic: Decreases NaCl and KCl reabsorption in thick ascending limb of the loop of Henle in the nephron

A

Furosemide

76
Q

EFFECTS:

  • Increased excretion of salt and water
  • reduces cardiac preload and afterload
  • reduces pulmonary and peripheral edema
A

Furosemide

77
Q

TOXICITY:

Hypovolemia, hypokalemia,
orthostatic hypotension,
ototoxicity,
sulfonamide allergy

A

Furosemide

78
Q

MOA:

Decreases NaCl reabsorption in the distal convoluted tubule

A

Hydrochlorothiazide

79
Q

EFFECTS:

Same as furosemide, but less efficacious

A

Hydrochlorothiazide

80
Q

TOXICITY:

Hyponatremia, hypokalemia,
hyperglycemia,
hyperuricemia, hyperlipidemia,
sulfonamide allergy

A

Hydrochlorothiazide

81
Q

Similar to spironolactone; more selective antialdosterone effect; no significant antiandrogen action

A

Eplerenone

82
Q

MOA:

• Block cytoplasmic aldosterone receptors in
collecting tubules of nephron
• possible membrane effect

A

Spironolactone

83
Q

EFFECTS:

  • Increased salt and water excretion
  • reduces remodeling
  • reduces mortality
A

Spironolactone

84
Q

TOXICITY:

Hyperkalemia, antiandrogen actions

A

Spironolactone

85
Q

MOA:

  • Inhibits ACE
  • reduces AII formation by inhibiting conversion of AI to All
A

Angiotensin-converting enzyme (ACE) inhibitors:

• Captopril

86
Q

EFFECTS:

  • Arteriolar and venous dilation
  • reduces aldosterone secretion
  • increases cardiac output
  • reduces cardiac remodeling
A

Angiotensin-converting enzyme (ACE) inhibitors:

• Captopril

87
Q

TOXICITY:

Cough, hyperkalemia, angioneurotic edema

A

Angiotensin-converting enzyme (ACE) inhibitors:

• Captopril

88
Q

MOA:

Antagonize AII effects at AT1 receptors

A

Angiotensin receptor
blockers (ARBs):
• Losartan

89
Q

TOXICITY:

Hyperkalemia; angioneurotic edema

A

Angiotensin receptor
blockers (ARBs):
• Losartan

90
Q

Select group of Beta blockers that reduce heart failure mortality

A

Metoprolol, bisoprolol

91
Q

Competitively blocks Beta1 receptors

A

BETA BLOCKERS

• Carvedilol

92
Q

EFFECTS:

  • Slows heart rate
  • reduces blood pressure
  • poorly understood effects
  • reduces heart failure mortality
A

BETA BLOCKERS

• Carvedilol

93
Q

TOXICITY:

Bronchospasm, bradycardia,
atrioventricular block,
acute cardiac decompensation

A

BETA BLOCKERS

• Carvedilol

94
Q

MOA:

Na+,K+ ATPase inhibition results in reduced
Ca2+ expulsion and increased Ca2+ stored in sarcoplasmic reticulum

A

CARDIAC GLYCOSIDE

• Digoxin

95
Q

EFFECTS:

  • Increases cardiac contractility
  • cardiac parasympathomimetic effect (slowed sinus heart rate, slowed atrioventricular conduction)
A

CARDIAC GLYCOSIDE

• Digoxin

96
Q

TOXICITY:

  • Nausea, vomiting, diarrhea
  • cardiac arrhythmias
A

CARDIAC GLYCOSIDE

• Digoxin

97
Q

MOA:

  • Releases nitric oxide (NO)
  • activates guanylyl cyclase
A

Venodilators:

• Isosorbide dinitrate

98
Q

EFFECTS:

  • Venodilation
  • reduces preload and ventricular stretch
A

Venodilators:

• Isosorbide dinitrate

99
Q

TOXICITY:

Postural hypotension, tachycardia, headache

A

Venodilators:

• Isosorbide dinitrate

100
Q

MOA:

Probably increases NO synthesis in endothelium

A

Arteriolar dilators:

• Hydralazine

101
Q

EFFECTS:

  • Reduces blood pressure and afterload
  • results in increased cardiac output
A

Arteriolar dilators:

• Hydralazine

102
Q

TOXICITY:

Tachycardia, fluid retention, lupus-like syndrome

A

Arteriolar dilators:

• Hydralazine

103
Q

MOA:

  • Releases NO spontaneously
  • activates guanylyl cyclase
A

Combined arteriolar and venodilator:

• Nitroprusside

104
Q

EFFECTS:

  • Marked vasodilation
  • reduces preload and afterload
A

Combined arteriolar and venodilator:

• Nitroprusside

105
Q

TOXICITY:

Excessive hypotension, thiocyanate and cyanide toxicity

A

Combined arteriolar and venodilator:

• Nitroprusside

106
Q

MOA:

  • Beta1–selective agonist
  • increases cAMP synthesis
A

Dobutamine

107
Q

EFFFECT:

Increases cardiac contractility,
output

A

Dobutamine

108
Q

TOXICITY:

Arrhythmias

A

Dobutamine and Dopamine

109
Q

MOA:

higher doses activate Beta and Alpha adrenoceptors

A

Dopamine

110
Q

EFFECTS:

  • Increases renal blood flow
  • higher doses increase cardiac force and blood pressure
A

Dopamine

111
Q

MOA:

  • Phosphodiesterase type 3 inhibitors
  • decrease cAMP breakdown
A

BIPYRIDINES

• Inamrinone, milrinone

112
Q

EFFECTS:

  • Vasodilators lower peripheral vascular resistance
  • also increase cardiac contractility

TOXICITY: Arrhythmias

A

BIPYRIDINES

• Inamrinone, milrinone

113
Q

MOA:

Activates BNP receptors,
increases cGMP

A

NATRIURETIC PEPTIDE

• Nesiritide

114
Q

EFFECTS:

  • Vasodilation
  • diuresis
A

NATRIURETIC PEPTIDE

• Nesiritide

115
Q

TOXICITY:

Renal damage, hypotension

A

NATRIURETIC PEPTIDE

• Nesiritide

Pharmacology (4 decks)

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