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Pharmacology > Drugs Used in Heart Failure > Flashcards

Drugs Used in Heart Failure Flashcards

0
Q

Characteristics of HF

A

Progressive and often fatal
Left ventricular dysfunction, reduced CO, insufficient tissue perfusion, signs of fluid retetion
5 million americans
Heart is unable to pump sufficient blood to meet the metabolic need of tissues
- Volume overload
- Inadequate tissue perfusion

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1
Q

The two forms of heart failure

A

Left ventricular systolic dysfunctions

Diastolic heart failure, also known as heart failure with preserved LV ejection fraction

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2
Q

HF: Causes

A 
Chronic hypertension
MI
CAD
dysarrhythmias
ageing of the myocardium
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3
Q

HF: Physiologic adaptations

A 
Reduced CO
Cardiac dilation
Increased sympathetic tone 
Water retention and increased blood volume
Natriuretic peptides
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4
Q

HF: Signs and Symptoms

A 
Decreased exercise tolerance
Fatigue
Shortness of breath
Tachycardia
Pulmonary and peripheral edema
Hepatomegaly
Distension of jugular veins
Progressive disorder
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5
Q

HF: Pathogenesis

A

Decreased contractility
Increased cardiac workload
- Increases in HR, preload, afterload

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6
Q

HF: Compensatory mechanisms

A

RAA stimulation
ADH release, ANF release
Sympathetic stimulation
Cardiac dilation and hypertrophy

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7
Q

Remodeling

A

Changes in cardiomyocytes, extracellular matrix, changes in heart size, shape and function

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8
Q

Drugs Used to Treat HF

A

Thiazide Diuretics
Loop (high-ceiling) diuretic
Potassium- sparing diuretic

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9
Q

Drugs that inhibit RAAS

A

ACE inhibitors
Angiotensin II receptor blockers
Aldosterone antagonists
Direct renin inhibitors

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10
Q

ACE inhibitors: Hemodynamic benefits

A

Arteriolar dilation
Venous adilation
Suppression of aldosterone release

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11
Q

ACE Inhibitor: Impact on cardiac remodeling

A

Favorable impact

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12
Q

ACE Inhibitors: Adverse effects

A 
Hypotension
Hyperkalemia
Intractable cough
Angioedema
Renal failure if patient has bilateral renal artery stenosis
Can cause fetal injury
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13
Q

Angiotensin II receptor blockers

A 
ARBs improve LV ejection fraction, reduce HF symptoms
Increase exercise tolerance
Decrease hospitalization
Enhance quality of life
Reduce mortality
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14
Q

Aldosterone antagonists: drugs

A

Spironolactone

Eplerenone

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15
Q

Aldosterone antagonists: Recommendations

A

Adding an aldosterone antagonist to standard HF therapy in patients with moderately severe or severe symptoms

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16
Q

Direct Renin Inhibitors

A

Benefits in HF about equal to ACE/ARBs

Aliskiren

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17
Q

What is the most common cause of secondary hyperaldosteronism?

A

Congestive heart failure

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18
Q

Beta-blockers: Action

A

With careful control of dosage, can improve patient status
Protect from excessive sympathetic stimulation
Protect against dysrhythmias

19
Q

Beta-blockers: Adverse effects

A

Fluid retention or worsening of HF
Fatigue
Hypotension
Bradycardia or heart block

20
Q

Digoxin (other cardiac glycosides): Actions

A

Positive inotropic
- Increase myocardial contractile force
- Alter electrical activity of the heart
- Favorably affect neurohormonal systems
Second-line agents

21
Q

Inotropic agents [acute care]

A

Dopamine
Dobutamine
Phosphodiesterase inhibitors

22
Q

Dopamine: Mechanism

A

Activates beta-adrenergic receptors in the heart, kidney ,and blood vessels
Increase HR
dilates renal blood vessels
Activates alpha1 receptors

23
Q

Dobutamine

A

Synthetic catecholamine

Selective activation of beta1- adrenergic receptors

24
Q

Phosphodiesterase inhibitors: Drugs

A

Inamrinone

Milrinone

25
Q

Vasodilators

A

Isossorbide dinitrate plus hydralazine

Intravenous vasodilators

26
Q

Intravenous vasodilators for acute care: Drugs

A

Nitroglycerin
Sodium nitroprusside
Nesiritide

27
Q

Nitroglycerin: Adverse effects

A

Hypotension

Resultant reflex tachycardia

28
Q

Sodium nitroprusside: Adverse effect

A

Profound hypotension

29
Q

Nesiritide: Adverse effect

A

Symptomatic hypotension

30
Q

Cardiac Glycosides: Drugs

A

Digoxin

31
Q

Digoxin: Origination

A

Foxglove plant

32
Q

Digoxin: Effects

A 
Positive inotropic action on the heart
Increases the force of ventricular contraction
Increases myocardial contractility
Inhibits sodium potassium ATPase promoting calcium accumulation in the myocytes
Increases exercise tolerance
Increased CO
Increased contractility
DOES NOT PROLONG LIFE
33
Q

Digoxin: Adverse Effects

A

Can cause severe dysrhytmias
Arrhythmia
Increases automaticity

34
Q

Digoxin: Status

A

alternative status

35
Q

Digoxin: Ionic interactions

A

K ( competes with digoxin to bind to Na-K-ATPase)
- Hyperkalemia reduces action of digoxin
- Hypokalemia increases digoxins action
Calcium
- Facilitates toxic effects of digoxin
- Hypercalcemia results in an increase risk of dig-induced arrhythmias
Magnesium
- Hypomagnesemia may cause arrhythmia

36
Q

Digoxin: Positive Inotropic Effects

A

Increased force and efficiency of contractions
- Increases CO
- Decreases heart size, venous pressure and BV
- Diuresis and relief from edema
Vagal effect
- Intensifies effect of vagus on the heart
- Increases sensitivity of SA node to negative chronotropic effects of Ach
- Reflex decrease in sympathetic tone
- Slow AV conduction

37
Q

Digoxin: Effects on ECG and contraction

A

Slowed AV and Bundle of HIS conduction (Prolongs PR interval)
Prolonged refractory period of AV node
Increased automaticity
- Premature ventricular contractions

38
Q

Digoxin: Effects on CHF

A 
Increased CO
   - Decreased sympathetic tone
   - Increased urine production
   - Decreased renin release
Bradycardia
Decreases afterload and preload
39
Q

Digoxin: Adverse Effects

A

Narrows margin of safety and therapeutic range

Cardiac dysrhythmias

40
Q

Digoxin: Cardiac dysrhythmias

A

Arterioventricular block, ventricular flutter, ventricular fibrillations
Predisposing factors
- Hypokalemia
- Elevated digoxin level

41
Q

Digoxin: Noncardiac adverse effects

A

Anorexia, nausea, vomiting, fatigue, visual effects

Useful warning symptoms early in digoxin toxicity so baseline assessment

42
Q

Digoxin: Measures to reduce adverse effects

A

Education

43
Q

Digoxin: Drug interactions

A

Diuretics (hypokalemia)
Beta blockers (decrease in contractility resulting in higher dose needed)
ACEI and ARBs (hyperkalemia)
Sympathomimetics (arrhythmia)
Quinidine (anticholinergic effects, sometimes used to decrease the bradycardia of digoxin, can increase digoxin levels)
Verapamil (can increase digoxin levels)

44
Q

Digoxin: Managing adverse effects

A

Withdraw digoxin
Monitor serum potassium or administer K
Administer lidocaine or phenytoin for arrhythmias
Cholestyramine, activated charcoal ( can bind digoxin in the gut where it wont be absorbed)

45
Q

Digoxin: Management of patients with AV block or bradycardia

A

Atropine

46
Q

Digoxin: Pharmacokinetics (absorption)

A 
Tables variable
Patients not switch brands
Crosses the placenta
Renal excretion
Digitalization

Pharmacology (13 decks)

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