Chapter 24 Heart Failure Drugs Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
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Transcript of Chapter 24 Heart Failure Drugs Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
Chapter 24
Heart Failure Drugs
Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs
Symptoms depend on the cardiac area affected Systolic dysfunction Diastolic dysfunction
• Less common
Heart Failure
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Cardiac defect Myocardial infarction Valve deficiency
Defect outside the heart Coronary artery disease Pulmonary hypertension Diabetes
Heart Failure: Causes
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Conduction System of the Heart
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Class I Class II Class III Class IV
The New York Heart Association
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Positive inotropic drugs Increase the force of myocardial contraction
Positive chronotropic drugs Increase heart rate
Positive dromotropic drugs Accelerate cardiac conduction
Drug Therapy for Heart Failure
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ACE inhibitors Angiotensin II receptor blockers Beta blockers Aldosterone antagonists B-type natriuretic peptides Phosphodiesterase inhibitors Cardiac glycosides
Drug Therapy for Heart Failure (cont’d)
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Prevent sodium and water resorption by inhibiting aldosterone secretion
Diuresis results, which decreases preload, or the left ventricular end-volume, and the work of the heart
Examples: lisinopril, enalapril, fosinopril, quinapril, captopril, ramipril, trandolapril, and perindopril
ACE Inhibitors
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Potent vasodilators; decrease systemic vascular resistance (afterload)
Examples: valsartan (Diovan), candesartan (Atacand), eprosartan (Teveten), irbesartan (Avapro), telmisartan (Micardis), olmesartan (Benicar), and losartan (Cozaar)
All ARBs are similar in action
Angiotensin II Receptor Blockers (ARBs)
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Beta blockers work by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system
Reduced heart rate, delayed AV node conduction, reduced myocardial contractility, and decreased myocardial automaticity result
Examples: metoprolol, carvedilol (Coreg)
Beta Blockers
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spironolactone (Aldactone) Potassium-sparing diuretic Also acts as an aldosterone antagonist, which has
been shown to reduce the symptoms of heart failure eplerenone (Inspra)
Selective aldosterone blocker
Aldosterone Antagonist
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hydralazine/isosorbide dinitrate (BiDil) First drug approved for a specific ethnic group,
namely African Americans dobutamine
Beta1-selective vasoactive adrenergic drug
Structurally similar to dopamine
Miscellaneous Drugs to Treat Heart Failure
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nesiritide (Natrecor) Used in the intensive care setting as a final effort to
treat severe, life-threatening heart failure, often in combination with several other cardiostimulatory medications
B-type Natriuretic Peptides
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Effects include diuresis (urinary fluid loss), natriuresis (urinary sodium loss), and vasodilation
Vasodilating effects on both arteries and veins Indirectly increases cardiac output Suppresses renin-angiotensin system
B-type Natriuretic Peptides:Mechanism of Action
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Classroom Response Question
Which patient is the best candidate to receive nesiritide therapy?
A.A patient with atrial fibrillation who has not responded to other drugs
B.A patient needing initial treatment for heart failure
C.A patient with reduced cardiac output
D.A patient with acutely decompensated heart failure who has dyspnea at rest
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Hypotension Dysrhythmia Headache Abdominal pain
B-type Natriuretic Peptides:Adverse Effects
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Work by inhibiting the enzyme phosphodiesterase
Results in: Positive inotropic response Vasodilation
milrinone (Primacor)
Phosphodiesterase Inhibitors
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Short-term management of heart failure Given when patient does not respond to
treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against long-term infusions
Phosphodiesterase Inhibitors:Indications
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milrinone Dysrhythmia Hypotension Angina (chest pain) Hypokalemia Tremor Thrombocytopenia
Phosphodiesterase Inhibitors:Adverse Effects
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No longer used as first-line treatment Originally obtained from Digitalis plant, foxglove Digoxin is the prototype Used in heart failure and to control ventricular
response to atrial fibrillation or flutter
Cardiac Glycosides
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Increase myocardial contractility Change electrical conduction properties of the
heart Decrease rate of electrical conduction Prolong the refractory period
• Area between SA node and AV node
Cardiac Glycosides:Mechanism of Action
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Positive inotropic effect Increased force and velocity of myocardial contraction
(without an increase in oxygen consumption) Negative chronotropic effect
Reduced heart rate Negative dromotropic effect
Decreased automaticity at SA node, decreased AV nodal conduction, and other effects
Cardiac Glycosides:Drug Effects
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Increased stroke volume Reduction in heart size during diastole Decrease in venous BP and vein engorgement Increase in coronary circulation Promotion of diuresis because of improved
blood circulation Palliation of exertional and paroxysmal nocturnal
dyspnea, cough, and cyanosis
Cardiac Glycosides:Drug Effects (cont’d)
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Heart failure Supraventricular dysrhythmias
Atrial fibrillation and atrial flutter
Cardiac Glycosides:Indications
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Classroom Response Question
A patient is in the emergency department with new onset atrial fibrillation. Which order for digoxin would most likely have the fastest therapeutic effect?
A.Digoxin 0.25 mg PO daily
B.Digoxin 1 mg PO now, then 0.25 mg PO daily
C.Digoxin 0.5 mg IV push daily
D.Digoxin 1 mg IV push now, then 0.25 mg IV daily
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digoxin (Lanoxin) Very narrow therapeutic window Drug levels must be monitored
• 0.5 to 2 ng/mL
Low potassium levels increase its toxicity Electrolyte levels must be monitored
Cardiac Glycosides:Adverse Effects
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digoxin (Lanoxin) (cont’d) Cardiovascular
• Dysrhythmias, including bradycardia or tachycardia
CNS• Headaches, fatigue, malaise, confusion, convulsions
Cardiac Glycosides: Adverse Effects (cont’d)
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digoxin (Lanoxin) (cont’d) Eye
• Colored vision (seeing green, yellow, purple), halo vision, flickering lights
GI• Anorexia, nausea, vomiting, diarrhea
Cardiac Glycosides: Adverse Effects (cont’d)
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digoxin immune Fab (Digibind) therapy Hyperkalemia (serum potassium greater than
5 mEq/L) in a digitalis-toxic patient Life-threatening cardiac dysrhythmias Life-threatening digoxin overdose
Digoxin Toxicity
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Classroom Response Question
A patient is receiving digoxin 0.25 mg daily as part of treatment for heart failure. The nurse assesses the patient before medication administration. Which assessment finding would be of most concern?
A. Apical heart rate of 58 beats/min
B. Ankle edema +1 bilaterally
C. Serum potassium level of 2.9 mEq/L
D. Serum digoxin level of 0.8 ng/mL
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Hypokalemia Use of cardiac pacemaker Hepatic dysfunction Hypercalcemia Dysrhythmias Hypothyroid, respiratory, or renal disease Advanced age
Conditions That Predispose to Digoxin Toxicity
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Assess history, drug allergies, contraindications Assess clinical parameters, including:
BP Apical pulse for 1 full minute Heart sounds, breath sounds
Heart Failure Drugs:Nursing Implications
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Assess clinical parameters (cont’d) Weight, I&O measures ECG Serum labs: potassium, sodium, magnesium, calcium,
renal, and liver function studies
Heart Failure Drugs:Nursing Implications (cont’d)
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Before giving any dose, count apical pulse for 1 full minute
For apical pulse less than 60 or greater than 100 beats/min Hold dose Notify prescriber
Heart Failure Drugs:Nursing Implications (cont’d)
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Hold dose and notify prescriber if patient experiences signs/symptoms of toxicity Anorexia, nausea, vomiting, diarrhea Visual disturbances (blurred vision, seeing green or
yellow halos around objects)
Heart Failure Drugs: Nursing Implications (cont’d)
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Check dosage forms carefully, and follow instructions for administering
Avoid giving digoxin with high-fiber foods (fiber binds with digitalis)
Patients should immediately report a weight gain of 2 lb or more in 1 day or 5 lb or more in 1 week
Heart Failure Drugs: Nursing Implications (cont’d)
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Nesiritide or milrinone Use an infusion pump Monitor I&O, heart rate and rhythm, BP, daily weights,
respirations, and so on
Heart Failure Drugs: Nursing Implications (cont’d)
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Monitor for therapeutic effects Increased urinary output Decreased edema, shortness of breath, dyspnea,
crackles, fatigue Resolution of paroxysmal nocturnal dyspnea Improved peripheral pulses, skin color, temperature
Monitor for adverse effects
Heart Failure Drugs: Nursing Implications (cont’d)
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A patient with a history of heart failure presents to the emergency department with difficulty breathing, cough, and edema of the lower extremities. The nurse anticipates administration of which type of medication?
A.Positive chronotrope
B.Negative chronotrope
C.Positive inotrope
D.Negative inotrope
Case Study
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The patient is prescribed an ACE inhibitor. The nurse understands the primary mechanism by which the ACE inhibitors exert their therapeutic effect in a patient in heart failure is:
A.to inhibit catecholamine release.
B.to inhibit acetylcholine release.
C.to inhibit aldosterone secretion.
D.to prevent vagal stimulation.
Case Study (cont’d)
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The patient is discharged home and returns to the emergency department 4 days later. The patient is admitted to the intensive care unit with acute decompensated heart failure with dyspnea at rest. The nurse anticipates administration of which medication?
A.atropine
B.carvedilol (Coreg)
C.lisinopril (Prinivil)
D.nesiritide (Natrecor)
Case Study (cont’d)
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