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

Copyright © 2014 by Mosby, an imprint of Elsevier Inc. 2

Cardiac defect Myocardial infarction Valve deficiency

Defect outside the heart Coronary artery disease Pulmonary hypertension Diabetes

Heart Failure: Causes


Conduction System of the Heart


Class I Class II Class III Class IV

The New York Heart Association


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


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)


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


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)


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


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


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


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


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


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


Hypotension Dysrhythmia Headache Abdominal pain

B-type Natriuretic Peptides:Adverse Effects


Work by inhibiting the enzyme phosphodiesterase

Results in: Positive inotropic response Vasodilation

milrinone (Primacor)

Phosphodiesterase Inhibitors


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


milrinone Dysrhythmia Hypotension Angina (chest pain) Hypokalemia Tremor Thrombocytopenia

Phosphodiesterase Inhibitors:Adverse Effects


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


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


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


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)


Heart failure Supraventricular dysrhythmias

Atrial fibrillation and atrial flutter

Cardiac Glycosides:Indications



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


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


digoxin (Lanoxin) (cont’d) Cardiovascular

• Dysrhythmias, including bradycardia or tachycardia

CNS• Headaches, fatigue, malaise, confusion, convulsions

Cardiac Glycosides: Adverse Effects (cont’d)


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)


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



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


Hypokalemia Use of cardiac pacemaker Hepatic dysfunction Hypercalcemia Dysrhythmias Hypothyroid, respiratory, or renal disease Advanced age

Conditions That Predispose to Digoxin Toxicity


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


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)


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)


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)


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



Nesiritide or milrinone Use an infusion pump Monitor I&O, heart rate and rhythm, BP, daily weights,

respirations, and so on



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



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


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)


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)


chapter 24 heart failure drugs copyright © 2014 by mosby, an imprint of elsevier inc

Documents

heart copyright

imprint of elsevier

heart failure drugs

heart examples

common heart failure

heart failure contd

lifethreatening heart

positive inotropic drugs