Quiz 7 Heart Failure Drugs

Question 1

Heart failure definition

Answer 1

Heart failure (HF) is a pathologic state in which the heart is unable to pump blood in sufficient amounts to meet the body’s metabolic needs (decreased CO)

Question 2

Symptoms of left-sided heart failure

Answer 2

• Pulmonary edema
• Coughing
• Dyspnea

Question 3

Symptoms of right-sided heart failure

Answer 3

• Jugular vein distention
• Ascites
• Pedal edema

Question 4

Diagnostic studies for heart failure

Answer 4

• BNP

- Echocardiography to determine ejection fraction (EF)

Question 5

Compensated v. decompensated heart failure

Answer 5

Compensated: under control mostly with meds

• clear lungs
• displaced cardiac apex

Decompensated: worsening/uncontrolled HF

• tachycardic
• tachypneic, with
• bilateral inspiratory rales
• jugular venous distention
• edema
• pale
• diaphoretic

Question 6

Positive inotropic, chronotropic, and dromotropic

Answer 6

↑ Contraction, ↑ HR, ↑ Conduction

Question 7

Goals of drug therapy for HF

Answer 7

• Improve symptoms
• Slow deterioration in myocardial function
• Reduce mortality

Question 8

MOA/Drug effects Loop Diuretics

Answer 8

MOA: decreases Na, Cl, and K reabsorption in thick ascending limb of the loop of Henle in the nephron which results in profound diuresis.

Effect: reduced blood volume decreases venous pressure (preload) and arterial pressure (afterload). Reduced pulmonary and peripheral edema.
Ex. Furosemide (Lasix)

Question 9

Indications Loop Diuretics

Answer 9

Acute and chronic HF

Question 10

Adverse Effects Loop Diuretics

Answer 10

• Hypokalemia (↑ risk of digoxin toxicity)

- Severe hypotension

Question 11

Nursing implications/patient education

Answer 11

Assess fluid volume status, lab values (K), advise patient to eat foods rich in Potassium (bananas, potatoes, dried fruit, tomatoes, spinach, citrus fruit)

Question 12

MOA/Drug effects ACEI (Inhibit RAAS)

Answer 12

MOA: inhibits ACE which prevents the conversion of angiotensin I to angiotensin II (a powerful vasoconstrictor). Also reduces aldosterone secretion. Suppress degradation of kinins (vasodilator).

Effect: arteriolar and venous dilation results in reduced preload, afterload, ↓ pulmonary & pedal edema, and increased cardiac output. ↑ kinins reduces cardiac remodeling.
Ex. lisinopril (Prinvil), captopril (Capoten), enalapril (Vasotec)

Question 13

Indications ACEI

Answer 13

Cornerstone of HF therapy

Question 14

Adverse Effects ACEI

Answer 14

A: angioedema
C: cough
E: extra Potassium (hyperkalemia)
hypotension

Question 15

MOA/Drug effects Beta-Blockers (Inhibit SNS)

Answer 15

MOA: protect heart from excessive sympathetic stimulation

Effect: Improve LV ejection fraction (1-3 months), slow the progression of HF, reduce need for hospitalization, and prolong survivial.
Ex. Carvedilol (Coreg), bisoprolol, sustained-release metoprolol (Toprol XL)

Question 16

Contraindications Beta Blockers

Answer 16

Heart block

Question 17

Adverse Effects Beta Blockers

Answer 17

• Fluid retention/ worsening HF
• Bradycardia/ heart block
• Hypotension

Question 18

Dosages Beta Blockers

Answer 18

Start low and go slow

Question 19

Things to know about Cardiac Glycosides

Answer 19

• Oldest group of cardiac drugs
• Comes from the foxglove plant
• Digoxin (Lanoxin) is the only cardiac glycoside available in the U.S.
• No longer used as first-line treatment

Question 20

MOA/Drug effects

Answer 20

MOA: inhibits the sodium-potassium adenosine triphosphatase pump.

Effect: positive inotropic effect increases the force of ventricular contraction which increases cardiac output. Increased CO, can reverse all the overt manifestations of HF.

Question 21

Indications Cardiac Glycosides

Answer 21

Second-line heart failure; atrial fibrillation

Question 22

Precautions Cardiac Glycosides

Answer 22

Lasix (secondary to risk of hypokalemia)

Question 23

Adverse effects Cardiac Glycosides

Answer 23

• Digoxin toxicity

- Cardiac dysrhythmia

Question 24

Therapeutic window Cardiac Glycosides

Answer 24

0.5 to 0.8 ng/mL

Question 25

Digoxin Toxicity S&S

Answer 25

• HR below 60 or new irregular rhythm
• Anorexia, nausea, confusion, and blurred, yellow tinged appearance of halos
• Antidote=digoxin immune Fab (Digibind)–>an antibody

Question 26

Nursing implications/patient education Cardiac Glycosides

Answer 26

• Monitor vital signs
• Monitor for EKG changes
• Monitor labs – K+, digoxin level (CRITICAL)
• Monitor for signs and symptoms of hypokalemia (lethargy, muscle weakness, leg cramps)

Question 27

MOA/Drug effects Vasodilator (Isosorbide Dinitrate plus Hydralize)

Answer 27

MOA: Isosorbide dinitrate causes selective dilation of veins which ↓preload and reduces congestive symptoms. Hydralize (Apresoline) causes selective dilation of arterioles which can improve cardiac output (decreased afterload) and renal blood flow (increase urine output/decrease volume).
Ex. Bidil (37.5 mg of hydralizine/ 20 mg isosorbide dinitrate)

Question 28

MOA/Drug effects B-type Natriuretic Peptide

Answer 28

MOA: A synthetic form of BNP produced by recombinant DNA technology. Causes suppression of RAAS, suppression of SNS, direct dilation of arterioles and veins (↓ preload and ↓ afterload).
Ex. nesiritide (Natrecor)

Question 29

Route B-type Natriuretic Peptide

Answer 29

Acutely decompensated CHF via continuous intravenous infusion only

Question 30

Nursing responsibilities/patient education Digoxin

Answer 30

• Take apical pulse for one minute before giving medication
• Hold dose and notify physician if bradycardia (heart rate less than 60 bpm) or new arrhythmias occur.
• Check potassium level prior to giving medication
• Check kidney function since you want to know they can excrete excess digoxin and avoid build up in body
• Immediately report weight gain of 2 or more pounds in 1 day or 5 or more pounds in 1 week