Heart Failure

Question 0

Left sided heart failure

Answer 0

Blood accumulates in left ventricle
Left ventricle thickens and enlarges (hypertrophy)
Cardiac remodeling
Blood backs up into the lungs
Cough and shortness of breath (pulmonary edema)

Question 1

Heart failure

Answer 1

Inability of ventricles to pump enough blood for body’s need; weakening of heart muscle (tissue) due to aging or disease. Left sided heart failure is far more common than right sided heart failure in US; #1 cause of right sided heart failure is left sided heart failuer

Question 2

Right sided heart failure

Answer 2

Blood backs up into veins
“Cor pulmonale” right sided heart failure caused by lung conditions
Causes peripheral edema and organ engorgement
Less common than left sided HF

Question 3

Pathophysiology of heart failure

Answer 3

Cardiac remodeling; physiologic adaptations to reduce cardiac output: cardiac dilation, increased sympathetic tone, water retention and increased blood volume, natriuretic peptides

Question 4

Preload

Answer 4

Ventricular end diastolic pressure; affects cardiac output. Degree myocardial fibers stretched prior to contraction; drugs that increase preload contractility will increase cardiac output

Question 5

Afterload

Answer 5

Affects cardiac output; pressure in aorta that must be overcome before blood is ejected from left ventricle, lowering blood pressure creates less afterload = less workload for the heart

Question 6

Treat Symptoms of Heart Failure

Answer 6

Slow heart rate (negative chronotropic agents), increase contractility (positive inotropes), reduce heart workload

Question 7

Management of heart failure: Stage A

Answer 7

No symptoms of HF, no structural or functional cardiac abnormalities; hypertension, CAD, diabetes, family history of cardiomyopathy, personal history of alcohol abuse, rheumatic fever, or treatment with a cardiotoxic drug. Management directed at reducing risk

Question 8

Management of heart failure: stage B

Answer 8

No signs and symptoms of HF, goal of management is to prevent development of symptomatic HF. Treatment is the same for stage A with addition of ACE inhibitors or ARBs

Question 9

Management of heart failure: stage C

Answer 9

Symptoms of HF; structural heart disease. Four major goals: relive pulmonary and peripheral congestive symptoms, improve functional capacity and quality of life, slow cardiac remodeling and progression of LV dysfunction, prolong life

Question 10

Management of heart failure: stage D

Answer 10

Marked symptoms of HF, advanced structural heart disease, repeated hospitalizations, best solution: heart transplant > LV mechanical assist device used until heart is available
Management: control of fluid retention, beta blockers pose high risk for worsening HF

Question 11

ACE Inhibitors

Answer 11

Prototype drug: Lisinopril (prinivil, zestril)
Mechanism of action: to enhance excretion of sodium and water
Primary use: decrease blood pressure and reduce blood volume; dilate veins
Adverse effects: first-dose hypotension, cough, hyperkalemia, renal failure, angioedema
-Reduce afterload, drug of choice for heart failure, lowers peripheral resistance and reduces blood volume, increases cardiac output

Question 12

ACE Inhibitors drug-drug interactions

Answer 12

NSAIDs: precipitate acute renal failure
Potassium supplements: hyperkalemia
Lithium - levels increased (inhibit elimination)
Potassium sparing diuretics: hyperkalemia

Question 13

Diuretics

Answer 13

Prototype drug: furosemide (lasix)/loop diuretic - decreases preload
Mechanism of action: to increase urine flow, reducing blood volume and cardiac workload
Primary use: to reduce edema and pulmonary congestion
Adverse effects: dehydration, electrolyte imbalance, hypotension, ototoxicity (specially loop diuretics)

Question 14

Thiazide diruetics

Answer 14

High-ceiling (loop) diuretics; most common for heart failure, if allergic to sulfa, loop diuretics should not be used. Potassium sparing diuretics

Question 15

Cardiac glycosides

Answer 15

Prototype drug: digoxin (lanoxin)
Mechanism of action: to cause more forceful heartbeat/slower heart rate
Primary use: to increase contractility or strength of myocardial contraction
Adverse effects: neutropenia, dysrhythmias, digitalis toxicity

Question 16

Cardiac (digitalis) glycosides

Answer 16

Digoxin (lanoxin, lanoxicaps, digitek); naturally occurring compound, profound effects on the mechanical and electrical properties of the heart, increases myocardial contractility, increased cardiac output

Question 17

Digoxin (Lanoxin) adverse effects

Answer 17

Noncardiac adverse effects: anorexia, nausea, vomiting, fatigue
-Cardiac dysrhythmias; predisposing factors: hypokalemia, elevated digoxin level (narrow therapeutic range), heart disease
Measures to reduce adverse effects: education

Question 18

Digoxon (lanoxin) drug interactions

Answer 18

Diuretics, ACE inhibitors and ARBs, sympathomimetics, quinidine, varapamil; pharmacokinetics: absorption, distributed widely and crosses the placenta, eliminated primarily by renal excretion, half-life about 1.5 days

Question 19

Beta-Adrenergic Blockers

Answer 19

Prototype drug: metoprolol (lopressor, tropol XL)
Mechanism of action: block cardiac action of sympathetic nervous system to slow heart rate and BP reducing workload of heart
Primary use: to reduce symptoms of heart failure and slow progression of disease
Adverse effects: fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block

Question 20

Beta Blockers

Answer 20

Action: with careful control of dosage, can improve patient status; protect from excessive sympathetic stimulation, protect against dysrhythmias
Adverse effects: fluid retention or worsening of HF, fatigue, hypotension, bradycardia or heart block

Question 21

Vasodilators

Answer 21

Drugs: hydralazine (apresoline); isosorbide dinitrate (isordil)
Mechanism of action: to relax blood vessels
Primary use: to lower blood pressure
-Used for clients who cannot take ACE inhibitors
Adverse reactions: reflex tachycardia, orthostatic hypotension

Question 22

Angiotensin II receptor blockers

Answer 22

ARBs improve LV ejection fraction, reduce HF symptoms, increase exercise tolerance, decrease hospitalization, enhance quality of lief, reduce mortality

Question 23

Aldosterone antagonists

Answer 23

Spironolactone (aldactone) and eplerenone (inspra); current studies recommend adding an aldosterone antagonist to standard HF therapy in patients with moderately severe or severe symptoms

Question 24

Direct renin inhibitors

Answer 24

Benefits in HF should be equal to those of ACE inhibitors or ARBs, aliskiren (tektuma) is being tested in HF, not yet approved for HF treatment

Question 25

Inotropic Agents

Answer 25

Sympathomimetics; dopamine (intropin)
-catacholamine, activates beta 1 adrenergic receptors in the heart, kidney, and blood vessels; increases heart rate, dilates renal blood vessels, activates alpha 1 receptors