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Flashcards in Heart Failure Deck (26):

Heart failure

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


Left sided heart failure

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)


Right sided heart failure

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


Pathophysiology of heart failure

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



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



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


Treat Symptoms of Heart Failure

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


Management of heart failure: Stage A

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


Management of heart failure: stage B

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


Management of heart failure: stage C

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


Management of heart failure: stage D

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


ACE Inhibitors

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


ACE Inhibitors drug-drug interactions

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



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)


Thiazide diruetics

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


Cardiac glycosides

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


Cardiac (digitalis) glycosides

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


Digoxin (Lanoxin) adverse effects

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


Digoxon (lanoxin) drug interactions

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


Beta-Adrenergic Blockers

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


Beta Blockers

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



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


Angiotensin II receptor blockers

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


Aldosterone antagonists

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


Direct renin inhibitors

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


Inotropic Agents

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