Heart Failure Flashcards
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)
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
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
Preload
Ventricular end diastolic pressure; affects cardiac output. Degree myocardial fibers stretched prior to contraction; drugs that increase preload contractility will increase cardiac output
Afterload
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
Diuretics
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
Vasodilators
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
