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Flashcards in Heart Failure Deck (22):

What are the 4 basic mechanisms of heart failure?

1. Increased blood volume/preload

2. Increased resistance to blood flow/afterload

3. Decreased contractility

4. Decreased filling 


Causes of increased volume/predload

Mitral regurg

Aortic regurg

Volume overload

L to R shunts

Chronic kidney disease


What can cause increased afterload?

Aortic stenosis or coarctation



What can cause decreased contractility?

Ischemic cardiomyopathy (MI)


Toxins (anthracycline, alcohol, cocaine)


What can cause decreased filling?

mitral stenosis


restrictive cardiomyopathy

hypertrophic cardiomyopathy

infiltrative cardiomyopathy


What's the difference between systolic/diastolic HF?

Systolic: impaired filling, concentric hypertrophy (thick walled heart), usually in older patients due to htn

Diastolic: impaired contraction, eccentric hypertrophy, all ages, related to coronary artery disease


What is the difference between compensated and decompensated heart failure?

Compensated: body counteracts heart failure

Decompensated: compensation ends --> congestion (orthopnea, ascites, edema, abdominojugular reflex), low perfusion (narrow pulse pressure, cool extremities)

Can be warm/cold or wet/dry



What's the difference between high output failure/low output failure?

High output: decreased vascular resistance (anemia, obseity, preg, etc)

Low output: decreased CO (low CO)

Both ultimately cause decreased fullness of the arterial vasculature


What are the 3 types of diuretics?

Loop diuretics: impair generation of hypertonic interstitium --> less ater reabsorption in collecting duct
**these are most effective***
- furosemide, bumetanide, torsemide

Thiazide: act on distal convuluting tubule & potentiate sodium and water excretion in the setting of loop diuretics
- hydrochlorothiazide

K+ sparing: spironolactone, eplerenone

All are given IV


When do you use diuretics? SE?

Treat excessive volume (preload)

Symptomatic relief

SE= dehydration, hypoalkemia, contraction alkalosis, ototoxicity


What is the mechanism of nitrates? 

Vascular smooth muscle vasodilation via producing NO in ET cells

Mostly venodilator, at low dose


When do you give nitrates?

Relive pulmonary congestion

Relieves chest pain if related to coronary artery vasoconstriction


What are the SE of nitrates?

HA, tachyphylaxis


What is the mechanism of action of hydralazine?

Arterial vasodilator

Treats htn by reducing afterload

SE=reflex tachycardia, lupus-like syndrome


What's the mechanism of action of ACEI? SE?

Inhibits angiotensin converting enzyme, blocking conversion of angiotensin I to II

Blocks the action of angiotensin II wich includes vasoconstriction, Na/H2O reabsorption, release of aldosterone, myocardial fibrosis (remodeling)

Effect is to promote vasodilation --> decrease BP & decrease afterload, facilitate natriuresis, reverse remodel the heart
** improves survival ***

SE: hypotension, renal insufficiency, hyperalkemia, cough, angioedema


Which meds improve survival?

Beta blockers 


Angiotensin receptor blockers

Aldosterone antagonists



What is the mechanism of angiotensin receptor blockers?

ARBs block AT1 receptor-- effectively same as ACEI

ARBs more effective bc angiotensin II can be generated via ACE escape pathway


SE=same as ACEI except cough (bc don't inhibit bradykinin pathway)


When are ARBs indicated?

In hypertensive patients

Heart failure pt's who can't tolerate ACEI

You can also administer ARBs with ACEI

Don't use in combination with aldosterone antagonists!!


What is the mechanism of action of beta blockers?

Block deleterious effect of catecholamines on the myocardium: negative inotrope via SNS blockade

Chronic beta receptor stimulation during heart failure --> downregulation and desensitization of beta receptors

Beta blockade allows for gradual re-upregulation of beta receptors (increased receptor density) while blocking the incessant catecholamine toxic effects on the myocardium


What are the effects and SE of beta blockers?

Negative inotrope

Morbidity and mortality benefit

SE: heart block, hypotension, fatigue, elevated TG's, decreased HDL, masks hypoglycemia


When should you not use beta blockers?

Don't give to pt's with decompensated CHF


What is the mechanism of aldosterone antagonists?

Modest diuretic: blocks Na reabsorption and K excretion of collecting duct

Reduced mortality when used in heart failure patients after best medical therapy


Gynecomastia with spironolactone (not eplerenone)