Heart Failure Flashcards
What are the 4 basic mechanisms of heart failure?
- Increased blood volume/preload
- Increased resistance to blood flow/afterload
- Decreased contractility
- 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
Htn
What can cause decreased contractility?
Ischemic cardiomyopathy (MI)
Myocarditis
Toxins (anthracycline, alcohol, cocaine)
What can cause decreased filling?
mitral stenosis
constriction
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
ACEI
Angiotensin receptor blockers
Aldosterone antagonists
Nitrates/hydralazine
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
Anti-hypertensives
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
SE=hyperalkemia
Gynecomastia with spironolactone (not eplerenone)
