Heart Failure Flashcards
What is heart failure
inability of the heart to maintain enough cardiac output to meet the metabolic demands of the body
What are causes of Heart failure
Ischemia (CAD)(m/c)
valvular defect
ETOH
viral
peripartum
Stress
chemo
familial
congenital
idiopathic
What are the AHA/ACC classifications
Stage A - D
what is stage A
cardiac risk factors
what is stage B
structural heart disease without HF
what is Stage C
structural heart disease with HF
what is Stage D
end-stage HF
what is AHA
American Heart Association
what is ACC
American College of Cardiology
What are the functional classification NYHA
Class 1-4 (symptoms)
starts at AHA/ACC stage B/C
what is class 1 NYHA classification
asymptomatic or mild sx with strenuous exercise, no limitations
what is class 2 NYHA classification
symptoms with ordinary activity; slight limitation
what is class 3 NYHA classifications
marked symptoms with ordinary activity; no symptoms at rest
what is class 4 NYHA classification
symptoms at rest
what are the goals of HF therapy
improve mortality
slow disease production
alleviate symptoms
what are the physiological goals of HF therapy
reduce myocardial work - afterload and preload reduction
improve output - contractility
reduce morphological changes - remodeling
What is systolic dysfunction
decreased ability of the heart to eject blood - due to impaired contractility or pressure overload
elevated ESV
reduced EF
eccentric ventricular remodeling and increased EDV and mass (myocytes elongate)
what is diastolic dysfunction
decreased relaxation (stiffness) of the heart with reduced SV
elevated EDV/EDP
EF may be preserved
concentric ventricular remodeling and increased ventricular mass (myocytes thicken)
what is the bodies natural response to HF
baroreceptor response
increase sympathetic tone - increased HR and contractility, increase peripheral vasoconstriction, increase release of renin
what does the activation of RRAS lead to
sodium and water retention
increase peripheral vascular tone (vasoconstriction)
What are the RAAS
ACE
ARBs
Aldosterone Antagonists
Renin inhibitors
what are Effective HF drug classes
RAAS
BB
Diuretics
Vasodilators
Inotropics
what is the MOA for ACEi
blocks the conversion of angiotension 1 to angitensin 2
what are the ACEi
captopril, enalapril, lisinopril
what are the benefits of ACEi
improved morbidity and mortality outcomes
reduces cardiac remodeling
slows progression of kidney disease
especially in diabetics
increase K+ reabsorption
improved survival
decreased LVH
slows progression of renal insufficiency, esp in diabetics
what are the AE of ACEi
dry cough
hyperkalemia
angioedema (rare)
skin reactions
contraindicated in pregnancy
what are ARBS
inhibitors of the RAAS
Loasartan, valsartan, candesartan, olmesartain
what is the MOA of ARBs
directly blocks angiotensin II type 1 receptors
does not affect bradykinin levels
what are the AE of ARBs
hypotension
hyperkalemia
worsening renal function
angioedema
contraindicated in pregnancy
what are the aldosterone antagonists that inhibit RAAS
spironolactone and eplerenone
recommended for stage C and D HF
what is the MOA for aldosterone antagonists
blocks the aldosterone (mineralocorticoid receptor)
decreases sodium and water retention
What are the AE of aldosterone antagonists
hyperkalemia
hypovolemia
gynecomastica
hypertriglyceridemia
induced CYP
renal dysfunction/failure
What is the angiotensin receptor-neprilysin inhibitors (ARNi)
sacubitril and valsartain
MOA: inhibits neprilysin - endopeptidase that degrades BNP, ANP, promotes diuresis and vasodilation
what are the AE of sacubitril
hypotension
hyperkalemia
dizziness
renal failure
cough
angioedema
contraindicated in pregnancy
where are B1 receptors
mainly on the heart and kidneys
where are B2 receptors
mainly on the lungs and vascular smooth muscle
when are BB not indicated in HF
NOT indicated for acute HF
what are the approved HF BBs in the US
carvedilol
metoprolol
bisoprolol
what are the benefits of BB
decreased cardiac O2 demand - increase HR, contractility and LV wall stress
improves survival after MI
improved LV hemodynamic function
improved survival in CHF
lowers BP
what are the AE of BB
cardiac: fatigue, dizziness, low exercise tolerance, bradycardia, sinus arrest, AV block, HF
Pulmonary: bronchoconstriction
CNS: sexual dysfunction, fatigue, depression
MEtabolic: change in glucose metabolism, may mask early signs of hypoglycemia (tachy)
what are symptoms of HF
SOB
Swelling of LE
Fatigue
Orthopnea
anorexia/distended abdomen
cough with frothy sputum
increased urination at night
confusion and/or impaired memory
what is the MOA for Loops diuretics
blocks reabsorption of Na+, Cl-, K+, HCO3-, Ca2+, Mg2+
promoted the excretion of water and electrolytes
decreased plasma volume - decreased preload and afterload
inidcations for diuretics
sympatomatic relief - only -volume overload
relief of pulmonary congestion
relief of peripheral edema
what are the AE of diuretics
hypovolemia
hypotension
electrolyte imbalance - hypokalemia, hyponatremia, hypocholoremia, hypomagnesemia
ototoxicity
hyperuricemia (gout)
hyperglycermia
what is Hydralazine
arteriole vasodilator
decreases afterload
what is isosorbide dinitrate
venodilator
converted to nitric oxide in the body
causes vasodilation
decreased preload and afterload
what are AE of vasodilators
headache
hypotension
tachy
what can hydralazine cause at high doses
rarely but may cause lupus-like syndrome including glomerulonephritis
what is the MOA of Digoxin
cardiac glycoside
inhibits NA-K-ATPase
alters Na+/Ca+ exchanger - increased intracellular Ca2+ and cardiac contractility
increase in vagal tone (decrease sym/renin release)
Parasympathomimetic effects - slows SA node firing and AV node conduction
when is digoxin indicated
Stage C and D and EF <25%
at low concentrations: reduced morbidity - improved symptoms, decreased admissions
what are the benefits of digoxin
increased cardiac contractility
- decrease symptoms of HF
-increase exercise tolerance
-decrease hospitalizations
useful for treatment of atrial arrhythmias
HF and AFib - win/win combo
what is higher levels of digoxin in the body associated with
decreased survival in HF
goal is 0.5 - 1.1 in HF
what are the AE of Digoxin
narrow TRUTH IS
factors that increase risk of toxicity: renal insufficiency, increased age, drug interactions (amiodarone, verapamil), metabolic factors (hypokalemia, hypomagnesemia, hypernatremia, hypercalcemia, acid-base disturbances)
what are signs and symptoms of Digoxin toxicity
Bradycardia (m/c)
AV block
tachyarrhythmia/ventricular automaticity
fatigue, n/v, delirium, blurred vision, anorexia, Diarrhea, abd pain, HA, dizziness, confusion
What are short term IV inotropic therapies
PDEi and B1 agonists
what are PDEi drugs
milrinon and inamrinone (formerly amrinone)
what is the MOA for PDEi
inhibit PDE type III to decrease breakdown of cAMP: increase cAMP
leads to enhanced activity of cAMP-dependent protein kinase (PKA), phosphorylation of voltage - dependent CA2+ channels and increase Ca2+ influx - vasodilation
what are the indications for Milrinone
acute hemodynamic and symptomatic relief in patients with advanced HFrEF (class III or IV)
short term support
routine use not supported
what is Dobutamine
B1 adrenergic receptor agonists
