Heart Failure Medication Flashcards
markers for cardiac injury
BNP
troponin T
troponin I
CK-MB
C-reactive protein
TNF alpha
Systolic Heart Failure - HFrEF
weakened pump
blood backs up and overloads heart
LVEF < 40%
diastolic heart failure - HFpEF
stiff or scarred relaxation
wont allow enough blood to fill the heart before it squeezes
LVEF > 50%
Acute decompensated heart failure
causes, results?
- most common cause: LV or diastolic dysfunction
- increase in ventricular filling presssure
Inotropic agents for acute events
(MOA, results, excreted)
cardiac glycosides (digoxin)
- inhibit phosphorylated alpha subunit residing in Na/KATPase channel
leads to contraction due to CA buildup
results in decreased drug action of digoxin
it is excreted via renal route
AE of digoxin (maintainence)
- Maintainance is < 1 ng/ml
- coadmin with Ca could result in malignant arrhythmia
Inotropes with vascular effects:
Dopamine (MOA)
- at low doses -> induces vasorelaxation bc of D2 receptors inhibit NE
- at moderate doses -> stim. B1 receptors increase cardiac contract and NE release
- at high doses -> stim. a receptor causing vasoconstriction
Dobutamine MOA
non-specific beta receptor agonist
- stimu. beta1 receptor resulting in increased contractility
- beta2 receptor results in vasodilation
Dobutamine adverse effects
tolerance may develop so add PDE3 inhibitor
PDE inhibitors (MOA)
inamrinone (PDE3) and sildenafil (PDE5)
- raise cellular cAMP levels
- positive inotropic effect with decreased resistance in both arteries and veins
PDE3 inhibitor (AE)
Inamrinone
- short term therapy
- can develop thrombocytopenia
PDE5 inhibitor
Sildenafil
- effective for ventricular systolic failure due to pulmonary artery hypertension
AE of MR antagonists (K+ sparing diuretics)
men develop gynecomastia substitute with eplerenone
can develop hyperkalemia which can be corrected with Ca or glucose and insulin
Diuretic Resistance
Plasmin and Prostasin
CAP1 cleaves gamma subunit of ENaC and activates ENaC channel
NSAIDs and diuretics
- prostaglandins enhance renal perfusion via RAAS
-NSAIDs decrease the renal perfusion and increase diuretic efficacy