Heart Failure Meds Flashcards
Loop diuretics characteristics
quickest to work!
used in pulmonary edema
PO onset: 1 hr
IV onset: 5 min
what happens if you push furosemide too quickly
ototoxicity– transient!
thiazide MOA
reduces blood volume
works on DISTAL tubule
results in excretion of water, Na, and K
decreases arterial resistance over time
considerations for thiazides
sulfa deriative! allergy!
K sparing MOA
competes with Al @ receptors in the distal tubule
ACE inhibitors characteristics
cornerstone of therapy in HF! imroves functional status and prolongs life!
MOA of ACE
STOP ANGIE arteriolar dilation: decreases afterload venous dilation: decreases preload suppress Al prevents cardiac remodeling
MOA of ARB
block receptors of AT2 after its formed.
ARNI MOA
increases natriuretic peptides
decreases effects of RAAS
considerations for ARNI
decrease in deaths + hospitalizations!!!
used INSTEAD of an ARB, have to be off of an ARB for 36 hours before starting this
Al Receptor blockers r/t HF
pts with HF can have 20x normal of Al.
REALLY WATCH K**
reduces symptoms, decrease hospitalizations, and prolongs life!
BB MOA
decrease HR
decrease contractility
slows conduction
CAN WORSE HF!!
which BB 3 are approved for HF?
carvedilol, metoprolol XL, bisoprolol
BB considerations for HF
used in combo with ACE and diuretics
start with SUPER low dose (1/10 or 1/20) and double every 2 weeks.
decreases sympathetic load on heart over time.
takes 3 mos to reach therapeutic effects
SE of BB
brady, decreased CO, AV heart block, rebound cardiac excitation, masks s/s of hypo in DM pts,
common SE of BB in HF
fatigue, dizziness, drowsy, headache, sexual dysfunction, depression
HCN channel blockers MOA
inhibits channels in SA node, slows HR
HCN SE
brady, HTN, afib, luminous phenomena
HCN pt teaching
check radial pulse, 50-60 is ok!
teach about visual changes– they’re transient
NSG considerations for BB and HCN
check BP and pulse before admin
wean off–
DM monitor blood sugar more closely
watch for s/s of heart failure (edema, wt, gain. SHOB)
cardiac glycoside MOA
slows the HR
increases force of contraction (this is unique to this drug)
increases cardiac output
Cardiac glycoside (digoxin) characteristics
narrow therapeutic range
doesn’t prolong life, can shorten it…
therapeutic levels with dig
0.5-0.8 ng/mL
hypokalemia and digoxin
K competes with dig @ Na/K pump
if k is low, more dig will bind and stay in the body
AE of digoxin (cardiac glycosides)
fatigue, dizziness, drowsiness, cardiac dysrhythmias
s/s of dig toxicity
N/V, anorexia, fatigue, visual disturbances
antidote of dib
digibind
expensive!!
considerations for dig
check apical pulse, hold if less than 60
teach pts to check pulse daily
d-d/d-f interactions: really normal things.. like antacids and high fiber foods!
Direct vasodilators MOA
isosorbide– relaxes venous SM
hydralazine– dilation of arterioles
SE of direct vasodilators
ortho hypo, reflex tachy, SLE syn (looks like lupus)
