Heart Failure Meds

Question 1

Loop diuretics characteristics

Answer 1

quickest to work!
used in pulmonary edema
PO onset: 1 hr
IV onset: 5 min

Question 2

what happens if you push furosemide too quickly

Answer 2

ototoxicity– transient!

Question 3

thiazide MOA

Answer 3

reduces blood volume
works on DISTAL tubule
results in excretion of water, Na, and K
decreases arterial resistance over time

Question 4

considerations for thiazides

Answer 4

sulfa deriative! allergy!

Question 5

K sparing MOA

Answer 5

competes with Al @ receptors in the distal tubule

Question 6

ACE inhibitors characteristics

Answer 6

cornerstone of therapy in HF! imroves functional status and prolongs life!

Question 7

MOA of ACE

Answer 7

STOP ANGIE
arteriolar dilation: decreases afterload
venous dilation: decreases preload
suppress Al
prevents cardiac remodeling

Question 8

MOA of ARB

Answer 8

block receptors of AT2 after its formed.

Question 9

ARNI MOA

Answer 9

increases natriuretic peptides

decreases effects of RAAS

Question 10

considerations for ARNI

Answer 10

decrease in deaths + hospitalizations!!!

used INSTEAD of an ARB, have to be off of an ARB for 36 hours before starting this

Question 11

Al Receptor blockers r/t HF

Answer 11

pts with HF can have 20x normal of Al.
REALLY WATCH K**
reduces symptoms, decrease hospitalizations, and prolongs life!

Question 12

BB MOA

Answer 12

decrease HR
decrease contractility
slows conduction

CAN WORSE HF!!

Question 13

which BB 3 are approved for HF?

Answer 13

carvedilol, metoprolol XL, bisoprolol

Question 14

BB considerations for HF

Answer 14

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

Question 15

SE of BB

Answer 15

brady, decreased CO, AV heart block, rebound cardiac excitation, masks s/s of hypo in DM pts,

Question 16

common SE of BB in HF

Answer 16

fatigue, dizziness, drowsy, headache, sexual dysfunction, depression

Question 17

HCN channel blockers MOA

Answer 17

inhibits channels in SA node, slows HR

Question 18

HCN SE

Answer 18

brady, HTN, afib, luminous phenomena

Question 19

HCN pt teaching

Answer 19

check radial pulse, 50-60 is ok!

teach about visual changes– they’re transient

Question 20

NSG considerations for BB and HCN

Answer 20

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)

Question 21

cardiac glycoside MOA

Answer 21

slows the HR
increases force of contraction (this is unique to this drug)
increases cardiac output

Question 22

Cardiac glycoside (digoxin) characteristics

Answer 22

narrow therapeutic range

doesn’t prolong life, can shorten it…

Question 23

therapeutic levels with dig

Answer 23

0.5-0.8 ng/mL

Question 24

hypokalemia and digoxin

Answer 24

K competes with dig @ Na/K pump

if k is low, more dig will bind and stay in the body

Question 25

AE of digoxin (cardiac glycosides)

Answer 25

fatigue, dizziness, drowsiness, cardiac dysrhythmias

Question 26

s/s of dig toxicity

Answer 26

N/V, anorexia, fatigue, visual disturbances

Question 27

antidote of dib

Answer 27

digibind

expensive!!

Question 28

considerations for dig

Answer 28

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!

Question 29

Direct vasodilators MOA

Answer 29

isosorbide– relaxes venous SM

hydralazine– dilation of arterioles

Question 30

SE of direct vasodilators

Answer 30

ortho hypo, reflex tachy, SLE syn (looks like lupus)