Heart Failure Drugs

Front 1

Which class of drugs do you never use in systolic heart failure

Back 1

non-dihydropyridine calcium channel blockers

Front 2

How would you treat someone with diastolic heart failure

Back 2

1) Give ace inhibitors and beta blockers

2) treat hypertension

3) diltiazem or verapamil= negative inotropic effects allow relaxation

Front 3

Describe stage A heart failure

Back 3

at risk ( has HTN, DM)
no structural abnormalities
no symptoms

Front 4

Describe stage B heart failure

Back 4

has structural abnormalities
no symptoms

Front 5

Describe stage C heart failure

Back 5

has structural abnormalities
has past or current symptoms

Front 6

describe stage D heart failure

Back 6

refractory heart failure requiring special interventions

Front 7

What is the only diuretic proven to prevent heart failure and decrease mortality in hypertensive patients

Back 7

thiazides

Front 8

which diuretic would u use for severe volume overload

Back 8

loop diuretics (bc they have the greatest natriuresis effect)

Front 9

What is a disadvantage of loop diuretics

Back 9

activate RAAS which may exacerbate hypertension

Front 10

how do you use diuretics in heart failure patients

Back 10

never use as a monotherapy!

use with Ace inhibitors and Beta blockers

Front 11

how would you use a diuretic in a patient with gut edema

Back 11

give diuretic as IV first until gut edema decreases

then give orally

Front 12

what kind of patients do you not give thiazides to

Back 12

decreased renal function

Front 13

what do you give to patients with decreased renal blood flow but has fluid overload

Back 13

sympathetic drugs (dopamine and dobutamine)

do NOT give NSAIDs (bc decreased prostaglandins decreases blood flow)

Front 14

what should u monitor in patients who are on diuretics

Back 14

1) weight = if gaining weight 2lbs/overnight or 5 lbs/week = increase diuretic dose

2) edema
3) postural hypotension
4) ELECTROLYTES!!!
5) BP
6) renal function

Front 15

what should the K and Mg levels be before you give diuretics to a patient in heart failure

Back 15

K >4 meq/L
Mg>2meq/L

or else will increased risk for arrythmias!

Front 16

Is digoxin used in heart failure for symptomatic relief or for decreasing mortality

Back 16

symptomatic only!

Front 17

how does digoxin affect mortality

Back 17

it decreases pump failure related deaths but increases sudden deaths (cancels out-> no effect on mortality)

Front 18

what is the MOA of digoxin

Back 18

inhibits Na/K atpase =increase Ca intracellularly = increase force of contraction of the heart (positive inotropy)

Front 19

what are the toxic effects of digoxin

Back 19

very narrow therapeutic index!!
1) anorexia
2) visual disturbances
3) cardiac effects (arrythmia, AV block, bradycardia)
4)confusion

Front 20

What do you monitor in patients on digoxin

Back 20

1) renal function
2) electrolyte= K!!! > 4meq/L
= if low= increased risk for arrythmias

Front 21

when do you use digoxin?

Back 21

never used first!

used only when beta blockers, ace-inhibitors and diuretics have failed to relieve symptoms

Front 22

Which group of heart failure patients does digoxin help?

Back 22

1) non ischemic
2) low ejection fraction
3) advance CHF
4) atrial fibrillation

Front 23

what is the appropriate serum level dose of digoxin

Back 23

0.6-1.0 (higher levels increase mortality)

Front 24

When is a digoxin serum level of 1.5-2.0 appropriate?

Back 24

only if RATE CONTROL is NEEDED ( atrial fib patients)

Front 25

when do you use Beta agonists like Dopamine and Dobutamine

Back 25

only in CHF exacerbations
-pulmonary edema
-pleural effusions

Front 26

why is the use of beta agonists (dopamine and dobutamine) limited and NOT recommended

Back 26

bc it INCREASES MORTALITY with long term use

Front 27

what is the MOA of brain natriuretic peptide (nesiritide)

Back 27

IV vasodilator
duiretic

Front 28

when do u use nesiritide

Back 28

when diuretic treatment isn't working

Front 29

what is a disadvantage of nesiritide

Back 29

very expensive

Front 30

what are the advantages of nesiritide

Back 30

1) less need to use diuretic
2) improves circulation in acute CHF patient
3) improves sob in acute chf patient
4) improves fatigue in acute chf patient
5) less likely than dobutamine to cause arrythmias

Front 31

what are the symptomatic benefits of ACE inhibitors

Back 31

1) decrease preload
2) decrease afterload
3) decrease sympathetics by decreasing RAAS

Front 32

What are the mortality benefits of ACE inhibitors

Back 32

1) reversal of LVH and myocardial remodeling

2) decreases angiotensin II and norepi = both are cardiotoxic

Front 33

what is the MOA of ace inhibitors

Back 33

1) prevent angiotensin II formation = decreases afterload due to less vasoconstriction

3) prevent aldosterone formation = decrease preload (due to less retention)

Front 34

what are the toxic effects of Ace inhibitors

Back 34

1) hypotension & dizziness
2) hyperkalemia
3) dry persistent cough = due to bradykinin
4) angioedema
5) renal insufficiency = serum creatinine may rise

Front 35

what are the contraindications for ace inhibitors

Back 35

1) K>5.5 meq/L
2) angioedema
3) pregnancy =bc it increases interuterine blood flow
4) bilateral renal stenosis = or history of anuria with previous use

Front 36

When do you use ace inhibitors in heart failure

Back 36

for all heart failure patients unless contraindicated

- slows progression of HF
-renal protective effects for diabetic patients

Front 37

how do you use ace inhibitors as far as dosing goes

Back 37

start with a lose dose and then gradually increase dose until goal is reached

Front 38

what are the erroneous reasons for underutilization of ace inhibitors

Back 38

1) increase in serum creatinine = expect this to transiently increase by 0.5

2) patient has reached optimal BP = fear of hypotension= must look at symptoms and not BP #

3) cough = must differentiate between heart failure cough or ace inhibitor induced cough

Front 39

what do u monitor in patients on ace inhibitors

Back 39

1) creatinine
2) Potassium

Front 40

How would you educate a patient about taking ace inhibitors

Back 40

1)improvements may not be seen for weeks to months

2)warn about cough
3) educate about improving survival and decreasing disease progression
4)warn about serious SE = like angioedema

Front 41

what is the moa of angiotensin 2 receptor blockers

Back 41

directly blocks angiotensin II receptors

- blocks more completely than Ace inhibitors
- blocks w/o the bradykinin effects

Front 42

when do you use ARBs

Back 42

only for a patient who cannot tolerate coughing from ace inhibitors

Front 43

what happens when you add ARB to ACE inhibitors

Back 43

1) improves morbidity (decreases hospitalizations)

2) no effect on mortality

Front 44

what is the drug combination that is known to decrease both morbidity and mortality in heart failure patients

Back 44

ace inhibitors + beta blockers

Front 45

what happens when you use beta blockers, ace inhibitors and ARBs all together

Back 45

increase in mortality ( unknown reason)

Front 46

what is the moa of nitrates

Back 46

activates guanylyl cyclase = increase cGMP = dilation in the venous side = decrease preload

Front 47

what is the moa of hydralazine?

Back 47

direct vasodilation of arterial smooth muscle = decrease afterload

Front 48

describe the benefits in mortality of using both nitrates and hydralazine at the same time

Back 48

mortality decrease not as much as ace inhibitors , but better than placebo

Front 49

why is the treatment with isosorbide dinitrate and hydralazine not the primary choice for treating heart failure patients

Back 49

bc it is more toxic than ace inhibitors or ARBs

Front 50

what are the toxic effects of isosorbide dinitrate + hydralazine treatment?

Back 50

1) SLE like rash from hydralazine
2) reflex tachycardia from hydralazine
3) headaches
4) dizziness
5) hypotension if taken with sildenafil

Front 51

when do you use isosorbide dinitrate and hydralazine

Back 51

only when ace inhibitors are contraindicated:
1) pregnancy
2) angioedema
3) hyperkalemia
4) renal insufficiency

Front 52

what does adding a vasodilator to ace-i, beta blockers and diuretic do

Back 52

decreases mortality in african americans

Front 53

What is the MOA of beta blockers

Back 53

blocks the effects of NE and other sympathetic neurotransmitters to the heart and vasculature

Front 54

what are the symptomatic benefits of beta blockers

Back 54

1) decreased contractility = improves heart function by attenuating effects of cathecolamines

2) decreases ventricular arrythmias

3) decreases cardiac hypertrophy

Front 55

which beta blocker is preferred for patients with high blood pressure

Back 55

carvedilol (non selective and alpha 1 blocker)

Front 56

which beta blockers are preferred in patients with low bp or pulmonary disease

Back 56

metoprolol
bisoprolol
- both are beta 1 selective

Front 57

which beta blockers are FDA approved for chf

Back 57

carvedilol
metoprolol

Front 58

what dose of metoprolol would you start with ?

Back 58

start with 12.5-25 mg and titrate up to 100-200mg

Front 59

what dose of carvedilol would you start with

Back 59

3.125-6.25 mg and titrate up to 25-50 mg

Front 60

what are the toxic effects of beta blockers

Back 60

1) edema
2) fatigue
3) fluid retention
--all 3 are due to decrease BP and HR---

4) dizziness and hypotension
= responds to diuretics

5) sexual dysfunction

Front 61

what are the contraindications against beta blockers

Back 61

1) unstable Heart failure = may need sympathetic kick to help with HR

2) copd/asthma (not with metoprolol)

3) av block

4) severe tachycardia

5) severe hypotension

Front 62

how are beta blockers used

Back 62

Used with ace inhibitors in all cases of stable heart failure unless CI

- symptoms may not improve for several months but MORTALITY WILL

Front 63

what is the moa of aldosterone antagonists like eplerenone and spironolactone

Back 63

blocks aldosterone effects in heart, kidney and vasculature
-may enhance loop diuretic effects

in kidneys: decrease Na/water retention = decrease preload
: decrease K/Mg loss = decreased arrythmias

in heart: decreases FIBROTIC ACTIONS in the myocardium= decreases heart stiffness

in vasculature: decreases vasoconstriction (decrease BP)

Front 64

what are the toxic effects of aldosterone antagonists

Back 64

1) HYPERKALEMIA =K must be <5 =if patient can't come in within 1-2 weeks to check K, do NOT prescribe

2) impotence and gynecomastia (give eplerenone for this)

Front 65

when do you use aldosterone antagonists in heart failure

Back 65

Given with ACE-i and Beta blockers = must make sure there's ADEQUATE RENAL FUNCTION and NOT hyperkalemic

- avoid if Cr>2 and K>5