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MOD 1 Quiz 2 > Phamacologic aspects of heart failure > Flashcards

Phamacologic aspects of heart failure Flashcards

1
Q

Goals?

A

improve ejection fraction
symptomatic relief of pulmonary edema
reduce cardiac remodeling

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2
Q

Ejection fraction=

A

SV/ EDV

increase it by increase preload, decrease afterload, increase contractility

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3
Q

main way to alleviate pulmonary edema?

A

decrease preload

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4
Q

Treat Stage A?

A

ACEI / ARB

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5
Q

Treat Stage B?

A

ACEI

Beta blocker

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6
Q

Treat Stage C?

A 
ACEI
Beta blocker
Loop diuretic
rare (thiazide, K sparing)
Digoxin
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7
Q

IV drugs for acutely decompensated heart failure?

A

Loop diuretics
Nitroglycerin
Nitroprusside
Nesiritide

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8
Q

Does ACEI relieve pulmonary edema?

A

No it doesn’t, Na and water loss is not sufficient to alleviate the edema associated with heart failure and after several months aldosterone levels return

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9
Q

ACE inhibitor MOA?

A

Increase bradykinin, decrease Ang II– arteriolar dilation, decrease afterload, increase stroke volume, increase CO

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10
Q

high levels of Ang II leads to?

A

cardiac hypertrophy and remodeling

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11
Q

ACEI end result?

A

prolong exercise tolerance
increase quality of life
decrease hospital readmissions for heart failure
decrease morbidity and mortality

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12
Q

How much start with ACEI?

A

start at low does and titrate up every 3-7 days to dose achieved in clinical trials

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13
Q

Advantages of ARB over ACEI?

A

no/less cough or angioedema

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14
Q

Beta blockers used for heart failure?

A

sustained release Metoprolol
Bisoprolol
Carbedilol

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15
Q

Carvedilol?

A

blocks beta 1, beta 2, alpha 1 receptors

antioxidant effects

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16
Q

MOA of beta blockers?

A

prevent or reverse cardiac hypertrophy and remodeling

prevent atrial/ ventricular arrhythmias

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17
Q

result beta blockers?

A

increase left ventricular ejection fraction
decrease ventricular volume
lessens symptoms of heart failure
decrease hospitalization for worsening HF
decrease mortality

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18
Q

major direct benefits of beta blocker?

A

reduce cardiac output

decrease mortality

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19
Q

Use beta blockers in all stage IV?

A

no, if symptoms at rest may not be able to tolerate a beta blocker

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20
Q

Clinical use of beta blocker?

A

Start at low does and titrate up every few weeks
benefit is not immediate
can exacerbate HF if too much is given

used in conjunction with ACEI, may have benefit in diabetics
Carvedilol and metoprolol are FDA approved

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21
Q

Initial and targe doeses for Metorpolol?

A 
Initial dose for class II 25 mg
12.5 mg for more severe

target dose 200 mg or highest tolerated dose

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22
Q

Adverse effects beta blocker as pertain to Heart Failure?

A

fluid retention and worsening heart failure
fatigue
bradycardia and heart block
hypotension
abrupt withdrawl can cause deterioration of cardiac function

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23
Q

Contraindications for beta blocker?

A

Acute decomponsated heart failure
-wait until patient is stable before starting
Dont give if already taking beta blocker for asthma
fixed airway disease is not necessarily a contraindication

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24
Q

When to take someone off a beta blocker with heart failure?

A

Leave on if taking chronic and symptoms appear, if recent initiation/ titration up then stop beta blocker

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25
Q

Effect of Furosemide on Preload? CO?

A

decrease preload by increasing Na excretion, reduce pulmonary and peripheral edema

little to no effect on heart failure

this decrease in wall may also improve systolic function

26
Q

Diuretic effect on heart failure frank starling?

A

move down the decomponsated curve without much of change to SV

27
Q

Clin use of diuretic for heart failure?

A

loop is the best
for Stage C and D (Edema)
only drugs that can adequately control fluid retention
no known effect on morbidity and mortality

28
Q

Adverse effects of Loop/ thaizide?

A

volume depletion (weigh themselves)
hypotension
worsening renal function
hypokalemia (can predispose patient to cardiac arrhythmia)

29
Q

K sparing diuretics use in heart failure pharm?

A

prevent hypokalemia associated with loop or thiazide diuretics

30
Q

Aldosterone and heart failure?

A

Aldosterone levels increase dramatically in heart failure to compensate by saving h20 and Na

ACEI only produce transient decrease

excessive aldosterone over time will cause vascular injury (hypertension) and cardiac remodeling (heart failure)

31
Q

Clin use of aldosterone antagonists?

A

patients with LVEF of 35% or less, already on ACEI and beta blocker and Stage C, Class II-IV
must monitor renal function and potassium concentrations

minimize risk of life threatening hyperkalemia
serum creatinine < 2.0 (female) 2.5 (male)
serum K < 5.0

32
Q

Big problem with aldosterone antagonists?

A

hyperkalemia

33
Q

Digoxin MOA?

A

Its a digitalis glycoside
cause a positive inotropic effect
block the ability of K to enter the cardiomyocyte in the Na/K ATPase which helps maintain Na concentration for the Na/Ca exchanger which is used in contraction of muscle

34
Q

Digoxin and postassium levels?

A

Works better with hypokalemia, hyperkalemia reduces the action Digoxin

thiazides and loops can cause hypokalemia

35
Q

Digoxin indirect effects?

A

increase vagal activity

sensitize baroreceptors and decrease sympathetic activity, decrease activity of SA and AV node

36
Q

Toxic effects Digoxin?

A

lower dose- sinus bradycardia, AV block

higher dose- increase sympathetic tone, Ca overload

37
Q

Calcium overload?

A

With digoxin, large build up of Ca in the cell, spontaneous release from SR, cause Delayed after Depolarization DAD, if large enough can reach threshold and cause an irregular contraction

cardiac arrhythmia can result

38
Q

Pharmacokinetics of DIgoxin?

A

Low therapeutic index, can easily overdose
short half life, 36-48 hours
might decrease hospitalizations
improve symptoms, quality of life, functional capacity and exercise tolerance
no effect on mortality

39
Q

Use digoxin for acute decomponsated HF?

A

not for acute

40
Q

Adverse effects of Digoxin?

A 
Cardiac arrythmias 
GI tract upset
CNS
Visual disturbance
Gynecomastia
41
Q

What is Digoxin immune Fab? Use Digoxin immune Fab?

A

digoxin ‘antidote’, Fab fragment of digoxin-specific antibody

Life threatening cases of digoxin toxicity

42
Q

Vasodilators?

A

Isosorbite dinitrate
Hydralazine

given together orally

43
Q

Hydralazine help someone with HF?

A

mainly dilates arteries

decrease afterload which increases ejection fraction

44
Q

Isosorbite dinitrate help someone with HF?

A

mainly dilates veins

decrease preload which decreases edema

45
Q

Isosorbite dinitrate and Hydralazine clin use?

A

African Americans already on diuretic, ACEI, beta blocker (Stage C Class III-IV)

In patients who cannont use and ACEI or ARB (C)

decrease mortality, not as good as ACEI

46
Q

Goal in treatment of acute decomponsated HF?

A

Relieve pulmonary congestion (reduce preload)

decrease pump failure (reduce afterload, increase contractility)

47
Q

Drugs for acute decomponsated?

A

Loop, Nitroglycerin, Nitroprusside, Nesiritide

48
Q

Loop treat acute decomponsated HF?

A

vasodilate, increase systemic venous capacitance, decrease left ventricular filling pressure

in addition to diuresis, decrease filling pressure

reduce pulmonary edema

49
Q

Concerned with loop?

A

excessive diuresis, hypotension, worse renal failure, electrolyte disturbance

50
Q

Clin use loop acute decompoinsated HF?

A

IV for volume overload

51
Q

Nitroglycerin?

A

increases NO mainly in veins

decrease preload, not much affect on afterload

52
Q

Nitroprusside?

A

increase NO in both arteries and veins
decrease preload
decrease afterload

53
Q

Nesiritde?

A

recombinant human Btype natriuretic peptide

54
Q

BNP?

A

hormone released from the ventricles, tries to counteract the vasoconstriction and Na retaining effects of NE, Ang II, and aldosterone

55
Q

Nestiride MOA?

A

activates guanyly cyclase on vascular smooth muscle cells, increase cGMP, dilate arteries, dilate veins

kidney, natriuresis

56
Q

Clin use Nestiride?

A

IV for acute decomponsated HF
added to diuretics for patients with evidence of severly symptomatic fluid overload in the absence of systemic hypotension, relief on angina, control of hypertension complicating HF

57
Q

Nestiride adverse effects?

A

Hypotension
Headache
not approved for intermittent IV infuison

58
Q

Treat stage D?

A

Dobutamine, Dopamine, Phosphodiesterase inhibitors (Inamrinone, Milrinone)

59
Q

Dobutamine?

A

activates beta 1 more than beta 2 or alpha receptors

Heart- Positive inotropic effect
Vasculature- Vasodilation

End result: increase force of contraction without significantly increase HR

60
Q

Dopamine MOA?

A

activates domaminergic, Beta, alpha receptors

low dose- vasodilate of renal, splanchnic, cerebrospinal, and coronary blood vessels
(increase renal blood flow, treat refractory edema)

high dose- positive inotropic

higher dose- vasoconstrict of arteries

61
Q

Phosphodiesterase Inhibitors?

A

increase cAMP, increase force of contraction, increase velocity of relaxation, vasodilation

62
Q

Problems with Phosphodiesterase inhibitors?

A 
intolerable side effects
minimal long term efficacy 
increase mortality with long term use
IV infusion, once stabilize wean off drug
short term, not long term

MOD 1 Quiz 2 (9 decks)

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