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pharm II exam 2 > CHF > Flashcards

CHF Flashcards

1
Q

differentiate between high output and low output heart failure

A
  • high output: heart is performing at maximum, but body needs more oxygen
    • ex: hyperthyroidism, anemia
  • low output: failure of heart; unable to keep up with normal demands of the body
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2
Q

sympathetic stimulation of the heart predisposes the heart to

A

arrhythymias

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3
Q

describe the frank starling law

A
  • as preload increases -> increased stretch -> increased contractility -> increased stroke volume
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4
Q

afterload is determined by

A
  • arterial resistance
    • aortic impedance
    • vascular resistance
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5
Q

what function of drugs will reduce preload? afterload? contractility?

A
  • preload: venodilators
  • afterload: arteriodilator drugs
  • contractility: B-blockers
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6
Q

why is contractility decreased in CHF

A

myocardial muscle fibers are stretched too far as ventricles become dilated

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7
Q

in CHF, what happens if you give a drug that decreases cardiac output

A
  • baroreceptor reflex will activate -> increased sympathetic stimulation of heart -> reflex tachycardia
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8
Q

list the cardiac contractility determinants

A
  1. sensitivity of contractile proteins to ca2+
  2. amount of Ca2+ released from SR
  3. amount of Ca2+ stored in SR
  4. amount of trigger Ca2+
  5. activity of Na-Ca exchanger: (NCX; pumps Ca2+ out)
  6. intracellular Na+ concentration and activity of Na/K ATPase
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9
Q

list other used names of Digitalis

A
  • cardiac glycoside
  • Digoxin
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10
Q

MOA of Digoxin

A
  • inhibits membrane sodium pump Na+/K+ ATPase
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11
Q

MOA of cardiac effects of digoxin

A

**inhibition of Na/K ATPase

  • increased intracellular Na+
  • decreased explusion of intracellular Ca2+
  • increased intracellular Ca2+ leads to increased SR Ca2+ stores
  • increased action-myosin interaction by Ca2+
  • increased contractility (positive inotropy)
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12
Q

explain how digoxin also slows heart rate in normal and failing hearts

A
  • Failing hearts, predominant tone is sympathetic
    • as digitalis increases myocardial contractility, sympathetic tone will be reduced
  • normal hearts: indirectly stimulates parasympathetics
    • Sensitization of arterial baroreceptors
    • Stimulation of central vagal nuclei
    • Increased SA node sensitivity to acetylcholine
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13
Q

is cardiac output increased by digitalis in a failing or normal heart

A
  • Cardiac output is increased by digitalis in the failing but not the in normal heart
    • Due to increased peripheral vasoconstriction in individuals with normal heart function
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14
Q

putting it together, list effects of digoxin

A
  • increases contractility
  • slows heart rate
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15
Q

digoxin

  • route of administration?
  • where is it excreted
A
  • oral
  • 80% excreted by kidneys, 20% by liver
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16
Q

what is the earliest sign of adverse effects of digoxin

A
  • all glycosides are toxic, narrow margin of saftey
  • earliest sign of toxicity: GI
    • N/V/D
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17
Q

adverse effects of Digoxin

A
  • CNS
    • HA, fatigue, drowsiness, hallucination
  • cardiac
    • arrhythmias: sinus bradycardia, ectopic ventricular beats, AV block, bigeminy
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18
Q

why should you measure K+ when patient is on digitalis

A

K+ and digitalis interact in two ways:

  • Both inhibit each other’s binding to Na+ , K+ -ATPase receptor thus K+ counteracts digitalis toxicity
  • K+ also reduces abnormal cardiac automaticity
  • **Therefore digitalis toxicity is treated with K+
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19
Q

intoxication treatment of digoxin

A
  1. minor (GI): discontinue or reduce digitalis
  2. moderate (arrhythmias): oral or IV potassium
  3. severe: digitalis immune fab
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20
Q

why is cardioversion not recommended in patients taking digoxin (unless patient is in V-Fib)

A
  • it will induce arrhythmias
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21
Q

Quinidine has what effect on digoxin

A
  • it displaces digoxin from tissue binding sites and enhances its toxicity
22
Q

hypokalemia has what effect on digitalis action

A
  • get more action -> increases toxicity
    • thiazides, loop diuretics
23
Q

what happens when digoxin is given with B-blocker

A

further decrease of SA or AV node acitivity

24
Q

why is digoxin not given with NE-releasing agents

A

catecholamines sensitize myocardium to digoxin -> increased toxicity

25
Q

List the phosphodiesterase inhibitors

A
  • inamrinone
  • milrinone
26
Q

inamrinone and milrinone have what main effect

A
  • positive inotropes
  • cause vasodilation
  • inodilators
27
Q

MOA of inamrinone and milrinone

A
  • inhibit cAMP phosphodiesterase
  • cause:
    • increase cAMP
    • increase in Ca2+ influx
    • significant vasodilating effect
28
Q

indication to use phosphodiesterase inhibitors

A
  • acute heart failure (pt is dying)
    • goal: increase cardiac output
29
Q

when should phosphodiesterase inhibitors not be used

A
  • long term
  • cause decreased survival compared to placebo due to arrhythmias
30
Q

low dose of dopamine has what effect

A
  • D1 receptors in kidney -> renal vasodilation
31
Q

moderate dose of dopamine has what effect

A
  • acts on B1 receptors in heart -> inotropic effect
32
Q

high dose of dopamine has what effect

A
  • acts on alpha receptors in vessels -> vasoconstriction
33
Q

when is dopamine given in heart failure? route of administration?

A
  • only in severe refractory CHF
  • IV
34
Q

MOA of dobutamine? route of administration?

A
  • selective B1-agonist
  • positive inotropic, less tachycardia
  • IV
35
Q

why are diuretics used in CHF

A
  • they decrease salt and water retention -> decreases venous pressure
    • decreased edema
    • decreased cardiac size
36
Q

list the drugs that reduce CHF mortality

A
  • aldosterone antagonist
  • B-blockers
  • ARBs
  • ACE inhibitors
37
Q

angiontensin II has what three primary effects

A
  1. direct vasoconstriction: result: increases afterload
  2. increases Na+ reabsorption in proximal tubule; releases aldosterone: result: increases preload
  3. alteres cardiovascular strucutre: result: increases remodeling
38
Q

which Potassium sparing diuretic action are used in CHF? why

A
  • Spironolactone (Aldactone®), Eplerenone (Inspra®)
  • Additional benefit by inhibiting aldosterone receptors
39
Q

ACE inhibitors have what common name ending

A

end in “…..pril”

40
Q

ARBs have what common name ending

A

end in sartan

41
Q

MOA of ACE-I

A
  • inhibits angiotensin converting enzyme
  • thus angiotensin I can’t become angiotensin II
42
Q

MOA of ARB

A
  • blocks angiotensin II from binding to the AT1 receptor
43
Q

DOC for treatment of CHF

A

ACE-inhibitors

  • effect: diminish cardiac workload
    • decrease afterload: reduce angiotensin II-induced vasoconstriction
    • decrease preload: reduce aldosterone release
44
Q

adverse effects of ACE-I

A
  • dry cough and angioedema
  • due to reduction in bradykinin metabolism
45
Q

B-blockers are used in what stages of CHF

A
  • effective only in early stages
  • dangerous in severe, end stage CHF due to negative inotropic effect
46
Q

List the vasodilators

A
  • sodium nitroprusside (nitropress)
  • isosorbide dinitrate
  • hydralazine
47
Q

why are vasodilators used in CHF

A
  • reduce preload (venodilation)
  • reduce afterload (arteriolar dilation)
  • or both
48
Q

MOA of Sacubitril/Valsartan (entresto)

A
  • contains two drugs: ARB and a neprilysin inhibitor
  • neprilysin inhibitor: leads to -> decreased vasoconstriction, decreased sodium retention, and decreased cardiac remodeling
49
Q

adverse effects of Sacubitril/Valsartan (entresto)

A
  • hypotension
  • hyperkalemia (ARB)
  • cough and angioedema
50
Q

Contraindications of Sacubitril/Valsartan (entresto)

A
  • pregnancy (ARB)
  • concurrent use with ACE inhibitor due to serious risk of angioedema

pharm II exam 2 (9 decks)

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