Antiarythmiques Flashcards

1
Q

Origines des troubles du rythme

A
  • troubles d’excitation < potentiel diastolique, pente de depolarisation du NS, potentiel seuil
  • troubles de conduction < re-entrees
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2
Q

Troubles d’excitation

A
  • surcharge calcique: DAD
  • QT long: EAD
  • hypokaliemie
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3
Q

Classes d’anti-arythmiques

A
  • classe I: bloquent canaux Na
    A: prolongent PA
    B: ralentissent PA
    C: pas d’effet sur la longueur
  • classe II: b-bloquants
  • classe III: prolongent periode refractaire, bloquent canaux K+
  • classe IV: anticalciques
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4
Q

IA

A

pas trop utilises

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5
Q

IB

A

lidocaine: bloque canaux Na actives et inactives
=> FV, TV, ischemie aigue

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6
Q

IC

A

flecainide: empeche extrasystoles (diminue excitabilite)
=> FA
x si pacemaker

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7
Q

II

A

sotalol: prolonge periode refractaire = allonge QT
=> arythmie SV ou V

! risque de TdP (surtout si bradycardie, hypokaliemie)

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8
Q

III

A

amiodarone: inhibe canaux Na inactives, inhibe canaux K+ (allonge QT), diminue rythme sinusal et conduction AV
(effet bB et AC)
=> arythmies SV et V

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9
Q

Effets secondaires amiodarone

A
  • hyperthyroidie (iode) -> hyperadrenergisme
  • fibrose pulmonaire (crepitants inspiratoires et expiratoires) >< IC
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10
Q

Interactions de l’amiodarone

A
  • CYP3A4
  • potentialise la digoxine
  • potentialise les anticoagulants coumariniques
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11
Q

C.I. amiodarone

A

grossesse

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12
Q

IV

A

verapamil: inotrope et chronotrope -, inhibe canaux Ca donc ralentit rythme NS et conduction NAV
=> arythmies SV

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13
Q

danger verapamil

A

pas avec b1-bloquant: risque de BAV

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14
Q

adenosine

A

bloque canaux K+ = hyperpolarisation
couples a prot Gai qui inhibe l’AMPc et diminue le Ca
=> TSV

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15
Q

interactions adenosine

A

dypiridamole la potentialise

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