Anti-Arrhythmics Flashcards

1
Q

how does NE beta 1 receptor activation lead to arrhythmia?

A

increases irritability of foci which may lead to arrhythmias (excess stimulation)

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2
Q

what does NE alpha receptor binding activate?

A

contraction/vasoconstriction

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3
Q

what does ACTIVATION of presynaptic alpha 2 receptor result in?

A

feedback inhibition of NE release (e.g., clonidine acts on this to decrease BP)

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4
Q

what does INHIBITION of presynaptic alpha 2 receptor result in?

A

increase release of NE

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5
Q

What are class I AADs?

A

sodium/fast channel blockers

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6
Q

What are class II AADs?

A

beta blockers

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7
Q

what are class III AADs?

A

potassium channel blockers

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8
Q

What phase do Class I AADs affect?

A

phase 0 (sodium influx)

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9
Q

What phase do Class II AADs affect?

A

phase 4

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10
Q

what phase do Class III AADs affect?

A

phase 2 (plateau phase- potassium efflux)

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11
Q

what phase do class IV AADs affect?

A

phase 2 (plateau phase- calcium influx)

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12
Q

what are class IV AADs?

A

calcium channel blockers

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13
Q

What are examples of Class IA AADs?

A

quinidine, ajmaline, procainamide, disopyramide

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14
Q

What are examples of Class IB AADs?

A

lidocaine, mexiletine, tocainide

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15
Q

What are examples of Class IC AADs?

A

encainide, flecainide, propafenone, moricizine

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16
Q

What are examples of Class II AADs?

A

carvedilol, propranolol, esmolol, timolol, metoprolol, atenolol, bisoprolol, nebivolol

17
Q

What are examples of Class III AADs?

A

amiodarone, sotalol, ibutilide, dofetilide, dronedarone

18
Q

What are examples of Class IV AADs?

A

verapamil, diltiazem

19
Q

What are examples of Class V AADs?

A

adenosine, digoxin, magnesium sulfate

20
Q

what are arrhythmia tx goals?

A
  1. fix abnormal automaticity by prolonging refractory period (phase 2-3)
  2. suppress re-entry by prolonging refractory period (phase 2-3)
  3. suppress triggered activity
21
Q

why has AAD use declined?

A

increased risk mortality and more effective defibrillators