Antiarrhythmic drugs Flashcards

1
Q

Procainamide MOA

A

Class 1a

  • Na+ channel blocker=primary
  • K+ channel blocker=secondary
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2
Q

Procainamide effects

A

Slows conduction velocity and pacemaker rate

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3
Q

Procainamide clinical applications

A

Atrial and ventricular arrhythmias

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4
Q

Procainamide side effects

A
  1. Torsades de pointes in pt’s with renal failure
  2. Hypotension
  3. Long term: Reversible lupus-related sx’s
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5
Q

Lidocaine MOA

A

Class 1b

  • Weak Na+ channel blocker
  • Minimal effect on normal tissue
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6
Q

Lidocaine Clinical applications

A

Ventricular arrhythmias (post-MI)

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7
Q

Lidocaine toxicity

A

Neurologic sx’s: CNS sedation or excitation

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8
Q

Who do we want to reduce Lidocaine dose in?

A
  1. HF pt’s

2. Liver dz pt’s

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9
Q

Flecainide MOA

A

Group 1c

-Strong Na+ channel blocker

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10
Q

Flecainide effects

A

No change in AP duration

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11
Q

Flecainide Clinical application

A

Treat supra ventricular arrhythmias (SVT) in pt’s with a NORMAL HEART

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12
Q

Who do we want to avoid giving Flecainide to?

A

Ischemic heart disease pt’s (post-MI)

Pro-arrhythmic

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13
Q

Class II drugs

A

Beta-Blockers

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14
Q

Beta-Blockers effects

A

Prolongation of AP duration

  1. Slows SA node automaticity
  2. Slows AV nodal conduction velocity
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15
Q

Beta-Blocker Clinical applications

A
  1. Atrial arrhythmias

2. Prevention of recurrent infarction an sudden death

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16
Q

Beta-Blocker toxicity

A
  1. Asthma
  2. AV block
  3. Acute HF
17
Q

Class III drug

A
  1. Amiodarone

2. Dofetilide

18
Q

Amiodarone MOA

A

Blocks K+ channels

19
Q

Amiodarone effects

A
  1. Prolongs QT (repolarization)

2. Prolongs AP= Prolongs effective refractory period!!!

20
Q

Amiodarone clinical applications

A
  1. Serious Ventricular arrhythmias

2. SVT

21
Q

Amiodarone toxicity

A
  1. Thyroid dysfunction: Hyper-hypothyroidsim
  2. Pulmonary fibrosis
  3. Optic neuritis
22
Q

Amiodarone drug interaction

A

Many, based on CYP metabolism

23
Q

What is considered the blue/ash man drug? Why? How do you protect against this?

A
  1. Drug: Amiodarone
  2. Photosensitivity: blue/gray skin
  3. WEAR SUNBLOCK
24
Q

What drug has to be initiated in the hospital? Why?

A

Dofetilide

–>Torsades de point toxicity

25
Q

Class IV drugs

A

Calcium channel blockers:

  1. Verapamil
  2. Diltiazem
26
Q

Effects of CCB

A
  1. Slows AV node conduction

2. Slows SA node

27
Q

Verapamil clinical application

A
  1. AV nodal arrhythmias-especially in prophylaxis
28
Q

Diltiazem clinical applications

A

Rate control in a-fib

29
Q

CCB side effects

A
  1. Constipation

2. Hypotension

30
Q

Magnesium clinical application

A
  1. Torsades de pointes

2. Digitalis induced arrhythmias

31
Q

Magnesium toxicity

A

Muscle weakness with overdose

32
Q

What does Magnesium oppose?

A

Calcium

33
Q

What ion is critical to functionality of Ca2+ channels and Na+/K+ ATPase pump?

A

Magnesium

34
Q

Potassium toxicity?

A
  1. Reentrant arrhythmia

2. Fibrillation or arrest in overdose

35
Q

Adenosine MOA

A

Increases K+ efflux of SA and AV node= hypwrpolarazing cell and decreasing frequency of cellular activation

36
Q

Adenosine clinical application

A

Paroxysmal SVT

37
Q

Adenosine toxicities

A
  1. Flushing
  2. Chest tightness-“heart will stop”
  3. Dizziness/Hypotension
  4. Dyspnea