Anti-Dysrhythmics PHARM Flashcards

1
Q

Propafenone
Vaughan Williams Classification Anti-Dysrhythmics

A

Class I
Blocks sodium channels
Phase 0 fast action potential in the heart
his-purkinje system, atrium/ventricle myocardium
prevents conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Propafenone
Indication

A

Acute treatment of AF

Pill in pocket cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Propafenone
MOA

A

Blocks sodium channels
blocks the fast AP in the ventricle/atrium myocardium and His-purkinje system

Decreases conduction atrium and ventricle

Prolonges PR and QT intervals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Propafenone
SE/AE

A

N/V/D/Constipation

Worsen dysrhythmias

Heart failure
More common first dose and/or Hx. MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Propafenone
Patient Educaiton

A

Report S&S heart failure
- dypsnea, SOB, nocturnal coughing, edema

Report S&S worsening dysrhythmias
- palpitations, fainting, dizziness, weakness, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Amiodarone
Vaughan Williams Classification of Anti-dysrhythmics

A

Class III
Blocks potassium channels
Blocks phase 4 of the fast action potential
His-purkinje, myocardium atrium/ventricle
Prolonges refractory period
slows automaticity/heart beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Amiodarone
Indication

A

LAST RESORT MEDICATION

Acute treatment atrial fibrillation
Pharmacological conversion
pill in pocket approach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Amiodarone
MOA

A
  1. Blocks potassium channels
    prolonges refractory of the atrium/ventricle myocardium
    slows heart beat

Prolonges PR and QT intervals

  1. Blocks sodium channels
    Phase 0 fast AP (atrium/ventricle) blocks conducion
  2. Blocks calcium channels (beta receptors)
    Phase 2 fast AP (atrium/ventricle) blocks contraction
    Phase 0 and 4, slow AP (SA and AV node) blocks conduction and automaticity

VERY STRONG DRUG
- decreases conduction
- decreases HR
- decreases contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Amiodarone
Pharmacokinetics

A

1/2 life is 25 to 110 days
four 1/2 lives to wash out (up to 1 year)
metabolized by CYP3A4
Lipid soluble
accumulates in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Amiodarone
SE/AE

A

TOXIC TO:

Heart: fatal dysrhythmias

Lungs: fibrosis, pneumonitis

Eyes: blindness, neuritis, neuropathy

Skin: Burn, blue colour

Thyroid: hypo/hyperthyroidism

Liver: failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Amiodarone
Prescriber Considerations

A

Do not combine with Class I (sodium blockers), Class II (beta blockers), or Class III (potassium blockers) - exacerbation cardiotoxicity

Do not combine with CYP3A4 inhibitors (non-dihydropyridine CCB)

Monitor
- Thyroid
- ECG
- Liver
- Vision
- X ray, PFT
- electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Sotalol
Vaughan Williams Classification Anti-dysrhythmic drugs

A

Class III
Blocks potassium channels
prevents phase 4 fast AP (ventricle/atrium, his-purkinje)
delays heart beat

Class II
Non-cardioselective beta blocker
blocks calcium channels
prevents phase 2 of the fast action potential (ventricle/atrium)
decreases contractility
prevents phase 0 of the slow action potential
decreases conduction

ECG findings
- prolonged QT interval
- prolonged PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sotalol
MOA

A
  • Decrease HR, conduction, contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sotalol
SE

A
  • bradycardia
  • AV heart blocks
  • heart failure
  • rebound tachycardia
  • impaired awareness hypoglycemia
  • hypoglycemia
  • insomnia, depression, hallucinations
  • life threatening QT dysrhtuhmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly