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CPT > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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1
Q

How do you generate an AP in cardiac myocytes? - make reference to the phases

A
  • 0: VGNC > influx of Na+ > rapid depolarisation
  • 1: K+ efflux > slight repolarisation
  • 2: Ca2+ influx > plateau
  • 3: K+ efflux > rapid repolarisation phase
  • 4: return to RMP by Na+/K+ATPase
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2
Q

How do you generate the pacemaker potential? - make reference to the phases

A
  • 4: HCN channels open Na+ influx > funny current - intial slow depolarisation
  • threshold potential reached
  • 0: influx of Ca2+ through L type Ca2+ channels > depolarisation
  • 3: efflux of K+ > repolarisation
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3
Q

What is the Vaughan Williams classification?

A
  • class I: block voltage gated Na+ channels
  • class II: beta blockers
  • class III: potassium channel blocker
  • class IV: calcium channel blocker
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4
Q

What are the sub types of class I antiarrhythmics?
Examples

A

Class IA - procainamide
Class IB - lidocaine
Class IC - flecainide

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5
Q

Example of class IB antiarrhythmics

A

Lidocaine

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6
Q

What are the uses of lidocaine?

A

Ventricular tachycardia
Not in atrial arrhythmias

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7
Q

What is the mechanism of action of lidocaine?

A

Class IB antiarrhythmic
- Weakly blocks voltage gated Na+ channels
- Decreases AP duration + effective refractory period

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8
Q

Adverse effects of lidocaine

A

Drowsiness + dizziness
N + V

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9
Q

Example of class IC antiarrhythmics

A

Flecainide

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10
Q

What are uses of flecainide?

A

Supraventricular arrhythmias
Premature ventricular contractions
Wolff- Parkinson White syndrome

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11
Q

What is the mechanism of action of flecainide?

A

Class IC antiarrhythmic
- blocks voltage gated Na+ channel
- slows phase 0/depolarisation
- prolong QT interval
- normal effective refractory period + AP

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12
Q

What are the adverse effects of flecainide?

A
  • Drowsiness + dizziness
  • N+V
  • pro-arrhythmia + sudden death with chronic use
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13
Q

Examples of class II antiarrhythmics

A

beta blockers
Bisoprolol
Propanolol
Atenolol
Metoprolol

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14
Q

What are the uses of class II antiarrhythmics?

A

Supraventricular tachycardias
Heart failure
After MI

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15
Q

What is the mechanism of action of class II antiarrhythmics?

A

Beta blockers
- block B adrenoreceptors
- decrease sympathetic activity on heart > reduces cAMP levels > reduces Ca2+ influx
- slows AP
- prolongs repolarisation at AV node
- increased PR interval

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16
Q

What are the adverse effects of class II antiarrhymics?

A

Hypotension
Fatigue
Bronchospasm

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17
Q

What are contraindications of class II antiarrhytmics?

A

Asthma
Acute heart failure
Partial AV block

18
Q

What the important drug drug interactions of class II antiarrhymics

A

B agonists
Verapamil + Diltiazem - CCBs

19
Q

Examples of class III antiarrhythmics

A

potassium channel blockers
Amiodarone + sotalol

20
Q

What are the uses of class III antiarrhythmics?

A

Broad anti-arrhythmic activity
(most arrhythmias)

21
Q

What is the mechanism of action of class III antiarrhythmics?

A

potassium channel blockers
- block potassium channel > prolong repolarisation by inhibiting K+ efflux > prolonged AP duration

22
Q

What are the adverse effects of amiodarone?

A
  • Pulmonary fibrosis
  • Hypo/hyperthyroidism
  • Photosensitivity
  • Hepatitis
  • Increased LDL cholesterol
  • Optic neuritis > transient blindness
23
Q

What are contraindications of amiodarone?

A

Active thyroid disease
Heart block

24
Q

What are the important drug drug interactions of class III antiarrhythmics

A

Amiodarone increases [plasma] of digoxin,warfarin + verapamil

25
Q

Examples of class IV antiarrhythmics

A

CCBs - non dihydropyridine
Verapamil
Diltiazem

26
Q

What are uses of class IV antiarrhythmics?

A

Control ventricles during Supraventricular tachycardia
Convert SVTs

27
Q

What is the mechanism of action of class IV antiarrhythmics?

A

calcium channel blockers
- block calcium channels
- decrease conduction through AV node > shorten phase 0 + prolonged repolarisation at AV node
- increased PR interval
- pronged plateau phase in cardiac myocytes
- prolong depolarisation + repolarisation

28
Q

What are the adverse effects of class IV antiarrhythmics?

A

Constipation
Bradycardia
Heart block

29
Q

What are important drug drug interactions of class IV antiarrhythmics?

A

Beta blockers

30
Q

What are the 2 pathways causing arrhythmia?

A
  • generate abnormal impulses
  • conduct impulses abnormally
31
Q

Do you treat arrhythmias via rate or rhythm control?

A

Most patients - rate control
Rhythm control in younger patients

32
Q

Examples of Class V antiarrhytmics

A

Digoxin
Adenosine
Ivabradine

33
Q

What affect does digoxin have on the heart?

A
  • cardiac glycoside
  • positive inotrope
  • AV node blockage
34
Q

What affect does ivabradine have on the heart?

A

Pacemaker current inhibitors
Slows heart rate

35
Q

What effect does adenosine have on the heart?

A

Stimulates A1 adenosine receptor > AV blockage
Short lasting

36
Q

Mnemonic to remember antiarrhythmics

A

Some Block Potassium Channels
- Class I: block Sodium channels
- Class II: Beta blockers
- Class III: block Potassium channels
- Class IV: block Calcium channels

37
Q

How to remember the action of Class I antiarrhythmics

A
  • IA - After - prolongs AP
  • IB - Before - shortens AP
  • IC - normal AP
38
Q

How do you use the names of B blockers to determine their selectivity?

A

A-N β1
O-Z β1 and β2
Not “olol” ending α and β

39
Q

Full name of HCN channels

A

Hyperpolarisation-activated cycling nucleotide gated channels

40
Q

What should you warn your patient of when prescribing amiodarone?

A

It may feel like their heart has stopped

CPT (29 decks)

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