Antiarrhythmics Flashcards

(39 cards)

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

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
Examples of class IV antiarrhythmics
**CCBs** - non dihydropyridine Verapamil Diltiazem
26
What are uses of class IV antiarrhythmics?
Control ventricles during Supraventricular tachycardia Convert SVTs
27
What is the mechanism of action of class IV antiarrhythmics?
**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
What are the adverse effects of class IV antiarrhythmics?
Constipation Bradycardia Heart block
29
What are important drug drug interactions of class IV antiarrhythmics?
Beta blockers
30
What are the 2 pathways causing arrhythmia?
- generate abnormal impulses - conduct impulses abnormally
31
Do you treat arrhythmias via rate or rhythm control?
Most patients - rate control Rhythm control in younger patients
32
Examples of Class V antiarrhytmics
Digoxin Adenosine Ivabradine
33
What affect does digoxin have on the heart?
- cardiac glycoside - positive inotrope - AV node blockage
34
What affect does ivabradine have on the heart?
Pacemaker current inhibitors Slows heart rate
35
What effect does adenosine have on the heart?
Stimulates A1 adenosine receptor > AV blockage Short lasting
36
Mnemonic to remember antiarrhythmics
**Some Block Potassium Channels** - **Class I**: block Sodium channels - **Class II**: Beta blockers - **Class III**: block Potassium channels - **Class IV**: block Calcium channels
37
How to remember the action of Class I antiarrhythmics
- **IA** - After - prolongs AP - **IB** - Before - shortens AP - **IC** - normal AP
38
How do you use the names of B blockers to determine their selectivity?
A-N β1 O-Z β1 and β2 Not “olol” ending α and β
39
Full name of HCN channels
Hyperpolarisation-activated cycling nucleotide gated channels