Anti-arrythmic drugs Flashcards

1
Q

Definition of an arrhythmia

A

Heart condition resulting in rate and/or timing of contraction which is insufficient to maintain a normal CO

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2
Q

Causes of abnormal impulse generation

A

Automatic rhythms - enhanced automaticity (more AP from SAN) or ectopic (AP not from SAN)
Triggered rhythms - conduction block (impulses not conducted from atria to ventricles) or reentry e.g WPW or post MI

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3
Q

Aim of drugs treating abnormal impulse generation

A

Decrease phase 4 slope in SAN

Raise VGNa channels threshold

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4
Q

Aim of drugs treating abnormal impulse conduction

A

Decrease conduction velocity

Increase effective refractory period

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5
Q

Prescribe phases of ventricular AP

A

0: Na influx
1: K efflux
2: Ca influx
3: K efflux
4: Na-K-ATPase mediated repolarisation

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6
Q

Which phases of ventricular AP make up the effective refractory period

A

0,1,2 and initial part of 3

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7
Q

Phases of pacemaker AP

A

0: Ca influx
2: peak of Ca influx
3: K efflux
4: HCN channel, funny current

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8
Q

What does gradient of phase 0 indicate

A

Conduction velocity

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9
Q

Treatment for sinus bradycardia

A

IV atropine

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10
Q

Treatment for stress induced arrhythmia

A

Beta blockers e.g bisoprolol or propranolol

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11
Q

MoA of atropine

A

Muscurinic antagonist which increases conduction through the AVN

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12
Q

Treatment for SVT

A

If systolic >90 vagal stimulation first, then IV adenosine

If systolic <90 do cardioversion

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13
Q

MoA of adenosine

A

Binds to A1 receptors in AVN and SAN which activates K channels.
This leads to hyper polarisation, inhibition of Ca channels and slows AVN conduction
‘Feeling of impending doom’

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14
Q

Treatment for pulseless VT

A

Defibrillator

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15
Q

Treatment for VT with pulse

A

If systolic <90 do cardioversion

If systolic >90 give amiodarone

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16
Q

Treatment for AF and atrial flutter

A

Systolic <90 do cardioversion

Systolic >90 give beta blockers, flecainide, amiodarone, digoxin

17
Q

MoA of digoxin

A

Inhibits Na-K-ATPase so has a positive ionotropic effect

Stimulates vagal activity so slows AVN conduction and increases effective refractive period

18
Q

Describe class 1A anti arrhythmia drugs and give examples

A

Procainamide, quinidine, disopyramide
Block Na channels and dissociate slowly during diastole (frequency dependent block) so they slow phase 0 and increases effective refractory period

19
Q

Describe class 1B anti arrhythmia drugs and give examples

A

Lidocaine
Block inactivated Na channels and dissociate rapidly in diastole
Ischaemic tissue more susceptible as more Na channels inactivated

20
Q

Describe class 1C anti arrhythmia drugs and give examples

A

Flecainide
Block Na channels and dissociate VERY slowly during diastole so significantly slow phase 0 and increase effective refractory period

21
Q

Describe class 2 anti arrhythmia drugs and give examples

A

Propranolol, bisoprolol, metoprolol

Have negative chronotropic effect as they increase refractory period in AVN

22
Q

Contraindications of class 2 anti arrhythmia drugs

A

Heart block

23
Q

Examples of class 3 anti arrhythmia drugs

A

Amiodarone

Sotalol

24
Q

MoA of amiodarone

A

Decreases AVN conduction

Slows phase 0 (Increases ERP)

25
Q

Side effects of amiodarone

A
Lung fibrosis
Hepatotoxic
Increased LDLs
Thyroid disease
Optic neuritis
26
Q

MoA of sotalol

A

Increase ERP
Slows phase 4
Slows AVN conduction

27
Q

Which anti arrhythmia drugs are most pro-arrhythmic

A

1A
1C
Sotalol

28
Q

Describe class 4 anti arrhythmia drugs and give examples

A

Verapamil

Diltiazem

29
Q

MoA of class 4 anti arrhythmia drugs

A

L type Ca channel blockers

Slow AVN conduction, negative ionotropic effect

30
Q

Contraindications of class 4 anti arrhythmia drugs

A

If patients on beta blockers as risk of asystole

31
Q

Treatment for secondary and tertiary heart blocks

A

Systolic >90 give atropine

Systolic <90 urgent pacemaker