Antidysrhythmic drugs Flashcards

1
Q

List the 4 stages of myocardial depolarisation.

A

0- Fast depolarisation, Na+ channels open, allowing an inward current
1- Na+ channels begin to close
2- Opening of Ca2+ channels, allows sustained contraction
3- Outward K+ movement
4- Slow depolarisation, due to Ca+ and Na+.

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2
Q

Which aspect of the ECG demonstrates ventricular conduction?

A

QT

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3
Q

What is used to classify dysrhythmias?

A

Site and rate

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4
Q

Compare types of atrial/supraventricular tachydysrhythmias.

A

Atrial fibrillation - persistent, irregular
Supraventricular tachycardia - rapid, regular (AV node or higher)
Paroxymal supraventricular tachycardia - intermittent

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5
Q

List drugs used to control ventricular rate.

A

Digoxin, Ca2+ channel blocker, beta-blocker

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6
Q

What is used to control sinus rhythm.

A

Direct current cardioversion

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7
Q

Compare types of ventricular dysrhythmias

A

Ventricular ectopics - premature contractions
Ventricular tachycardia - rapid, regular
Ventricular fibrillation - irregular

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8
Q

What are the two major mechanisms of dysrhythmias?

A

Abnormal pulse generation and abnormal impulse conduction/repolarisation.

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9
Q

List mechanisms of abnormal impulse generation.

A

Altered normal automaticity

Ectopic aytomaticity

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10
Q

List mechanisms of abnormal impulse conduction/depolarisation.

A

Conduction block
Re-entry circuits
After-depolarisations

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11
Q

What are the different types of conduction block?

A

1st AV block - prolonged PR interval
2nd AV block - impulses not conducted, no QRS
3rd AV block - no conduction

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12
Q

What are re-entry circuits?

A

Retrograde conduction re-exiting tissue that has already passed through the refractory period

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13
Q

What is the caused of QT prolongation in after-depolarisation?

A

Impaired K+ efflux.

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14
Q

When are antidysrhythmic drugs used?

A

Bradydysrhythmics: acutely
Tachydysrhythmics: only for life-threatening dysrhythmias or for moderate/severe symptoms

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15
Q

What drugs are used for bradycardia?

A

Acute - atropine, adrenaline, isoprenaline

Chronic - Stop bradycardic medication, pacemaker

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16
Q

List the classes of antidysrhythmics.

A

Class I - Na+ channel blockers, block conduction, phases 0, 4
Class II - beta blockers
Class III - block cardiac K+ channels and other actions, phase 3
Class IV - Ca2_ channel blockers, particularly in nodal tissue

17
Q

Describe class I antiarrhythmics.

A

Local anaesthetic properties

Block fast Na+ current at phase 0, slow cardiac conduction, depress automaticity.

18
Q

When are class I antuarrythmics used?

A

Used for ventricular and supraventricular dysrhythmias, often I.V.
Can be pro-dysrhythmic

19
Q

What gives class I antiarhythmics some selectivity?

A

Use dependent block of Na+ channels

20
Q

Lis the subclasses of class I antiarrhythmics

A

Class I A - prolongs AP
Class I B - shortens AP
Class I C - does not change AP duration

21
Q

Describe class II antidysrhythmics.

A

Reduce effects of Adr, NA and SNS (i.e. catecholamine toxicity).
Decrease sinus node automaticity and affect atrio-ventricular communication.

22
Q

When are class II antidysrhythmics used?

A

AF (exercise, mental stress), post-MI

23
Q

Describe class III antidysrhythmics.

A

Prolong AP by blocking K+ efflux, prolong refractory period (QT interval)
Can be pro-dysrhythmic as increase ventricular conduction (QT interval)

24
Q

Give examples of class III antidysrhythmics.

A
Sotalol - beta blocker with class III activity
Amiodarone - serious ADRS - thyroid, lungs, liver, deposits in eyes and skin)
25
Q

Describe Class IV antidysrhythmics.

A

Block slow Ca2+ influx responsible for conduction in nodal tissues. Suppress automaticity.
ADRs: headache, flushing, hypotension, peripheral oedema.

26
Q

When is verapamil used?

A

oral for AF and to prevent recurrence of paroxysmal supraventricular tachycardia. Care when combining with beta-blockers.

27
Q

List the unclassified antidysrhythmic drugs.

A

Digoxin

Adenosine (I.V.)

28
Q

What is the mechanism of action of adenosine in dysrhythmia?

A

Promptly converts supraventricular tachycardia to sinus rhythm
As well as working on adenosine receptors, stimulates pathways pathways similar to ACh absent in ventricles, hyperpolarises conduction tissue.

29
Q

What is the effect of digoxin in dysrhythmia?

A

Blocks atrio-ventricular conduction, slows ventricular rate in AF (may cause AV block)
Central vagal stimulation

At high doses, causes depolarisation and increased abnormal automaticity and ventricular dysrhythmia