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
Describe Class IV antidysrhythmics.
Block slow Ca2+ influx responsible for conduction in nodal tissues. Suppress automaticity. ADRs: headache, flushing, hypotension, peripheral oedema.
26
When is verapamil used?
oral for AF and to prevent recurrence of paroxysmal supraventricular tachycardia. Care when combining with beta-blockers.
27
List the unclassified antidysrhythmic drugs.
Digoxin | Adenosine (I.V.)
28
What is the mechanism of action of adenosine in dysrhythmia?
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
What is the effect of digoxin in dysrhythmia?
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