Arrhythmias and anti-arrhythmic drugs Flashcards

1
Q

Defects in impulse conduction

A

Re-entry
Conduction block
Accessory tracts

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2
Q

Defects in impulse formation

A

Altered automacity

Triggered activity

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3
Q

Altered automacity (physiological)

A

Modulation of SA node activity by the ANS

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4
Q

Altered automacity (pathological)

A

Latent pacemaker takes over SA node function

  • when SA node firing frequency is low
  • if a latent pacemaker fires faster than the SA node rate
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5
Q

Triggered activity (EAD)

A

Can occur in phase 2 or 3 of the ventricular AP

Prolonged AP

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6
Q

Triggered activity (DAD)

A

Normal AP is followed by a depolarising event

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7
Q

Re-entry

A

Conduction pathway of heart divides into 2 branches.
AP comes down the branches but collides with each other at a point so AP’s can’t progress further.

Uni-directional block: 
AP can't progress down normal route of 2 branches and can therefore only go down 1 branch. 
Slow backwards (retrograde) AP can occur at the non functioning branch so AP conducts slowly back up to the start of branch 1 again and the process repeats.
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8
Q

First degree heart block (conduction block)

A

Prolonged PR interval

Treatment: none

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9
Q

Mobitz type 1 second degree heart block (conduction block)

A

PR interval progressively increases until a QRS complex is missed resulting in a missed ventricular beat.

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10
Q

Mobitz type 2 second degree heart block (conduction block)

A

PR interval is normal
Every ‘nth’ impulse fails to go through the AVN (i.e. no QRS complex)
Some P waves followed by QRS complexes, some not
QRS:Non-QRS - 2:1 or 3:1 ratio usually
Management: ventricular pacing

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11
Q

Third degree -complete- heart block (conduction block)

A

Atria and ventricles work independently
P waves don’t link to QRS complexes
Management: ventricular pacing

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12
Q

Accessory tract pathways

A

Usually - only point of electrical contact between A&V is AV node.

Bundle of Kent - extra tissue between A&V which bypasses the AVN. Impulse is conducted more quickly than that through AVN

Eg: WPW syndrome where delta wave excites ventricle before the normal QRS complex

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13
Q

Anti-arrhythmic drugs: Class IA

A
Blocks voltage activated Na+ channels 
Moderate rate 
Cardiac AP - phase 0
Prolongs refractory period
eg: disopyramide
Rhythm control
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14
Q

Anti-arrhythmic drugs: Class IB

A
Blocks voltage activated Na+ channels
Fast rate
Cardiac AP - phase 0
Prevents premature beats 
Rhythm control
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15
Q

Anti-arrhythmic drugs: Class IC

A
Blocks voltage activated Na+ channels 
Slow rate 
Cardiac AP - phase 0
Depress conduction
eg: flecanide
Rhythm control
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16
Q

Anti-arrhythmic drugs: Class II

A
Blocks B-adrenoceptors 
(eg: metoprolol) 
Cardiac AP - phase 4
Decreased rate of depolarisation at SA/AV node 
Rate control
17
Q

Anti-arrhythmic drugs: Class III

A
Blocks voltage activated K+ channels 
EG: amiodarone, sotalol 
Cardiac AP - phase 3
Prolongs AP duration 
Increased refractory period 
Rhythm control
18
Q

Anti-arrhythmic drugs: Class IV

A
Blocks voltage activated Ca2+ channels
EG: verapamil 
Cardiac AP - phase 2
Slows conduction in SA and AV nodes 
Decreases force of contraction
Rate control
19
Q

Adenosine

A

Useful to treat SVT but not VT
Very short acting
Administration route: IV bolus

20
Q

Arrhythmia investigations

A
ECG 
24 hr ECG 
Exercise ECG 
Echo
CXR 
Electrophysiological study - induce arrhythmia to study mechanism