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CVS II > Anti Arrhythmic Drugs > Flashcards

Anti Arrhythmic Drugs Flashcards

1
Q

What’s the QT duration in ECG?

A

refractory phase of non-nodal AP

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2
Q

Define arrhythmia

A

abnormalities in heart rhythm

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3
Q

Symptoms of arrhythmia?

A

palpitations, dizzy, faint, fatigue, unconscious, cardiac arrest, blood coagulation (stroke, MI)

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4
Q

Causes of arrhythmia?

A

cardiac ischemia (MI, angina), heart failure, hypertension, coronary vasospasm, heart block, excess sympathetic stimulation

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5
Q

Origin of arrhythmia?

A

supraventricular (above ventricles SAN, atria, AVN) or ventricular

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6
Q

Effect of arrhythmia on heart rate?

A

Tachycardia (>100 bpm) or Bradycardia (<60 bpm)

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7
Q

How does arrhythmia affect CO?

A

lead to incorrect filling + ejection –>incorrect CO

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8
Q

What are common arrhythmias?

A

atrial fibrillation (AF), supraventricular tachycardia (SVT), heart block, ventricular tachycardia (VT), ventricular fibrillation (VF)

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9
Q

What’s atrial fibrillation (AF)?

A

Quivering atria activity (no P wave)
Irregular ventricular contraction
‘Clot-producing’ – risk of stroke

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10
Q

What’s supraventricular tachycardia (SVT)?

A

P wave buried in T wave

Fast ventricular contractions

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11
Q

What’s heart block?

A

Failure of conduction system (SA, AV, or bundle of his)

Uncoordinated atria/ventricular contractions

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12
Q

What’s ventricular tachycardia (VT)?

A

Fast, regular

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13
Q

What’s ventricular fibrillation (VF)?

A

Fast, irregular

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14
Q

Why’s there no P waves in atrial fibrillation (AF)?

A

atria depolarising + repolarising all the time

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15
Q

How does atrial fibrillation (AF) cause stroke?

A

blood not ejected from atria so clot,can move to L ventricle -> aorta -> brain ->

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16
Q

Mechanisms of arrhythmogenesis?

A

Abnormal Impulse Generation

Abnormal Conduction

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17
Q

Causes of abnormal impulse generation?

A

Automatic rhythms -↑ SAN activity, ectopic activity

Triggered rhythms -Early after depolarisations (EADs), delayed-after depolarisations (DADs)

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18
Q

Causes of abnormal conduction?

A

Re-entry electrical circuits

Conduction block

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19
Q

What’s ectopic pacemaker activity

A 
other heart areas have pacemaker activity to safeguard against SAN damage
SAN= 60-70/s
AVN= 40-60 /s
Bundle of His= 30-40/s 
Purkinje fibres= 15-25/s
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20
Q

How’s ectopic pacemaker activity increased?

A

sympathetic nerve activity by increasing: HR, AVN conduction, excitability of ventricular tissue

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21
Q

How does ectopic pacemaker increased activity cause arrhythmia?

A

continuous/enhanced sympathetic stimulation –> stress, heart failure –> arrhythmia

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22
Q

How does early after depolarisations (EADs) + delayed-after depolarisations (DADs) cause arrhythmia?

A 
Abnormal levels of Ca2+ in SR
Ca2+ leaks into cytosol - diastolic leak
Stimulate Na/Ca exchanger (NCX)
1 Ca2+ out and 3 Na+ in – depolarisation
Altered ion channel activity - no refractory period
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23
Q

How are re-entry pathways produced?

A

damaged myocardium so some heart areas more conductive

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24
Q

Why do AP stop conducting?

A

surrounding tissue refractory

25
Q

How is heart block produced?

A

fibrosis / ischaemic damage of conducting pathway-AVN issue

26
Q

What’s 1st degree heart block?

A

PR interval > 0.2 s

27
Q

What’s 2nd degree heart block?

A

> 1 atria impulses fail to stimulate ventricles

28
Q

What’s 3rd degree heart block?

A

complete block, atria + ventricles beat independently of one another

29
Q

Why do the ventricles contract at slow rate?

A

SAN pacemaker potential generating activity in atrium but disconnected to ventricles so bundle of his + purkinje fibres generate own electrical activity (ectopic)

30
Q

Why can heart block cause?

A

unconsciousness, Adams-Stokes attacks – syncope

31
Q

Goals of arrhythmia treatment?

A
  • Restore sinus rhythm + normal conduction

- Prevent more serious + fatal arrhythmia occurring

32
Q

What can anti-arrhythmia drugs do?

A

Reduce conduction velocity
Alter refractory period
Reduce automaticity (decrease EADs, DADs, ectopics)

33
Q

What’s the anti-arrhythmia drugs classification based on?

A

Vaughan Williams classification system

34
Q

What’s class I anti-arrhythmia drug?

A

Na+ channel blockers (non-nodal tissue)

-reduces upstroke

35
Q

What’s class II anti-arrhythmia drug?

A

β blockers (nodal and non-nodal tissue)

-reduces sympathetic on heart so affects both AP

36
Q

What’s class III anti-arrhythmia drug?

A

K+ channel blockers (non-nodal tissue)

-not repolarising quickly, increasing AP length increases refractory period

37
Q

What’s class IV anti-arrhythmia drug?

A

Ca2+ channel blockers (nodal and non-nodal tissue)

-affects upstroke in nodal + plateau in non-nodal

38
Q

Features of class I anti-arrhythmia drugs?

A

Block Na+ channels in non-nodal tissue (atria/ventricles)

Has use-dependence : only block Na+ channels in high frequency firing tissue cause in INACTIVATED state

39
Q

Describe how class I anti-arrhythmia drugs work on high frequency firing tissue

A
  • binds to inactivated Na+ channel
  • fast dissociating drug (off channels in <0.5 s)
  • still bound to inactivate site when next impulse arrives
  • inhibits high frequencies
40
Q

Describe how class I anti-arrhythmia drugs work on normal frequency firing tissue

A
  • binds to inactivated Na+ channel
  • fast dissociating drug (off channels in <0.5 s)
  • drugs comes off inactivate site for next impulse
  • no effect on normal firing
41
Q

What’s Lidocaine?

A 
class I anti-arrhythmia drug
for fast arrhythmia (VT + VF)
42
Q

Describe how class II anti-arrhythmia drugs work

A

Blocks β1 in heart so reducing sympathetic :
decrease in SAN + AVN firing rate
decrease [Ca2+] so reduce ventricular excitability

43
Q

What’s Atenolol?

A 
class II anti-arrhythmia drug
reduce VT after myocardial infarctions + slow conduction via AVN to reduce ventricular firing rate in SVT
44
Q

Describe how class III anti-arrhythmia drugs work

A
  • inhibit K+ channels responsible for repolarisation in atria/ventricles
  • increases QT duration so slower repolarisation
  • maintains depolarisation
  • Na+ channels inactivated so can’t fire more AP
45
Q

What’s Amiodaron?

A 
class III anti-arrhythmia drugs
for SVT + VT
46
Q

What’s Sotalol?

A 
class III anti-arrhythmia drugs + combined class II actions
for SVT + VT
47
Q

Describe how class IV anti-arrhythmia drugs work

A

Block L-type vgcc:
affects phase 0 firing of SAN + AVN
affects phase 2 of atria/ventricle
affects vascular smooth muscle so vasodilation of blood vessels + reduce BP

48
Q

What’s Verapamil?

A 
class IV anti-arrhythmia drug
cardiac specific - control ventricular response rate in SVT
49
Q

What’s Diltiazem?

A 
class IV anti-arrhythmia drug
cardiac + vascular smooth muscle - control ventricular response rate in SVT
50
Q

What’s Adenosine?

A

non-classified
decreases activity in SAN + AVN
used for SVT

51
Q

What’s Atropine?

A

non-classified
Mus antagonist
reduce para activity
used to treat sinus bradycardia after MI

52
Q

What’s Digoxin?

A

non-classified
central effects, increases vagus activity, decrease HR + conduction
used for AF

53
Q

How can anti-arrhythmic drugs be pro-arrhythmic?

A
  • Class III drugs increases QT duration, long QT syndrome –> EADs + DADs - arrhythmia
  • Classes I, II, IV increase refractory period (less SA, AV, atria/ventricular firing) + reduce conduction time
  • Class IV reduce contractility
54
Q

What’s torsades de pointes?

A

ventricular tachycardia

55
Q

Goal of sinus tachycardia + treatment?

A

Slow down SAN

Class II, III

56
Q

Goal of AF + treatment?

A

Reduce atria activity, return of atria output, prevent clot formation
II, III, IV, digoxin + anticoagulants

57
Q

Goal of SVT + treatment?

A

Reduce ventricular response rate

Class II, III, IV

58
Q

Goal of heart block + treatment?

A

Coordinate atria/ventricular contractions

pacemaker

59
Q

Goal of VT + VF + treatment?

A

Reduce ventricular activity, return ventricular output

Class I, II, III

CVS II (19 decks)

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