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CVS II > Anti Arrhythmic Drugs > Flashcards

Anti Arrhythmic Drugs Flashcards

(59 cards)

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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?

Study These Flashcards
A

surrounding tissue refractory

25
How is heart block produced?
fibrosis / ischaemic damage of conducting pathway-AVN issue
26
What's 1st degree heart block?
PR interval > 0.2 s
27
What's 2nd degree heart block?
>1 atria impulses fail to stimulate ventricles
28
What's 3rd degree heart block?
complete block, atria + ventricles beat independently of one another
29
Why do the ventricles contract at slow rate?
SAN pacemaker potential generating activity in atrium but disconnected to ventricles so bundle of his + purkinje fibres generate own electrical activity (ectopic)
30
Why can heart block cause?
unconsciousness, Adams-Stokes attacks – syncope
31
Goals of arrhythmia treatment?
- Restore sinus rhythm + normal conduction | - Prevent more serious + fatal arrhythmia occurring
32
What can anti-arrhythmia drugs do?
Reduce conduction velocity Alter refractory period Reduce automaticity (decrease EADs, DADs, ectopics)
33
What's the anti-arrhythmia drugs classification based on?
Vaughan Williams classification system
34
What's class I anti-arrhythmia drug?
Na+ channel blockers (non-nodal tissue) | -reduces upstroke
35
What's class II anti-arrhythmia drug?
β blockers (nodal and non-nodal tissue) | -reduces sympathetic on heart so affects both AP
36
What's class III anti-arrhythmia drug?
K+ channel blockers (non-nodal tissue) | -not repolarising quickly, increasing AP length increases refractory period
37
What's class IV anti-arrhythmia drug?
Ca2+ channel blockers (nodal and non-nodal tissue) | -affects upstroke in nodal + plateau in non-nodal
38
Features of class I anti-arrhythmia drugs?
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
Describe how class I anti-arrhythmia drugs work on high frequency firing tissue
- 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
Describe how class I anti-arrhythmia drugs work on normal frequency firing tissue
- 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
What's Lidocaine?
``` class I anti-arrhythmia drug for fast arrhythmia (VT + VF) ```
42
Describe how class II anti-arrhythmia drugs work
Blocks β1 in heart so reducing sympathetic : decrease in SAN + AVN firing rate decrease [Ca2+] so reduce ventricular excitability
43
What's Atenolol?
``` class II anti-arrhythmia drug reduce VT after myocardial infarctions + slow conduction via AVN to reduce ventricular firing rate in SVT ```
44
Describe how class III anti-arrhythmia drugs work
- 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
What's Amiodaron?
``` class III anti-arrhythmia drugs for SVT + VT ```
46
What's Sotalol?
``` class III anti-arrhythmia drugs + combined class II actions for SVT + VT ```
47
Describe how class IV anti-arrhythmia drugs work
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
What's Verapamil?
``` class IV anti-arrhythmia drug cardiac specific - control ventricular response rate in SVT ```
49
What's Diltiazem?
``` class IV anti-arrhythmia drug cardiac + vascular smooth muscle - control ventricular response rate in SVT ```
50
What's Adenosine?
non-classified decreases activity in SAN + AVN used for SVT
51
What's Atropine?
non-classified Mus antagonist reduce para activity used to treat sinus bradycardia after MI
52
What's Digoxin?
non-classified central effects, increases vagus activity, decrease HR + conduction used for AF
53
How can anti-arrhythmic drugs be pro-arrhythmic?
- 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
What's torsades de pointes?
ventricular tachycardia
55
Goal of sinus tachycardia + treatment?
Slow down SAN | Class II, III
56
Goal of AF + treatment?
Reduce atria activity, return of atria output, prevent clot formation II, III, IV, digoxin + anticoagulants
57
Goal of SVT + treatment?
Reduce ventricular response rate | Class II, III, IV
58
Goal of heart block + treatment?
Coordinate atria/ventricular contractions | pacemaker
59
Goal of VT + VF + treatment?
Reduce ventricular activity, return ventricular output | Class I, II, III

CVS II (19 decks)

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