Arrhythmias Flashcards

(59 cards)

1
Q

What is an arrhythmia?

A

An irregular heart beat

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2
Q

How are arrhythmias classified?

A

Site (atrial,nodal, ventricular) and type (irregular, tachycardia brachycardia)

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3
Q

How can irregular heart beat progress?

A

Flutter then fibrillation

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4
Q

Which sort of arrhythmia has greatest impact on cardiac output, how can they progress?

A

Ventricular arrhythmias, can progress to ventricular fibrillation (fatal)

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5
Q

What is the most common type of arrhythmia?

A

Atrial fibrillation

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6
Q

What happens in bradycardia, what can cause it?

A

Slow heart rate e.g. sinus dysfunction or heart slowing drugs e.g. beta blocker

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7
Q

What can bradycardia lead to?

A

Atrial fibrillation, cardiac arrest

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8
Q

What is treatment for bradycardia?

A
Ach receptor (M2) antagonist (e.g. atropine) to prevent slowing vagal stimulation of heart.
Implantation of pacemaker device.
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9
Q

What is atrial fibrillation, what’s the role of ectopic sites?

A

Irregular, rapid atrial contraction.

Ectopic sites where action potentials and thus atrial systoles are initiated from all over.

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10
Q

What is the effect of atrial fibrillation on ventricles?

A

AVN only intermittently activated by chaotic activity of atria so irregular ventricular function

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11
Q

How is atrial fibrillation treated?

A

Slow atrial contractions (e.g. verapamil, amiodarone, beta blocker, ivabradine)
Electrical shock treatment to restore normal rhythm

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12
Q

What is heart block?

A

Toxic effect of cardiac glycosides or, infarct encompasses AVN so wave of activity not transmitted from atria to ventircles

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13
Q

What happens to beating of atria and ventricles in heart block?

A

Atria beat at pace set by SAN but ventricles beat independently at pace set by ventricular pacemaker cells

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14
Q

What happens to hearts pumping in heart block?

A

Loss of efficiency

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15
Q

What happens in 1st degree heart block?

A

Slower conduction through AVN

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16
Q

How do you diagnose 1st degree heart block?

A

Prolonged PR interval (>0.25 secs)

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17
Q

What is 2nd degree heart block?

A

Block of AVN so partial conduction (not all impulses conducted through AVN)

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18
Q

How do you diagnose second degree block on ECG?

A

P wave blocked from initiating a QRS complex

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19
Q

What happens in 3rd degree block?

A

No conduction, ventricles contract independently of atria (at intrinsic rate of 30-40bpm)

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20
Q

How do you treat heart block?

A

Artificial pacemaker

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21
Q

How can ectopic pacemaker activity arise?

A

Ischaemic damage to SAN so other cells undertake pacemaker activity

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22
Q

Where do secondary pacemakers arise?

A

AVN and purkinjie fibres

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23
Q

What assumes pacemaker role when SAN is blocked?

A

AVN

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24
Q

What assumes pacemaker role when AVN blocked?

A

Funny current in Purkinje fibres can initiate slow pacemaler potential

25
List some anti dysrhythmic drugs?
``` By modifying AP: Local anaesthetics (lidocaine) Beta blockers Amiodarone Verapamil Ivabradine Adenosine ```
26
How does use of beta blockers and amiodarone vary based on time frame?
Beta blocker: acute | Amiodarone: chronic
27
How do L.A treat arrhythmias?
Bind VGNC Reduce abnodmal propagation Reduce abnormal impulses
28
How do LA reduce abnodmal propagation?
Extend effective refractory period (until drug dissociates from channel) so reduces risk of propagating abnodmal impulses and prevent ectopic beat occuring after sinus rhythm
29
How do LA reduce abnormal impulses?
Reduce excitability (decreased open Na+ channel so reduce spontaneous depolarisation)
30
In what state does Lidocaine bind sodium channel?
Active state
31
When do sodium channels reactivate (lidocaine)?
When lidocaine begins to dissociate
32
How is lidocaine's efficiency frequency dependent?
High frequency impulses (e.g. tachycardia, fibrilaiton) should be suppressed more than low frequency ones (e.g. sinus rhythm) as an impulse arriving soon after drug begins to dissociate will be suppressed more than impulse arriving later
33
What are the risks of lidocaine?
Reduced contractility of myocardium Block Na+ entry, so more Na+ comes in via NCX to compensate, so more Ca2+ pumped out, less Ca2+ in cell so less contractility and heart failure
34
How can lidocaine actually cause dysrhythmia?
Less Ca2+ in cell (due to NCX activity) so decreased contractility and cardiac failure Reduced perfusion of coronary arteries and ischaemia so dysrhythmia.
35
Examples of beta blockers?
Atenolol, propanolol
36
By reducing sympathetic drive, what do beta blockers do?
Reduce myocardial oxygen demand and debt Reduce pacemaker currents induced by sympathetic stimulation Reduce disaprity and shortening of action potentials associated with sympathetic drive
37
What are the chronic effects of beta blockers?
Increase AP length Reduce cardiac workload and debt Reduce platelet stickiness (reduce thromobosis and risk of myocardial ischaemia)
38
How can beta blockers increase action potential length?
Decrease K+ current that repolarises cell, increase effective refractory period, so antidsyrhythmic
39
What does ischaemia and sympathetic drive contribute to?
Arrhythmias
40
What is the side effect of beta blockers?
Fall in contractility (block SNS inotropic effects)
41
What does Amiodarone do?
Lengthen AP Reduce cardiac workload Enhances LA activity Effective refractory period
42
How can amiodarone lengthen APs?
Decrease K+ current that repolarises membrane (stage 3 cardiac AP)
43
How does reducing cardiac workload help treat arrhythmias?
Reduce myocardial infarction
44
What are side effects of amiodarone?
Reduced cardiac contractility, skin photosensitivity, thyroid disturbances
45
What is verapamil used for?
Nodal (i.e. when ca2+ current causing arrhyhmias) and ischaemic arrhythmias
46
What does Verapamil block?
L-type Ca2+ channels
47
What are the effects of verapamil?
Reduce excitability of ischaemic cells (in which depolarising current carried by Ca2+) Reduces effect of calcium in cell (causes cell uncoupling through impacting gap junctions) increase conduction and decreased spontaneous depolarisation of purely indivdual cells to encourage heart to act as syncytium
48
Why are most anti arrhythmia drugs potentially dangerous?
Negatively inotropic | Reduce coronary perfusion and thus may lead to future dysrhythmias
49
How can adenosine treat arrhythmias?
Parasympathomimetic acting on A1 receptors to activate IKAch so hyperpolarises membrane and decreasing heart rate by blocking AVN
50
What does ivabradine bind to?
Block HCN4 if channels in the SAN
51
How does ivabradine treat angina and arrhythmias?
Slows cardiac pacemaker activity, reducing myocardial oxygen demand
52
What is adenosine used for?
Supraventricular tachycardia originating in the AVN
53
Why can cardiac glycosides be used for arrhythmias, how?
Slow down heart rate, slow down refracory period of AVN
54
What sort of arrhythmia can atropine treat?
Bradycardia | 2nd or 3rd degree heart block
55
What are the discharge rates of AVN and purkinje fibres?
40-60bpm and 20-40bpm
56
What does flecainide do?
Inhibits Na+ channel, slowing upstroke of cardiac action potential
57
Why use flecainide over lidocaine?
Stronger blocker of Na+ channels
58
A compound that opens K+ channels in the atrioventricular node
Adenosine
59
What arrhythmia are cardiac glycosides used to treat?
Atrial fibrillation