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Cardiovascular physiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

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
Q

List some anti dysrhythmic drugs?

A 
By modifying AP:
Local anaesthetics (lidocaine)
Beta blockers
Amiodarone
Verapamil
Ivabradine 
Adenosine
26
Q

How does use of beta blockers and amiodarone vary based on time frame?

A

Beta blocker: acute

Amiodarone: chronic

27
Q

How do L.A treat arrhythmias?

A

Bind VGNC
Reduce abnodmal propagation
Reduce abnormal impulses

28
Q

How do LA reduce abnodmal propagation?

A

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
Q

How do LA reduce abnormal impulses?

A

Reduce excitability (decreased open Na+ channel so reduce spontaneous depolarisation)

30
Q

In what state does Lidocaine bind sodium channel?

A

Active state

31
Q

When do sodium channels reactivate (lidocaine)?

A

When lidocaine begins to dissociate

32
Q

How is lidocaine’s efficiency frequency dependent?

A

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
Q

What are the risks of lidocaine?

A

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
Q

How can lidocaine actually cause dysrhythmia?

A

Less Ca2+ in cell (due to NCX activity) so decreased contractility and cardiac failure
Reduced perfusion of coronary arteries and ischaemia so dysrhythmia.

35
Q

Examples of beta blockers?

A

Atenolol, propanolol

36
Q

By reducing sympathetic drive, what do beta blockers do?

A

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
Q

What are the chronic effects of beta blockers?

A

Increase AP length
Reduce cardiac workload and debt
Reduce platelet stickiness (reduce thromobosis and risk of myocardial ischaemia)

38
Q

How can beta blockers increase action potential length?

A

Decrease K+ current that repolarises cell, increase effective refractory period, so antidsyrhythmic

39
Q

What does ischaemia and sympathetic drive contribute to?

A

Arrhythmias

40
Q

What is the side effect of beta blockers?

A

Fall in contractility (block SNS inotropic effects)

41
Q

What does Amiodarone do?

A

Lengthen AP
Reduce cardiac workload
Enhances LA activity Effective refractory period

42
Q

How can amiodarone lengthen APs?

A

Decrease K+ current that repolarises membrane (stage 3 cardiac AP)

43
Q

How does reducing cardiac workload help treat arrhythmias?

A

Reduce myocardial infarction

44
Q

What are side effects of amiodarone?

A

Reduced cardiac contractility, skin photosensitivity, thyroid disturbances

45
Q

What is verapamil used for?

A

Nodal (i.e. when ca2+ current causing arrhyhmias) and ischaemic arrhythmias

46
Q

What does Verapamil block?

A

L-type Ca2+ channels

47
Q

What are the effects of verapamil?

A

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
Q

Why are most anti arrhythmia drugs potentially dangerous?

A

Negatively inotropic

Reduce coronary perfusion and thus may lead to future dysrhythmias

49
Q

How can adenosine treat arrhythmias?

A

Parasympathomimetic acting on A1 receptors to activate IKAch so hyperpolarises membrane and decreasing heart rate by blocking AVN

50
Q

What does ivabradine bind to?

A

Block HCN4 if channels in the SAN

51
Q

How does ivabradine treat angina and arrhythmias?

A

Slows cardiac pacemaker activity, reducing myocardial oxygen demand

52
Q

What is adenosine used for?

A

Supraventricular tachycardia originating in the AVN

53
Q

Why can cardiac glycosides be used for arrhythmias, how?

A

Slow down heart rate, slow down refracory period of AVN

54
Q

What sort of arrhythmia can atropine treat?

A

Bradycardia

2nd or 3rd degree heart block

55
Q

What are the discharge rates of AVN and purkinje fibres?

A

40-60bpm and 20-40bpm

56
Q

What does flecainide do?

A

Inhibits Na+ channel, slowing upstroke of cardiac action potential

57
Q

Why use flecainide over lidocaine?

A

Stronger blocker of Na+ channels

58
Q

A compound that opens K+ channels in the atrioventricular node

A

Adenosine

59
Q

What arrhythmia are cardiac glycosides used to treat?

A

Atrial fibrillation

Cardiovascular physiology (11 decks)

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