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Arrhythmia Flashcards

1
Q

What is an arrhythmia?

A

This is a condition in which there are disturbances in the electrophysiology of the heart

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2
Q

What are the 2 causes of arrhythmia?

A

Abnormal impulse formation
Abnormal impulse conduction

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3
Q

What are the 2 types of abnormal impulse formation?

A

Triggered rhythms
Automatic rhythms

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4
Q

What can cause a triggered rhythm?

A

Ectopic foci
Enhanced normal automaticity

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5
Q

What is an ectopic beat?

A

This is a beat that originates in places other than the sino-atrial node

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6
Q

What is meant by enhanced normal automaticity?

A

This is an increased frequency of action potentials from the sino-atrial node

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7
Q

What are some possible causes of enhanced normal automaticity?

A

Ischaemia
Abnormal catecholamine production

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8
Q

What is meant by an automatic rhythm?

A

This is the formation of an abnormal after-depolarisation

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9
Q

What are the 2 types of abnormal after-depolarisation?

A

Early after depolarisation (Phase 2 or 3)
Delayed after depolarisation (Phase 4)

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10
Q

What are the 2 types of abnormal impulse conduction?

A

Conduction block
Re-entry

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11
Q

What is conduction (Heart) block?

A

This is when there’s an obstruction of the normal impulses that travel down the heart

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12
Q

What are the 2 types of re-entrant rhythms?

A

Circus movement (Re-entrant tachycardia)
Reflection

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13
Q

What are some forms of cardiac abnormality that can lead to an arrhythmia?

A

Congenital heart defects
Accessory pathway formation

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14
Q

How can the autonomic nervous system cause arrhythmias?

A

Increased sympathetic tone causes a tachycardia, while increased vagal tone causes a bradycardia

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15
Q

What are some metabolic conditions that can cause tachycardias?

A

Hypoxia
Hyperthermia
Hypercapnia
Myocardial stretch

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16
Q

What are some metabolic conditions that can cause bradycardias?

A

Hypothermia
Hyperkalaemia

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17
Q

What are some symptoms of general arrhythmia?

A

Palpitations
Dyspnoea
Faintness
Shock
Syncope
Death
Anxiety
Heart failure

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18
Q

What are some investigations required in arrhythmia?

A

12-Lead ECG
Stress ECG or 24-hour Holter ECG
Blood testing
CXR
Echocardiography
Electrophysiological study

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19
Q

What occurs in an electrophysiological study?

A

An arrhythmia can be induced, to study the arrhythmia and map the arrhythmia
The region causing the arrhythmia can then be cauterised via catheter radioablation

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20
Q

What are the 2 types of tachycardia?

A

Broad complex tachycardia
Narrow complex tachycardia

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21
Q

What is meant by a broad complex tachycardia?

A

This is a fast heart rate with a QRS duration of >0.12 seconds (3 small squares)

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22
Q

What is meant by a narrow complex tachycardia?

A

This is a fast heart rate with a QRS duration of <0.12 seconds (3 small squares)

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23
Q

What are the 4 main differentials of narrow complex tachycardia?

A

Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter

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24
Q

What are the 4 main differentials of broad complex tachycardia?

A

Ventricular tachycardia
Polymorphic ventricular tachycardia
Atrial fibrillation with bundle branch block
SVT with bundle branch block

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25
Q

What is ventricular tachycardia?

A

This is an arrhythmia resulting in a regular, fast heart rate, usually caused by an underlying disease

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26
Q

What are some possible causes of ventricular tachycardia?

A

Coronary artery disease
Previous MI
Cardiomyopathy
Iatrogenic
Idiopathic

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27
Q

What are the 2 forms of ventricular tachycardia?

A

Monomorphic ventricular tachycardia
Polymorphic ventricular tachycardia

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28
Q

What pathways lead to monomorphic ventricular tachycardia?

A

Enhanced automaticity
Re-entrant circuit in the ventricle

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29
Q

What pathways lead to polymorphic ventricular tachycardia?

A

Abnormal ventricular re-polarisation

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30
Q

What are some causes of polymorphic ventricular tachycardia?

A

Long QT syndrome
Drug toxicity
Electrolyte imbalance

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31
Q

What are some symptoms of ventricular tachycardia?

A

Pre-syncope
Syncope
Hypotension
Cardiac arrest

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32
Q

What is the average heart rate range in ventricular tachycardia?

A

120 - 220 bpm

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33
Q

How will monomorphic ventricular tachycardia appear on ECG?

A

Constant QRS morphology
Broad complex rhythm
Rapid rate

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34
Q

How will polymorphic ventricular tachycardia appear on ECG?

A

Broad QRS complexes that very in amplitude

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35
Q

What is Torsades de pointes?

A

This is a specific polymorphic ventricular tachycardia, associated with long QT intervals and QRS complexes that appear to twist around the isoelectric line

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36
Q

What does Torsades de pointes translate to?

A

Twisting of the points

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37
Q

What are some possible causes of Torsades de pointes?

A

Type I anti-arrhythmics (Na+)
Type III anti-arrhythmics (K+)

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38
Q

What does Torsades de pointes look like on ECG?

A

Long QT
Long QRS
Twisting of the QRS complexes about the isoelectric line

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39
Q

How is unstable ventricular tachycardia, with a pulse treated?

A

Direct Current Cardioversion (DCCV)

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40
Q

How is pulseless ventricular tachycardia treated?

A

Defibrillation (Shockable rhythm of cardiac arrest)
Adrenaline
Amiodarone

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41
Q

How is stable ventricular tachycardia treated?

A

1st - Amiodarone (Type III)
2nd - Lignocaine (Type I)
3rd - Direct current cardioversion (DCCV)

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42
Q

How is Torsades de pointes treated?

A

IV magnesium

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43
Q

What is ventricular fibrillation?

A

This is an arrhythmia that involves very rapid and irregular ventricular activation, with no mechanical effect

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44
Q

What is the pathway of arrhythmia in ventricular fibrillation?

A

Ventricular ectopic beat

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45
Q

What are some causes of ventricular fibrillation?

A

Ischaemic heart disease
Cardiomyopathy
Electrolyte imbalance
Overdose of cardio toxic drugs

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46
Q

How does ventricular fibrillation usually present?

A

It is not supportive of life and so causes cardiac arrest, presenting with rapid unconsciousness and cessation of respiration

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47
Q

How does ventricular fibrillation present on ECG?

A

Bizarre irreglar waveform
No recognisable QRS complexes
Random frequency and amplitude
Uncoordinated electrical activity

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48
Q

How is ventricular fibrillation managed acutely?

A

Defibrillation
Amiodarone
Adrenaline

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49
Q

How is ventricular fibrillation managed long term?

A

Implantable cardiovertor defibrillator (ICD)

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50
Q

What are premature ventricular complexes?

A

These are ventricular ectopics, often caused by random electrical discharges outside the atria

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51
Q

What are some causes of premature ventricular complexes?

A

Left ventricular hypertrophy
Heart failure
Myocarditis
Ischaemic heart disease
Electrolyte imbalance

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52
Q

How will ventricular ectopics present on ECG?

A

These will appear as isolated, random, abnormal broad QRS complexes, within the regular sinus rhythm

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53
Q

What is bigeminy?

A

This is a condition where every other beat is a ventricular ectopic beat

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54
Q

How will bigeminy present on ECG?

A

This will show as a normal beat, followed closely by an ectopic beat

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55
Q

How are premature ventricular complexes managed?

A

Reassurance
Referral in cases of underlying causes
ß-Blockers to control symptoms

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56
Q

What is atrial fibrillation?

A

This is an arrhythmia leading two chaotic and disorganised atrial activity, which produces an irregular heart beat

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57
Q

What are some common causes of atrial fibrillation?

A

Hypertension
Heart failure
MI
Hyperthyroidism
Rheumatic heart disease
Sepsis
Electrolyte disturbances

58
Q

What is the name given to idiopathic atrial fibrillation?

A

Lone atrial fibrillation

59
Q

What are some possible underlying genetic conditions in lone atrial fibrillation?

A

Brugada syndrome
Long QT syndrome

60
Q

Describe the pathophysiology of atrial fibrillation?

A

This is caused by the presence of ectopic foci in the muscle sleeves of the ostia of the pulmonary veins, providing an atrial, premature beat which allows fro the conduction of multiple actin potential through the atria

61
Q

What is the usual range of atrial contraction rate in atrial fibrillation?

A

300 - 600 bpm
The AV node delays these and causes a rate of around 150 in the ventricles

62
Q

How does atrial fibrillation increase stroke risk?

A

Increased rate leads to loss of atrial kick and decreased filling times, meaning that there’s a reduced cardiac output, which reduces CO and allows stasis of blood which increases stroke risk

63
Q

What are the 3 classes of atrial fibrillation?

A

Paroxysmal - < 48 hours
Persistent - > 48 hours but cardiovertable
Permanent - cannot be cardioverted

64
Q

What are some lifestyle risk factors of atrial fibrillation?

A

Obesity
Alcohol abuse
Infection

65
Q

How can atrial fibrillation present?

A

Asymptomatic (30%)
Rapid palpitations
Pre-syncope and syncope
Chest pain
Dyspnoea
Sweatiness
Fatigue

66
Q

What is the main clinical sign of atrial fibrillation?

A

Irregularly irregular pulse

67
Q

How will atrial fibrillation present on ECG?

A

F waves
Absence of P waves
Atrial rate >300bpm
Variable ventricular rate

68
Q

What is the 1st line treatment of atrial fibrillation in the elderly?

A

ß-Blockers
Rate limiting calcium channel blockers
Digoxin

69
Q

What is the second line treatment of atrial fibrillation in the elderly?

A

AV node ablation

70
Q

What is the first line treatment of atrial fibrillation in younger patients?

A

Direct current cardioversion
Pharmacological cardioversion (Type I or III)

71
Q

What is the second line treatment of atrial fibrillation in younger patients?

A

Left atrial catheter ablation
Maze procedure

72
Q

Who is most at risk of thromboembolic stroke in atrial fibrillation?

A

Thyrotoxicosis
Hypertrophic cardiomyopathy
Age >75
Hypertension
Heart failure
Diabetes

73
Q

How is risk of thromboembolic stroke calculated in atrial fibrillation patients?

A

CHA2DS2-VASc score
Score >2 indicates long term anticoagulation

74
Q

What is given to patients at higher risk of thromboembolic stroke in atrial fibrillation?

A

Warfarin (Requires INR testing often)
DOAC

75
Q

What is atrial flutter?

A

This is a form of atrial tachycardia, characterised by a succession of rapid atrial depolarisation

76
Q

What pathway causes arrhythmia in atrial flutter?

A

Re-entrant rhythm in either atrium, which is recirculated in a self perpetuating loop

77
Q

Can atrial flutter progress to atrial fibrillation?

A

Yes

78
Q

How will atrial flutter present on ECG?

A

Atrial rate >300bpm
Ventricular rate ~150bpm
QRS normal
Saw tooth waves

79
Q

What is the first line management strategy in acute paroxysmal cardiac arrhythmia?

A

Direct current or pharmacological cardioversion

80
Q

What is the usual treatment for recurrent atrial flutter?

A

Catheter ablation
Class III anti-arrhythmics
AV nodal blocking agents (Adenosine)

81
Q

Does atrial flutter also carry a risk of thromboembolic stroke?

A

Yes - CHA2DS-VASc score

82
Q

What is a supraventricular tachycardia?

A

This is a narrow complex tachycardia, resulting from repeated re stimulation of the AV node via a re-entrant rhythm

83
Q

How will supra ventricular tachycardia present on ECG?

A

QRS complex follows by a T wave and then a QRS complex, with the P waves being lost in the T wave

84
Q

What are the 3 types of supra ventricular tachycardia?

A

Atrioventricular nodal re-entrant tachycardia
Atrioventricular re-entrant tachycardia
Atrial tachycardia

85
Q

What are the 4 stages of management of supra ventricular tachycardia?

A
  1. Vagal manœuvres
  2. Adenosine IV
  3. Verapamil or ß-Blocker
  4. Synchronised DC cardioverison
86
Q

What are the 3 main vagal manoeuvres?

A

Valsalva manœuvre
Carotid sinus rhythm
Diving reflex

87
Q

What is a vagal manoeuvre?

A

This is a manoeuvre to stimulate the vagus nerve, increasing the activity of the parasympathetic nervous system, which can slow heart rate

88
Q

What is the valsalva manouvre?

A

This is the action of increasing intrathoracic pressure, usually by asking a patient to blow hard against resistance, including blowing into a syringe for 10-15 seconds

89
Q

What is meant by carotid sinus massage?

A

This is a vagal manoeuvre in which the baroreceptors in the carotid sinus are stimulates, by massaging one side of the neck
Massaging both simultaneously can cause syncope

90
Q

What is the diving reflex?

A

This is a vagal manoeuvre that involves submerging a patients face in cold water

91
Q

How does adenosine work?

A

This works by slowing cardiac conduction, primarily through the AV node or accessory pathway

92
Q

How is adenosine given?

A

It has a half life of only around 10 seconds, so a large bolus is needed via a grey cannula into the antecubital fossa to reach the heart immediately

93
Q

What are some conditions in which adenosine is contraindicated?

A

Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential arrhythmia

94
Q

What are some possible side effects of adenosine?

A

Brief period of asystole or bradycardia
Feeling of dying
Sense of impending doom

95
Q

What 3 doses of adenosine are trialled in supra ventricular tachycardia?

A

Initially 6mg bolus
Then 12mg bolus
Then 18mg bolus

96
Q

What is meant by atrial tachycardia?

A

This is a supra ventricular tachycardia in which the electrical signal originates outside the atria, not the SA node

97
Q

What is meant by atria-ventricular nodal re-entrant tachycardia (AVNRT)?

A

This is a supraventricular tachycardia in which the re-entry point is through the AV node

98
Q

What is atrio-ventricular re-entrant tachycardia?

A

This is a supra ventricular tachycardia in which the re-entry point is an accessory pathway between the atria and ventricles

99
Q

What are some possible causes of sinus tachycardia?

A

Anxiety
Fever
Hypotension
Anaemia
Sepsis
Pain

100
Q

How is sinus tachycardia usually treated?

A

Treatment of underlying cause
ß-Blockers

101
Q

What are some possible causes of sinus bradycardia?

A

Physiological (e.g. in athletes)
Drugs (e.g. ß-Blockers)

102
Q

How is sinus bradycardia treated?

A

Atropine (If acute)
Pacing if there is haemodynamic compromise

103
Q

What is sick sinus syndrome?

A

This encompasses many conditions that cause dysfunction in the SA node, usually caused by idiopathic degenerative fibrosis of the sinoatrial node, resulting in sinus bradycardia, sinus arrhythmia and prolonged pauses, with an increased risk of atrial fibrillation

104
Q

What is asystole?

A

This refers to an absence of electrical activity in the heart

105
Q

What are some risk factors for asystole?

A

Mobitz type II heart block
Type III heart block
Previous asystole
Ventricular pauses longer than 3 seconds

106
Q

How are unstable patients with an increased risk of asystole managed?

A

1st - IV atropine
2nd - Inotropes (e.g. isoprenaline or adrenaline)
3rd - Temporary cardiac pacing
4th - Permanent implantable pacemaker

107
Q

What is atropine?

A

This is an anti-muscarinic medication, which inhibits the parasympathetic nervous system

108
Q

What are some side effects of atropine

A

Pupil dilatation
Dry mouth
Urinary retention
Constipation

109
Q

What are the 3 main classes of heart block?

A

1st degree
2nd degree
3rd degree

110
Q

What is meant by 1st degree heart block?

A

An AV nodal delay of >0.2 seconds, but presenting with no complications

111
Q

What are the 2 types of 2nd degree heart block?

A

Mobitz type I
Mobitz type II

112
Q

What is meant by Mobitz type I heart block?

A

Progressive lengthening of the PR interval eventually leads to a dropped beat

113
Q

What is meant by Mobitz type II heart block?

A

Beats are dropped at regular intervals, usually at 2:1 or 3:1 intervals

114
Q

What is meant by 3rd degree heart block?

A

This is full heart block, where there is no communication between the SA and AV node, meaning the ventricles and atria contract separately without each other

115
Q

What is Wolff-Parkinson-White syndrome?

A

This is a condition causing the formation of an extra-electrical pathway, connecting the atria and ventricles

116
Q

What is the name given to the accessory pathway formed in Wolff-Parkinson-White syndrome?

A

Bundle of Kent

117
Q

What are some ECG changes in Wolff-Parkinson-White syndrome?

A

Short PR interval
Wide QRS complex
Delta waves

118
Q

What is the definitive treatment of Wolff-Parkinson-White syndrome?

A

Radiofrequency ablation of the accessory pathway

119
Q

What can occur is a patient with Wolff-Parkinson-White syndrome develops atrial fibrillation or flutter?

A

This is lead to a chaotic rhythm that passes through the accessory pathway, causing a polymorphic wide complex tachycardia

120
Q

What medications are contraindicated in those with WPW and AF due to increased risk of polymorphic VT?

A

ß-Blockers
Ca2+ channel blockers
Digoxin
Adenosine

121
Q

What is meant by inotropy?

A

Modification of the force of contraction

122
Q

What is meant by lusitropy?

A

Modification of the rate of relaxation (Length of diastole)

123
Q

What is mean by chronotropy?

A

Modification of heart rate

124
Q

What is a class I anti-arrhythmic drug?

A

Sodium channel blockers

125
Q

What are the 3 types of class I anti-arrhythmic drugs?

A

Ia - Moderate
Ib - Weak
Ic - Strong

126
Q

What is a class II anti-arrhythmic drug?

A

ß-blockers

127
Q

What is a class III anti-arrhythmic drug?

A

Potassium channel blockers

128
Q

What is a class IV anti-arrhythmic drug?

A

Calcium channel blockers

129
Q

How do class I anti-arrhythmics work?

A

They block Na+ chanels and so slow the depolarisation (Phase 0) of the myocytes, preventing contraction

130
Q

In what conditions are class I anti-arrhythmics indicated in?

A

Ventricular arrhythmia
Ischaemic tissue
Inherited long QT syndrome

131
Q

What are some examples of class I anti-arrhythmics?

A

Lidocaine
Mexilitine

132
Q

How does lidocaine work?

A

It blocks open or inactive sodium channels, so blocks contraction and nerve impulses in damaged, depolarised tissue

133
Q

How do class II anti-arrhythmics work?

A

They antagonise ß1 adrenoceptors
These adrenoceptors activate Gas which activates adenylyl cyclase
This converts AMP to cAMP
cAMP increases levels of protein kinase A
Protein kinase A increases the rate of the funny current
Therefore ß-blockers slow the funny current and so slow heart rate

134
Q

What are some examples of ß1 cardioselective ß-blockers?

A

Atenolol
Bisoprolol
Carvedilol

135
Q

What are some examples of non-selective ß-blocker?

A

Propranolol
Sotalol

136
Q

In which condition are ß-blockers contraindicated in?

A

Asthma as they also act on ß2 receptors, which causes bronchospasm

137
Q

What conditions are ß-blockers indicated in?

A

Sustained ventricular arrhythmias
Atrial tachycardia
Angina
Hypertension

138
Q

How do class III anti-arrhythmics work?

A

They block K+ and thus decrease levels of K+ influx and so prolong the plateau in myocytes (Phase 2), therefore prolonging the refractory period

139
Q

What is an example of a type III anti-arrhythmic?

A

Amiodarone (Also has type I, II and IV properties)

140
Q

What is the risk of most type III anti-arrhythmic drugs?

A

Can prolongue the QT interval and so become pro-arrhythmic, with an increased risk of Torsades de pointes

141
Q

How do class IV anti-arrhythmics work?

A

They block Ca2+ channels, and thus prolong the depolarisation phase of sino-atrial nodal potentials

142
Q

What are some examples of class IV anti-arrhythmics?

A

Verapamil
Diltiazem

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