Cardiology: Tachycardia Flashcards

1
Q

What happens in atrial fibrillation?

A

1) Factors that cause dilation of the atria through inflammation and fibrosis result in discrepancies in the refractory periods within the atrial tissue (left atrium loses refractoriness before the end of atrial systole)
2) This causes electrical re-entrant pathways within the atria and recurrent uncoordinated atrial contraction, typically at 300-600 bpm
3) Delay at the AV node means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response

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2
Q

What is the most common sustained cardiac arrhythmia?

A

AF

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3
Q

What are cardiac causes of AF?

A

1) Ischaemic heart disease (most common)
2) HTN
3) Rheumatic heart disease
4) Pericarditis/myocarditis

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4
Q

What are non-cardiac causes of AF?

A

1) Dehydration
2) Endocrine e.g. hyperthyroidism
3) Infective e.g. sepsis
4) Pulmonary e.g. pneumonia or PE
5) Environmental toxins e.g. alcohol abuse
6) Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia

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5
Q

What are the 4 classifications of AF?

A

1) Acute - lasts < 48h
2) Paroxysmal - lasts < 7 days and is intermittent
3) Persistent - lasts > 7 days but is amenable to cardioversion
4) Permanent - lasts > 7 days and is not amenable to cardioversion

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6
Q

What are symptoms of AF?

A

1) Palpitations
2) Chest pain
3) Shortness of breath
4) Dizziness

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7
Q

What are signs of AF?

A

1) Irregularly irregular pulse with variable volume
2) Single waveform on the JVP (due to loss of a wave)
3) Apical to radial pulse deficit
4) Variable intensity first heart sound
5) Features suggestive of underlying cause or complications e.g. HF

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8
Q

What does an ECG show in AF?

A

Irregularly irregular HR + absent p waves

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9
Q

What is fast AF?

A

When the ventricular rate > 100 bpm (requires immediate treatment)

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10
Q

How do you assess a patient with fast AF?

A

Assess for haemodynamic stability using an ABCDE approach - shock, syncope, chest pain, pulmonary oedema

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11
Q

How do you treat a patient with fast AF who is haemodynamically unstable?

A

DC cardioversion

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12
Q

What are the principles of management in AF?

A

1) Consider reversible causes e.g. infection, dehydration, abnormal electrolytes
2) If AF persists or reversible causes are not present then decisions should be made about rate control, rhythm control or electrical cardioversion

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13
Q

What is the first line strategy for managing AF?

A

Rate control

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14
Q

When do you not offer rate control as the first line strategy to people with AF?

A

1) AF has a reversible cause
2) Heart failure thought to be primarily caused by AF
3) New-onset AF
4) When rhythm control would be more suitable based on clinical judgement

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15
Q

What is the first line initial monotherapy rate control for AF?

A

Beta blocker e.g. bisoprolol or rate-limiting CCB e.g. diltiazem

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16
Q

When would you consider digoxin monotherapy for rate control in AF?

A

For people with non-paroxysmal AF only if they are sedentary

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17
Q

What is the most commonly used beta-blocker in AF?

A

Bisoprolol

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18
Q

When can beta blockers not be used for AF?

A

Hypotension - bisoprolol will drop BP

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19
Q

Which beta blocker cannot be used as a rate control agent in AF?

A

Sotalol - bc of its rhythm control action

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20
Q

Which non-dihydropyridine CCBs are used in AF for rate control?

A

Diltiazem or verapamil

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21
Q

Why are non-dihydropyridine CCBs not frequently used in hospital settings for AF?

A

Bc they are negatively ionotropic - therefore CI in HF

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22
Q

How is digoxin used in AF for rate control?

A

1) Usual for patients who are hypotensive or have co-existent HF
2) Often used second line in conjunction with beta blockers if fast AF remains refractory
3) Avoid in younger patients - increases cardiac mortality

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23
Q

How can rhythm control be achieved in AF?

A

1) Electrical cardioversion
2) Pharmacological cardioversion

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24
Q

Why is cardioversion/rhythm control not considered in most cases of chronic AF or those who have failed cardioversion before?

A

Bc they are unlikely to be successfully cardioverted

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25
Q

How do you rhythm control new acute AF (onset < 48h) ?

A

DC cardioversion with sedation

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26
Q

How do you rhythm control AF with onset > 48h or uncertain onset?

A

Patient must be anticoagulated for at least 3 weeks before DC cardioversion can take place
(OR patient can have TOE to rule out a thrombus in the left atrial appendage before cardioversion)

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27
Q

Which drugs are used for pharmacological cardioversion/rhythm control in AF?

A

1) Flecainide
2) Amiodarone
3) Sotalol

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28
Q

When and how is flecainide used for pharmacological cardioversion/rhythm control in AF?

A

1) Preferred in young patients with structurally normal hearts (can induce fatal arrhythmias in structurally abnormal hearts)
2) Given regularly or when symptoms come on

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29
Q

When and how is amiodarone used for pharmacological cardioversion/rhythm control in AF?

A

1) V effective drug in controlling rate + rhythm
2) But massive list of significant side effects so should normally only be given to older, sedentary patients

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30
Q

When and how is sotalol used for pharmacological cardioversion/rhythm control in AF?

A

1) Beta blocker with additional K channel blocker action
2) Used for those that don’t meed the demographics for either flecainide or amiodarone

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31
Q

What is the main complication of AF?

A

Embolic stroke - long term anticoagulation reduces this risk

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32
Q

Which score stratifies risk of embolic stroke and thromboembolism for AF patients with non-valvular AF?

A

CHADS2VASc score

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33
Q

What are the components of the CHADS2VASc score?

A

1) Congestive heart failure - 1 point
2) Hypertension - 1 point
3) Age > 75 - 2 points
4) Diabetes - 1 point
5) Stroke/TIA previously - 2 points
6) Vascular disease known - 1 point
7) Age 65-74 - 1 point
8) Sc - Female - 1 point

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34
Q

When should patients be anticoagulated according to the CHADS2VASc score?

A

Males scoring 1 or more, females scoring 2 or more
(max score = 9 = 15% annual stroke risk)

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35
Q

Which score stratifies bleeding risk?

A

HASBLED (considered as a risk of anticoagulation)

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36
Q

What are the components of the HASBLED score?

A

1) Hypertension - 1 point
2) Abnormal renal or liver function - 2 points if both
3) Stroke previous - 1 point
4) Bleed - major, previous - 1 point
5) Labile INR - 1 point
6) Elderly > 65 - 1 point
7) Drugs/alcohol - 1 point for drug or alcohol use (2 if both)

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37
Q

Which score is recommended by 2021 NICE AF guidelines to assess bleeding risk when deciding whether to anticoagulate a patient?

A

ORBIT score

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38
Q

What are the components of the ORBIT score?

A

1) Sex
2) Low Hb - 2 points
3) Age > 74 - 1 point
4) Bleeding history - 2 points
5) eGFR < 60 - 1 point
6) Concomitant use of anti-platelets - 1 point

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39
Q

What is currently considered to be the anticoagulation treatment of choice in AF?

A

DOACs e.g. edoxaban, apixaban, rivaroxaban, dabigatran

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40
Q

What are the benefits of DOACs for AF?

A

1) Do not require monitoring
2) Generally associated with less bleeding risks than warfarin

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41
Q

What is the con of DOACs for AF?

A

Most have approximately 12 hour half-lives therefore if patients miss doses they are not covered

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42
Q

Which is the only oral anticoagulant licensed for valvular AF?

A

Warfarin

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43
Q

How does warfarin need to be prescribed?

A

1) Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic)
2) Requires regular INR monitoring - INR can be affected by many drugs and foods

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44
Q

What is the half life of warfarin?

A

40 hours - anticoagulant effects lasts days

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45
Q

When is LMWH e.g. enoxaparin used for AF?

A

Rarely for patients who cannot tolerate oral treatment - involves daily treatment dose injections

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46
Q

When is atrial ablation an option for AF treatment?

A

For some patients who have uncontrolled symptoms and have an identifiable locus in their left atrium

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47
Q

What are complications of AF (from uncontrolled HR, embolism or anticoagulation)?

A

1) HF
2) Systemic emboli - ischaemic stroke, mesenteric ischaemia, acute limb ischaemia
3) Bleeding - GI, intracranial

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48
Q

What defines a narrow complex tachycardia?

A

QRS complex < 120ms (three small squares on ECG)

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49
Q

How do you assess a patient with narrow complex tachycardia?

A

ABCDE

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50
Q

How do you manage a narrow complex tachycardia (incl. AF) in a patient that shows adverse features (shock, syncope, acute pulmonary oedema or myocardial ischaemia (chest pain)?

A

Synchronised DC cardioversion
(Emergency/immediate synchronised direct current cardioversion/shock)

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51
Q

How is a broad complex tachycardia defined?

A

QRS complex > 120ms

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52
Q

What are adverse features in a patient with narrow complex tachycardia?

A

1) Shock
2) Syncope
3) Acute pulmonary oedema
4) Myocardial ischaemia - chest pain

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53
Q

What do you need to know to determine management in a haemodynamically stable patient with narrow complex tachycardia?

A

Whether it is regular or irregular

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54
Q

How do you manage regular narrow complex tachycardia (SVT) in a haemodynamically stable patient?

A

1) Vagal manoeuvres - carotid sinus massage or valsalva manoeuvres
2) Then IV adenosine 6mg
3) Then IV adenosine 12mg
4) then IV adenosine 18mg

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55
Q

What is the first line management of a regular narrow complex tachycardia in a haemodynamically stable patient?

A

Vagal manoeuvres - carotid sinus massage or valsalva manoeuvres

56
Q

What is second line management of regular narrow complex tachycardia in a haemodynamically stable patient if vagal manoeuvres fail?

A

IV adenosine 6mg

57
Q

What is third line management of regular narrow complex tachycardia in a haemodynamically stable patient?

A

IV adenosine 12mg

58
Q

What is fourth line management of regular narrow complex tachycardia in a haemodynamically stable patient?

A

IV adenosine 18mg

59
Q

What is the most likely diagnosis in irregular narrow complex tachycardia?

A

Atrial fibrillation

60
Q

What condition do you manage irregular narrow complex tachycardia?

A

AF

61
Q

What is another name for regular narrow complex tachycardias?

A

Supraventricular tachycardias (SVT)

62
Q

What are the two types/causes of narrow complex tachycardias?

A

1) SVT (regular)
2) AF (irregular)

63
Q

How do you manage acute AF (irregular narrow complex tachycardia) in a haemodynamically stable patient with onset < 48h?

A

Rhythm control
1) LMWH followed by flecainide (if no heart disease)
2) LMWH followed by amiodarone (if heart disease)

64
Q

In which patients can you use flecainide to rhythm control acute AF with onset < 48h?

A

Healthy - NO heart disease

65
Q

How do you manage acute AF (irregular narrow complex tachycardia) in a haemodynamically stable patient with onset > 48h?

A

Rate control
1) Metoprolol or bisoprolol or verapamil
2) Digoxin if signs of heart failure
3) Anticoagulation

66
Q

How do you manage acute narrow complex tachycardia in a patient who is not haemodynamically stable?

A

Synchronised DC shock

67
Q

What condition is an irregular broad complex tachycardia presumed to be?

A

VF

68
Q

Is VF pulse or pulseless?

A

Always pulseless

69
Q

What do the QRS complexes look like in VF?

A

Polymorphic + irregular

70
Q

Which guidelines dictate VF management

A

ALS

71
Q

What are the initial priorities in VF?

A

BLS
1) Ensure airway is patent
2) Check for signs of life (pulse and breathing)
3) Commence CPR

72
Q

Is VF shockable?

A

Yes

73
Q

What is first line management of VF?

A

Defibrillation - unsynchronised cardioversion using 200J biphasic shock

74
Q

What type of shock do you give in VF?

A

200J biphasic shock

75
Q

How do you manage VF?

A

1) Check airway, signs of life + commence CPR
2) Defibrillation - unsynchronised cardioversion using 200J biphasic shock
3) Resume chest compressions (CPR) for 2 mins before re-checking rhythm
4) After the 3rd shock - 1mg adrenaline IV (10ml 1:10,000) + 300mg amiodarone IV
5) Continue to administer adrenaline every 3-5 mins after every alternate shock

76
Q

What is the medical management of VF/pulseless VT?

A

After 3rd shock
1) IV adrenaline 1mg (10ml 1:10,000) + IV amiodarone 300mg
Every 3-5 mins after every alternate shock:
2) IV adrenaline 1mg (10ml 1:10,000)

77
Q

What are the features of ventricular tachycardia on ECG?

A

Absent P waves + monomorphic regular broad QRS complexes

78
Q

What is the rhythm in VF?

A

Irregular

79
Q

What is the rhythm in VT?

A

Regular

80
Q

How do you manage pulseless VT?

A

Same as VF
1) Check airway, signs of life + commence CPR
2) Defibrillation - unsynchronised cardioversion using 200J biphasic shock
3) Resume chest compressions (CPR) for 2 mins before re-checking rhythm
4) After the 3rd shock - 1mg adrenaline IV (10ml 1:10,000) + 300mg amiodarone IV
5) Continue to administer adrenaline every 3-5 mins after every alternate shock

81
Q

How long do you carry out CPR for after unsynchronised shock (defibrillation) before re-checking the rhythm?

A

2 minutes

82
Q

How do you manage VT or torsades de pointes with a pulse and adverse features (shock, syncope, myocardial ischaemia (chest pain) or heart failure (acute pulmonary oedema)?

A

1) Synchronised DC shock - up to 3 attempts
2) Seek expert help
3) IV amiodarone 300mg over 10-20 mins
4) IV amiodarone 900mg over 24h

83
Q

What is the first line management of VT with pulse and adverse features?

A

Synchronised DC shock

84
Q

What is medical management of VT or torsades de pointes with pulse and adverse features?

A

After 3 attempts of synchronised DC shock + seeking expert help:
1) IV amiodarone 300mg over 10-20 mins
2) IV amiodarone 900mg over 24h

85
Q

How do you manage VT with pulse and NO adverse features?

A

AMIODARONE
1) IV amiodarone 300mg over 20-60 mins
2) IV amiodarone 900mg over 24h

86
Q

What is Torsades de Pointes (TdP)?

A

A form of polymorphic VT caused by QT prolongation

87
Q

Is torsades de pointes regular or irregular?

A

Can be either

88
Q

What does torsades de pointes look like on ECG?

A

QRS complexes twisting around the isoelectric line

89
Q

What are causes of torsades de pointes?

A

1) Congenital long QT syndromes e.g. Romano Ward syndrome, Jervell and Lange-Neilsen syndrome
2) Medication - antiarrhythmics, erythromycin/clarithromycin, TCAs, antipsychotics, ketoconazole
3) MI
4) Renal/liver failure
5) Hypothyroidism
6) AV block
7) Toxins

90
Q

What medications can cause torsades de pointes?

A

1) Antiarrhythmics
2) Antibiotics e.g. erythromycin/clarithromycin
3) TCAs
4) Antipsychotics
5) Ketoconazole

91
Q

What are cardiac causes of torsades de pointes?

A

1) Congenital long QT syndromes e.g. Romano Ward syndrome, Jervell and Lange-Neilsen syndrome
2) MI
3) AV/heart block

92
Q

What are other causes of torsades de pointes?

A

1) Renal/liver failure
2) Hypothyroidism
3) Toxins

93
Q

How do you manage torsades de pointes in haemodynamically unstable patients?

A

Same as VT - synchronised DC shock + IV amiodarone

94
Q

How do you manage torsades de pointes in haemodynamically stable patients?

A

1) IV magnesium sulphate - 2g over 10 mins
2) Stop offending drugs that prolong the QT interval
3) Correct electrolyte abnormalities esp. hypokalaemia and hypomagnesaemia
4) Consider isoprenaline infusion and temporary/permanent pacing

95
Q

What is the most important first line treatment in torsades de points in haemodynamically stable patients?

A

IV magnesium sulphate (2g over 10 mins)

96
Q

What can be used in patients with recurrent torsades de pointes despite initial therapy with magnesium sulphate?

A

Isoprenaline infusion + temporary/permanent pacing

97
Q

Which electrolyte abnormalities are especially important to correct in torsades de pointes?

A

Hypokalaemia + hypomagnesaemia

98
Q

Which part of the heart is affected in narrow complex tachycardia?

A

Atria

99
Q

Which part of the heart is affected in broad complex tachycardia?

A

Ventricles

100
Q

What are indications for transcutaneous pacing in tachyarrhythmias?

A

Patients unresponsive to medical management e.g. patients with SVT failing to respond to vagal manoeuvres and adenosine

101
Q

Which tachyarrhythmias require pacemakers?

A

Those that are resistant to pharmacological therapy

102
Q

What type of permanent pacemakers are used in tachyarrhythmias resistant to pharmacological therapy?

A

1) These forms of permanent pacing are typically dual chamber (with one lead in the right atrium and one lead in the right ventricle)
2) Bi-ventricular pacemaker (in which a 3rd wire is placed in a branch of the coronary sinus, to allow left ventricular pacing and ventricular synchronisation) is an option if the left ventricular ejection fraction is <35%

103
Q

What type of arrhythmia does Wolff Parkinson White syndrome (WPW) lead to?

A

Supraventricular tachycardia (SVT)

104
Q

What causes WPW?

A

1) A congenital accessory electrical pathway connects the atria to the ventricles bypassing the AV node
2) The accessory pathway leads to the potential for re-entrant circuits to form leading to SVTs

105
Q

Who is more affected by WPW?

A

Men (2:1)

106
Q

How does WPW present?

A

Asymptomatic OR
1) Palpitations
2) Dizziness
3) Syncope

107
Q

What do you see on an ECG in WPW?

A

1) Delta waves - slurred upstroke in QRS
2) Short PR interval < 120ms
3) Broad QRS
4) OR narrow complex tachycardia if a re-entrant circuit has developed

108
Q

What investigations are done for WPW?

A

1) ECG
2) 24h ECG monitoring - if paroxysmal symptoms
3) Routine bloods - incl. TFTs if non-cardiac causes of tachycardia are suspected
4) Echo - to assess ventricular function
5) Intracardiac electrophysiological studies to map the location of the accessory pathway

109
Q

What investigation is done in WPW if patients have paroxysmal symptoms?

A

24h ECG

110
Q

Why is an echo done in WPW?

A

To assess ventricular function

111
Q

What investigation can be done in WPW to map the location of the accessory pathway?

A

Intracardiac electrophysiological studies

112
Q

How do you treat WPW?

A

1) Radiofrequency ablation of the accessory pathway
2) Drug treatment e.g. amiodarone or sotalol to avoid further tachyarrhythmias (CI in heart disease)
3) Surgical (open heart) ablation - rarely done, only used in complex cases

113
Q

How do you definitively treat WPW?

A

Radiofrequency ablation of the accessory pathway

114
Q

How can you try and avoid further tachyarrhythmias in WPW?

A

Drug treatment - e.g. amiodarone or sotalol (CI in structural heart disease)

115
Q

Which two drugs are contraindicated in WPW for long term use and why?

A

Digoxin and NDP-CCBs e.g. verapamil - they may precipitate VF

116
Q

How do you manage an SVT in an unstable patient with WPW?

A

Urgent DC cardioversion (regardless of rhythm)

117
Q

What are signs of an unstable WPW patient with SVT?

A

1) BP < 90/60
2) Signs of systemic hypoperfusion
3) Fast AF

118
Q

What is an orthodromic AV reciprocating tachycardia?

A

Narrow QRS complex + short PR interval (in WPW)

119
Q

In which condition is a orthodromic and antidromic AV reciprocating tachycardia seen?

A

WPW

120
Q

How do you manage a WPW stable patient with orthodromic AV reciprocating tachycardia (narrow QRS + short PR)?

A

Like SVT
1) Vagal manoeuvres (carotid sinus massage or valsalva manoeuvre)
2) IV adenosine

121
Q

What happens in orthodromic AV reciprocating tachycardia in WPW?

A

1) One limb of the aberrant circuit involves the AV node
2) So slowing conduction through the AV node helps terminate the tachycardia

122
Q

What is antidromic AV reciprocating tachycardia?

A

Wide QRS complex

123
Q

How do you treat stable WPW patients with antidromic AV reciprocating tachycardia, AF or atrial flutter?

A

IV procainamide or flecainide (antiarrhythmics) - help prevent rapid conduction through the accessory pathway

124
Q

What can be used in stable WPW patients with ortho/antidromic AV reciprocating tachycardia, AF or atrial flutter if symptoms persist?

A

DC cardioversion

125
Q

What is Brugada syndrome?

A

Genetic condition caused by sodium channelopathies

126
Q

Where is the mutation in Brugada syndrome?

A

Sodium channels

127
Q

In which patients is incidence of Brugada syndrome high?

A

Southeast Asian males

128
Q

What is Brugada syndrome a common cause of?

A

Sudden cardiac death

129
Q

How does Brugada syndrome present?

A

Asymptomatic OR
1) Palpitations
2) Syncope
Due to AV nodal re-entrant tachycardias (AVNRTs), VT or VF

130
Q

What arrhythmias can Brugada syndrome cause?

A

AV nodal re-entrant tachycardias (AVNRTs), VT or VF

131
Q

How is Brugada syndrome diagnosed?

A

Characteristic ECG changes + at least one clinical criterion:
1) VF or polymorphic VT
2) Family history of sudden cardiac death under the age of 45
3) Syncope or ECG signs in the family
4) Inducible VT
5) Nocturnal agonal breathing

132
Q

What is a key clinical sign in Brugada syndrome?

A

Nocturnal agonal breathing

133
Q

What investigations are used for diagnosis of Brugada syndrome?

A

1) ECG
2) Genetic testing
3) Family history
4) Special provocation tests e.g. ajmaline

134
Q

What risk factors can increase the risk of arrhythmia in Brugada syndrome?

A

1) Fever
2) Excess alcohol intake
3) Dehydration
4) Medication
5) Electrolyte abnormalities

135
Q

What advice should patients with Brugada syndrome be given?

A

To avoid risk factors for arrhythmia (e.g. excess alcohol) or take prompt action e.g. taking paracetamol if they have any fever

136
Q

Which medications can increase the risk of arrhythmia in Brugada syndrome?

A

1) Antiarrhythmics e.g. flecainide
2) Verapamil
3) Antidepressants e.g. amitriptyline

137
Q

What is definitive management of Brugada syndrome?

A

ICD - to reduce the risk of sudden death from arrhythmias e.g. VT or VF