Arrythmia and AF Flashcards

1
Q

What is the role of the SAN and where is it located?

A

Located in the RA near the opening of SVC. It is the pacemaker of the heart and starts depolarisation. It coordinates contraction of atria and sends impulses to the AVN.

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2
Q

What is the role of the AVN and where is it located?

A

Located in the RA near tricuspid valve on the inter-atrial septum. It acts as an electrical gatekeeper between atria and ventricles, by delaying impulse to ventricles allowing time for atria to contract and blood to fill the ventricles. Sends impulses to bundle of His.

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3
Q

What is the role of the His-purkinje fibres?

A

Spreads electrical impulses synchronously throughout RV and LV, allowing ventricles to contract at the same time.

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4
Q

What does the p wave indicate?

A

Atrial depolarisation.

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5
Q

What does the QRS complex indicate?

A

Ventricular depolarisation. Normal duration = 120 msec.

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6
Q

What does the T wave indicate?

A

Ventricular repolarisation.

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7
Q

What is the PR interval and what does it show?

A

Beginning of p wave to beginning of QRS complex. It shows the slow conduction through AVN. Time taken for atria to contract. Normal duration = 200 msec.

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8
Q

What is the QT interval and what does it show?

A

Beginning of QRS to end of T wave. It shows repolarisation of ventricles.

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9
Q

What is the ST segment and what does it show?

A

It is the isoelectric section of ECG between the end of S wave and beginning of T wave. It is the time between ventricular depolarisation and ventricular repolarisation.

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10
Q

What is normal resting HR, bradycardia and tachycardia?

A

Normal: 60-100bpm
Bradycardia: <60bpm
Tachycardia: >100bpm

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11
Q

What is the normal rate of PR interval and QRS complex?

A

PR interval: <200msec/<5 small squares.
QRS complex: <120msec/<3 small squares.

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12
Q

How many msec is one small square and one large square on ECG?

A

Small square: 40msec
Large square: 200msec

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13
Q

How would you calculate rate on ECG?

A

300/number of large squares between RR interval
OR
1500/number of small squares between RR interval

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14
Q

Define paroxysmal AF

A

Recurrent episodes (≥30 seconds in duration) that terminate spontaneously within 48 hours.

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15
Q

What are the 2 differentials for an irregularly irregular pulse?

A

Atrial fibrillation and ventricular ectopics.

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16
Q

How would you differentiate between AF and ventricular ectopics?

A

Using an ECG. Also, ventricular ectopics disappear over a certain HR threshold, therefore a regular HR during exercise suggests ventricular ectopics over AF.

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17
Q

Define valvular AF

A

Patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve.

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18
Q

Define non-valvular AF

A

AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis.

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19
Q

Flecainide should be avoided in…

A

Atrial flutter

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20
Q

What is INR?

A

International normalised ratio. It’s a calculation of how the prothrombin time of the patient compares with the prothrombin time of a normal health adult. An INR of 1 indicates a normal prothrombin time. An INR of 2 indicates that the patient has a prothrombin time twice that of a normal healthy adult (it takes them twice as long to form a blood clot).

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21
Q

Describe the advantages of DOACs compared to warfarin

A

No monitoring is required.
No major interaction problems.
Equal or slightly better than warfarin at preventing strokes in AF.
Equal or slightly less risk of bleeding than warfarin.

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22
Q

Should aspirin be offered to prevent a stroke in a patient with AF?

A

No - there is no role for aspirin in preventing stoke in AF. This used to be recommended, but not any longer.

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23
Q

Describe the complications of AF (cardiac and non-cardiac)

A

Cardiac: HF, tachycardia-induced cardiomyopathy, ischaemia, sudden cardiac arrest.
Non-cardiac: thromboembolic events (stroke, TIA, mesenteric ischaemia, ischaemic limb), collapse, bleeding events (anticoagulation).

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24
Q

Describe some vagal manoeuvres

A

Valsalva manoeuvre - forced expiration against a closed glottis (covering mouth and nose).
Carotid sinus massage - massaging carotid artery for 5-10 secs whilst patient lying on back with head turned to one side.

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25
Q

Is it safe to prescribe non-dihydropyridine calcium channel blockers with beta blockers?

A

No as both classes are negatively inotropic and chronotropic, which together may cause HF, bradycardia and potentially asystole.

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26
Q

What are the 4 possible ECG rhythms in cardiac arrest?

A

VF, pulseless VT, pulseless electrical activity (PEA) and asystole.

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27
Q

How would you distinguish between SVT and VT?

A

Use adenosine as it blocks the AVN, therefore if it’s SVT the HR should slow.

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28
Q

Why are anti-arrhythmic drugs (e.g. beta blockers, calcium channel blockers, adenosine) contraindicated in patients with WPW syndrome that develop AF or atrial flutter?

A

Increased risk of causing a polymorphic wide complex tachycardia because anti-arrhythmic reduce conduction through AVN, promoting conduction through the accessory pathway. Increasing the risk that the chaotic atrial activity will pass through accessory pathway into ventricles.

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29
Q

Define bigeminy

A

Where ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic etc.

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30
Q

Define sick sinus syndrome

A

Aka sinus node dysfunction. It comprises a variety of disturbances affecting both generation of electrical activity from the sinus node and transmission within the atria. Examples include sinus bradycardia, sinus arrest/pause, tachy-brady syndrome.

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31
Q

Describe the antimuscarinic side effects of atropine

A

Pupil dilatation, urinary retention, dry eyes and constipation.

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32
Q

What is the most common arrhythmia?

A

Atrial fibrillation (AF).

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33
Q

Describe the pathophysiology of AF

A

Disorganised atrial electrical activity causes independent contraction of cardiomyocytes leading to fibrillation of the atria. Contraction of atria is uncoordinated, rapid and irregular.

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34
Q

Why does AF increase an individuals risk of ischaemic stroke?

A

Blood stasis in atria causes thrombus formation, which can lead to an embolism.

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35
Q

Name 5 causes of AF

A

Sepsis, mitral valve stenosis/regurgitation, IHD, thyrotoxicosis, hypertension.

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36
Q

What feature on examination would suggest AF?

A

Irregularly irregular pulse.

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37
Q

Describe the hallmark ECG features of AF

A

Irregularly irregular rhythm.
Absent p waves.
Irregular, fibrillating baseline.
Narrow QRS complex tachycardia.

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38
Q

Which scan is routinely requested in patients with new-onset AF?

A

Transthoracic echocardiogram.

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39
Q

What is the purpose of rate control in AF?

A

To allow the ventricles to fill with blood more efficiently.

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40
Q

What drugs can be used for rate control in AF?

A

Beta blockers, rate limiting calcium channel blockers (verapamil, diltiazem), digoxin.

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41
Q

How can rhythm control be achieved in AF?

A

Through cardioversion or long-term medication.

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42
Q

When would pharmacological cardioversion be indicated over electrical cardioversion in AF?

A

Pharmacological - AF presenting < 48 hours or severely haemodynamically unstable.
Electrical - AF presenting > 48 hours and stable.

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43
Q

How long must patients be anticoagulated for before electrical cardioversion?

A

3 weeks prior.

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44
Q

What drugs would be used for pharmacological cardioversion?

A

Flecainide or amiodarone (if patient has structural heart disease).

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45
Q

What is the first line medication for long term management of rhythm control in AF?

A

Beta blockers.

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46
Q

Describe the ‘pill in pocket approach’ for paroxysmal AF

A

Patient takes flecainide when they feel their symptoms starting. They must have infrequent episodes without any underlying structural heart disease.

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47
Q

What part of the heart does thrombus formation predominately occur in AF?

A

Left atrial appendage.

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48
Q

Describe the risks and benefits of anticoagulants

A

Slight increase bleeding risk. However bleeds are more reversible than strokes and have fewer long-term consequences. Benefits - it reduces stroke risk by 2/3.

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49
Q

What is the first line medication for anticoagulation in AF?

A

DOACs e.g. apixaban, rivaroxaban, dabigatran.

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50
Q

What other medications can be used for anticoagulation in AF?

A

Warfarin

51
Q

What tool is used for assessing stroke risk in AF?

A

CHA2DS2-VASc

52
Q

What tool can be used to assess bleeding risk in patients with AF?

A

ORBIT score.

53
Q

What are the 2 shockable rhythms?

A

VT and VF

54
Q

What are the 2 non-shockable rhythms?

A

Pulseless electrical activity and asystole.

55
Q

What is a re-entrant circuit?

A

Continuous wave of depolarisation in a circular path.

56
Q

Give 2 examples of tachyarrhythmias that are generated from a macro re-entrant circuit

A

Atrial flutter and AVRT

57
Q

How can you differentiate from SVT and VT from an ECG?

A

SVT - narrow QRS complex (<120 ms).
VT - wide QRS complex (>120 ms).

58
Q

What is an accessory pathway?

A

Abnormal connection between atria and ventricles away from AVN.

59
Q

How would you treat an unstable patient with tachycardia?

A

Up to 3 synchronised shocks or IV amiodarone.

60
Q

How would you treat AF?

A

Rate control with beta blocker or diltiazem.

61
Q

How would you treat atrial flutter?

A

Beta blocker to control rate.
Radiofrequency ablation of re-entrant circuit.

62
Q

How would you treat SVT?

A

Vagal manoeuvres or adenosine.

63
Q

How would you treat VT?

A

IV amiodarone.

64
Q

Describe the ECG features for atrial tachycardia

A

Fast and narrow QRS complexes and abnormal p waves.

65
Q

What blood tests would you do for an arrhythmia?

A

FBC (anaemia), U&Es (electrolyte balance) and TFTs.

66
Q

How fast do atria contract with atrial flutter?

A

300bpm

67
Q

Describe the ECG features for atrial flutter

A

Sawtooth pattern.

68
Q

What are the 2 types of SVT?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT).

69
Q

What causes AVNRT?

A

Additional conduction pathways within the AVN creating a short circuit.

70
Q

Describe the ECG features for AVNRT

A

Rapid, narrow QRS complex, absent p waves.

71
Q

What causes AVRT?

A

Accessory pathway.

72
Q

The condition with an accessory pathway due to pre-excitation of ventricles is known as…

A

Wolff-Parkinson White syndrome.

73
Q

What is the accessory pathway called in WPW syndrome?

A

Bundle of Kent.

74
Q

Describe the ECG features for WPW syndrome

A

Short PR interval, early slurred upstroke in QRS complex (delta wave), wide QRS complex.

75
Q

How would you definitively treat WPW syndrome?

A

Radiofrequency ablation of accessory pathway.

76
Q

Describe the MOA of adenosine

A

Slow cardiac conduction through AVN.

77
Q

What is the long-term management for paroxysmal SVT?

A

Beta blockers, calcium channel blockers or amiodarone.
Radiofrequency ablation.

78
Q

Describe the pathophysiology of VT

A

Rapid, recurrent ventricular depolarisation commonly due to scarring of ventricles following MI.

79
Q

Describe the ECG features for VT

A

Regular, rapid wide QRS complexes.

80
Q

Polymorphic VT is also known as…

A

Torsades de pointes

81
Q

Torsades de pointes occurs secondary to…

A

QT interval prolongation.

82
Q

What electrolyte imbalances can cause Torsades de pointes?

A

Hypokalaemia, hypomagnesaemia, hypocalcaemia.

83
Q

Would would you treat Torsades de pointes?

A

IV magnesium.

84
Q

Describe the ECG pattern for Torsades de pointes

A

Height of QRS complex progressively gets smaller, then larger, then smaller etc.

85
Q

Describe the pathophysiology of VF

A

Ventricular muscles contract independently.

86
Q

Describe the ECG features for VF

A

No p waves, QRS complexes or T waves.
No coordinated electrical activity.

87
Q

What are ventricular ectopics?

A

Premature ventricular beats from random electrical discharges from outside the atria.

88
Q

Describe the ECG features for ventricular ectopics

A

Individual random, abnormal, broad QRS complexes on background of normal ECG.

89
Q

Describe the ECG features for sinus pause/arrest

A

Transient absence of p waves lasting >= 2 secs.

90
Q

What causes heart block?

A

Abnormal conduction through AVN.

91
Q

What is a first degree heart block?

A

Delayed conduction through AVN.

92
Q

Describe the ECG features for first degree heart block

A

Constant prolongation of PR interval (>200 ms).

93
Q

What is a second degree heart block?

A

Intermittent failure of conduction through AVN.

94
Q

Describe the ECG features for Mobitz type 1 (Wenckebach)

A

Progressive lengthening of PR interval followed by an absent QRS complex.

95
Q

Describe the ECG features for Mobitz type 2

A

Constant PR interval, occasionally followed by no QRS complex.

96
Q

What is a fixed 2:1 heart block?

A

2 p waves for every QRS complex.

97
Q

What is third degree heart block?

A

Complete heart block - complete failure of conduction through AVN.

98
Q

Describe the ECG features for third degree heart block

A

P waves have no association with QRS complexes.

99
Q

What is a bundle branch block (BBB)?

A

Disturbance in normal conduction down right/left bundle branches, causing a delay in ventricular depolarisation.

100
Q

Describe the QRS morphology in RBBB

A

M in V1 & W in V6

101
Q

RBBB may indicate what?

A

Disease of right side of heart e.g. PE or pulmonary pathology.

102
Q

Describe the QRS morphology in LBBB

A

W in V1 & M in V6

103
Q

A new onset LBBB may indicate what?

A

STEMI

104
Q

Left axis deviation is caused by?

A

Blockage of left anterior fascicle.

105
Q

Right axis deviation is caused by?

A

Blockage of left posterior fascicle.

106
Q

Define asystole and what arrhythmias can cause it?

A

Cessation of electrical and mechanical activity of the heart.
VF or VT.

107
Q

Describe the management for bradycardias

A

IV atropine.
IV isoprenaline.
Pacemaker.

108
Q

In AF should you offer anticoagulation based on sex alone?

A

No

109
Q

A single episode of paroxysmal atrial fibrillation, even if provoked, should still prompt consideration of what?

A

Anticoagulation

110
Q

A 67-year-old man with a background of asthma presents with dyspnoea and tachycardia. An ECG is performed and shows absent p-waves and irregular rhythm.

His oxygen saturations are 94% on room air, his respiratory rate is 17 breaths/minute and his heart rate is 130 bpm. He is apyrexial and his blood pressure is 130/80mmHg.

Which drug would be the most appropriate to control the rate?

A

Diltiazem (beta blockers are contraindicated in asthma).

111
Q

AVN block is more common following what type of MI?

A

Inferior MI

112
Q

What is the most common cause of death following a MI?

A

VF

113
Q

What is a side effect of adenosine?

A

Flushing and chest pain.

114
Q

What is a bifasicular block?

A

RBBB + left/right axis deviation

115
Q

What is a trifasicular block?

A

Bifasicular block + 1st degree heart block

116
Q

What is Brugada syndrome and describe it’s ECG changes

A

Rare form of inherited cardiovascular disease witch may present with sudden cardiac death.
Convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave.

117
Q

What is the management for Brugada syndrome?

A

Implantable cardioverter-defibrillator.

118
Q

Electrical cardioversion is synchronised to which wave?

A

R wave

119
Q

What tests should be performed prior to starting amiodarone?

A

TFTs, LFTs, U&E, CXR

120
Q

What ECG changes are associated with hypothermia?

A

J waves

121
Q

Where should the intraosseous route be given in adults?

A

Proximal tibia (distal femur and distal tibia in paediatrics).

122
Q

What are the first line investigations for palpitations?

A
  • 12 lead ECG.
  • TFTs.
  • U&Es.
  • FBC.
  • Next step: Holter monitor.
123
Q

ECG changes with hypercalcaemia?

A

Shortening of QT interval

124
Q

Hypercalcaemia ECG

A

Shortening of the QT interval