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The Cardiovascular System > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What should be the only pathway for electrical activity to pass between the atria and ventricles?

A

AV node

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2
Q

What is an arrhythmia?

A

An irregular heart beat

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3
Q

What are the two main classes of arrhythmia?

A
  1. Supraventricular (SVT)
  2. Ventricular (VT)

These classifications are based on the origin of the arrhythmia

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4
Q

What does “supraventricular” confer about the location of the arryhtmia’s origin?

A

It is above the ventricles and within the atria, SA node, AV node or His origin

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5
Q

Name 3 tachycardic SVT arrhythmias

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. Ectopic atrial tachycardia
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6
Q

Name 2 bradycardic SVT arrhythmias

A
  1. Sinus bradycardia
  2. Sinus pauses
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7
Q

What are AV node arryhthmias due to?

A

Re-entrant rhythms

e.g. AVN re-entrant tachycardia (SVT arrhythmia)

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8
Q

Where and why do ventricular arrhythmias arise?

A

Arise in ventricles due to ectopic beats from latent pacemakers

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9
Q

What is supraventricular paroxysmal tachycardia?

A

A re-entrant tacycardia

This comes and goes spontaneously

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10
Q

Wolf-Parkinson-White syndrome involves which type of arrhythmia?

A

Paroxysmal supraventicular tachycardia

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11
Q

What are the three types of venticular arrythmias?

A
  1. Ventricular tachycardia
  2. Ventricular fibrillation
  3. Asystole - the heart fails to beat
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12
Q

What are ectopic beats

A

Beats arising from outwith the SA node

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13
Q

Which factors may promote tachycardia and ectopic beats?

A
  • Hyperthermia
  • Hypoxia
  • Hypercapnia
  • Cardiac dilatation
  • Hypokalaemia (prolongs repolarisation)
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14
Q

Which factors may induce bradycardia and heart block?

A
  • Hypothermia
  • Hyperkalaemia
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15
Q

What are afterdepolarisations?

A

Depolarisations occurring, for various reasons, within phase 2 of the myocitic action potential

They may induce a second heart beat

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16
Q

Afterdepolarisations are associated with use of which drug and why?

A

Digoxin

It leads to a calcium overload in cells making contractions easier

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17
Q

Deficiency of which element will potentiall lead to afterdepolarisations and why?

A

Potassium

Hypokalaemia leads to afterdepolarisations because a lack of potassium means cells cannot depolarise as easy since potassium is used for depoalrisation

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18
Q

What is the name of the accessory pathway utilised in WPW syndrome?

A

The bundle of Kent

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19
Q

How is sinus tachycardia treated?

A

Beta blockers

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20
Q

What is micro re-entry?

A

This is when the AV nodal re-entrant tachycardia circuit uses the circuit within the AVN

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21
Q

Micro re-entry is most common in which type of person?

A

Young woman

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22
Q

Acutely, how are SVT arrhythmias treated?

A

Increase vagal tone via:

  • Valsalva manouvre
  • Carotid sinus massage
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23
Q

How are SVTs treated long term to slow the conduction in the AVN?

A
  • Adenosine
  • Verapamil
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24
Q

Problematic accessory tracts are treated by what?

A

Radiofrequency abalation

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25
Q

What is first degree AV block?

A

There is no block

The PR interval is increased

There is no treatment

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26
Q

What are the two types of second degree heart block?

A
  1. Mobitz type I
  2. Mobitz type II
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27
Q

Describe Mobitz type I

A

PR interval gradually increases until a QRS comple does not occur

The cycle then resets

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28
Q

Describe Mobitz type II

A

The is pathological and usually involves a ratio of P waves to QRS complexes since only some P waves can get through

Common ratios are 2:1 and 3:1

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29
Q

What is third degree heart block?

A

No potentials from the SA node will make it through the AV node so there is no coordination between atrial and ventricular coordination

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30
Q

What is the treatment for third degree heart block?

A

Ventricular pacing

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31
Q

How do ventricular arrythmias present on ECG?

A

Wide QRS

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32
Q

How can ventricular tachycardia often be identified on ECG?

A
  • Wide QRS
  • No P waves (present, yet not visible)
  • Large T wave opposite to QRS deflection

This is for monomorphic VT which involves just one circuit so all the beats are the same

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33
Q

What is polymorphic VT and how does it present on ECG?

A

This happens all over the ventricles so there are numerous circuits leading to completely irregular patterns

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34
Q

Give an example of polymorphic VT

A

Torsades de Pointes

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35
Q

How can VT be treated acutely, and why is this treatment useful?

A

Adenosine

It can aid the diagnosis depending on its effect as it has a short half life

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36
Q

When a VT is unstable, how is it treated?

A

Direct current cardioversion (DCCV)

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37
Q

If VT is stable, how is it treated?

A

Anti-arrhythmic drugs

38
Q

How is VT treated long term?

A
  • Re-vascularisation to correct ischaemia
  • No anti-arrhythmic drugs as these worsen outcomes long-term
  • Cardioverter defibrillation use if life threatening
  • VT catheter ablation
  • Beta blockers
39
Q

What is ventricular fibrillation?

A

Ventricular activity is chaotic and leads to the heart losing its ability to function as a pump

40
Q

How is ventricular fibrillation treated?

A
  • Defibrillation
  • CPR
41
Q

What is the most serious potential consequence of atrial fibrillation?

A

Stroke

42
Q

Which 3 main categories can atrial fibrillation be classified under?

A
  1. Paroxysmal - episodes terminate spontaneously last < 48 hours
  2. Persistent - episodes are not self terminating - last > 48 hours
  3. Permanent - continuous AF which cannot be cardioverted, or attempts to do so may be inappropriate

The first detected episode of AF is often also described as a form

43
Q

What are the symptoms of AF?

A
  • Palpitations
  • Dyspnoea
  • Chest pain
  • Pre-syncope (dizziness) or syncope
  • Fatigue
44
Q

What are the sign(s) for AF?

A

An irregularly irregular pulse

45
Q

What is used for diagnosis of AF and why?

A

ECG

Other conditions can give an irreguarly irregular pulse such as ventricular ectopics

46
Q

What are the two components of AF management?

A
  1. Rate/rhythm control
  2. Reducing stroke risk (anticoagulation)
47
Q

How do rate and rhythm control vary?

A
  1. Rate - accepts there will be an irregular pulse, yet aims to slow down the pulse
  2. Rhythm - attempts to return the patient to normal sinus rhythm (cardioversion)
48
Q

Which two methods can be used for cardioversion?

A
  1. Drugs
  2. Synchronised DC electrical shocks
49
Q

What is used for first line in AF to control the rate?

A

Either:

  • Beta blocker
  • Rate limiting calcium channel blocker (diltiazem)
50
Q

Assuming first line rate control treatment fails for AF, what is second line?

A

Combination therapy using any 2 of the following drugs:

  1. Beta blocker
  2. Diltiazem
  3. Digoxin
51
Q

What is a normal rate for atrial fibrillation?

A

Can be >300bpm

52
Q

In theory, in atrial fibrillation, the ventricular contraction rate should match the atrial rate since there is nothing wrong with the conduction pathway in this sense.

Why is it that this doesn’t happen when atrial contraction rates get very high?

A

The AV node cannot conduct impulses at this rate and this is the rate limiting factor for ventricular contraction

53
Q

Why is it dangerous when patients switch from AF to sinus rhythm?

A

There is high risk of an embolism being pushed out the atria when they contract properly

This can lead to stroke

54
Q

Before attempting cardioversion, what must be confirmed about the patient’s disease or pharmacological status?

A

They have had symptoms for less than 48 hours

or

Have been anticoagulated prior to cardioversion

This is to avoid the risks of stoke via embolism release

55
Q

What is the scoring strategy used to determine the most appropriate anticoagulation strategy depending on the patient’s risk of stroke?

A

CHA2DS2-VASc

56
Q

Which invasive procedure can allow for sinus rhythm in AF to be restored?

A

Catheter abalation of atrial focus

(or surgery)

57
Q

What treatment is given, or considered, when a patient has the following CHA2DS2-VASc scores:

a) 0
b) 1 (female)
c) 1 (male)
d) 2

A

a) None
b) None
c) Consider anticoagulation
d) Offer anticoagulation rather than consider

58
Q

What are the components of CHA2DS2-VASc?

A

C - Congestive heart failure (points = 1)

H - Hypertension (points = 1)

A2 - Age >= 75 (points = 2); age 65-74 (points = 1)

D - Diabetes (points = 1)

S2 - Prior stroke or TIA (points = 2)

V - Vascular disease (points = 1)

S - Sex - female (points = 1)

59
Q

If AF has an onself of <48 hours how may a patient be cardioverted?

A

Electrical - DC cardioversion

Pharmacologically - Amiodarone (structure heart disease), flecainide or amiodarone (without structural disease)

60
Q

If it is confirmed the onset of AF was under 48 hours, what should be done after cardioversion in such patients?

A

Nothing

Further anticoagulants are unnecessary

(they are already anticoagulated by heparin for example, before cardioversion)

61
Q

If the patient has had AF for >48 hours what should be done before cardioversion?

A

The patient must be anticoagulated for at least 3 weeks beforehand

62
Q

If the patient has had AF for >48 hours what cardioversion technique is recommended?

A

Electrical cardioversion

Patients should then be anticoagulated for at least 4 weeks

63
Q

What is the main drug used for pharmaclogical cardioversion of atrial fibrillation?

A

Amiodarone

(or flecainide, if no evidence of structural heart disease)

64
Q

Following a stroke or TIA, what is the anticoagulant of choice?

A

Warfarin

65
Q

In acute stroke patients, why is anticoagulation therapy delayed?

A

Risk of haemorrhage

66
Q

When would digoxin be the preffered agen to control rate in patients with AF?

A

If the patient has coexistent heart failure

(otherwise, beta blocker or calcium channel blockers are used)

67
Q

Which agents can maintain sinus rhythm in patients with a history of AF?

A
  • Amiodarone
  • Flecainide
  • Sotalol
68
Q

What is lone AF?

A

AF in the absence of underlying heart disease

Possibly genetic

69
Q

What is the gold standard for terminating AF via cardioversion?

A

Electrical cardioversion

This is more effective than the pharmacological option

70
Q

In AF, where is the ectopic focus commonly located?

A

Ostia of pulmonary veins

71
Q

Where does ventricular tachycardia originate?

A

Ventricular ectopic focus

72
Q

What are the two main types of VT?

A

Monomorphic VT - Mostly caused by MI (all waves are the same on ECG)

Polymorphic VT - all waves on ECG are different as there are many areas producing ectopic beats

73
Q

Give a common example of polymorphic VT

A

Torsades de pointes

74
Q

How is VT managed if the patient has low systolic BP (<90mmHg), chest pain, heart failure or heart rate >150bpm?

A

Immediate cardioversion

75
Q

If antiarrhythmic drugs fail for VT management what must be used?

A

Electrical cardioversion

Syncronised DC shocks

76
Q

Which drugs will be used in VT?

A
  • Amiodarone
  • Lidocaine
77
Q

Which drug is strictly not used to treat VT?

A

Verapamil

78
Q

If drug therapy fails what can de done for patients with VT?

A
  • Implantable cardioverter-defibrillator (ICD) - particularly useful for patients with LV dysfunction
  • EPS - electrophysiological study
79
Q

Name some drugs that can induce a long QT interval

A
  • Amiodarone
  • Sotalol
  • Class 1a antiarrhythmic drugs
80
Q

What are some causes for a long QT interval?

A
  • Hypokalaemia
  • Hypocalcaemia
  • Acute MI
  • Myocarditis
81
Q

Which sign on an ECG is distinctive of Torsades de pointes?

A

Long QT interval

(may also deteriorate into VF)

82
Q

How is long QT interval treated?

A

Magnesium sulphate (IV)

83
Q

What causes Wolff-Parkinson-White syndrome?

A

Accessory pathway (bundle of Kent) between atria and ventricles

(can be left or right sided)

84
Q

Which type of arrhythmia is associated with WPW syndrome?

A

Atrioventricular re-entry tachycardia (AVRT)

85
Q

What are possible ECG features for WPW syndrome?

A
  • Short PR
  • Delta waves
  • Left/right axis deviation depending on side of accessory pathway
86
Q

How is type A (left sided - by far the most common) differentiated with type B (right sided) WPW syndrome?

A

There is a dominant R wave in V1 in type A that is not present in type B

87
Q

What is the management for WPW syndrome?

A

Radiofrequency ablation of the accessory pathway

Sotalol, amiodarone or flecainide

88
Q

When treating WPW syndrome, which drug should be avoided if there is coexistent AF?

A

Sotalol

(may increase transmission through accessory pathway by prolonging AV refractory period)

89
Q

What are cannon A waves and where are they seen?

A

Visible pulsations in the JVP

90
Q

What causes cannon A waves?

A

Particular associated with third degree heart block, when atria and ventricles contract simultaneously

A large pressure is pushed against the AV valves which radiated back up the jugular vein

This is also associated with pulmonary hypertension

91
Q

What defines first degree heart block?

A

Lengthened PR interval

(PR > 0.2 seconds)

The Cardiovascular System (24 decks)

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