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Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is the definition of an arrhythmia?

A

An abnormal cardiac rhythm where the normal HR is between 60 - 100 bpm

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2
Q

What can arrhythmias result in?

A
  • Sudden death
  • Syncope
  • Heart failure
  • Chest pain
  • Dizziness
  • Palpitations
  • No symptoms at all
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3
Q

What are the two main types of arrhythmia?

A
  • Tachycardia

- Bradycardia

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4
Q

What is the definition of bradycardia?

A

Heart rate is slow (less than 60bpm during the day and less than 50bpm at night)

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5
Q

What is the definition of tachycardia?

A

Heart rate is fast - more than 100bpm

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6
Q

What can tachycardias be subdivided into?

A

Supraventricular tachycardias and ventricular tachycardias

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7
Q

Where do supraventricular tachycardias arise from?

A

From the atrium or the AV junction

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8
Q

Where do ventricular tachycardias arise from?

A

The ventricles

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9
Q

What are the four types of supraventricular tachycardia?

A
  1. Atrial fibrillation
  2. Atrial Flutter
  3. AV reentrant tachycardia (AVRT) e.g. Wolf-Parkinson-White syndrome
  4. AV nodal reentrant tachycardia (AVNRT)
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10
Q

What are the two types of ventricular tachycardia?

A
  1. Ventricular tachycardia

2. Ventricular fibrillation

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11
Q

How does atrial fibrillation develop?

A

Risk factors cause stress to the atrium leading to tissue heterogeneity. These different tissue properties then cause unpredictable contractions of the atria. Multiple wavelets then conduct around the atria and can collide to create daughter wavelets. No unified atrial contraction - chaotic irregular atrial rhythm caused -

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12
Q

What are the causes of AF?

A
  • Idiopathetic
  • Hypertension
  • Any condition that causes increase in pressure
  • Heart failure
  • Coronary artery disease
  • Vascular heart disease
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13
Q

What are the risk factors of AF?

A
  • Older than 60
  • Diabetes
  • High blood pressure
  • Coronary artery disease
  • Prior MI
  • Structural heart disease (valve problems or congenital defects)
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14
Q

What is the dangerous risk of AF and why?

A

Risk of stroke as the blood isn’t being pumped properly from the atria to the ventricles and so can stagnate and cause a clot which can then travel to the brain.

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15
Q

What are the symptoms of AF?

A
  • May have no symptoms
  • Palpitations - thumping
  • Dyspnea - shortness of breath
  • Chest pain
  • Fatigue - as heart pumping at high bpm but delivering blood less effectively
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16
Q

What would show in the ECG in AF?

A
  • Absent P waves
  • Rapid irregular QRS complexes
  • Absence of an isoelectric baseline
  • Variable ventricular rate
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17
Q

What is the acute management for AF?

A
  • Cardioversion - depolarise all the tissues and allow the SAN to take over.
  • Ventricular rate control - achieved by drugs that block the AV node e.g calcium channel blockers or beta blockers
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18
Q

What are the two strategies used in the management for long term and stable AF?

A

Rate control or rhythm control

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19
Q

How would you control the rate in long term AF?

A
  • AV nodal slowing agents plus oral anticoagulation
  • Beta-blocker e.g. Bisoprolol
  • Calcium channel blocker e.g. Verapamil or Diltiazem
  • If above fails then try Digoxin and then consider Amiodarone
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20
Q

How would you control the rhythm in long term AF?

A
  • Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia
  • Appropriate anti-coagulation
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21
Q

When is rhythm control advocated over rate control?

A

In younger, symptomatic and physically active patients

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22
Q

How do you assess the risk of a stroke?

A

Use the CHA2DS2-VASc score

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23
Q

What is atrial flutter?

A

Atrial flutter is usually an ORGANISED atrial rhythm with an atrial rate typically between 250-350bpm

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24
Q

What is atrial flutter caused by?

A

It’s caused by a re-entry circuit within the right atrium, which overrides the SAN

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25
Q

What are the causes of atrial flutter?

A
  • Idiopathic (30%)
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
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26
Q

How does the re-entry circuit occur in atrial flutter?

A

Heart cells become irritated due to an underlying condition this causes them to change their properties and the re-entry circuit to develop

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27
Q

What are the symptoms of atrial flutter?

A
  • Palpitations
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
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28
Q

What are the ECG findings on an atrial flutter?

A
  • Narrow complex tachycardia
  • No normal P waves (flutter waves, F waves - ‘Sawtooth’ appearance) represent re entry circuits causing contraction
  • Each F wave cannot induce ventricle contraction due to longer refractory period of AV node - so QRS present every few F waves E.g. 2:1 atrial to ventricular
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29
Q

What is the treatment of atrial flutter?

A
  • Electrical cardioversion but anticoagulate before e.g low molecular weight heparin e.g. Enoxaparin or Dalteparin if acute i.e. atrial flutter started less than 48 hours ago
  • Radiofrequency catheter ablation - ablation of the tricuspid valve isthmus
  • Block offending re-entrant wave and restoring normal rhythm
  • IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias
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30
Q

What are the risks of atrial flutter?

A
  • Prolonged tachycardia lead to ventricles decompensating = Heart failure
  • Atria not contracting effectively so blood stagnates and clots = Stroke
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31
Q

What is AV reentrant tachycardia (AVRT)?

A
  • It is formed by the normal conduction system and an accessory pathway connecting the ventricles to the atria resulting in circus movement.
  • Impulses can travel from atria to ventricle (anterograde) or from ventricle back to atria (retrograde)
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32
Q

What syndrome is an example of AVRT?

A

Wolf-Parkinson-White syndrome

33
Q

What is Wolf-Parkinson-White-Syndrome

A

Where the accessory pathway by passes the AV node and causes early abnormal depolarisation which is called pre excitation

34
Q

How is the pre excitation in Wolf-Parkinson-White-Syndrome reflected on the ECG?

A
  • Short PR interval

- Wide QRS complex that begins as a slurred part known as a delta wave

35
Q

Why does the QRS complex start to slur in Wolf-Parkinson-White-Syndrome?

A

As part of the ventricle is contracting before the rest due to the pre excitation phase

36
Q

Explain what happens in WPW syndrome?

A

In WPW there is an extra bit of conduction tissue called the Bundle of kent that carries impulses from the atria to the ventricles without going through the SAN. The signal bi-passing the SAN causes the ventricles to contract early (pre-excitation). This combines with the signal that comes through the SAN node. Ventricles are contracting early which makes the PR interval shorter and the overall QRS complex is longer.

37
Q

What are the symptoms of WPW?

A

Often asymptomatic but when it does present it presents with

  • Palpitations
  • Severe dizziness
  • Dyspnea
  • Syncope - fainting
38
Q

What is AV nodal reentrant tachycardia (AVNRT)?

A
  • Slow (alpha) pathway ends up going back up the fast (beta) pathway due to its fastest refractory period and its restimulation before the beta pathway can be stimulated again. This results in a loop where the atria and the ventricles are contracting at the same time.
39
Q

What is the presentation of AVNRT?

A
  • Rapid regular palpitations with abrupt onset and sudden termination
  • Severe dizziness
  • Dyspnea
  • Syncope
  • Polyuria (due to the release of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)
40
Q

What would the ECG show in AVNRT?

A

P waves are not seen or are seen directly before the QRS complex due to the atria and the ventricles contracting at basically the same time.

41
Q

What are the treatment options for AVNRT and AVRT?

A
  • Radiofrequency catheter ablation - basically destroying the accessory pathway or the slow pathway in the case of AVNRT
  • Vagal manoeuvres - activating the vagus nerve which will then temporarily block the AVN (breath holding, carotid massage)
  • If manoeuvres are not effective then IV adenosine
  • Cardioversion
42
Q

What is radiofrequency catheter ablation?

A

Radio waves are used to destroy the tissue that is causing the irregular heart beat

43
Q

What is the definition of long QT syndrome?

A

When the QT interval is over 1/2 of a cardiac cycle or greater than 440ms for males and greater than 460ms for females at a rate of 60bpm.

44
Q

What is the cause of long QT syndrome?

A

Caused by abnormal repolarization of some of the heart cells either from congenital abnormalities or from medication.

45
Q

If long QT syndrome gives rise to a recurrent circuit what will this cause?

A

Polymorphic QRS complexes

46
Q

What is the presentation of LQTS?

A
  • Palpitations

- Syncope

47
Q

What is the treatment for LQTS?

A
  • Treat underlying cause

- If acquired long QT then give IV isoprenaline (contraindicated for congenital long QT)

48
Q

What are the two types of ventricular tachycardia?

A
  • Premature ventricular tachycardia

- Focal ventricular tachycardia

49
Q

What is premature ventricular tachycardia?

A

Single beats coming from the ventricles. Can lead to sudden death if over 250bpm.

50
Q

What is the problem that premature ventricular contraction causes?

A

There is less time for the ventricles to fill between each beat so less blood is pumped to the body and to the brain.

51
Q

What is focal ventricular tachycardia?

A

This is when pacemaker cells in the ventricles get irritated and start firing quicker than the cells in the SAN node. Usually these fire a lot slower and so never get a chance to cause an impulse.

52
Q

Why might the cells become stressed or irritated in focal ventricular tachycardia?

A
  • Medications/ drugs e.g. meth
  • Ischaemia - scarred or dead tissue can lead to signals moving around the dead tissue and can create a reentrant ventricular tachycardia
53
Q

What does the ECG look like in ventricular tachycardia?

A

More frequent QRS complexes

54
Q

What is the difference between a monomorphic and a polymorphic ECG pattern?

A 
Monomorphic = all QRS complexes look the same - as a result of the impulse coming from the same place each time - could be recurrent or focal 
Polymorphic = QRS complexes are difference - as a result of the impulses coming from different areas of the ventricle - could be as a result of different pacemaker cells firing
55
Q

What is the treatment for ventricular tachycardia?

A
  • Cardioversion with drugs

- Radiofrequency catheter ablation

56
Q

What do you branch bundle blocks cause in an ECG?

A

Wide QRS complexes

57
Q

What is a right bundle branch block?

A

No depolarization down right branch - activation of the RV is delayed as depolarisation has to spread across the septum from the left ventricle.

58
Q

What are the causes of a bundle branch block?

A
  • Pulmonary embolism
  • Ischaemic heart disease (fibrous tissue blocks electrical impulse)
  • Atrial/ Ventricular septal defect, R heart failure, RV hypertrophy
59
Q

What does a bundle branch block cause in the heart sound?

A

A wide physiological splitting of the second heart sound

60
Q

What ECG changes do you see in a right bundle branch block?

A
  • Broad QRS > 120 ms
  • RSR’ pattern in V1-3 (V1-3 are leads that represent RV) (‘M-shaped’ QRS complex)
  • Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
  • MaRRow
61
Q

What is a left bundle branch block?

A

The impulse has to spread from the right ventricle across the septum to the left ventricle.

62
Q

What ECG changes do you get in a left bundle branch block?

A
  • QRS duration to > 120 ms
  • Eliminates the normal septal Q waves in the lateral leads.
  • V1 - deep S waves = W waves
  • I, aVL, V5 and V6 - tall R waves
  • WiLLiaM
63
Q

What physiological sound do you get in left bundle branch block?

A

reverse splitting of the second heart sound

64
Q

What are the three types of AV block?

A

First degree, second degree and third degree

65
Q

What are the characteristics of first degree heart block (husband, P, comes home late but at the same time)?

A
  • Not block but delay
  • Prolonged PR interval > 0.22s
  • Every atrial depolarisation is followed by conduction to the ventricles but with delay
66
Q

What are the cause of first degree block?

A
  • Hypokalemia
  • Myocarditis
  • Inferior MI
  • Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
67
Q

What is the presentation and management of first degree block?

A

There are no symptoms and no treatment is required.

68
Q

What are the three variations of second degree block?

A
  1. Mobitz type I (Weinkebach)

2. Mobitz type II

69
Q

What are the characteristic of Mobitz type I (husband p comes home later each now)?

A

Progressive lengthening of PR interval then failure of proper conduction, so a beat is ‘dropped’ and there is a missing P wave on the ECG

70
Q

What are the causes of Mobitz type I?

A

Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin. Also Inferior MI.

71
Q

What is the presentation and possible treatment for Mobitz type I?

A

Usually benign and does not need treatment until causing symptoms (light headedness, dizziness and syncope)

72
Q

What are the characteristics of Mobitz type II (husband always home at the same time but sometimes he doesn’t come home at all)?

A

PR interval is constant but then there is atrial depolarization without ventricular depolarization (‘drops a beat’).

73
Q

What are the causes of Mobitz type II?

A

Anterior MI, Mitral valve surgery, SLE and Lyme disease, Rheumatic fever

74
Q

What does Mobitz type II result in?

A

Shortness of breath, postural hypotension and chest pain

75
Q

Should a pacemaker be used in Mobitz type II?

A

Yes as there is a high risk of developing sudden complete AV block

76
Q

What is third degree heart block (husband and wife living seperate)?

A
  • Complete absence of AV conduction
  • None of the supraventricular impulses are conducted to the ventricles
  • Ventricle cells recognise not getting impulse to create own electrical rhythm = ventricular escape rhythm
77
Q

How will third degree heart block present?

A

Typically, the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation

78
Q

What are the causes of third degree block?

A
  • Structural heart disease e.g. transposition of great vessels
  • Ischaemic heart disease e.g. acute MI, Hypertension
  • Endocarditis
  • Lyme disease
79
Q

What are the treatment options for third degree block?

A

It depends on the etiology, one option is a permanent pacemaker or IV atropine.

Cardio (9 decks)

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