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Cardiology > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What is first degree heart block?

A

This occurs when the electrical signal from the SA node is conducted to the ventricles, but the conduction is delayed more than normal

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2
Q

What are the criteria for the diagnosis of first degree heart block on ECG?

A

PR interval being longer than normal (>0.2s)

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3
Q

What can cause first degree heart block?

A
  • Coronary Artery Stenosis
  • Acute rheumatic Carditis
  • Digoxin Toxicity
  • Electrolyte disturbances
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4
Q

What are the different types of second degree heart block?

A
  • Wenckeback (Mobitz type 1)
  • Mobitz type 2
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5
Q

What is the general definition of second degree heart block?

A

When excitation intermittently fails to pass through the AV node or the bundle of His

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6
Q

What is a Wenckbach?

A

Mobitz type 1 Second degree heart block

This is characterised by progressive lengthening of the PR interval, and then failure to conduct an atrial beat. This is then followed by a conducted beat with a shorter PR interval, after which the cycle repeats.

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7
Q

What is a mobitz type II second degree heart block?

A

This occurs when most beats are conducted with a constant PR interval, but occasionally atrial depolarisation occurs without subsequent ventricular depolarisation.

The PR interval of the conducted atrial beats is normal.

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8
Q

What is important to remember about Mobitz type II second degree heart blocks?

A

They can descend into complete heart block

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9
Q

What are the subtypes of type II 2nd degree heart block?

A
  • 2:1 Block
  • 3:1 block
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10
Q

What is 2:1 type II 2nd degree heart block?

A

When there are alternate conducted and non-conducted atrial beats. In the case of 2:1, this means that there is one conducted beat, followed by two non-conducted beats. This gives twice as many P waves as QRS complexes.

The PR interval again remains constant for conducted beats.

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11
Q

What is 3:1 type II 2nd degree heart block?

A

There are three P waves to every QRS complex. This means that only 1/3 of the P waves are conducted. The PR interval of the conducted P waves remains constant.

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12
Q

What are the causes of wenckebach phenomena?

A
  • Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
  • Increased vagal tone (e.g. athletes)
  • Inferior MI
  • Myocarditis
  • Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
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13
Q

What is the mechanism of third degree heart block?

A

Atria are contracting but there is no conduction to the ventricles (no relationship between P and QRS complex). Ventricles are excited by a slow escape rhythm which takes over, from a depolarising focus with the ventricular muscle.

This causes the QRS complexes to become abnormally shaped due to the abnormal spread of depolarisation from ventricular focus. The complexes can also become broader than normal.

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14
Q

What are causes of third degree heart block?

A

MI

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15
Q

What can cause mobitz type II heart block?

A
  • Anterior MI - septal infarction with necrosis of the bundle branches
  • Idiopathic fibrosis of the conducting system
  • Cardiac surgery
  • Inflammatory conditions - rheumatic fever, myocarditis, Lyme disease
  • Autoimmune - SLE, systemic sclerosis
  • Infiltrative myocardial disease - amyloidosis, haemochromatosis, sarcoidosis
  • Hyperkalaemia.
  • Drugs - beta-blockers, calcium channel blockers, digoxin, amiodarone.
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16
Q

What is the difference between mobitz type I and mobitz type II heart block in terms of mechanism?

A

Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), whereas Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).

Mobitz I is produced by progressive fatigue of the AV nodal cells, whereas Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.

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17
Q

What are causes of complete heart block?

A
  • Inferior myocardial infarction
  • AV-nodal blocking drugs - calcium-channel blockers, beta-blockers, digoxin
  • Idiopathic degeneration of the conducting system
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18
Q

What is atrial flutter?

A

When the atrial rate is > 250/min and there is no flat baseline between the P-waves, atrial flutter is present.

Any arrhytmia should be identified from the lead in which P-waves can most easily be seen

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19
Q

What are the criteria for atrial flutter?

A
  • P-waves seen at a rate >250/min - often in a sawtoothed appearance.
  • Ventricular activation remains constant
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20
Q

What is atrial fibrillation?

A

When the atrial muscle fibres contract independently of ventricular muscle fibres. The AV node is bombarded with depolarisation waves of varying strength from the independently fibrillating cardiac muscles.

Depolarisation spreads down the bundle of His at irregular intervals in an all or nothing fashion. This means that the depolarisation is of constant intensity. However, the ventricles contract irregularly (rhythm wise).

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21
Q

What are the characteristics of atrial fibrillation on an ECG?

A
  • No P waves, and an irregular baseline
  • Irregular QRS complex, which are normally shaped
  • Waves can be seen in V1 which resemble atrial flutter
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22
Q

How much does cardiac output drop by in atrial fibrillation?

A

10-20%

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23
Q

What is the main risk from atrial fibrillation?

A

Embolic stroke

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24
Q

Why is atrial fibrillation associated with left or right atrial enlargement?

A

An enlarged atrium increases the potential for re-entrant circuits

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25
Q

What are causes of AF?

A
  • MI
  • Heart failure/Ischaemia
  • Hypertension
  • Hyperthyroidism
  • PE
  • Pneumonia
  • Caffeine
  • Alcohol
  • Decreased K+, Mg2+
  • Cardiomyopathy
  • Constrictive pericarditis
  • Sick Sinus syndrome
  • Lung Cancer
  • Endocarditis
  • Atrial myxoma
  • Haemochromatosis
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26
Q

Why is atrial fibrillation potentially dangerous?

A

Compromisation of cardiac output -> Hypertension and pulmonary congestion

Blood stasis in the atria -> thrombus formation (particularly left atrial appendage)

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27
Q

What are the main aspect of approaching the management of AF?

A
  1. Ventricular rate control
  2. Restore sinus rhythm
  3. Assessemtn for need to anticoagulate
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28
Q

What are the symptoms of someone with AF?

A

Can be asymptomatic

If symptomatic

  • Chest pain
  • Palpitations
  • Dyspnoea
  • Syncope
  • Fatigue/Faintness
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29
Q

What are signs of AF?

A
  • Irregularly Irregular rhythm
  • Apical pulse rate > radial pulse rate
  • S1 of variable intensity
  • Signs of LVF
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30
Q

What is re-entry?

A

A reentry arrhythmia occurs when the electrical wave front in the heart gets caught in a loop. When this happens, the depolarization will repeatedly cycle through the tissue utilized in the loop until something interrupts it.

For re-entrance to occur, there has to be a unidirectional block within a conducting pathway.

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31
Q

What are the ECG characteristics of AF?

A
  • Absent P-waves
  • Irregular baseline
  • Irregular QRS - normally shaped
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32
Q

If someone presented with Chest pain, palpitations and syncope, what investigations would you do?

A
  • ECG
  • Bloods - U+E’s, Troponin, TFTs
  • ECHO
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33
Q

What are the different classifications of AF?

A
  • First detected
  • Paroxysmal
  • Persistent
  • Permanent
34
Q

How would you manage someone with Acute AF who was very unwell or showing signs of haemodynamic instability?

A
  • Give Oxygen and take U+E’s
  • Emergency cardioversion - if unavailable - IV amiodarone 300 mg over 1hr
35
Q

What is haemodynamic instability?

A

If a person is hemodynamically stable, it means that he/she has a stable heart pump and good circulation of blood. Hemodynamic instability is defined as any instability in blood pressure which can lead to inadequate arterial blood flow to organs.

36
Q

If someone was haemodynamically stable with symptomatic AF, how would you manage them?

A

Assess for heart failure

  • No heart failure - B-Blockers (bisoprolol) or CCB (Verapimil, diltiazim)
  • Heart failure - Digoxin or amiodarone

Determine thromboembolism risk (CHA2DS2-VASc Score)

  • <48hrs + no TE on ECHO - DC/Pharmacological Cardioversion
  • >48hrs + no TE on ECHO - Establish LMWH, then DC cardioversion
  • TE on ECHO - LMWH + Warfarin/DOAC, then cardioversion after 3-4 weeks
37
Q

How would you assess someone with AF for thrombus?

38
Q

How would you manage someone with chronic AF?

A
  • Rate control
  • Rhythm control
  • Anticoagulation
39
Q

When treating chronic AF, what would you do to try and control rate?

A
  • 1st choice - B-blockers (bisoprolol) or CCB (verapimil, diltiazem)
  • 2nd choice - digoxin or amiodarone (if digoxin fails)
40
Q

When would you use digoxin or amiodarone to treat acute AF as a first line?

A

If the patient has heart failure

41
Q

When treating chronic AF, what would you do to try and control rhythm?

A
  • DC cardioversion
  • Ablate and pace - ablate AV node, insert pacemaker
  • Pulmonary vein ostial ablation
  • Maze procedure
42
Q

How would you anticoagulate someone with Chronic AF?

A
  • Warfarin/DOACs
  • Can use aspirin instead
43
Q

What are indications for cardioversion in someone with acute AF?

A
  • < 48 hrs - Very unwell/haemodynamically unstable + presentation within 48 hour window
  • >48 hours - anticoagulation for 3 weeks prior to cardioversion, and continue for 4 weeks after cardioversion (longer if high risk for stroke)
  • Thrombus ruled out by TOE
44
Q

What are supraventricular tachycardias?

A

An abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart. The atria contract faster than 150/min

45
Q

What is the maximum rate at which the AV node can conduct atrial depolarisation?

A

About 200/min - anything beyond this and AV block occurs, with some P-waves not followed by QRS complexes

46
Q

What are the different SVT’s?

A
  • Sinus node tachycardia
  • AV node re-entry tachycardia
  • AV re-entry tachycardia
  • Atrial Flutter
  • Atrial Fibrillation
47
Q

What is sinus tachycardia?

A
  • Normal response to things like exercise, fear, pain etc.
  • These are sinus rhythms which exceed 100 bpm
48
Q

What is AV node re-entry tachycardia?

A

https://www.youtube.com/watch?v=36MT8hR-gDg

Two functionally and anatomically different pathways present within the AV node. One of these pathways conducts quicker with a long refractory period, and the other conducts more slowly with a quicker refractory period.

In sinus rhythm, the fast one is involved in depolarisation of the ventricles. If depolarisation occurs early, this is conducted by the slow pathway as the fast pathways is still refractory. It then travels back through the fast pathway which is no longer refractory (slow-fast conduction)

49
Q

What are the characteristic features on AVNRT on ECG?

A
  • Characterised by no P-waves, or P-waves directly before or after the QRS complex
  • Regular normal QRS complex
50
Q

What is AV re-entry tachycardia?

A

Can cause Wolff-Parkinson White syndrome

Characterised by an abnormal connection of myocardial fibres from the ventricle back to the atrium (accessory pathway). This results from incomplete separation of the atria during development

Conduction occurs through this pathway without the delay of the AV node, meaning that the ventricles are excited early. The accessory pathway conductivity and location are significant factors, and the location can be determined

https://www.youtube.com/watch?v=36MT8hR-gDg

51
Q

What is Wolff Parkinson white syndrome?

A

Caused by congenital accessory conduction pathway between atria and ventricles.

A constellation of symptoms associated with WPW ECG patterns. Symptoms can include an tachycardia, palpitations, shortness of breath, lightheadedness, or syncope.

52
Q

What are the most common arrythmias that people with WPW present with?

A
  • AVRT
  • Atrial Flutter
  • Atrial Fibrillation
53
Q

What is the name of the accessory pathway found in WPW?

A

Bundle of kent

54
Q

What are the characteristic features of WPW on ECG?

A
  • Delta-Wave
  • Short PR interval
  • Wide QRS complex
  • Dominant R-wave in V1 - type A
  • Deep S-wave in V1 - type B
55
Q

What is ventricular fibrillation?

A

https://www.youtube.com/watch?v=kETghJagzOY

This is a very rapid ventricular activation with no mechanical effect. It is caused by uncoordinated contraction of the ventricles, which causes them to quiver. This rhythm rarely resolves by itself.

56
Q

What are cardiac causes of Ventricular fibrillation?

A
  • Myocardial ischemia / infarction
  • Cardiomyopathy (dilated, hypertrophic, restrictive)
  • Channelopathies e.g. Long QT (acquired / congenital) causing TdP –> VF and Brugada syndrome
  • Aortic stenosis
  • Aortic dissection
  • Myocarditis
  • Cardiac tamponade
  • Blunt trauma (Commotio Cordis)
57
Q

What are respiratory causes of VF?

A
  • Tension pneumothorax
  • Pulmonary embolism
  • Primary pulmonary hypertension
  • Sleep apnoea
  • Bronchospasm
  • Aspiration
58
Q

What are environmental causes of VF?

A
  • Electrical shocks, drowning, hypothermia
  • Sepsis
59
Q

What are the characteristic features of VF on ECG?

A
  • Chaotic irregular deflections of varying amplitude
  • No identifiable P waves, QRS complexes, or T waves
  • Rate 150 to 500 per minute
  • Amplitude decreases with duration (coarse VF -> fine VF)
60
Q

What is ventricular tachycardia?

A

https://www.youtube.com/watch?v=xAfj5AHxC2I

A type of tachycardia which originates in the ventricles and is usually broad complex tachycardia (QRS >140 bpm). This causes heart rate to exceed 150-200 bpm.

The ventricular rate of contraction starts driving the heart beat, rather than the SA node

61
Q

What can cause ventricular tachycardia?

A
  • IHD
  • Previous MI
  • Cardiomyopathies
  • Ion Channel Disorders
  • Congenital Heart disease
62
Q

What are the characteristic features of VT on ECG?

A
  • Very broad complexes (>160ms).
  • Absence of typical RBBB or LBBB morphology.
  • Extreme axis deviation (“northwest axis”)
  • AV dissociation (P and QRS complexes at different rates).
  • Capture beats/Fusion beats
  • Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.
  • Josephson’s sign – Notching near the nadir of the S-wave.
63
Q

What are the different subtypes of VT?

A
  • Monomorphic - Beats match each other in each lead
  • Polymorphic - beat to beat variation
64
Q

What is a capture beat?

A

Occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.

The sinus node “captures” the ventricles producing a narrow-complex beat

65
Q

What is a fusion beat?

A

Occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.

The first of the narrower complexes is a fusion beat (the next two are capture beats).

66
Q

What is concordance?

A

QRS complexes are either all positive or all negative

67
Q

What can cause sinus bradycardia?

A
  • Athletic training
  • Fainting attacks
  • Hypothermia
  • Myxoedema
68
Q

What can cause sinus tachycardia?

A
  • Exercise
  • Fear
  • Pain
  • Haemorrhage
  • Thyrotoxosis
69
Q

What is sinus arrest?

A

The SA node transiently ceases to generat electrical impulses that normally stimulate the myocardium.

It is defined as lasting from 2.0 seconds to several minutes. If the SA node begins depolarising again, normal rhythm can be resumed. If not, other pacemaker regions within the heart take over depolarisation.

70
Q

When is no impulse regarded as sinus arrest?

A

if it lasts > 2 seconds

71
Q

What rate is the Atrial escape rhythm?

72
Q

What rate is the junctional escape rhythm?

73
Q

What rate is the ventricular escape rhythm?

74
Q

What is an atrial ectopic beat?

A

Also known as supraventricular ectopic

Occurs when the atria depolarise earlier than it should. The accompanying heartbeat is called an extra systole. The term ectopic refers to the depolarisation occurring in an abnormal location. These have abnormal p-waves. QRS complexes remain the same.

75
Q

What is a ventricular ectopic beat?

A

These are caused by early firing of the ventricles. They have abnormal QRS complexes, which are typically wide and can be of almost any shape. These are common and usually of no importance.

76
Q

Why are ventricular ectopics potentially dangerous?

A

When they occur in the T-wave of a preceding beat, they can induce VF and are thus potentially dangerous.

77
Q

What are the different criteria used in the CHA2DS2-VASc score used to assess for risk of stroke in AF?

A
  • Congestive HF - 1 point
  • Hypertension - 1 point
  • Age > 75 - 2 point
  • Diabetes mellitus - 1 point
  • Prior Stroke/TIA - 2 point
  • VAScular disease - 1 point

Anything above 1 and you should consider anticoagulation

78
Q

If someone had a CHA2DS2-VASc score of 0 with AF, what anticoagulant therapy would you start them on?

A

None, or aspirin

79
Q

If someone had a CHA2DS2-VASc score of 1 with AF, what anticoagulant therapy would you start them on?

A

Aspirin or Warfarin

80
Q

If someone had a CHA2DS2-VASc score of >/=2 with AF, what anticoagulant therapy would you start them on?

81
Q

What mnemonic can you use to for determining the causes of atrial fibrillation?

A

PIRATES

  • PE, Pulmonary disease, Post-operative
  • IHD, Idiopathic
  • Rheumatic valvular disease
  • Anemia, Alcohol, Age, Autonomic tone
  • HyperThyroid
  • Elevated BP (hypertension), Electrocution
  • Sleep apnea, Sepsis, Surgery

Cardiology (29 decks)

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