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Study Notes - Cardiology > *Arrhythmias > Flashcards

*Arrhythmias Flashcards

1
Q

What is an arrhythmia?

A

Abnormality of heart rate or rhythm

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2
Q

What are the 2 broad anatomical types of arrhythmias?

A

Supraventricular

Ventricular

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3
Q

What are the names of the 3 internal tracts that connect the SA node and AV node?

A

Anterior, middle and posterior internodal tracts

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4
Q

What are ectopic beats?

Name when you have several of these in a row?

A

Beats or rhythms that originate in places other than the SA node (when the latent pacemaker fires at a rate faster than the SA node)
Ectopic rhythm - ectopic focus dictates the entire rhythm

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5
Q

Are ectopic beats/ rhythms dangerous?

A

Depends how the affect the cardiac output

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6
Q

How can arrhythmias be categorised based on rate?

A

Tachyarrhymias

Bradyarrhytmias

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7
Q

What are the 4 types of atrial tachycardia? (SVT)

A

Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia
Sinus tachycardia

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8
Q

What are the 2 types of atrial bradycardia?

A

Sinus bradycardia

Sinus pauses

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9
Q

What are the 3 types of atrioventricular node arrhythmias?

A

AV node re-entry
Accessory pathways
AV block

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10
Q

What are the 4 types of ventricular arrhythmias??

A

Premature ventricular complex
Ventricular tachycardia
Ventricular fibrillation
Asystole

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11
Q

What are the clinical causes of arrhythmias? (5)

A

Abnormal anatomy e.g. left ventricular hypertrophy, accessory pathways
Autonomic e.g. sympathetic stimulation (nervousness, hyperthyroidism), increased vagal tone
Metabolic e.g. hypoxic myocardium, ischaemic myocardium, electrolyte imbalances
Inflammation e.g. viral myocarditis]Drugs
Genetics (mutations of cardiac ion channels) e.g. congenital long QT syndrome

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12
Q

What are the 5 mechanisms of arrhythmias?

A

Defects in impulse formation (altered automaticity, triggered activity)
Defects in impulse conduction (re-entry, accessory tracts, conduction block)

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13
Q

What is altered automaticity?

A

When a latent pacemaker takes over the SA nodes function as the normal pacemaker of the heart (causes escape or ectopic beats) - can occur physiologically when the ANS modulates the SA nods activity e.g. caused by drugs, ischaemia

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14
Q

What is triggered activity?

A

When abnormal action potentials are triggered by a preceding action potential resulting in the heart cells beating twice e.g. tornadoes de points

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15
Q

What is re-entry?

A

Self-sustaining electrical circuit stimulates an area of the myocardium to be stimulated repeatedly

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16
Q

What is conduction block?

A

Any disease that disrupts electrical conduction may reduce conduction or cause heart block

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17
Q

What are accessory pathways?

A

Additional electrical conduction pathway between 2 areas of the heart e.g. WPW

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18
Q

What effect does hypothermia have on phase 4 of AP slope?

A

Decreases it (altered automaticity)

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19
Q

What effect does hyperthermia have on phase 4 of action potential slope?

A

Increases it (altered automaticity)

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20
Q

What effect do hypoxia and hypercapnia have on phase 4 of AP slope?

A

increase it (altered automaticity)

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21
Q

What effect does hypokalaemia have on phase 4 of AP slope?

A

Increases it (also prolongs repolarisation and increases ectopics)

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22
Q

Symptoms of arrhythmias?

A

Palpitations (a noticeably rapid, strong or irregular heart beat)
SOB
Diziness
Syncope
Sudden cardiac death
Worsen pre-exisiting conditiosn e.g. angina

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23
Q

Investigations of arrhythmias? (&)

A 
12 lead ECG
CXR
Echocardiogram
Stress ECG
24 hours ECG hotter monitoring
Event recorder
Electrophysiological (EP) study
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24
Q

Why is an ECG done for arrhythmias?

A

To assess rhythm

Signs of previous MI, pre-excitation (WPW)

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25
Q

What sign on an ECG suggests a previous MI?

A

Pathological Q waves

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26
Q

Why perform an exercise ECG in a patient with suspected arrhythmia?

A

To assess for ischaemia

Exercise induced arrhythmia

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27
Q

Why perform a 24 hour hotter ECG in a patient with suspected arrhythmia?

A

To assess for paroxysmal arrhythmia

To link symptoms to underlying heart rhythm

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28
Q

Why perform an echo in a patient with suspected arrhythmia?

A

To assess for structural heart disease

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29
Q

Why perform an electrophysiological study in a patient with a suspected arrhythmia?

A

To trigger the arrhythmia and study its mechanism

Opportunity to treat by ablation at the same time

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30
Q

What are the symptoms of atrial ectopic beats?

A

Asymptomatic

palpitations

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31
Q

Treatment of atrial ectopic beats?

A

Generally no treatment but patients may find B blockers helps (avoid stimulants e.g. caffeine)

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32
Q

When is sinus bradycardia physiological?

A

Athlete

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33
Q

What is sick sinus syndrome?

A

Sinus node dysfunction causing bradycardia +/- rest, senatorial block, or SVT alternating with bradycardia/ asystole

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34
Q

What are causes of sinus bradycardia?

A

Drugs e.g. beta blockers
Ischaemia
Lots more

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35
Q

Treatment of sinus bradycardia?

A

Atropine (if acute, e.g. MI)

Pacing if haemodynamic compromise e.g. hypotension, CHF, angina, collapse

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36
Q

Causes of sinus tachycardia?

A

Physiological in anxiety, fever, hypotension, anaemia

Inappropriate due to drugs, etc.

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37
Q

Treatment of sinus tachycardia?

A

Treat underlying cause

B-adrenergic blockers

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38
Q

What is an example of a paediatric vagal manoeuvre (used to treat SVT)?

A

ice water to face for infants

Blow through straw (valsalva) for child or adolescents

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39
Q

What is the most common cause of SVT?

A

Atriventricular re-entry

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40
Q

What causes atrioventricular re-entry anatomically?

A

A small re-entry circuit involving the atrioventricular node and surrounding atrial tissue

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41
Q

What is wolf-parkinson-white?

A

Presence of an accessory pathway between the atria na ventricles causing ventricular pre-excitation

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42
Q

What type of abnormality does WPW cause on an ECG?

A

Delta waves

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43
Q

Acute management of SVT?

A

Vagal manoeuvres
IV adenosine (extremely short half life so have to push it in as fast as you can)
IV verapamil

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44
Q

Chronic management of SVT?

A

Avoid stimulants
Radifrequency ablation
Anti-arrhythmic drugs (Class II or IV)

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45
Q

What is cardiac ablation?

A

Selective cauterisation of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

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46
Q

What does cardiac ablation involve?

A

Placement of catheters in heart via femoral veins
Intracardiac ECG recorded during sinus rhythm, tachycardia and during pain manoeuvres
Catheter placed over focus/ pathway and tip heated

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47
Q

What causes AV node conduction disease?

A 
Ageing process
Acute MI
Myocarditis
Infiltrative disease e.g. amyloid
Drugs e.g. B blcokers, Calcium channel blockers
Calcific aortic valve disease
Post-aortic valve diseases
Genetic e.g. Lenore's disease, myotonic dystroph
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48
Q

1st degree heart block?

A

PR interval prolonged (greater than 0.2 seconds)

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49
Q

Treatment of 1st degree heart block?

A

None - long term follow up recommended as more advanced block may develop

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50
Q

What are the 2 types of 2nd degree heart block?

A

Mobitz I

Mobitz II

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51
Q

What is Mobitz I?

A

Prolong PR interval cumulating in a droped ventricular beat (QRS complex)

52
Q

what is Mobitz II?

A

Regularly more than one P wave to each QRS complex in a 2:1, 3:1 or 4:1 ratio

53
Q

Treatment of mobitz II?

A

Permanent pacemaker

54
Q

Treatment of mobitz I?

A

Ventricular pacing

55
Q

What is third degree heart block?

A

Complete atrioventricular dissociation: regular P waves, regular QRS complexes but no association between the 2

56
Q

Treatment of 3rd degree heart block?

A

Ventricular pacing

57
Q

What is trancutaneous pacing?

A

Using a defibrillator to pace the heart during an emergency (other type is transvenous)

58
Q

What are the 2 types of pacemakers available?

A 
Single chamber (paces the right atria or right ventricle only)
Dual chamber (paces the RA and RV)
59
Q

What is a single chamber pacemaker used for?

A 
Atrial = isolated SA node disease but normal AV node
Ventricular = AF with slow ventricular rate
60
Q

What is a dual chamber pacemaker used for?

A

Maintains AV synchrony - AVN disease

61
Q

What are premature ventricular complexes?

A

ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia

62
Q

What causes premature ventricular complexes?

A

May not have structural heart disease
Ischaemic heart disease
Hypertension with left ventricular hypertrophy
Heart failure
May be marker for inherited arrhythmia syndrome

63
Q

Symptoms of premature ventricular complexes?

A

Usually asymptomatic

64
Q

Treatment of premature ventricular ectopics?

A

Beta blockers

65
Q

What is a broad complex tachycardia in a patient with no history of cardiac disease?

A

VT

66
Q

What is ventricular tachycardia?

A

Tachycardia originating from a ventricular focus

67
Q

Is VT life threatening?

A

Yes

68
Q

What type of patients does VT occur in?

A

Usually those with significant heart disease e.g. coronary artery disease
Rarely, cardiomyopathy
Inherited syndrome e.g. long QT, Brugada syndrome
(look for cause of VT .e.g electrolytes (hypokalaemia, hypomagnesaemia, ischaemia, hypoxia, medications)

69
Q

what is long QT syndrome?

A

a rare inherited or acquired heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsades de pointes

70
Q

What is Brugada syndrome?

A

a genetic disease that is characterised by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death.

71
Q

Difference between monomorphic and polymorphic VT?

A

in mono. QRS = symetrical

In poly. QRS = unsymetrical

72
Q

What is ventricular fibrillation?

A

Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump

73
Q

Treatment of VF?

A

Defibrillation and cardiopulmonary resuscitation

74
Q

Treatment of VT?

A

DC cardioversion if unstable
If stable consider pharmacologic cardioversion with AAD
If unsure if VT or something else, consider adenosine to make a diagnosis

75
Q

what long term treatments are available for VT?

A

Implantable cardiovertor defibralltors

CHF therapies

76
Q

What is normally the cause of ventricular arrhythmias?

A

Structural problems

77
Q

What causes atrial flutter?

A

rapid heart rate causes by re-entry circuits in the atrium

78
Q

Appearance of atrial flutter on ECG?

A

Saw tooth appearance

79
Q

What is atrial fibrillation caused by physiologically?

A

Rapid, unsynchronised and chaotic electrical activity which causes conduction of irregular signals to the ventricles due to multiple weavlets of re-entry and ectopic focus around the pulmonary veins

80
Q

What results in increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6) and increased S wave depth in the right-sided leads (III, aVR, V1-3)?

A

Left ventricular hypertrophy

81
Q

Type of heart beat in A Fib?

A

Irregular

82
Q

What are the 3 different types of AFib?

A

Paroxysmal
Persistent
Permanent (chronic)

83
Q

What is paroxysmal AFib?

A

Reverts to sinus rhythm spontaneously - often recurrent

84
Q

What is persistent AFib?

A

AF that is not self terminating/ has lasted longer than 7 days but can be terminated through treatment

85
Q

What is permanent AFib?

A

Continuos AF that cannot be successfully terminated

86
Q

What does incidence of AFib increase with?

A

Age

87
Q

Associated diseases/ causes of AFib?

A 
Hypertension
Congestive heart failure
Sick sinus syndrome - "tachy brady syndrome"
Coronary heart disease
Thyroid disease
Familial
Valvular heart disease
Alcohol abuse
Congenital heart disease
Cardiac surgery
Other rarer causes e.g. COPD

Either classified into cardiac or non-cardiac cause

88
Q

What is lone (idiopathic) AFib?

A

Absence of any underlying cause for AF (diagnosis of exclusion)

89
Q

Symptoms of AFib?

A 
Palpitations
Pre-syncope (dizziness)
Syncope
Chest pain
Dyspnoea
Sweatiness
Fatigue
Can be asymptomatic
Symptoms often worse at the onset of AF
90
Q

Termination of atrial fib?

A

pharmacological cardioversion with anti-arrhythmic drugs (30% effective)
Electrical cardioversion (90% effective)
Spontaneous reversion to sinus rhythm

91
Q

What are the anti-arrhythmic drug examples that can be used to terminate and prevent atrial fib?

A

Flecainide
Sotalol
Amiodarone

92
Q

ECG of atrial fib?

A

Atrial rate greater than 300 bpm

93
Q

Rhythm in Atrial Fib?

A

Irregularly irregular

94
Q

Ventricular rate in atrial fib?

A

Variable (dependent upon AV node conduction properties, sympathetic and parasympathetic tone, presence of drugs which act on the AV node)

95
Q

Recognition of atrial fib on ECG?

A

Absence of P waves, presence of f waves - ventricular rate is irregular

96
Q

What pharmacological agents are useful in controlling ventricular rate in AF by decreasing conduction in the AV node?

A

Beta blcokers

Calcium channel blcokers

97
Q

Ventricular rate in A fib?

A

Irregular
Can be slow, normal or fast (and ranging between these) - depends on AV node conduction properties, sympathetic and parasympathetic tone, presence of drugs which act on the aV node (e.g. flecanide, sotolol, amiodarone)

98
Q

What is it called when AF goes so fast that it looks regular but it actually its?

A

Pseudoregularisation

99
Q

How does AF cause a reduced cardiac output?

A

Lost atrial kick and decreased killing time

100
Q

If the patient has hypertrophic cardiomyopathy, what can AFib result in?

A

Congestive heart failure

101
Q

What does ventricular rates less than 60bpm in AF suggest?

A

AV conduction disease

102
Q

Management of AF?

A

Rhythm control (maintain SR predominantly)
OR
Rate control: Accept AF but control ventricular rate
Anti-coagulation for both approaches if high risk for thromboembolism

103
Q

Rate control during AFib?

A

Pharmacological therapy to slow down AVN conduction:
Digoxin
Betablcokers
Verapamil, diltizam
Give the above alone or in combination
If the above doesnt work, the aV node can be completely ablated and a pacemaker fitted

104
Q

Rhythm control of Afib?

A

Restoration of NSR:
Pharmacological cardioversion (anti-arrhythmic drugs e.g. amiodarone)
Direct current cardioversion
Maintenance of NSR:
Anti-Arrhythmic drugs
Catheter ablation of atrial focus/ pulmonary veins
Surgery (Maze procedure)

105
Q

Treatment of paroxysmal AF?

A

Rhythm control:
Cardiovert (pharma/ DC)
Anti-Arrhythmic drugs to prevent
Anti-coag

106
Q

Treatment of persistent or permanent AF?

A 
Rate control (digoxin, beta blocker, verapamil or diltiazem)
Anti-coagulation if high risk
DC cardioversion if structurally normal heart
107
Q

what is tornadoes de pointes?

A

a specific form of polymorphic VT in patients with a long QT interval. It is characterized by rapid, irregular QRS complexes, which appear to be twisting around the ECG baseline - it can be acquired or congenital (very deadly form of vt)

108
Q

Heart rate in torsades de points?

A

200-250 bpm

109
Q

Rhythm in torsades de pointes?

A

Irregular (In comparison to normal VT)

110
Q

Recognition of tornadoes de pointes?

A

Long QT interval
Wide QRS
Continuously changing QRS morphology

111
Q

Events leading to Torsdaes de points?

A 
hypokalaemia
Prolongation of AP duration (drug induced)
Renal impairment (increased drug levels)
112
Q

What is the scoring system used to assess risk of thromboembolism in atrial fib?

A

CHADVASC score

113
Q

What is the CHADSVASC score

A

C Congestive heart failure (or Left ventricular systolic dysfunction) 1
H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1
A2 Age ≥75 years 2
D Diabetes Mellitus 1
S2 Prior Stroke or TIA or thromboembolism 2
V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1
A Age 65–74 years 1
Sc Sex category (i.e. female sex) 1

Score is 1 maybe antii-cogaulant
If 2 or greater then you should be on anti-coagulants

114
Q

What puts patients at a high risk of thromboembolism?

A 
Valvular heart disease
Age greater than 75 especially female
Hypertension
Heart failure
Previous TE/stroke
Coronary artery disease or diabetes and greater than 60yo
Thyrotoxicosis
115
Q

Indications for anti-coag in AF?

A 
Valvular AF (mitral valve disease)
Non valvular AF if:
Age greater than 75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD/ DM
Daibetes
116
Q

Bleeding risk assessment for AF?

A 
HAS BLED
Hypertension 1
Abnormal renal or liver function 1 or 2
Stroke 1
Bleeding 1
Labile INRs 1
Elderly (age greater than 65) 1
Drugs or alcohol 1 or 2
(if score is greater than 3 = high risk)
117
Q

Why type of ablation is done in AF to maintain sinus rhythm?

A

Ablating AF focus

118
Q

What type of ablation is done in AF to control rate?

A

Ablation of AVN to stop fast conduction to the ventricles

119
Q

Is Atrial flutter regular or irregular?

A

Regular - usually paroxysmal and is rapid

120
Q

Where is the re-entry circuit in atrial flutter?

A

Right atrium

121
Q

How long can episodes of Atrial flutter last?

A

Seconds to years

122
Q

What does chronic atrial flutter usually progress to?

A

Atrial fibrillation

123
Q

Risk of atrial flutter?

A

May result in thrombi-embolism

124
Q

Characteristic feature of Atrial flutter on eCG?

A

Regular rapid rate with saw root F wave

125
Q

Treatment of Atrial flutter?

A

RF ablation
Pharmacological therapy to slow the ventricular rate = restores sinus rhythm, and maintains sinus rhythm once converted
Cardioversion
Warfarin for prevention of thromboembolism

Study Notes - Cardiology (25 decks)

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