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Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Sinoatrial node (SAN)

A

In the roof of the right atrium.

Primary pacemaker of the heart due to the ability of nodal cells to spontaneously depolarise.

Inherent rate of depolarisation of the SAN is faster than other areas of the heart which have pacemaker properties meaning in normal conditions an impulse originates from the SAN.

A wave of depolarisation spreads from the SAN across the right and left atria - seen as a P wave on the ECG and causing atrial contraction.

The SAN has automaticity, but this is modulated by autonomic tone, at rest vagal tone predominates.

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2
Q

Which part of the ECG represents the depolarisation from the SAN?

A

p wave

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3
Q

Atrioventricular node (AVN)

A

The atria and ventricles are electrically insulated from each other by the fibrous skeleton, which is bridged only by the AVN.

Cells of the AVN have slower conduction, delaying transmission of impulses, seen as the PR interval on the ECG, this allows for final diastolic filling of the ventricle prior to ventricular systole.

The AVN is also influenced by autonomic tone.

The AVN can act as a subsidiary pacemaker.

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4
Q

Which part of the ECG represents the delay in conduction from the AVN?

A

PR interval

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5
Q

His-Purkinje Network

A

From the AVN the impulse reaches the Bundle of His (aka distal AVN).

This divides into the right and left bundle branches, the latter further dividing into the left anterior fascicle and left posterior fascicle.

The bundle branches are a specialised conduction systems allowing for rapid propagation of impulses through the ventricles.

Impulses are transmitted from the branching bundles to the Purkinje fibres which form a rapidly conducting network of fibres transmitting impulses to ventricular myocardial cells.

This rapid depolarisation of the ventricle is seen as the QRS complex on the ECG and triggers ventricular contraction.

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6
Q

What does the QRS complex on an ECG represent?

A

The rapid depolatisation of the centricles due to the network of Purkinje fibres

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7
Q

How should the dog be lying for an ECG?

A

Right lateral recumbency

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8
Q

P wave of an ECG

A

Atrial depolarisation.

Duration corresponds to the time it takes for both atria to fully depolarise.

P wave amplitude is directly proportional to the atrial mass.

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9
Q

When could you see a prolonged p wave?

A

(P mitrale) may be seen with atrial, especially left atrial, dilation or interatrial conduction delay

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10
Q

When can you see increased p wave amplitude?

A

may be seen with atrial enlargement (especially right atrial dilation- P Pulmonale).

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11
Q

What is wandering pacemaked?

A

Regular variation in P wave amplitude associated with variation in vagal tone, commonly seen with sinus arrhythmia.

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12
Q

What can cause absent p waves?

A

either hidden during tachycardia, or absent due to SAN or atrial disease, or electrolyte abnormalities (hyperkalaemia).

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13
Q

Ta wave

A

Atrial repolarisation, rarely seen as hidden by the QRS complex.

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14
Q

PR interval

A

The time it takes for a depolarisation wave to be conducted through the atria, AVN and Bundle of His.

PR interval increases with reduction in heart rate.

Prolonged PR interval = 1st degree AV block, may be seen with increased vagal tone, conduction system disease, electrolyte abnormalities, drugs (beta blockers) etc.

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15
Q

QRS complex

A

Ventricular depolarisation.

Q corresponds to the first negative deflection; R corresponds to the first positive deflection, S corresponds to a second negative deflection

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16
Q

What does a tall QRS suggest?

A

an increase in ventricular mass (i.e. left ventricular enlargement).

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17
Q

What does a low amplitude QRS suggest?

A

effusions, intrathoracic mass, broad chested dogs, poor electrode contact, hyperkalaemia, obesity, hypothyroidism.

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18
Q

What does a wide QRS suggest?

A

Ventricular ectopic or intraventricular conduction disturbance (e.g. bundle branch block).

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19
Q

T wave

A

Ventricular repolarisation.

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20
Q

Causes of t wave changes

A

myocardial hypoxia,
electrolyte abnormalities (especially potassium),
severe systemic disease,
drug toxicities.

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21
Q

ST segment

A

Corresponds to phase 2 of the action potential, the period during which electrical activity is transmitted to mechanical contraction.

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22
Q

What can cause abnormalities of the ST segment?

A

(depression/elevation) may be associated with hyperkalaemia, myocardial ischaemia and hypoxia, trauma.

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23
Q

QT interval

A

The time it takes for both ventricular depolarisation and repolarisation.

Longer with slower heart rates and vice versa.

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24
Q

Long QT interval

A

can be a risk factor for ventricular arrhythmias.

Causes of long QT: electrolyte abnormalities, drugs (potassium channel blockers), hypothermia etc.

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25
Q

How to calculate an instantaneous (beat to beat) heart rate from ECG

A

Calculated from a single R-R interval, this is a good representation of the mean heart rate if the rhythm is regular.

Calculated via 60000/R-R interval in ms (as there are 60000ms in a minute).

Or if counting boxes: at 50mm/s, 3000/ no of boxes (at 50mm/s each box is 20ms), at 25mm/s, 1500/no of boxes (at 25mm/s each box is 40ms).

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26
Q

How to calculate an average heart rate from ECG

A

Better for an irregular rhythm.

Count the number of complexes in a 3 second interval, which is 15cm at 50mm/s or 7.5cm at 25mm/s, and multiply by 20.

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27
Q

Sinus rhythm

A

P wave before every QRS

Narrow QRS complexes (dogs <70ms; cats <40ms)

P and QRS complexes are positive in leads I, II, III, aVF

Variable T wave morphology

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28
Q

Sinus arrhythmia

A

Cyclic variation in heart rate associated with respiration

Increased HR on inspiration, decreased on expiration - decreased and increased vagal tone

P wave morphology may vary = wandering pacemaker

Narrow QRS complexes

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29
Q

Supraventricular arrhythmias on ECG

A

Narrow QRS complexes

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30
Q

Ventricular tachyarrhythmias on ECG

A

Wide and bizarre QRS complexes

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31
Q

Types of supraventricular arrhythmias

A

Supraventricular premature complexes aka atrial premature complexes (SVPC/APC)

Supraventricular tachycardia (SVT)

Atrial fibrillation (AF)

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32
Q

Supraventricular premature complexes aka atrial premature complexes (SVPC/APC)

A

Narrow QRS complex

Early complex

Altered P’ wave may be seen (or may be hidden in the preceding T wave)

Occurs when an ectopic focus in the atria or atrioventricular junction depolarises the atria prematurely

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33
Q

Supraventricular tachycardia (SVT)

A

Fast, regular rhythm

Narrow QRS complex (same morphology as sinus beats)

P’ wave morphology differs from a sinus P wave

P’ wave may be before/within/after the QRS

Important differential = sinus tachycardia!

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34
Q

Cause of supraventricular techycardia (SVT)

A

A narrow QRS complex tachycardia due to either an ectopic focus within the atria (atrial tachycardia; most common), or the atrioventricular junction (junctional tachycardia), or a re-entry circuit.

Paroxysmal or sustained.

SVTs are most commonly associated with structural heart disease, so echocardiography is indicated; electrolyte disturbances and endocrinopathies can also be associated with some supraventricular arrhythmias.

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35
Q

Acute/emergency management of supraventricular tachycardia (SVT)

A

Vagal manoeuvres, e.g. ocular pressure, gag reflex, may slow or break the rhythm.

IV esmolol (fast acting B-blocker)

IV diltiazem (calcium channel blockers)

IV sotalol (potassium channel blocker)

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36
Q

Chronic/oral management of supraventricular tachycardia (SVT)

A

PO diltiazem

PO sotalol

PO amiodarone

Radiofrequency ablation (accessory pathway)

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37
Q

Atrial fibrillaiton on ECG

A

Fast, irregular (chaotic) rhythm

No P waves

Narrow QRS complex

+/- f waves

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38
Q

Cause of atrial fibrillation

A

Atrial fibrillation can only occur if there is a critical atrial mass to allow propagation of small wavelets of depolarisation to occur; therefore, AF is most often associated with cardiac disease and significant atrial dilation.

However giant breed dogs may develop AF without signs of structural heart disease (referred to as lone AF, which may be slow).

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39
Q

Rate control for atrial fibrillation

A

Diltiazem +/- digoxin.
Used together these drugs have synergistic effect at controlling the ventricular rate in AF.

Aim of treatment: 24-hour mean heart rate (from a Holter) <125 bpm, which is associated with improved survival.

Treat the underlying cardiac disease and congestive heart failure.

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40
Q

Rhythm control for atrial fibrillation

A

If there is significant structural heart disease or AF has been longstanding, it is usually not possible to convert the rhythm back to sinus, and if this is achieved, the rhythm will usually revert back to AF. However acute onset AF in a structurally normal heart may be convert to sinus rhythm.

DC electrical cardioversion: use of a defibrillator under general anaesthesia to deliver a shock of electricity.

Amiodarone may convert the rhythm to sinus or increase the likelihood of electrical cardioversion being successful.

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41
Q

Ventricular arrhythmias

A

Ventricular premature complexes (VPCs)

Ventricular tachycardia

Ventricular fibrillation

Accelerated idioventricular rhythm

42
Q

Ventricular premature complexes (VPCs) on ECG

A

Wide and bizarre QRS

T wave opposite polarity to QRS

P waves not associated with QRS

43
Q

Cause of ventricular premature complexes (VPCs)

A

An ectopic focus may arise in the ventricular myocardium.

Because this does not follow the normal His-Purkinje conduction system but instead depolarisation has to spread cell-to-cell, this is a slow process, creating a wide & bizarre QRS complex.

The repolarisation wave (T wave) is in the opposite direction to the QRS complex.

Ventricular rhythms may be associated with structural heart disease or systemic disease

44
Q

Ventricular tachycardia on ECG

A

Wide QRS complexes

Fast, regular rhythm

Paroxysmal or sustained

No associated p waves

Dangerous rhythm

45
Q

Cause of Ventricular tachycardia

A

Due to an ectopic focus within the ventricles, usually regular.

May be sustained or paroxysmal.

Dangerous arrhythmia with risk of ventricular fibrillation and sudden cardiac death.

Ventricular arrhythmias may be associated with systemic disease (especially abdominal) such as hypovolaemia, hypoxia, splenic masses, SIRS, sepsis, trauma, or may be associated with cardiac disease. Therefore, extra-cardiac diagnostics should also be pursued.

46
Q

Ventricular fibrillation

A

Terminal rhythm requiring CPR and electrical defibrillation.

Complete loss of co-ordinated ventricular depolarisation/repolarisation resulting in a chaotic ECG.

Undulations of different shapes and sizes without any deiscernible P, QRS, or T

47
Q

Accelerated idioventricular rhythm

A

A ventricular rhythm slower than ventricular tachycardia, at <150-180 bpm.

Most often associated with extracardiac disease (GDV, post-splenectomy, SIRS etc).

As the rate is lower than a ‘true’ ventricular tachycardia, accelerated idioventricular rhythm is normally not haemodynamically unstable and antiarrhythmic treatment is therefore not needed.

Monitor the rhythm and look for underlying extra-cardiac disease if not already known and assess volume status and analgesia.

48
Q

Criteria of malignancy in ventricular arrhythmias

A

Criteria associated with greater haemodynamic instability/ higher risk of sudden cardiac death

Burden

Complexity

R on T phenomenon

R-R interval

49
Q

Burden of a ventricular arrhythmia

A

this is an important part of screening and diagnosing both DCM and ARVC.

There is no clear cut-off for the percentage of ventricular arrhythmias which warrant initiation of treatment, and this should be taken into account with the complexity of the arrhythmias.

50
Q

Complexity of a ventricular arrhythmia

A

Couplets and triplets are more malignant than single VPCs and bigeminy; ventricular tachycardia being the most malignant.

51
Q

R on T phenomenon

A

where a ventricular depolarisation begins on the preceding T wave.

52
Q

R-R interval

A

coupling interval >260/minute is associated with increased risk of sudden cardiac death.

53
Q

Emergency management of ventricular tachycardia

A

IV lidocaine bolus followed by a CRI is first line therapy.

IV amiodarone bolus and CRI.

Sotalol

54
Q

Chronic oral management of ventricular arrhythmias

A

PO sotalol- good first line choice in most cases, unless severe systolic dysfunction.

PO mexiletine- minimal myocardial depressant effect, high risk of GI side effects.

PO amiodarone- not a first line drug, advise speaking to a cardiologist before using, however useful in life-threatening ventricular arrhythmias especially if severe systolic dysfunction or concomitant supraventricular arrhythmias.

55
Q

Bradyarrhythmias

A

Escape beats/rhythms

Atrial standstill

Atrioventricular block

Sinus arrest

Sick sinus syndrome

56
Q

Escape beats/rhythms on ECG

A

Wide QRS complex with no associated p wave

Occurs after a pause in sinus beats

57
Q

Cause of escape beats/rhythms

A

During bradyarrhythmias, subsidiary pacemakers may become the dominant pacemakers to keep the heart beating, the intrinsic rate of these subsidiary pacemakers is lower than the sinoatrial node; such rhythms are referred to as escape rhythms.

58
Q

Classification of escape beats

A

Junctional (i.e. arising from the atrioventricular region) with narrow QRS complexes,

or ventricular with wide QRS complexes.

59
Q

Atrial standstill on ECG

A

No p waves

Slow HR

Tall spiky T waves associated with hyperkalaemia

60
Q

Cause of atrial standstill

A

Atrial standstill with a sinoventricular rhythm is most commonly associated with hyperkalaemia (Addison’s disease, urethral obstruction).

The SAN still drives the rhythm and there is conduction from the SAN to the AVN, but the atrial cardiomyocytes do not depolarise (no P waves).

Atrial cardiomyopathy (rare, reported in English Springer spaniels and Labradors) may also cause atrial standstill, with no atrial activity (no P waves) and a junctional or ventricular escape rhythm.

61
Q

Treatment of atrial standstill

A

Correct the hyperkalaemia

Unless atrial cardiomyopathy - requires pacemaker

62
Q

First degree AV block

A

delayed conduction through the AVN with a prolonged PR interval but the P:QRS ratio remains 1:1.

Typically associated with high vagal tone.

63
Q

Second degree AV block

A

Intermittent failure of AVN conduction resulting in non-conducted P waves.

Can be Mobitz type 1 or type 2

64
Q

Mobitz type 1

A

Wenckebach phenomenon

there is gradual lengthening of the PR interval before a non-conducted P wave (intermittent failure of AV conduction).

Often associated with high vagal tone.

Lazy bouncer

65
Q

Mobitz type 2

A

Fixed PR interval, single or multiple non-conducted P waves, often a fixed ratio.

Can be considered as low grade (if only 1 or 2 non-conducted P waves in a row) or high grade (>2 non-conducted P waves in a row), the latter is more likely to be symptomatic.

Associated a 6 with pathological disease of the AVN.

Picky bouncer

66
Q

Third degree AV block

A

there is persistent failure of AVN conduction resulting in no relationship between P waves and QRS complexes.

The ventricles depolarise via a junctional or ventricular escape rhythm.

This always represents disease of the AVN.

67
Q

Sinus arrest

A

A pause of >3 times the normal R-R interval

Causes
○ Part of SSS (sick sinus syndrome)
○ Drugs (amiodarone, digoxin)
○ Electrolyte imbalances
○ Myocarditis
○ Idiopathic

68
Q

Sick sinus syndrome

A

This is an umbrella term for a number of arrhythmias resulting from dysfunction of the sinus node with resultant clinical signs; the AVN may also be affected and escape rhythms may also fail.

69
Q

ECG findings of sick sinus syndrome

A

Sinus bradycardia

Low mean heart rate on Holter

Intermittent sinus arrest

Intermittent first and second degree AV block

+/- supraventricular tachycardia

70
Q

Signalment of sick sinus syndrome

A

WHWT, cairns, miniature Schnauzers, and terriers are more commonly affected.

71
Q

Clinical signs of sick sinus syndrome

A

may present with lethargy, reduced exercise capacity or syncope (associated with long pauses).

72
Q

Management of sick sinus syndrome

A

Some dogs may respond to medical management for a short period of time; most often a pacemaker is required.

73
Q

Vaughan WIlliams classification of antiarrhythmic drugs

A

I: sodium channel blockers

II: Beta blockers

III: potassium channel blockers

IV: calcium channel blockers

N/A: Na/K ATPase pump inhibitor, Vagomimetic

74
Q

Class I: Sodium channel blockers - mechanism of action

A

Blocking sodium channels depresses the rapid depolarisation phase in working myocardial cells, so reduces automaticity and slows conduction velocity.

Work more effectively at higher heart rates.

More effective in ventricular than atrial myocardial cells.

75
Q

Class I: Sodium channel blockers - main use

A

ventricular arrhythmias

76
Q

Class I: Sodium channel blockers - main side effects

A

gastrointestinal (especially nausea), but also neurological signs (depression) possible with higher/repeated doses.

77
Q

Class I: Sodium channel blockers - examples

A

Lidocaine

Mexiletine

78
Q

Lidocaine

A

IV only.

First line emergency management of ventricular tachycardia.

CRI after initial bolus

Rapid onset of action

Adverse effects: neurological (depression, agitation, seizures), nausea.

79
Q

Mexiletine

A

Similar mechanism of action to lidocaine, but different pharmacokinetics, so can be given orally.

Adverse effects: gastrointestinal (anorexia, vomiting, diarrhoea)- always give with food. Lethargy, ataxia, bradycardia, hypotension less commonly reported.

Unlikely to be available in many first opinion practices unless ordered in specifically.

80
Q

Class II: beta blockers - mechanism of action

A

Beta-adrenergic antagonists.

Nonselective vs selective B1 blockade.

Exert antiarrhythmic effects indirectly by decreasing the cardiac effects of adrenergic stimulation resulting in decrease rate of SAN discharge, decreased rate of conduction through the AVN and decreased automaticity of ectopic foci.

81
Q

Class II: beta blockers - main uses

A

Slow AVN conduction

Slow rate in atrial arrhythmias

Ventricular arrhythmias

82
Q

Class II: beta blockers - main adverse effects

A

Adverse effects related to excessive attenuation of sympathetic tone including negative inotropy.

NEVER use in uncontrolled heart failure patients who may be reliant on increased sympathetic tone to maintain cardiac output.

Must not be stopped suddenly (dose must be tapered), due to up-regulation of beta receptors.

83
Q

Class II: beta blockers - examples

A

Atenolol

Esmolol

84
Q

Atenolol

A

B1 selective (cardio-selective).

Decreases heart rate, slows AVN conduction, prolongs repolarisation in myocardial cells.

Not frequently used as an antiarrhythmic but can have use in supraventricular and ventricular tachyarrhythmias.

Useful in hyperthyroid cats with tachyarrhythmias.

Adverse effects: bradycardia, hypotension, myocardial depression.

85
Q

Esmolol

A

Ultrashort acting non-selective beta blocker.

Can use in acute management of very rapid supraventricular tachycardias.

86
Q

Class III: potassium channel blockers - mechanism of action

A

Prolong repolarisation in nodal and working myocardial cells (thus lengthen the QT interval).

87
Q

Class III: potassium channel blockers - main uses

A

Ventricular arrhythmias

Supraventricular arrhythmias

88
Q

Class III: potassium channel blockers - main adverse effects

A

Care if the QT is already prolonged or there are marked electrolyte disturbances (which may lengthen the QT).

89
Q

Class III: potassium channel blockers - examples

A

Solatol

Amiodarone

90
Q

Solatol

A

Potassium channel blocker with non-selective beta blocker properties.

Ventricular and supraventricular arrhythmias- good first line choice for chronic oral therapy.

Peak effect within 2-4 hours of oral administration

Negative inotropic effect due to beta blocker properties generally tolerated, but care if severe systolic dysfunction.

Adverse effects: QT prolongation, reduced systolic function, bradycardia, hypotension.

91
Q

Amiodarone

A

Classified as a class III but has properties of all classes.

Supraventricular and ventricular arrhythmias.

Minimal myocardial depression.

Takes several weeks to reach steady state so requires loading.

Can be used IV for emergency management of ventricular arrhythmias

Adverse effects (cumulative doses): hepatic and thyroid dysfunction. GI signs, anaemia and neutropenia also possible

Unlikely to be on the shelf in most first opinion practices- would advise speaking to a cardiologist before using if not familiar.

92
Q

Class IV: calcium channel blockers - mechanism of action

A

Non-dihydropyridine calcium channel blockers have antiarrhythmic and vascular effects via blockade of slow L-type calcium channels (so reducing calcium influx across cell membranes) involved in excitation contraction coupling and vascular smooth muscle contraction.

Decrease the rate of depolarisation in the SAN and reduce rate of conduction through the AVN.

Main effect in nodal tissue

93
Q

Class IV: calcium channel blockers - main uses

A

Supraventricular arrhythmias

94
Q

Class IV: calcium channel blockers - main adverse effects

A

bradycardia, hypotension (vasodilation), lethargy, anorexia.

May cause decrease in myocardial contractility- however much lower risk than beta blockers and generally well tolerated even in dogs with systolic dysfunction.

95
Q

Class IV: calcium channel blockers - examples

A

Diltiazem

Digoxin

96
Q

Diltiazem

A

Only mild negative inotropic effect, generally well tolerated.

Supraventricular arrhythmias. First line +/- digoxin for atrial fibrillation.

97
Q

Digoxin

A

Parasympathomimetic effects.

Used to control the ventricular rate in atrial fibrillation. Synergistic effect with diltiazem associated with better rate control.

Adverse effects: gastrointestinal (anorexia, vomiting, diarrhoea), cardiac (pro-arrhythmic), neurological (depression, weakness).

Narrow therapeutic window. Risk of digoxin toxicity increases in cases with hypokalaemia, anorexia, and cachexia.

Assess serum digoxin concentration 5-7 days post initiation/dose change, 6-8hrs post pill.

98
Q

Treatment options for bradyarrhythmias

A

Use atropine response test to determine if vagally mediated

Medical management
- treat underlying disease
- increase rate of discharge

Pacemaker implantation

99
Q

Atropine response test

A

For bradyarrhythmias

Used to determine if a bradyarrhythmia is vagally mediated (profound sinus arrhythmia, sinus arrest, first degree AV block, type 1 second degree AV block).

Atropine = anticholinergic.

A positive response is indicated by an increase in heart rate >150 bpm, abolition of sinus arrest, significant improvement in AV block.

100
Q

Medical management of bradyarrhythmias

A

Treat underlying disease if vagally mediated or electrolyte disturbances.

Otherwise, limited efficacy.

Attempt to increase rate of discharge of the SAN, conduction through the AVN etc via terbutaline (B2 agonist), theophylline (xanthine derivative).

101
Q

Pacemaker implantation

A

Transvenous pacemaker implantation is often the only treatment likely to significantly reduce clinical signs and improve exercise tolerance in patients with significant bradyarrhythmias (third degree AV block, atrial standstill (not due to hyperkalaemia, SSS).

Cardiology (10 decks)

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