Arrhythmias

Question 1

What adverse features should you assess when approaching patient with tachycardia?

Answer 1

shock
syncope
myocardial ischaemia
heart failure

Question 2

Treatment of narrow QRS tachycardia

Answer 2

Regular rhythm

• vagal maneuvers
• adenosine 6mg rapid IV bolus (if no effect, given 12mg, then further 12 mg)
• Record ECG continuously
• if sinus rhythm is achieved –> probable re-entry paroxysmal SVT.
• if not achieved –> possible atrial flutter

Irregular rhythm

• control rate with beta blocker or diltiazem
• if in heart failure - consider digoxin or amiodarone
• consider anticoagulation if at high risk of thromboembolism

Question 3

Treatment of broad QRS tachycardia

Answer 3

Regular rhythm

• IF VT or uncertain rhythm –> amiodarone
• IF known to be SVT with bundle branch block –> treat as for regular narrow complex tachycardia

Irregular rhythm
- could be - AF with bundle branch treat as for narrow complex OR pre-excited AF - consider amiodarone

Question 4

Treatment of SVT with bundle branch block

Answer 4

• vagal maneuvers
• adenosine 6mg rapid IV bolus (if no effect, given 12mg, then further 12 mg)
• Record ECG continuously
• if sinus rhythm is achieved –> probable re-entry paroxysmal SVT.
• if not achieved –> possible atrial flutter

Question 5

What structures of the heart, may a supra ventricular arrhythmia arise from?
- Would the QRS be broad or narrow?

Answer 5

Sinus
Atria
Junctional

NARROW

Question 6

What structures of the heart, may a ventricular arrhythmia arise from?
- Would the QRS be broad or narrow?

Answer 6

VENTRICLES

BROAD

Question 7

What is tachycardia?

• 3 main mechanisms
• symptoms
• When would the QRS complex be broad or narrow?

Answer 7

> 100 beats/min

3 main mechanisms
Increased automaticity
- Repeated spontaneous depolarisation of ectopic focus, often in response to catecholamines

Re-entry

• Ectopic beat and sustained by re-entry circuit
• Re-entry circuit – occurs when there are 2 alternative pathways with different conducting properties (AV node and an accessory pathway or area of normal and an area of ischaemic tissue)

Triggered activity

• Can cause ventricular arrhythmias in patients with coronary artery disease
• Form of secondary depolarisation arising from incompletely repolarised cell membrane

Symptoms
- Syncope – heart unable to contract/relax properly at extreme rates

QRS complex may be broad or narrow

• Broad – arises from ventricle
• Narrow – arises from atria

Question 8

What is bradycardia?

• mechanisms
• What may cause it?

Answer 8

<60/min

Mechanisms
Reduced automaticity
- E.g. sinus bradycardia
- Normal at rest and in high resting vagal tone

Blocked or abnormally slow conduction
- E.g. AV block

Pathology

Intrinsic: degenerative processes, congenital, tissue damage, tissue inflammation, infections, abnormal autonomic effects

Extrinsic: exposure to toxins, drugs, electrolyte abnormalities

Hypothyroidism

Inferior wall MI/ increased intracranial pressure

High vagal tone in young adults – common cause of sinus bradycardia and Mobitz I AV block

Question 9

What is chronotropic incompetence?

Answer 9

Inability to accelerate sinus rate with exercise

Question 10

What is AV conduction disturbance?

• what are the types?
• symptoms
• management

Answer 10

AV conduction disturbance occurs when atrial depolarisation fails to reach ventricles or when atrial depolarisation is conducted with a delay

First degree: PR interview >200ms due to AV nodal conduction delay

Second degree: failure of conduction from atria to ventricles

• Mobitz I: progressive prolongation of PR interval with dropped beats. Characterised by progressive failure of conduction, likely to produce narrow QRS and will improve with atropine.
• Mobitz II: constant PR interval and subsequent loss of conduction. Characterised by failure of His-Purkinje cells and occurs in context of pre-existing LBBB/bifascicular block. May worsen with atropine.
• Fixed ratio: P:QRS ratio

Third degree (complete block): absence of AV conduction. Perfusing rhythm is maintained by

• Junctional: escape rhythm in bradycardia or arrest of SAN. Activation of junction may occur with/without AV block
• Ventricular: escape rhythm from ventricles when there is AV block/sinus bradycardia → syncope/ sudden cardiac death

AV dissociation is when atrial and ventricles do not activate in synchronous fashion

• Isorhythmic: atrial rate=ventricular rate but p-wave is not conducted
• Interference: when p-waves and QRS rates are similar but occasionally, atria conduct to ventricles

Symptoms

• Low cardiac output – fatigue, lightheadedness, syncope
• Hypotension
• Feature of exercise intolerance and chest pain
• May manifest after beta-blocker, calcium-channel blocker or digoxin
• Cannon a-waves in JVP

Management

• Unstable: atropine and temporary pacing
• Stable w/ sinus node dysfunction
• Reversible: treatment of underlying cause, adjunct theophylline for symptomatic relief
• Reversible w/severe symptoms: temporary pacing
• Irreversible: reassurance
• Irreversible w/ severe symptoms: permanent pacing
• May need pacemaker.

Question 11

What are the types of second degree AV failure

Answer 11

Mobitz I: progressive prolongation of PR interval with dropped beats. Characterised by progressive failure of conduction, likely to produce narrow QRS and will improve with atropine.

Mobitz II: constant PR interval and subsequent loss of conduction. Characterised by failure of His-Purkinje cells and occurs in context of pre-existing LBBB/bifascicular block. May worsen with atropine.

Question 12

What is sinus arrhythmia?

• what causes it?
• what should you suspect if it is absent?

Answer 12

Change to HR during respiration

• Increases during inspiration
• Slows during expiration

Due to normal parasympathetic nervous system activity (vagus nerve), can be pronounced in children

If absent during respiration/ position change → ?autonomic neuropathy

Question 13

Sinus bradycardia

• what is it?
• when does it occur?
• what are some causes?
• Would you treat it?

Answer 13

<60/min

May occur in healthy people at rest, athletes

Asymptomatic → no treatment

Symptomatic acute → IV atropine 0.6-1.2 mg

Recurrent/persistent symptomatic → consider pacemaker implantation

Causes:

• MI
• Sinus node disease (sick sinus syndrome)
• Hypothermia
• Hypothyroidism
• Cholestatic jaundice
• Raised intracranialpressure
• Drugs – B-blockers, digoxin, verapamil

Question 14

Sinus tachycardia

• what is it?
• what causes it?

Answer 14

> 100/min

Increased sympathetic activity – exercise, emotion, pregnancy, pathology

Causes:

• Anxiety
• Fever
• Anaemia
• Heart failure
• Thyrotoxicosis
• Phaeochromocytoma
• Drugs – Beta-agonists (bronchodilators)

Question 15

Sino atrial disease

• what is this also known as?
• when may it occur?
• what is the pathology?
• how does it present?
• what is the treatment?

Answer 15

Sick sinus syndrome

Occur at any age – most common elderly

Pathology – fibrosis, degenerative changes or ischaemia of SA (sinus) node

Variety of arrhythmias

Presentations – palpitations, dizzy spells or syncope due to intermittent tachycardia/bradycardia or pauses within no atrial or ventricular activity (SA block or sinus arrest)

Common features:

• Sinus bradycardia
• Sinoatrial block (sinus arrest)
• Paroxysmal atrial fibrillation
• Paroxysmal atrial tachycardia
• Atrioventricular block

Troublesome symptoms → Permanent pacemaker

Atrial pacing may prevent AF

• Improves symptoms but not prognosis
• Only in symptomatic patients

Question 16

Atrial ectopic beats

• what are they?
• what are the symptoms?
• what are ECG findings?
• what should you suspect in someone with very frequent ectopic beats?
• when would you treat?
• what is the treatment?

Answer 16

extrasystoles, premature beats

Usually no symptoms – sensation of missed beat/abnormally strong beat

ECG – premature QRS
- P wave – different morphology as atria activate from abnormal site

Very frequent ectopic beats → ?about to go into AF

Rarely treated unless bad symptoms – Beta-blocker

Question 17

Atrial tachycardia

• what is the pathology?
• What drug may cause it?
• what would be seen on ECG?
• what is the treatment?

Answer 17

Due to increased atrial automaticity, sinoatrial disease, digoxin toxicity

ECG

• Narrow-complex tachycardia
• Abnormal P wave morphology
• May have AV block if atrial rate is rapid

Treatment

• Beta-blockers reduces automaticity
• Class I or II anti-arrhythmic drug
• Ventricular response in rapid atrial tachycardias may be controlled by AV node-blocking drugs
• Catheter ablation – target ectopic site (consider if recurrent with drugs)

Question 18

Atrial flutter

• pathology
• what would the atrial rate be?
• what would you see on ECG?
• when should you suspect it?
• How would you diagnose it?
• What is the management?
• What drug should be avoided?

Answer 18

Large (macro) re-entry circuit
- Usually within right atrium encircling the tricuspid annulus

Atrial rate = 300/min, usually associated with 2:1, 3:1, 4:1 AV block, with corresponding HR of 150, 100 or 75 min)

ECG = saw-toothed flutter waves
- In regular 2:1 AV block – may be difficult to identify flutter waves as they may be buried in QRS complexes and T waves

Suspect if there is a narrow complex tachycardia of 150/min

Diagnosis

• Carotid sinus pressure
• IV adenosine – temporarily increase degree of AV block → revealing flutter waves

Management

• Control ventricular rate – Digoxin, beta-blockers, verapamil
• In some cases – may try to restore sinus rhythm by direct current cardioversion or by using IV amiodarone
• Prevent recurrent episodes – Beta-blocker or amiodarone

AVOID flecainide

• May be used for acute treatment or prophylaxis
• AVOID due to risk of slowing the flutter circuit and facilitating 1:1 AV nodal conduction
• May cause paradoxical tachycardia and haemodynamic compromise
• If used – must give with AV node-blocking drug – e.g. beta-blocker

Catheter ablation – 90% of cure. Use if have persistent symptoms

Question 19

Atrial fibrillation

• Does the prevalence rise with age?
• what is the pathology?
• what would ECG show?
• What could be the underlying cause?
• How would a patient present?
• How may symptoms differ in an elderly patient?
• What are potential complications?
• What investigations would you do?
• What is the treatment?

Answer 19

Prevalence rises with age

Abnormal automatic firing & multiple interacting re-entry circuit loops around atria

• Episodes initiated by rapid bursts of ectopic beats from conducting tissue in pulmonary veins or from diseased atrial tissue
• Becomes sustained due to re-entrant conduction within atria or continuous ectopic firing
• Atria beat rapidly but in uncoordinated and ineffective manner
• Ventricles activated irregularly at rate determined by conduction through AV node → irregularly irregular
• Associated with dilation of atria with fibrosis/ inflammation causes difference in refractory periods within atrial tissue and promotes electrical re-entry→ AF→ degeneration into other tachyarrhythmias (AT, flutter, AV nodeal re-entrant tachycardia/AV re-entrant tachycardia e.g. WPW)
• Increased coronary flow is not compensated, predisposing patient to left ventricular dysfunction and subsequent symptoms of chest discomfort, dizziness, SOB

ECG

• Normal but irregular QRS complexes
• Absent P waves – may have baseline irregular fibrillation waves

May be first manifestation of heart disease

• Coronary artery disease (e.g. acute MI)
• Valvular heart disease – esp. rheumatic, mitral valve disease
• Hypertension
• Sinoatrial disease
• Hyperthyroidism
• Alcohol
• Cardiomyopathy
• Congenital heart disease
• Chest infection
• Pulmonary embolism
• Pericardial disease
• Idiopathic (lone atrial fibrillation – structurally normal heart)

Presentations

• Palpitations
• Breathlessness/ dizziness
• Fatigue
• Heart failure – if have poor ventricular function or valve disease – due to loss of atrial function and HR control
• Chest pain – if have underlying coronary artery disease

Elderly – may be asymptomatic if associated with rapid ventricular rate → discovered routinely
- Focal neurological (hemiplegia/dysphasia)

Associated with significant morbidity and 2x increase in mortality

• Stroke
• Systemic embolism

Management

• Assessment – history, ECG, ECHO, thyroid function tests
• Electrolytes – hyper/hypokalaemia, hyper/hypomagnesaemia
• Troponin
• Thyroid function tests
• CXR = pneumonia, pericarditis, HF can precipitate new-onset AF
• Cardiomegaly, left atrial dilatation
• ECHO – left atrial dilatation, valvular disease

Question 20

What is paroxysmal AF?

- Treatment?

Answer 20

Intermittent episodes which self-terminate within 7 days

In many cases turns into permanent - due to electrical remodelling
- AF for many months → structural remodelling – atrial fibrosis and dilatation

IF well tolerated – may not need treatment

1st line – beta-blockers

• Especially if associated with coronary artery disease, hypertension, cardiac failure
• Reduce ectopic firing which initiates AF

Class Ic drugs – propafenone or flecainide

• Avoid in patients with coronary artery disease or left ventricular dysfunction
• Flecainide – prescribe with rate limiting beta-blocker as it occasionally precipitates atrial flutter

Class III drugs – amiodarone

• SEs restrict use to patients in whom other measures have failed
• Dronedarone – alternative; Contraindicated: heart failure, significant left ventricular impairment

NOT digoxin / verapamil – but they do limit HR by blocking AV node

Ineffective drug therapy or SE – try catheter ablation

• Disconnect pulmonary veins from LA electrically, preventing ectopic triggering of AF
• Lines of conduction block can be created within atria to prevent re-entry
• Works in 75% with prior drug-resistant episodes
• May need repeat procedure
• Risks: tamponade, stroke

Question 21

Persistent AF

- What are the two forms of treatment?

Answer 21

Prolonged episodes that can be terminated by electrical or chemical cardioversion

Treatment two forms:

• Rhythm control – restore and maintain sinus rhythm
• Rate control – accept AF will be permanent and use treatments to control ventricular rate and to prevent embolic complications

Rhythm control

• If have troublesome symptoms but treatable underlying cause
• Electrical cardioversion (75% success)
• Present for <48 hours → IV heparin and immediate cardioversion
• Stable, no structural heart disease → IV flecainide (restore rhythm in 8 hours)
• Structural/ischaemic heart disease → IV amiodarone (central venous catheter)

Electrical cardioversion – DC shock = alternative

• Often effective if drugs fail
• Other situations – only use when patient has been established on warfarin (INR > 2.0 for 4 weeks) and eliminated underlying problems (hypertension, alcohol excess)

Elderly – tagert INR <3.0 due to increased risk of intracranial haemorrhage. Alternatively use direct thrombin (e.g. dabigatran) and factor Xa (e.g. rivaroxaban) inhibitors – no blood monitoring required.

Anticoagulation for at least 3 months post cardioversion

Recurrence occurs – try cardioversion again but consider pre-treatment with amiodarone

Rate control

• Digoxin, beta-blockers, rate-limiting Ca antagonists (verapamil, diltiazem) – reduce ventricular rate by increasing degree of AV block
• Beta-blockers & rate-limiting calcium antagonists more effective than digoxin at controlling HR during exercise & additional benefits in pts with hypertension or structural heart disease.
• Combination therapy (e.g. digoxin and atenolol) is often advisable but rate-limiting calcium channel antagonists should not be used with β-blockers because of the risk of bradycardia

Question 22

Permanent AF

- what is the treatment

Answer 22

Treatment as for persistent

Ventricular rate control

• 1st line: bisoprolol
• 2nd line: non-dihydropyridine calcium channel blocker e.g. verapamil/diltiazem
• 3rd line: digoxin (poor rate control, monotherapy reserved for older patients), dual therapy with bisoprolol/ calcium blocker)

?ABLATE

?amiodarone class III antiarrhythmic: severe s/e e.g. iodine moiety→ thyroid issues, pneumonitis, slate grey appearance, neuropathy, liver issues

Restoration of sinus rhythm/maintenance

• Elective cardioversion (ECHO to detect thrombi, amiodarone if high failure risk)
• Flecainide, dronedarone, amiodarone (best in LVSD, other two drugs contraindicated or if flecainide ci in structural problems e.g. MI)
• ?ablate: pulmonary vein isolation

Prevention of thromboembolic events
- Apixaban, edoxaban

Question 23

What is the treatment for unstable AF?

Answer 23

synchronized DC cardio version with/without amiodarone

reasons for being unstable - shock, MI, syncope, HF

Question 24

What is the treatment for stable <48hr AF?

Answer 24

Rate control: beta blocker e.g. bisoprolol/ metoprolol

Rhythm control: synchronised DC cardioversion OR flecainide (ci: structural heart disease)

Begin heparin if delayed

Question 25

What is the treatment for stable >48hr AF?

Answer 25

Rate control: bisoprolol/diltiazem

Rhythm control: anticoagulated 3-4 weeks prior to DC cardioversion

Question 26

What scoring system should be used to asses risk of thromboembolism in AF?
- what factors does this consider?

Answer 26

CHADS-VASc: HF, HTN, Age (65-74, >74), DM, Stroke Hx, Vascular disease, Sex

Maximum score = 9

Question 27

Atrioventricular nodal re-entry tachycardia

• pathophsyiology
• what would HR be?
• How long do espiodes last?
• presentation?
• ECG
• management

Answer 27

Due to re-entry in a circuit involving AV node and its 2 right atrial input pathways: a superior ‘fast’ pathway and an inferior ‘slow’ pathway

Regular tachycardia – 120-240/min

Often in absence of structural heart disease

Episodes may last few secs – many hours

Presentation:

• Aware of rapid, very forceful, regular heartbeat
• May have chest discomfort, lightheadedness, breathlessness
• May have polyuria due to release of atrial natriuretic peptide

ECG

• Tachycardia with normal QRS complexes
• May have rate-dependent bundle branch block

Management

• Do not always need to treat
• Can stop episode by carotid sinus pressure or valsalva manoeuvre
• Adenosine (3–12 mg rapidly IV in incremental doses until tachycardia stops) or verapamil (5 mg IV over 1 min) will restore sinus rhythm in most cases.
• Intravenous β-blocker or flecainide can also be used.

In rare cases, if have severe haemodynamic compromise, tachycardia should be terminated by DC cardioversion.

In patients with recurrent SVT, catheter ablation = most effective therapy and will permanently prevent SVT in more than 90% of cases.

Alternatively, prophylaxis with oral β-blocker, verapamil or flecainide may be used but commits predominantly young patients to long-term drug therapy and can create difficulty in female patients, as these drugs are normally avoided during pregnancy.

Question 28

Wolff-Parkinson-White syndrome

Answer 28

Abnormal band of conducting tissue connects atria and ventricles = ‘accessory pathway’

• Comprises rapidly conducting fibres - resemble Purkinje tissue - conduct very rapidly & rich in sodium channels.
• Initiation of contraction by accessory pathway → tachycardia

50% - only conducts in retrograde direction (from ventricles to atria) → no change in ECG in sinus rhythm

50% - also conducts antegradely (from atria to ventricles) → AV conduction in sinus rhythm is mediated via both AV node and accessory pathway, → distorting QRS complex.

Premature ventricular activation via pathway:
- Shortens PR interval
- ‘Slurred’ initial deflection of QRS complex = delta wave
This is known as a manifest accessory pathway.

As AV node & accessory pathway have different conduction speeds and refractory periods → a re-entry circuit can develop, causing tachycardia

When associated with symptoms = Wolff–Parkinson–White syndrome.

ECG almost indistinguishable from AVNRT

Carotid sinus pressure or IV adenosine can terminate the tachycardia.

If atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because accessory pathway lacks the rate-limiting properties of the AV node

• This is known as pre-excited atrial fibrillation
• May cause collapse, syncope and sudden death.
• Should be treated as emergency, usually with DC cardioversion.

Symptomatic patients → 1st line treatment = Catheter ablation
- Nearly always curative.

Alternatively, prophylactic anti-arrhythmic drugs, such as flecainide or propafenone, can be used to slow conduction in, and prolong the refractory period of, the accessory pathway.

Long-term drug therapy is not the preferred treatment for most patients

NO Amiodarone – due to SE & ablation is safer and more effective.

Digoxin and verapamil shorten the refractory period of the accessory pathway and should not be used.

Question 29

Ventricular ectopic beats

Answer 29

Ventricular ectopic beats (extrasystoles, premature beats)
• QRS complexes in sinus rhythm narrow as ventricles are activated rapidly and simultaneously via the His–Purkinje system.
• Complexes of ventricular ectopic beats (VEBs) - premature, broad and bizarre because ventricles are activated sequentially rather than simultaneously.
• The complexes may be unifocal (identical beats arising from a single ectopic focus) or multifocal (varying morphology with multiple foci).
• ‘Couplet’ and ‘triplet’ = two or three successive ectopic beats.
• A run of alternating sinus and ventricular ectopic beats is known as ventricular ‘bigeminy’.
• Ectopic beats produce low stroke volume because left ventricular contraction occurs before filling is complete.
• Pulse → irregular, with weak or missed beats (
• Usually asymptomatic but may have irregular heart beat, missed beats or abnormally strong beats (due to increased output of post-ectopic sinus beat).
• Significance of VEBs depends on presence/absence of underlying heart disease.

Question 30

Ventricular ectopic beats in otherwise healthy subjects

Answer 30

• VEBs frequently found in healthy people
• Prevalence increases with age.
• Ectopic beats in patients with otherwise normal hearts - more prominent at rest and disappear with exercise.
• Treatment not necessary, unless patient is highly symptomatic (β-blockers or, in some situations, catheter ablation).
• Sometimes manifestation of otherwise subclinical heart disease - coronary artery disease or cardiomyopathy.
• No evidence that anti-arrhythmic therapy improves prognosis but always investigate very frequent VEBs → ECHO (?structural heart disease) & exercise stress test (?underlying ischaemic heart disease).

Question 31

Ventricular ectopic beats associated with heart disease

Answer 31

• Frequent VEBs often occur during acute MI but need no treatment.
• Persistent, frequent (over 10/hr) VEBs in patients who have survived acute phase of MI indicate poorer long-term outcome.
• Other than β-blockers, anti-arrhythmic drugs do not improve & may worsen prognosis.
• Common in patients with heart failure of any cause, including cardiomyopathy.
• Associated with adverse prognosis, but this is not improved by anti-arrhythmic drugs.
• Effective treatment of the heart failure may suppress ectopic beats.
• Also feature of digoxin toxicity, and may occur as ‘escape beats’ in patients with bradycardia.
• Treatment = treat underlying condition.

Question 32

Ventricular tachycardias

Answer 32

• Occurs most commonly in settings of: acute MI, chronic coronary artery disease, cardiomyopathy
• Occurs when there is extensive ventricular disease - impaired left ventricular function or a left ventricular aneurysm.
o VT may cause haemodynamic compromise or degenerate into ventricular fibrillation
• Caused by abnormal automaticity or triggered activity in ischaemic tissue, or by re-entry within scarred ventricular tissue.
• Presentation: palpitation or symptoms of low cardiac output, e.g. dizziness, dyspnoea or syncope.
• ECG – tachycardia, broad, abnormal QRS complexes, rate > 120/min (
• May be difficult to distinguish from SVT with bundle branch block or pre-excitation (WPW syndrome).
o Features in favour of VT:
• History of MI
• AV dissociation (pathognomonic)
• Capture/ fusion beats (pathogonomic)
• Extreme left axis deviation
• Very broad QRS complexes (>140 ms)
• No response to carotid sinus massage or IV adenosine
• Patients recovering from MI sometimes have periods of idioventricular rhythm (‘slow’ VT) at a rate only slightly above preceding sinus rate & <120/min.
o Reflect reperfusion of infarct territory → may be good sign.
o Usually self-limiting & asymptomatic, & do not require treatment.
o Other forms of sustained VT will require treatment, often as an emergency.
• VT occasionally occurs in patients with otherwise healthy hearts (‘normal heart VT’), usually because of abnormal automaticity in the right ventricular outflow tract or one of the fascicles of the left bundle branch.
o Prognosis is good and catheter ablation can be curative.
• Management
o Prompt action to restore sinus rhythm is required and should usually be followed by prophylactic therapy.
o Synchronised DC cardioversion = treatment of choice if systolic BP is <90 mmHg.
o If arrhythmia well tolerated, IV amiodarone may be given as a bolus, followed by a continuous infusion.
o IV lidocaine can be used but may depress left ventricular function, → hypotension or acute heart failure.
o Hypokalaemia, hypomagnesae- mia, acidosis and hypoxaemia should be corrected.
o Beta-blockers effective at preventing VT by reducing ventricular automaticity.
o Amiodarone can be added if additional control is needed.
o Class Ic anti-arrhythmic drugs should not be used for prevention of VT in patients with coronary artery disease or heart failure because they depress myocardial function and can be pro-arrhythmic (increase likelihood of a dangerous arrhythmia).
o In patients at high risk of arrhythmic death (e.g. those with poor left ventricular function, or where VT is associated with haemodynamic compromise), use of an implantable cardiac defibrillator is recommended.
o Rarely, surgery (e.g. aneurysm resection) or catheter ablation can be used to interrupt the arrhythmia focus or circuit in patients with VT associated with a myocardial infarct scar.

Question 33

Torsades de pointes

Answer 33

• Form of polymorphic VT is a complication of prolonged ventricular repolarisation (prolonged QT interval).
• ECG - rapid irregular complexes that oscillate from an upright to an inverted position and seem to twist around the baseline as the mean QRS axis changes
• Usually non-sustained and repetitive, but may degenerate into ventricular fibrillation.
• During periods of sinus rhythm, ECG will usually show a prolonged QT interval (> 0.43 s in men, > 0.45 s in women when corrected to a heart rate of 60/min).
• Common causes (long QT interval):
o Bradycardia
o Electrolyte disturbance
• Hypokalaemia
• Hypomagnesaemia
• Hypocalcaemia
o Drugs
• Disopyramide, flexainide (other class Ia, Ic anti-arrhythmic drugs)
• Sotalol, amiodarone (and other class III anti-arrhythmic drugs)
• Amitripytline (and other tricyclic antidepressants)
• Chlorpromazine (and other phenothiazines)
• Erythromycin (other macrolides…)
o Congenital syndromes – K and Na channels
• Long QT1: gene affected KCNQI: K+ channel (30-35%)
• Long QT2: gene affected HERG: K+ channel (25-30%)
• Long QT3: gene affected SCNSA: Na+ channel (5-10%)
• Long QT4-12: rare
• Long QT syndrome subtypes have different triggers, which are important when counselling patients.
o Adrenergic stimulation (e.g. exercise) -long QT type 1
o Sudden noise (e.g. an alarm clock) - long QT type 2.
o During sleep – type 3
• Treatment should be directed at underlying cause.
• Intravenous Mg (8 mmol over 15 mins, then 72 mmol over 24 hrs) should be given in all cases.
• Atrial pacing will usually suppress arrhythmia through rate-dependent shortening of QT interval.
• Intravenous isoprenaline is a reasonable alternative to pacing but should be avoided in patients with the congenital long QT syndromes.
• Long-term therapy may not be necessary if underlying cause can be removed.
• Beta-blockers effective at preventing syncope in patients with congenital long QT syndrome.
• Some, particularly those with extreme QT interval prolongation (> 500 ms) or certain high-risk genotypes should be considered for implantation of a defibrillator.
• Left stellate ganglion block may be of value in patients with resistant arrhythmias.
• Brugada syndrome - related genetic disorder that may present with polymorphic VT or sudden death.
o Defect in Na channel function
o Abnormal ECG (right bundle branch block and ST elevation in V1 and V2 but not usually prolongation of the QT interval).
o Implantable defibrillator.

Question 34

AV block

Answer 34

• AV conduction influenced by autonomic activity
• Causes: fibrosis, CAD, AV nodal blocking agents (beta-blockers, Ca channel blockers, digoxin, adenosine), anti-arrthymic (Na channel blockers, Class III agents e.g. amiodarone, sotalol)
• Other aetiologies
o High vagal tone in athletes
o Cardiomyopathy e.g. hypertrophic, sarcoid, amyloid, haemochromatosis
o Adjacent valvular calcification
o Poster catheter ablation for arrhythmia
o Electrolyte imbalance
o Neuromuscular disorders e.g. myotonic dystrophy, Kearns-Sayre syndrome (mitochondrial disease with progressive external opthalmoplegia), Erb dystrophy, peroneal muscular atrophy
o Transient vagotonia: endotracheal suction, micturition, inferior MI
• Presentation: fatigue, dyspnoea, junctional escape rhythm
• May be intermittent and only evident when conducting tissue is stressed by rapid atrial rate
o → Atrial tachyarrhythmias often associated with AV block
• 1st degree
o AV conduction delayed → PR interval prolonged (>0.20s)
o Rarely causes symptoms
• 2nd degree
o Dropped beats occur as some impulses from atria fail to conduct to ventricles
o Mobitz type 1
• Progressive lengthening of successive P intervals → dropped beat
• Cycle repeats itself → Wenckebach phenomenon (due to impaired conduction in AV node; may be physiological; sometimes observed at rest/during sleep in athletic young adults with high vagal tone)
o Mobits type 2
• PR interval of conducted impulses remain constant but some P waves not conducted
• Usually caused by disease of His-Purkinje system
• Risk of asystole (flat line on ECG)
o 2:1 AV block
• Alternate P waves conducted → impossible to distinguish between Mobitz type I and type II block
• 3rd degree (complete AV block)
o AV conduction fails completely – atria and ventricles beat independently (AV dissociation)
o Ventricular activity maintained by escape rhythm arising in AV node or bundle of His (narrow QRS complexes) or distal Purkine tissues (broad QRS complexes)
o Distal escape rhythm tend to be slower and less reliable
o Slow (25-50/min), regular pulse
• Only varies with exercise in case of congenital complex AV block
o Compensatory increase in stroke volume → large volume pulse
o Cannon waves visible in neck
o Intensity of first heart sound varies due to loss of AV synchrony
o Aetiology
• Congenital
• Acquired
• Idiopathic fibrosis
• MI/ischaemia
• Inflammation – acute (aortic root abscess in infective endocarditis); chronic (sarcoidosis, Chagas’ disease)
• Trauma – cardiac surgery
• Drugs – digoxin, beta-blocker
• Stoke-Adams attacks
o Recurrent syncope
• Caused by episodes of ventricular asystole in complete heart block or Mobitz type II 2nd degree AV block
• Or due to sinoatrial disease
o Sudden loss of consciousness – occurs without warning & results in collapse
o Brief anoxic seizure (due to cerebral ischaemia) may occur if prolonged asystole
o Pallor and death-like appearance during attack → once heart starts beating again, have characteristic flush
o Recovery rapid
• Epilepsy → slow recovery
o Similar symptoms to sinoatrial disease and neurocardiogenic syncope
• Management
o AV block complicating acute myocardial infarction
• Common in acute inferior MI – usually transient
• As right coronary artery supplies AV node
• Usually have reliable escape rhythm
• If remains well – no treatment required
• Symptomatic 2nd/3rd degree AV blocks – may respond to atropine (0.6mg IV, repeated as required), or temporary pacemaker
• Most will resolve in 7-10 days
o 2nd/3rd degree AV heart block complicating acute anterior MI
• Indicates extensive ventricular damage involving both bundle branches
• Poor prognosis
• May go into asystole → temporary pacemarker
• If present with asystole → IV atropine or IV isoprenaline – help to maintain circulation until temporary pacing electrode can be inserted
• External (transcutaneous) pacing can provide effective temporary rhythm support
o Chronic AV block
• Symptomatic bradyarythmias → permanent pacemaker
• Asymptomatic 1st degree or Mobitz type 1 2nd degree block (Wenckebach phenomenon) → no treatment but may indicate serious underlying heart disease
• Asymptomatic Mobitz type 2 2nd or 3rd degree AV heart block – due to risk of asystole and sudden death

Question 35

Stoke-Adams attack

Answer 35

Due to AV block

Recurrent syncope
• Caused by episodes of ventricular asystole in complete heart block or Mobitz type II 2nd degree AV block
• Or due to sinoatrial disease
o Sudden loss of consciousness – occurs without warning & results in collapse
o Brief anoxic seizure (due to cerebral ischaemia) may occur if prolonged asystole
o Pallor and death-like appearance during attack → once heart starts beating again, have characteristic flush
o Recovery rapid
• Epilepsy → slow recovery
o Similar symptoms to sinoatrial disease and neurocardiogenic syncope

Question 36

Bundle branch block
- pathology
-

Answer 36

• Conduction block in right or left bundle branch can occur due to many pathologies:
o Ischaemic or hypertensive heart disease
o Cardiomyopathies
• Depolarisation proceeds through a slow myocardial route in affected ventricle rather than through rapidly conducting Purkinje tissues that constitute the bundle branches.
→ delayed conduction into LV or RV
→ broadens QRS complex (≥ 0.12 s)
→ produces characteristic alterations in QRS morphology

Question 37

RBBB

Answer 37

can occur in healthy people
o Normal variant
o Right ventricular hypertrophy or strain – e.g. pulmonary embolism
o Congenital heart disease - e.g. atrial septal defect
o Coronary artery disease
o Activation of right ventricle is delayed as depolarisation has to spread across the septum from LV
o Delayed RV→secondary R wave in right precordial leads (V1-3) and wide slurred S wave in lateral waves
o Abnormal secondary repolarisation with ST depression/ T wave inversion in right precordial leads
o Normal axis

Question 38

LBBB

Answer 38

o Often signifies important underlying heart disease.
• Coronary artery disease
• Hypertension
• Aortic valve disease – aortic stenosis
• Cardiomyopathy
• IHD
• Anterior MI
• Lenegre disease
• Hyperkalaemia
• Digoxin toxicity
o Normally, the septum is activated from left to right, producing Q waves in lateral waves
o In LBBB, septal depolarisation becomes right to left due to the block→ eliminates q wave in lateral leads
o Right to left depolarisation produces tall R wave (I,V5-6) and deep S waves in right precordial leads (V1-3)→left axis deviation

Question 39

Which arrhythmias may result in cardiac arrest?

Answer 39

VF (IHD)
Pulseless ventricular tachycardia (IHD)
- Torsades de pointes in patients with underlying prolonged QT interval - ma be related to hypomagesaemia

Asystole

Question 40

How would you treat cardiac arrest?

Answer 40

Shockable rhythms - adrenaline 1mg IV every 3-5 mins

Non-shockable rhythms - adrenaline 1mg IV every 3-5 mins, consider reversible causes - hypoxia, hypovolemia, potassium status