Arrhythmia management

Arrhythmia management
Dr Andrew Crofton
Emergency Registrar

Introduction
 Regular rhythm has <10% variation in beat-to-beat length
 Check by marking off 5 beats and moving
 Conduction defects
 Bundle branch blocks: Pre-existing or rate-related
 Accessory pathways
 Hyperkalaemia
 Sodium channel blockade
 Pacing

The bradycardic unstable patient
 Transcutaneous pacing is Class I treatment
 Most patients achieve capture at 100mA
 Start at lowest current that achieves capture
 IV narcotics/benzodiazepines are necessary
 Atropine is Class IIA treatment
 500mcg q5min IV until desired response achieved (up to 3mg)
 Transient effect so prepare for transcutaneous/venous pacing
 Use cautiously in ischaemia
 Can be used cautiously in heart transplant patients but often no response due to lack of vagal
innervation
 Adrenaline 2-10mcg/min IV infusion
 Dopamine 2-10mcg/kg/min IV infusion

The tachycardic unstable patient
 Synchronised cardioversion applies current well away from vulnerable period of
inducing VF (10ms after peak of R wave) (for all others)
 Defibrillation applies current as soon as button pressed (for VF)
 200J either way
 Complications
 Myocardial damage (rare if <325 J)
 Induced arrhythmias
 More likely if on digoxin, quinidine, electrolyte abnormalities or MI
 Thromboembolism
 1.2-1.5% of chronic AF patients (if unstable risk outweighed by benefit)
 Hypotension

Stable narrow-complex tachycardia
 Regular
 Attempt vagal manoeuvres (10mL syringe)
 Adenosine 6mg IV, 12mg IV, 12mg IV
 If converts
 Likely AVRT or AvnRT
 Does not convert
 Likely atrial flutter, ectopical atrial tachycardia, junctional tachycardia
 Control rate and consider underlying cause and manage accordingly
 Irregular
 Probable AF, atrial flutter or MAT
 Control rate and consider underlying cause and manage accordingly

Stable wide-complex tachyarrhythmia
 Regular rhythm
 Possible VT or unknown
Amiodarone 150mg IV over 10 min
Repeat if necessary to total 2.2g over 24 hours
Prepare for synchronised cardioversion
 Definite SVT with aberrancy
Treat as for SVT

Stable wide-complex tachyarrhythmia
 Irregular rhythm
 WPW with AF
 Avoid AV nodal blockers
 Consider amiodarone and expert consultation
 Torsades de pointe
 Magnesium 1-2g over 5-60min
 Polymorphic VT
 Prepare for synchronised cardioversion
 AF with aberrancy
 Follow narrow complex irregular algorithm

Sinus arrhythmia
 Definition
 Variation >0.12s between longest and shortest P-P interval
 Normal sinus P waves and P-R intervals
 1:1 AV conduction
 Normal finding in young people often due to Bainbridge reflex (vagal tone changes
with respiration)
 No treatment required

Premature atrial contractions
 Definition
 Ectopic P wave that appears before next expected sinus beat
 Ectopic P wave that has a different shape and axis
 Ectopic P wave may or may not be conducted through AV node (depends if reaches AV node
in absolute refractory period (not conducted) or in relative refractory period (delayed
conduction – long PR))
 May conduct aberrantly if reaches bundle branch while still in refractory period
 Common at all ages and usually do not indicate cardiac disease
 Frequent PAC’s seen in chronic lung disease, IHD, digitalis toxicity, increased stress,
caffeine, tobacco
 May precipitate sustained atrial tachycardia, flutter or fibrillation
 Treatment
 Cease any toxins and treat any underlying disorder, if present

Bradydysrhythmias
 Bradycardia (ventricle and atria at same slow rates)
 Includes sinus bradycardia, junctional rhythm, idioventricular rhythm and hyperkalaemia-
related sinoventricular rhythm
 AV blocks
 Second-degree AV block (usually type 2), 3rd degree AV block, slow AF/flutter
 80% of bradydysrhythmias are due to factors outside the conduction system e.g.
toxicity, ACS, hypoxia
 Emergent treatment is only required if:
 HR <50 and accompanied by hypotension or hypoperfusion OR
 Needs resuscitative treatment
 Structural disease of the infranodal system
 Needs close monitoring and pacing available at all times

Bradydysrhythmias
 Atropine
 Vagolytic
 Effective for sinus bradycardia and junctional rhythms but not useful (nor particularly
harmful) for idioventricular rhythms, second-degree type 2 or third-degree AV block

Sinus bradycardia
 Definition:
 Atrial rate <60/min
 May be:
 Physiological (e.g. athletes)
 Pharmacological (e.g. digoxin, opioids, beta-blocker, CCB)
 Pathological (e.g. acute inferior MI, raised ICP, carotid sinus hypersensitivity or
hypothyroidism)
 Treat if signs of hypoperfusion and <50 as per algorithm

Sick sinus syndrome
 Heterogenous group of diseases causing intermittent tachy- and bradyarrhythmias
 Tachyarrhythmias usually: AF, junctional tachycardia, SVT or atrial flutter
 Bradyarrhythmias usually: Sinus bradycardia, prolonged sinus arrest, SA block
usually with AV nodal block and inadequate AV nodal escape rhythms
 Causes
 Ischaemia, rheumatic disorders, myocarditis, pericarditis, metastatic tumors, surgical
damage and cardiomyopathies
 Symptoms
 Syncope, near syncope, palpitations, dyspnoea, chest pain or CVA

Sick sinus syndrome
 Exacerbating factors
 Disease: Abdominal pain, raised ICP, thyrotoxicosis, hyperkalaemia, increased vagal tone
 Drugs: Beta-blockers, CCB, digoxin, quinidine, procainamide, disopyramide
 Diagnosis often requires Holter monitoring
 Treatment: Avoid antiarrhythmics as worsen one or the other part
 NEED PACEMAKER URGENTLY

Sinus tachycardia
 Definition:
 Atrial rate usually 100-160
 Physiological: Children, exercise, anxiety, emotion
 Pharmacological: Atropine, salbutamol, adrenaline, alcohol, nicotine, caffeine
 Pathological: Sepsis, pain, fever, hypoxia, anaemia, hypovolaemia, PE
 Treat underlying disorder ONLY

SVT
 Defined as any tachyarrhythmia arising from above AV node
 Commonly describes AVRT and AvnRT
 60% have AvnRT and 20% have AVRT (involving bypass tract)
 The rest have re-entry involving some other site
 Occurs in 2% of patients after AMI
 HR usually 150-200J in adult
 Rates >220 suggest accessory pathway (AVRT)
 In a normal heart, rates of 160-200 may be tolerated for days

SVT - ECG
 p waves
 May be seen in latter part of QRS in lead V1 in 30% of AVNRT
 Indicates typical slow-fast AVNRT with short R-P interval
 If later in the T wave, suggests fast-slow AVNRT with long R-P interval
 More commonly seen in AVRT
 ST elevation in aVR – 70% sensitive and specific for accessory pathway
 ST depression is common and not predictive of IHD
 ST-T wave changes can persist for days following reversion
 Electrical alternans seen in 20% of SVT and is not predictive of pericardial effusion

SVT
 Causes
 Idiopathic
 Structural heart disease
 Thyrotoxicosis
 Precipitants
 Alcohol
 Caffeine
 Sympathomimetics
 Ischaemia
 Hypokalaemia
 Pregnancy
 Cannabis

SVT - AVnRT
 Re-entry circuit within AV node
 60% of cases
 Initiated by ectopic atrial impulse reaching AV node in relative refractory period
 Mostly slow-fast (i.e. slow antegrade and fast retrograde conduction)
 ECG characteristics
 P wave buried in QRS complex and usually not visible
 1:1 conduction
 Normal QRS complex
 Causes
 Normal heart
 Rheumatic heart disease, acute MI, acute pericarditis, mitral valve prolapse or a pre-excitation syndrome
 Pregnant patients with tachyarrhythmias have a higher rate of foetal distress

SVT - AVnRT
 Treatment
 Vagal manoeuvres (success rate 20-25%)
 15% without augmentation and 40% with augmentation
 Valsalva in supine position is most effective (need strain for at least 10 seconds) using 10mL
syringe
 Ice pack on face reserved for infants with 6-7 seconds and nose held closed (diving reflex)
 Carotid sinus massage
 10 seconds at a time, first on non-dominant cerebral hemisphere
 Never bilateral
 CI: Known AV nodal block, digoxin or carotid artery stenosis

SVT
 Adenosine
 >90% of re-entrant SVT converted but 1/3 revert back. Increased efficacy if higher heart rate
 This is the only Class I therapy
 First choice if infants, structural heart disease or borderline perfusion
 Elimination half-life 10 seconds
 50% suffer facial flushing, distress and chest pain
 Early recurrence seen in 25% of patients
 6mg then 12mg
 Potentiated by carbamazepine and dipyramidole so use 3mg (blocks nucleoside transport into cells)
 Theophylline and caffeine antagonise effect at adenosine receptors so use higher dose
 20% reduced reversion rate if caffeine in last 4 hours
 Also use lower dose if central line or heart transplant patients
 Initially cleared from serum rapidly by intracellular uptake (nucleoside transporter) then deamination by adenosine
deaminase in cytosol or phophorylation by adnosine kinase
 Not contraindicated in WPW when QRS is narrow

SVT - AvnRT
 Verapamil and diltiazem are second-line therapy (Class IIA)
 Diltiazem 15-20mg IV over 2 min then continuous infusion 4-20mg/hr
 Can repeat bolus in 15 min if needed
 Verapamil 2.5-5mg IV over 2 min, can repeat at 15min if necessary
 First choice if young adult without structural heart disease and narrow QRS
 Reversion rate 80% with 5mg and 95% with 10mg
 Progressively less effective for HR >175
 Probably more effective than adenosine if caffeine ingested in last 4 hours
 Pre-treatment with 5mL of 10% calcium gluconate decreases hypotensive effects without impairing
cardioversion success
 CI: CCF or COAD
 Calcium should be available – 500-1000mg IV of calcium chloride q10min if necessary
 Mean SBP drop of 20mmHg and MAP drop of 10mmHg with verapamil

SVT
 Beta-blockers
 Class IIA recommendation also
 Metoprolol 5mg IV q5min up to 3 doses
 Esmolol 500mcg/kg IV over 1 min. Can repeat after 2-5min then infusion 50mcg/kg/min
 Propranolol 0.1mg/kg divided into 3 equal doses given slowly 2 min apart
 CI: CCF or COAD
 Esmolol effective in 50% of re-entrant SVT
 Hypotension seen in 50% but rapidly reversible if esmolol used
 Propranolol IV also 50% success rate (80% with AvnRT and 15-20% with accessory pathway
AVRT)
 Electrical cardioversion rarely required (20-100J biphasic)

SVT - Prophylaxis
 Flecainide
 Digoxin and verapamil in combination
 Need high doses
 Radiofrequency ablation of accessory pathways

SVT - AVRT
 Re-entry usually occurs with antegrade conduction via AV node (hence narrow
complex – orthodromic conduction)
 85% of re-entrant SVT seen with WPW are narrow complex (orthodromic)
 Retrograde P wave is often seen after the QRS as arises from atrial stimulation via
retrograde accessory pathway transmission
 Inverted in II, III, aVF (as arising from Bundle vs. sinus node)
 Antidromic conduction results in wide complex tachy-arrhythmias that are difficult
to differentiate from VT
 Only 5% of accessory pathways are in this

SVT - AVRT
 Types
 Lown-Ganong-Levine syndrome
 James fibres (atriohisian connection)
 Continuation of posterior internodal tract connecting atrium with proximal His bundles
 Usual delay in AV node is bypassed
 Get short PR as a result with normal QRS (as still initiated from Bundle of His)
 No Delta wave

SVT - AVRT
 Types continued
 Mahaim bundles
 Bundles of myogenic tissue
 Impulses go via AV node but then some impulses bypass infranodal conducting system
 Get ventricular activation from two sources simultaneously – bypass tract and normal conducting system
 Results in delta wave then normal QRS after this
 Kent bundles
 Myogenic tissue bypassing AV node altogether
 Most common source for WPW syndrome
 Short PR (<120ms), delta wave, broad QRS >100ms
 Repolarisation abnormalities occur due to altered depolarisation and include ST and T wave discordant
changes

SVT – AVRT
 Paroxysmal re-entrant SVT occurs in 40-80% of WPW patients
 AF in 10-20% of WPW patients
 Atrial flutter in 5% of WPW patients
 Most patients with WPW have longer refractory periods in bypass tract than AV node (but minority have opposite)
 Can result in wide complex tachycardia transmitting atrial fib/flutter at 1:1
 Any patient with a ventricular rate >300 should raise suspicion of pre-excitation syndrome
 Treatment
 Narrow-complex orthodromic AVRT treated like AvnRT
 As AV node is involved, any AV nodal blocking agent will help
 Wide-complex antidromic AVRT is usually associated with a short refractory period in the bypass tract, with high risk of rapid
ventricular rates and VF
 AVOID beta-blockers, CCB and adenosine
 Best treated with cardioversion
 Amiodarone and flecainide are options with Cardiology input

WPW
 SVT with WPW
 Verapamil contraindicated when antidromic conduction present as may convert atrial rate to
ventricular rate and precipitate VF
 AF with WPW
 Flecainide
 Drug of choice if structurally normal heart w/o CAD
 Slow conduction in accessory pathway
 150mg IV over 30 minutes (2mg/kg)
 Electrical cardioversion
 If unstable or flecainide contraindicated
 Adenosine
 Unlikely to be of benefit and may enhance ventricular response through AV blockade
 Verapamil and digoxin enhance conduction via accessory pathway and are CI

WPW
 1-2% of patients with WPW actually present with an arrhythmia
 80% AVRT
 15-30% AF
 5% A flutter
 1-3% of population have accessory pathways
 Can have pseudo-old infarction pattern

Atrial flutter
 Exact mechanism unknown
 Regular atrial rate of 250-350
 Sawtooth flutter waves – superiorly directed and most easily seen in II, III, aVF (usually inverted)
 AV block, usually 2:1 and ventricular rate 125-175
 There is no isoelectric segment
 Often flutter waves only visible in one lead
 Flutter wave and QRS ALWAYS meet above the baseline
 May transmit 1:1 if bypass tract or atrial rate slowed by medications to allow AV nodal
conduction
 Often better tolerated than AF at high ventricular rates due to organised atrial actiity

Atrial flutter
 Causes
 Ischaemic heart disease
 Acute MI (occurs in 2% of AMI)
 Congestive cardiomyopathy
 PE
 Myocarditis
 Blunt chest trauma
 Digoxin toxicity

Atrial flutter
 Diagnostic manoeuvres if flutter waves difficult to identify (e.g. adenosine)
 Management
 Chemical cardioversion rarely successful
 Verapamil 10% (but 90% effective if AMI-related)
 50J will cardiovert 80%
 100J will cardiovert 95%
 Atrial overdrive pacing (>400) an option
 Anticoagulate as for AF
 Rate control as for AF
 Conservative approach waiting for reversion is often appropriate if 2:1 block

Atrial fibrillation
 Most common sustained arrhythmia – lifetime risk over 40yo = 25%
 0.4-2% of population
 4% if over 60, 7% if over 65, >10% if >85yo
 1.6% per annum if over 75
 Causes 25% of strokes in patients >80yo
 90% of ‘lone fibrillators’ revert within 48 hours and 60% will cardiovert with 100J
 Atrial fibrillation waves – best seen in V1,2,3, aVF
 Irregularly irregular ventricular response
 QRS <120ms unless pre-existing BBB, accessory pathway or rate-related BBB
 Usual ventricular response is 140-180/min but slower in diseased AV node or AV nodal blocking agents
 More rapid ventricular response may be seen in bypass tracts
 Asymptomatic in 20%

Atrial fibrillation
 Predisposing factors
 Increased atrial size and mass
 Usually one of four conditions underlying:
 Rheumatic heart disease
 IHD (40%)
 Thyrotoxicosis
 HTN
 Also
 Chronic lung disease
 Pericarditis
 Acute alcohol intoxication (holiday heart – high spontaneous reversion rate)
 PE
 Atrial septal defect
 Clinical hyperthyroidism in 1%

AF
 Classification
 Primary
 Secondary (30%)
 Recurrent (>=2 episodes)
 Paroxysmal (terminates spontaneously or with intervention within 7 days)
 Sustained (>7 days)
 Occult (only with prolonged ECG monitoring)
 Long-standing (>1 year and rhythm control attempted)
 Permanent (attempts at rhythm control abandoned)
 Non-valvular AF – Absence of:
 Rheumatic mitral disease
 Mechanical or bioprosthetic heart valve
 Mitral valve repair

AF
 Observation strategy
 Usually the least appropriate if RVR
 Indications
 Holiday heart
 Acute stimulant intoxication (benzos first-line)
 Significant underlying heart disease with stress response e.g. febrile
 Unlikely to respond to chemical rhythm control and chemical rate control poses risk of
cardiac decompensation
 If haemodynamically stable, treat underlying cause and reconsider strategy at 48 hours
 If rhythm control required, electrical is method of choice

AF
 Spontaneous reversion
 <1 hour: 25%
 <6 hours: 40%
 <24 hours: 50%
 <48 hours: 65%
 >1 week: Rare
 Without anticoagulation therapy
 Up to 5% of patients with chronic AF have at least one embolic episode each year
 Conversion from chronic AF to sinus rhythm carries 1-5% risk of arterial embolism

Atrial fibrillation
 Treatment
 If stable, rate control is first priority to resting HR of <110
 If no evidence of CCF or a bypass tract:
 Beta-blockers: Metoprolol 5mg IV q5min up to 15mg or esmolol or propranolol
 CCB: Diltiazem 15-20mg IV over 2 min, followed by infusion 4-20mg/hr
 IV amiodarone second-line: 5mg/kg IV over 30-60min followed by 15mg/kg/day infusion (can cause
cardioversion though)
 Can add digoxin if fails
 If CCF evident (LVEF <40%) but no bypass tract:
 IV digoxin or amiodarone (CI in pregnancy)
 Digoxin 400-600mcg IV loading dose repeated at 4-6 hours
 If accessory pathway evident:
 DC cardioversion, amiodarone or flecainide are options

Atrial fibrillation
 Rate control
 Potential candidates
 Age >65
 Sedentary
 Asymptomatic
 Coronary artery disease
 HTN
 Large atria
 No cardiac failure
 Structural heart disease esp. MV
 Do not use rate control if HR <90 as suggests intracardiac conduction disturbance and high
risk of severe bradycardia

AF
 Rate control
 Optimum HR depends on diastolic/systolic ratio
 70-80: No valve disease, normal coronaries
 60-70: AS, MS, LVH, CAD (prolongs diastole)
 80-90: AR, MR (shortens diastolic regurg time)
 90-115: Sepsis, exercise
 Optimum agent: No difference although diltiazem theoretically less likely to cause hypotension
 Metoprolol
 1mg aliquots up to 5-15mg total IV
 Causes less negative inotropy than verapamil
 Need early oral therapy to maintain rate control

AF
 Digoxin
 May be no better than placebo (esp. in shock, sepsis, hypoxia)
 500mcg slow IV injection then 250mcg q4-6hr to total 1500mcg

Atrial fibrillation
 Cardioversion
 Indicated if unstable OR if <48 hours duration OR if definitively anticoagulated for at least 3
weeks OR if TOE has confirmed no atrial thrombus
 Continue for at least 4 weeks after cardioversion (in those not requiring long-term anticoagulation)
 Pharmacological cardioversion
 Effective in 50% of patients with recent onset AF
 Electrical cardioversion is more effective, has shorter hospital stay and is quicker
 Does not require sedation or fasting
 Severe HF, significant AS – Amiodarone
 CAD, moderate HF, abnormal LVH – Amiodarone or Vernakalant
 No structural heart disease – IV Flecainide, Ibutilide, Propafenone, Vernakalnt, Procainamide
 Procainamide

Atrial fibrillation
 Cardioversion continued
 85% convert with 100J and >95% if 210J (start with 100J – or 200J if obese)
 Can try 4-5 attempts in a row until successful
 More likely to be effective if short duration and atria not dilated
 Amnesia as important as analgesia (fentanyl + prop)

AF
 Chemical cardioversion
 Amiodarone
 5mg/kg IV loading dose over 30-60min (50% by 24 hours, 90% by 48 hours)
 Can continue 600mg over 24 hours
 Flecainide
 2mg/kg IV over 30 minutes
 300mg orally if >70kg or 200mg if <70kg
 Can repeat
 60% reversion within 3 hours and 80% within 8 hours
 Not recommended if IHD or structural heart disease or >55yo
 Sotalol
 Useful if hypertension, CAD with good LV function
 Rate control properties probably more beneficial
 80-160mg IV or PO

Atrial fibrillation
 Rhythm control
 First choice if new onset AF but risk of thromboembolism
 20% lower stroke risk than rate control in the long-term
 No survival benefit if older or higher risk patients
 55% remain in sinus rhythm at 1 year on treatment (vs. 30% if no treatment)
 <50% of those in whom rhythm control is attempted are in sinus rhythm at 5 years
 Consider if:
 Young
 Lone AF
 Symptomatic
 Secondary to treated or corrected precipitant
 Cardiac failure

AF
 Rhythm control
 Risk factors for failed reversion
 Age >65
 Cardiac failure
 Late presentation > 48 hours
 Previous AF
 Recurrence whilst on antiarrhythmic therapy
 Structural cardiac lesions
 Left atrial dilation
 Secondary AF

Atrial fibrillation
 Anticoagulation
 Bleeding risk with aspirin is same as warfarin and NOACs but aspirin does NOT prevent stroke
 Stroke risk/year
 0.1% lone fibrillators <60yo with normal echo
 5% in AF without structural heart disease
 10% in AF with rheumatic heart disease
 25% if mitral stenosis
 1.5-2.5% if warfarinised or on aspirin
 Risk increased 3x in patients with moderate-to-severe LA enlargement
 European Society Cardiology
 CHADS2-VASC score 0 = No anticoagulation
 1 – Anticoagulation should be considered (strongly in men)
 2 or more – Anticoagulation indicated
 Warfarin if mechanical heart valves or moderate/severe mitral stenosis irrespective of CHADS—VASC score

Atrial fibrillation – CHADS2-VASC
 CCF +1
 HTN >140/90 on at least 2 occasions or current antihypertensive therapy +1
 Age 75 or older +2
 DM +1
 Previous stroke, TIA or thromboembolism +2
 Vascular disease +1
 Age 65-74 +1
 Sex (female) +1

AF
 Anticoagulation has 60% relative risk reduction for stroke
 Absolute risk reduction
 2.7% per year for primary prevention
 8.4% per year for secondary prevention
 25% relative risk reduction of death
 1% risk of haemorrhage per year overall

Atrial fibrillation - HASBLED
 HTN +1
 Abnormal LFT/renal fx +1 point each
 Stroke +1
 Bleeding history or disposition +1
 Labile INR +1
 Elderly >65yo +1
 Drug (NSAID/antiplatelet)/alcohol use +1 point each

Atrial fibrillation – Bleeding risk factors
 Modifiable
 HTN (esp. SBP >160)
 Labile INR
 Antiplatelets/NSAId
 Excess alcohol (>=8 drinks/week)
 Potentially modifiable
 Anaemia
 Impaired renal fx
 Impaired liver fx
 Reduced platelet count or function

Atrial fibrillation – Bleeding risk factors
 Non-modifiable
 Age >65
 Hx of major bleeding
 Previous stroke
 Dialysis-dependent kidney disease or transplant
 Cirrhotic liver disease
 Malignancy
 Genetic factors
 Biomarker-based bleeding factors
 hsTn
 Serum creatinine

AF - NOACs
 Overall reduce risk of ICH by 0.2%/year vs. warfarin
 Increase risk of GI haemorrhage 0.25%/year vs. warfarin
 Same risk of ischaemic stroke
 Apixaban appears most effective with 0.3%/year lower incidence of stroke and 1%
redution in major bleeding vs. warfarin
 Dabigatran is inferior to warfarin if prosthetic valves
 DOACs considered appropriate for non-mechanical valvular AF (except rheumatic
MS)

Atrial fibrillation – NOAC’s
 Apixaban
 ARISTOTLE trial 5mg BD reduced embolism by 21% compared to warfarin, 31% reduction in
major bleeding and 11% reduction in all-cause mortality
 Rates of haemorrhagic stroke, ICH were lower on apixaban
 Rates of GI bleeding were similar
 Dabigatran
 RE-LY trial 150mg BD reduced embolism by 35% compared with warfarin without a significant
increase in bleeding
 GI bleeding increased by 50%
 110mg BD was non-inferior to warfarin with 20% fewer bleeding episodes
 Edoxaban
 ENGAGE AF-TIMI 48 trial 60mg daily non-inferior to warfarin

Atrial fibrillation - NOACs
 Rivaroxaban
 ROCKET-AF trial Non-inferior to warfarin 20mg daily. Did not reduce mortality, ischaemic
stroke or major bleeding
 Increased GI bleeding but significant reduction in haemorrhagic stroke and ICH
 Meta-analysis
 10% lower mortality in NOAC vs. warfarin with significantly reduced ICH and
haemorrhagic stroke
 GI haemorrhage 1.25x more llikely on NOAC. ICH halved on NOACs

Atrial fibrillation – Left atrial appendage
occlusion
 More research needed for Watchman device given high complication rates
 May be a suitable alternative for patients with absolute contraindications to
NOAC’s or warfarin OR those who suffer strokes despite anticoagulation
 May be interventional or percutaneous
 Large randomised control trial of surgical LAA occlusion performed concomitantly
with open heart surgery or AF ablation is underway

Atrial fibrillation – Combination antiplatelet
and OAC therapy
 Triple therapy dramatically increases bleeding risk
 OAC monotherapy without antiplatelets is recommended for stable CAD without ACS and/or
intervention in last 12 months
 Short-term triple therapy with OAC, aspirin and clopidogrel recommended for those treated for
ACS
 Prasugrel or ticagrelor should be avoided in triple therapy unless a clear need (e.g. stent thrombosis
despite aspirin and clopidogrel)
 This is due to increased major bleeding risk compared to clopidogrel
 The WOEST trial looked at OAC + clopidogrel vs. triple therapy
 Bleeding lower in dual therapy group
 Rates of MI, stroke, stent thrombosis did not differ
 All-cause mortality lower in dual therapy group at 1 year (2.5 vs 6.4%)
 Trial too small but may be future therapy

Atrial fibrillation – Combination therapy
National Heart Foundation Guideline

Atrial fibrillation – Management of
bleeding on NOACs or warfarin
 APTT useful only for dabigatran
 PT for warfarin
 Dabigatran cleared by dialysis
 If recent intake of NOAC (<2-4hr) activated charcoal can be considered
 For warfarin
 FFP more rapid than Vitamin K
 Prothrombin complex concentrates faster than FFP
 Combination offers best chance of survival in ICH
 NOAC
 Prothrombin complex
 Specific antidotes
 Idarucizumab humanised antibody fragment for dabigatran
 Andexanet alpha, modified human recombinant Factor Xa reverses anti-Xa effect in minutes

Management of bleeding
National Heart Foundation Guideline

AF – Long-term Rx
 Maintenance of SR if successfully cardioverted
 Amiodarone most effective (65% in SR at 1 year)
 Sotalol 40% in SR at 1 year
 Flecainide
 Pill in pocket of 600mg PO intermittently also proven benefit

Multifocal atrial tachycardia (MAT)
 At least three different site of atrial ectopy
 Frequently confused with AF or atrial flutter
 P waves – 3 or more different morphologies
 Changing P-P, P-R and R-R intervals
 Atrial rhythm usually 100-180/min
 Causes
 Typically elderly, COAD, CCF, sepsis or methylxanthine toxicity
 Digoxin is an unlikely cause of MAT
 Treatment
 Directed towards underlying disorder
 Cardioversion has no effect on atrial ectopy
 Poor prognostic indicator in illness

Terminology re: ectopic beats
 Compensated pause
 If the coupling interval (Interval between normal complex and ectopic complex) + the
return cycle (interval between ectopic complex and next normal complex) is equal to 2x
the dominant cycle interval (regular R-R)
 Uncompensated pause
 Coupling interval + return cycle is less than 2x DC

Junctional arrhythmias
 Impulse arises from AV node or Bundle of His above the bifurcation with spread
retrogradely towards atria and anterogradely to ventricles
 AV dissociation may occur if junctional escape rate is faster than the sinus node
rate and junctional impulse is blocked from retrograde transmission
 P wave often buried in QRS

Junctional arrhythmias –
Junctional premature contractions
 Ectopic P wave different morphology and often inverted in II, III, aVF (i.e. directed
superiorly/retrograde)
 Ectopic P wave may lie before or after normal QRS complex
 Shorter than normal PR interval
 Premature ectopic QRS complex
 Uncommon in healthy hearts. Occur in CCF, digoxin toxicity, IHD and AMI (esp. inferior)
 No specific treatment. Treat underlying disorder

Junctional arrhythmias –
Junctional rhythm
 Typically sinus node overdrive suppresses all other pacemakers
 If sinus node discharge is <60 or is blocked, junctional escape beats can occur
 Rate 40-60
 Typically do not conduct retrogradely to the atria, so typically get QRS complex without P waves either before or
after
 Accelerated junctional rhythms can occur at 60-100 or junctional tachycardia >100. Typically this will capture both
atria and ventricles.
 Seen with digoxin toxicity, acute rheumatic fever, or inferior MI
 Typically seen in sinus bradycardia, slow phase of sinus arrhythmia, AV block or in the pause after premature beats
 Sustained junctional escape rhythms seen in CCF, myocarditis, hypokalaemia and digoxin toxicity
 Treatment
 If sustained, treat underlying cause, consider atropine
 Consider potassium supplementation to high-normal
 Consider digoxin toxicity and treatment thereof

Ventricular arrhythmias
- Premature ventricular contractions
 P waves do not precede QRS
 Retrograde P waves may be present
 QRS is premature and wide
 ST segment and T waves are directed opposite to the major QRS deflection
 Usually don’t affect the sinus node so get a fully compensated post-ectopic pause (vs. PAC with uncompensated pause due to SA node reset)
 May see fixed coupling interval (<0.04s) if single ectopic focus (with uniform or multiform PVC’s depending on ventricular depolarisation pattern)
 May see fusion beats
 Very common, even without structural heart disease
 Occur in most patients with IHD and universally in AMI
 Also seen in digoxin toxicity, CCF, hypokalaemia, alkalosis, hypoxia and sympathomimetic drugs
 Unclear if these are an indicator of morbidity/mortality
 Treatment
 Treat underlying cause
 If >3 in a row = non-sustained VT
 No evidence that lignocaine therapy or oral antiarrhythmic therapy for chronic PVC’s has any mortality benefit

Ventricular arrhythmias – Ventricular
parasystole
 Independent ectopic pacemaker (usually in ventricles) competes with dominant pacemaker
(entrance block)
 Ectopic pacemaker has an innate rate so coupling interval is different each time
 Variation in coupling interval
 Common relationship between interectopic beat intervals
 Fusion beats may be seen
 Usually associated with severe IHD, AMI, hypertensive heart disease or electrolyte disturbance
 Infrequently can lead to VT or VF
 Treatment of underlying disease is crucial
 Anti-arrhythmics indicated if symptomatic episodes or subsequent VT/VF

Ventricular arrhythmias – Accelerated
idioventricular rhythm (AIVR)
 Ectopic rhythm of ventricular origin seen in reperfusion of AMI
 Wide and regular QRS complexes
 Rate 40-100
 Runs of 3-30beats/min usually
 Begins with fusion beat
 Some association with VT (but not VF)
 Usually causes no symptoms but loss of atrial kick may reduce CO
 Treatment
 Any suppression i.e. with lignocaine can cause asystole if this is the only pacemaker
 Atrial pacing if reduced CO is problematic

Ventricular arrhythmias –
Ventricular tachycardia (VT)
 3 or more sequential depolarisations from a ventricular pacemaker at >100/min
 Wide QRS >0.10
 Rate >100 (usually 150-200)
 QRS axis usually constant
 QRS <120ms in 5% of episodes
 Monomorphic vs. polymorphic
 Polymorphic – QRS complex of multiple morphologies in single lead
 Torsade de pointes is a specific subtype of polymorphic VT in which QRS swings from positive
to negative axis in a single lead and QT is prolonged
 Sustained vs. non-sustained vs. recurrent
 Cannon a waves indicate AV dissociation

Ventricular arrhythmias –
Ventricular Tachycardia
 Most common causes are IHD and AMI
 Most common within 30 minutes of AMI (re-entrant mechanism)
 Increased automaticity >12 hours after infarction
 Less common causes include HOCM, mitral valve prolapse, drug toxicity (digoxin, quinidine, procainamide and sympathomimetics)
 Hypoxia, alkalosis and electrolyte abnormalities
 Cannot be differentiated from SVT by clinical criteria alone
 Treat all wide complex tachycardia as VT until proven otherwise
 Treatment
 Unstable – Synchronised cardioversion 100-200J (90% effective)
 90% successful if rate <200/min and 70% successful if rate >200 (opposite of SVT)
 Stable
 Amiodarone 150mg over 10 min, repeated up to 2g total then infusion
 Procainamide
 Lignocaine 1-1.5mg/kg IV every 5 min, repeated until effect

VT – Chemical cardioversion
 Lignocaine
 More effective in ischaemic VT due to depression of automaticity
 Initial bolus 100mg (20% effective) and second bolus of 50mg effective in another 10%
 Even less effective if not ischaemic
 Sotalol
 1.5mg/kg over 5 minutes
 Only if haemodynamically stable and QTc normal
 65% reversion rate
 Amiodarone
 150mg over 5-10 minutes (30% effective at 1 hour)
 Second dose over 10-20 minutes if fails
 600mg over next 24 hours
 Adenosine
 May treat unrecognised SVT with aberrancy and probably safe in VT

VT – Overdrive pacing
 Set rate to 120% of current rate of VT
 Start pacing by increasing current until electrical and mechanical capture achieved
 After 20-30 seconds, gradually wind back rate to test if overdrive pacing has taken
over pacemaker function and terminated VT
 Does not necessarily require sedation
 Can precipitate VF

VT in special situations
 Digitalis toxicity – Digibind
 Chloral hydrate toxicity – Beta-blockade
 Sodium channel blocker – Bicarb
 Hypothermia – Active warming
 Stimulants – Benzos, alpha and beta-blockers
 Electrolyte imbalance – Replace/treat

VT – Fascicular tachycardia
 Rare but may occur with structural heart disease
 Usually misdiagnosed as SVT with RBBB
 Key to diagnosis is recognition of VT features e.g. fusion/capture/AV dissociation
 Usually originates in posterior fascicle
 ECG features
 Mimics SVT with aberrancy
 Relatively narrow QRS 0.11-0.14
 RBBB pattern
 Usually left axis
 Right axis deviation if from anterior fascicle
 Rx
 Verapamil
 Does not respond to adenosine or standard anti-VT therapy

Right Ventricular Outflow Tract VT
 Shows LBBB morphology with rightward axis
 May be part of ARVD
 Treated with adenosine +- IV verapamil

Ventricular arrhythmias
- Torsades de pointes
 Typically short runs 5-15 seconds at 200-240/min
 Seen in serious myocardial disease with prolonged QT
 Risk factors for drug-induced TdeP
 Age >65
 Female
 Renal impairment
 Electrolyte disturbances
 Arrhythmias with long pauses
 Genetic predisposition
 >1 drug administered known to cause prolonged QT

Ventricular arrhythmia - Torsades
 Treatment
 Cardioversion 200J if pulsless or in extremis
 Magnesium 1-2g IV over 60-90s then infusion 1-2g/hr (rarely helpful if normal QT) =
10mmol bolus)
 Withdraw offending agents
 Correct electrolyte disturbances
 Pacing if TdeP secondary to bradycardia or heart block (chemical or electrical)

Torsades de pointes vs. Polymorphic VT
 Torsades specifically relates to a subtype of polymorphic VT associated with long
QT and is managed with magnesium
 Polymorphic VT with normal QT duration is associated with myocardial ischaemia,
infarction or post-cardiac surgery should be managed as for monomorphic VT (and
not with magnesium)
 QT prolongation
 A risk for TdeP only if due to T wave prolongation (JT interval >380ms) NOT if due to
QRS prolongation
 Risk increases 6% for every 10% increase in QTc above 500ms

VT vs. SVT with aberrancy
 Age >35, IHD, CCF or CABG strongly suggest VT
 Suggest VT
 AV dissociation (seen in 10% of VT patients) and 75% specific for VT
 Fusion beats (,10% of VT)
 Capture beats (<10% of VT)
 Josephson’s sign (notching near nadir of S wave)
 Brugada’s sign (onset of QRS to nadir of S wave >0.1s) (2.5 squares)
 Onset of R wave to deepest part of S wave >100ms is >95% specific for VT
 QRS >0.14s
 Post-ectopic fully compensatory pause
 Constant coupling intervals
 All positive or all negative deflections (20% sensitivity but 90% specificity)
 Northwest (extreme) axis
 Absence of typical RBBB or LBBB morphology (although 35% of ischaemic VT has LBBB morphology)
 RSR= with taller left rabbit ear (vs. RBBB taller right rabbit ear - most specific)

VT vs. SVT with aberrancy
 Suggest SVT with aberrancy
 Preceding ectopic P wave
 Varying BBB
 Varying coupling intervals
 Historical criteria
 2 or more of the following = 95% probability of VT
 Age >35
 Active angina
 Previous AMI

Brugada Method for VT vs. SVT with
aberrancy
 VT diagnosed if, analysed in sequence, any of these 4 are present:
 Absence of RS complexes in all praecordial leads
 R to S interval >100ms in one or more praecordial leads
 AV dissociation
 V1: Monophasic R, qR, QS or RS + V6: rS, QS, qR or S > R
 SVT diagnosed if none of above present

Griffith method
 VT diagnosed if no to either criteria for SVT
 SVT diagnosed if both criteria below present:
 QRS morphology classic for BBB
 LBBB
 rS or QS in V1 and V2
 Time to S wave nadir in V1 or V2 >70ms
 R wave and no Q wave in V6
 RBBB
 rSR’ in V1
 RS in V6
 R wave > S wave in V6
 No AV dissociation

Vereckai method
 VT diagnosed if, analysed in sequence, any of the following 4 present in aVR
 Initial R wave
 Initial r or q wave >40ms
 Notch on initial descending limb of predominantly negative QRS
 Slow conduction at beginning of QRS
 Ratio of vertical distance travelled in voltage during initial 40ms (Vi) and terminal 40 s (Vt)
 Vi/Vt < 1 i.e. vertical amplitude of first 40ms in aVR less than the terminal 40s

Pava method
 VT diagnosed if time from isoelectric line to peak of R wave in II > 50ms
 Otherwise SVT

SVT with aberrancy
 Aberrant wide complex QRS may be due to
 Pre-existing BBB
 Rate-related conduction block (common)
 Ventricular pre-excitation syndrome (e.g. WPW)
 Toxic-metabolic condition
 Aberrancy defined as QRS >120ms

Ventricular arrhythmias - VF
 May be primary or secondary to VT and prolonged LV failure/shock
 Digoxin toxicity, quinidine toxicity, hypothermia, blunt chest trauma, severe electrolyte abnormality
or myocardial irritation by intracardiac catheter or pacemaker lead
 Amplitude becomes less with time and becomes asystole within 1-3 minutes
 3% of asystole is actually fine VF
 Rate 300-600/min
 Treatment
 200J defibrillation (x3 if witnessed monitored)
 Five cycles of CPR
 Check pulse/rhythm
 If ongoing VF, continue above + amiodarone 300mg IV bolus or lignocaine 1.5mg/kg IV
 Consider beta-blocker if VF storm ??

VF
 Special circumstances
 Active cooling if <30
 Bicarb if sodium channel blockade
 K replacement if hypokalaemic

Electrical storm
 Recurrent VT/VF despite conventional initial therapy
 Treatment with additional antiarrhythmics may potentiate
 Especially if prolonged QTc
 Thought to be driven by sympathetic activity (so adrenaline questionable)
 Defibrillate each episode
 Correct K, Mg 10mmol
 Beta-blockade may be beneficial

Conduction Disturbances
- Sinoatrial block aka exit block
 First-degree SA block
 Cannot be seen on ECG
 Second-degree SA block
 Some impulses get through, others do not
 Suspect if expected P wave and QRS do not occur
 Variable (Wenckebach-type)
 Progressive shortening of P-P interval before dropped complex
 Constant-type
 Interval encompassing missed beat is an exact multiple of the cycle length
 Third-degree SA block
 May be due to sinus node failure, sinus node stimulus inadequate to activate atria or atrial
unresponsiveness

Conduction disturbances – Sinoatrial block
 Causes
 Acute rheumatic fever, acute inferior MI, myocarditis, digoxin, quinidine, salicylates, beta-
blockers, CCB’s
 Vagal stimulation alone rarely
 Treatment
 Atropine can increase sinus node rates
 Cardiac pacing for recurrent or symptomatic bradycardia

Conduction disturbances
- Sinus arrest
 P-P interval bears no relationship to baseline sinus node discharge rate
 Same conditions that cause sinus block can cause sinus arrest
 If prolonged, can see AV junctional escape beats
 Especially common in digoxin toxicity and aging, as in sick sinus syndrome
 Treatment
 Atropine if symptomatic
 Cardiac pacing for symptomatic bradycardia

- AV block
 First-degree: No treatment necessary
 Second-degree:
 Type 1 Wenckebach
 Symptomatic: atropine 0.5mg IV q5min or transcutaneous pacing
 Type 2
 Implies structural damage, permanency and may progress to complete heart block (especially in AMI)
 If symptomatic: Transcutaneous pacer pads applied and atropine provided (60% effective)
 Third-degree
 Nodal blocks seen in 8% of inferior MI
 Infranodal blocks wit broad complex escape rhythms may be seen in large anterior infarcts
 Usually symptomatic
 Treatment: Transcutaneous pacing. Atropine may be effective for nodal escape rhythms

First-degree AV block
 PR >200ms
 Av node is usually level of block but can be at an infranodal level
 Occasionally seen in normal hearts
 Commo causes include increased vagal tone, medication toxicity, inferior MI and
myocarditis
 If no evidence of other cardiac disease, has no prognostic value
 In the setting of inferior MI, may herald complete heart block
 Close monitoring is all that is required if in setting of ischaemia

Second-degree (Type 1) Wenckebach AV
block
 Progressive prolongation
 4:3 ratio indicates 3 of 4 atrial impulses are conducted to the ventricles
 Can have fixed ratio like this or can be variable
 This block almost always occurs at level of AV node
 Often due to reversible depression of the AV nodal conduction
 Occurs as each successive depolarisation produces prolongation of the refractory period of the AV
node
 As next atrial impulse comes along it meets the AV node earlier in its relative refractory period and
conduction occurs more slowly each time until atrial impulses reaches AV node in the absolute
refractory period
 Usually transient and associated with inferior MI, medication toxicity, myocarditis or after cardiac
surgery
 May be physiological in rapid atrial rates
 If very slow or unstable, atropine will be effective in most

Second-degree Type 2 AV block
 PR interval remains constant both before and after nonconducted atrial beats
 Usually occurs in infranodal system, often with coexistant BBB or fascicular blocks
(therefore often wide QRS)
 Even if QRS complex is narrow, the block is usually infranodal
 High-grade if more than one consecutive P wave is not conducted
 If 2:1 cannot differentiate between type 1 and type 2
 If wide complex, typically infranodal
 If narrow complex, 50:50 infranodal/AV nodal site of block
 Consider worst-case and assume type 2 block in this situation
 Treatment – Pacing pads, close monitoring. Atropine usually not helpful as infranodal in
most cases

Third-degree AV block
 If occurs at AV node level, junctional escape rhythm at 40-60 occurs with narrow
QRS as originates above bifurcation of Bundle of His
 If at infranodal level, get wide ventricular escape rhythm at <40/min
 May be narrow if from His bundle or may be wide if bundle branch or Purkinje system
pacemaker
 Nodal complete heart block occurs in 8% of inferior MI and may last for days
 Infranodal AV block with wide QRS suggests structural damage to infranodal
system as seen with extensive anterior MI
 If in context of ischaemia, mortality is increased even with pacing as suggests
extensive infarct

 Unifascicular blocks
 No treatment required. Treat underlying cause if known
 Bifascicular blocks
 Generally no treatment required. Treat underlying cause if known
 Placement of ventricular demand pacemaker indicated if symptomatic bradycardia
 If AMI with pre-existing or new bi- or trifascicular block, prophylactic ventricular demand
pacemaker insertion is indicated
 Trifascicular blocks
 Placement of ventricular demand pacemaker indicated if symptomatic bradycardia
 If AMI with pre-existing or new bi- or trifascicular block, prophylactic ventricular demand
pacemaker insertion is indicated

Brugada syndrome
 Eight different genetic mutations lead to channelopathy in transmembrane sodium, calcium or potassium
ion channels
 Highest incidence in Southeast Asians
 Responsible for up to 60% of idiopathic VF
 Clinical features
 Majority asymptomatic and only found via incidental ECG
 50% of patients with Brugada pattern suffer malignant arrhythmia
 2-year death rate for missed diagnosis from ED is 30%
 Average age at presentation is 30yo
 Symptomatic patients may present with palpitations, near to complete syncope, or seizures due to VT
 Characteristic ECG changes are not always present
 Fever and provocative testing with flecainide may provoke ECG abnormalities associated with Brugada syndrome

Brugada syndrome
 Need Brugada pattern + at least one of:
 Syncopal episode
 VF
 Polymorphic VT
 SCD in relative <45yo
 ST segment elevation in family member

Brugada syndrome in leads V1-3
 Type 1:
 Coved-shaped ST elevation >2mm followed by inverted T wave
 Type 2:
 ST elevation >2mm
 Trough in ST segment at least 1mm deep
 Positive or biphasic T wave (Saddleback)
 Type 3:
 Coved-shaped or saddleback pattern ST segment with 1-2mm elevation only

Brugada syndrome
 Type 1 considered diagnostic if appropriate clinical or family history
 Type 2 and 3 suggestive but not diagnostic
 Require further evaluation
 In those with aborted sudden cardiac death, risk of recurrent VF is 50% within 5 years
 Tall R wave in aVR due to delayed conduction in RVOT associated with higher risk of
arrhythmia
 Treatment
 Must recognise
 Avoid sodium channel blockers and treat fever
 ICD is the only proven therapy to terminate malignant ventricular dysrhythmias and prevent sudden
death
 Quinidine can be helpful to reduce the incidence of dysrhythmias as adjunct to ICD

Long QT syndrome
 13 variants of congenital long QT syndrome
 1/2000 live births
 QTc >440ms in males or >460ms in females
 Risk of dysrhythmias increases with QTc
 Moderate risk QTc 480-499ms
 High risk QTc >500ms
 Syncope is the most common symptom and torsades the most common dysrhythmia
 Avoid channel blockers, impair cardiac repolarisation, prolong the QT or provoke tachydysrhythmias
 Beta-blockers are initial treatment of choice (propranolol and nadolol are first-line)
 Exercise is a trigger where swimming is notably dangerous

Arrhythmogenic RV dysplasia
 Autosomal dominant inheritance
 More common in males
 Usually symptomatic at 15-40yo
 Fibrosis of subendocardial areas of myocardium with RV dilation and hypokinesis
 Aneurysms in inferior/apical/infundibular walls
 Signs of RVH may be present
 ECG
 Anterior TWI or widened QRS V1-3
 Right axis deviation may be present
 Epsilon waves (25% of cases only)

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