Patient PBL Case 1
Atrial Fibrillation
Atrial fibrillaion (AF) is a supraventricular tachyarrhythmia characterized by disorganized atrial electrical activity and progressive deterioration of atrial electromechanical function.
ECG findings: absence of P waves, rapid oscillations (or fibrillatory [f] waves) that vary in amplitude, frequency, and shape; and an irregular ventricular response.


Classification of atrial fibrillation
Paroxysmal AF – Episodes of AF that typically lasts less than 24 hours but can last up to 7 days; these terminate spontaneously
Persistent AF -- Episodes of AF than last more than 7 days and require either pharmacologic or electrical intervention to terminate
Permanent AF - Continuous AF, that has failed cardioversion, or where cardioversion has never been attempted
· Lone AF - AF in individuals (usu <60yo) without structural or cardiac or pulmonary disease, with low risk for thromboembolism.

Atrial fibrillation (AF) is caused by multiple reentrant waveforms within the atria, which bombard the atrioventricular (AV) node, commonly leading to a tachycardia that is irregularly irregular.

The rate at which atrial fibrillation causes a ventricular contraction is dependent upon the refractory state of the AV node. There is loss of atrial contraction and its contribution to ventricular filling, also referred to as loss of atrial kick.
In addition, this loss of contraction can lead to stagnation of blood in the atrium and can promote thrombus formation. Patients may be at risk for embolization when atrial fibrillation converts to sinus rhythm as organized atrial contractions can now cause the dislodging or fragmentation of the atrial thrombus into the systemic circulation.

In summary, clinical presentations are typically due to the following:

Loss of atrial kick (synchronized atrial mechanical activity
Irregularity of ventricular response
Inappropriately rapid heart rate

Causes of AF
CVS causes
Non CVS causes
Non CVS Respiratory Causes
Long-standing hypertension
Ischemic heart disease
Any form of carditis
Infiltrative heart disease of any type
Sick sinus syndrome
Low levels of potassium, magnesium, or calcium
Sympathomimetic drugs, alcohol, electrocution
Noncardiovascular respiratory causes include the following:
Pulmonary embolism
Lung cancer
Lone atrial fibrillation is idiopathic and defined as the absence of any known etiologic factors plus normal ventricular function by echocardiography. Most patients with lone atrial fibrillation are younger than 65 years, although age is not used to define lone atrial fibrillation.


Treatment and Management of SVTs (Sarah)

1. Vagal maneuvers--
- valsalva
-diving reflex-- splash face with cold water
-carotid massage-- be careful-- in those with carotid stenosis, can cause stroke
-pressing down on eyelids
-standing on head
-urination or defecation

2. If heart rate cannot be slowed using vagal maneuvers:
- if stable, determine rhythm, and treat accordingly.
-if unstable, and px has chest pain, dyspnea, altered consciousness, low BP, CHF, HR>150 or acute MI, cardiovert.

3. Tx for different SVTs:
AF/Atrial flutter
- General Mx= control rate, anticoagulate, and consider rhythm cardioversion. (drug cardioversion preferred)
acute atrial fibrillation/flutter
- ventricular rate control: first choice Ca2+ channel blockers-- diltiazem> verapamil, or beta- blocker eg. metoprolol. 2nd line-- antiarrhythmic agents eg. amiodarone, digoxin.
- if atrial fibrillation> 48 hrs, anticoagulate (heparin) unless contraindicated.
- Cardiovert: if onset <48 hrs, DC cardioversion or administration of antiarrhythmics, eg. amiodarone, ibutilide, procainimide, sotalol. Drug cardioversion preferred!
- if onset> 48 hrs, avoid cardioversion --
-administer anticoagulants for 3 wks then cardiovert and continue anticoagulating for 4 wks.
- or, administer anticoagulant (heparin), then take transesophageal echo. If clear of clots, cardiovert within 24 hrs, then anticoagulate for 4 weeks.
- if ejection fraction low (<40%), avoid beta-blockers, verapamil, procainamide, ibutilide. Only conversion agent allowed is amiodarone, within 48hr period. If outside 48hr period, anticoagulate.
- if patient is young, HR>300, and EKG shows delta wave, consider WPW
-avoid AV node blockers-- eg. adenosine, beta blockers, Ca2+ blockers, digoxin.
-if <48 hrs, administer rate control and cardioversion-- amiodarone, sotalol, flecainide unless EF abnormal or CHF-- then give amiodarone.
-if >48 hrs, anticoagulate and DC cardioversion

chronic atrial fibrillation/flutter
-rate control shown to be as effective as rhythm control in chronic AF. Use beta-blocker, or Ca2+ blocker-- if this fails, add digoxin (beware bradycardia).
-anticoagulate with warfarin, or aspirin if warfarin contraindicated/ px <65 y/o, no hypertension, diabetes, LV dysfunction, rheumatic valve disease, past TIA/MI.
- IF px is young or 1st presentation, consider rhythm control

narrow complex tachycardias:
-if unstable, (ill/hemodynamically unstable)-- DC cardioversion
In GENERAL, Mx for stable SVT:
-vagal stimulation
-get 12-lead ECG/clinical exam, determine specific rhythm disorder

- if EF normal, Ca blocker>beta blocker> digoxin> DC cardioversion.
- if EF low/CHF present, NO cardioversion, digoxin, amiodarone, diltiazem.

-multifocal atrial tachycardia: (seen in COPD)
-treat hypoxia, hypercapnia with O2
-if EF normal, and rate>110 bpm Ca2+ blocker, beta-blocker, amiodarone
- if EF<40%, CHF-- amiodarone, diltiazem
junctional tachycardia: (rare)
-attempt vagal maneuvers
-adenosine usually cardioverts junctional rhythm to sinus rhythm
- if it recurs, treat with beta-blocker, amiodarone

- NOTE: adenosine preferred as Rx in pregnant women.

4. ongoing treatment for recurrent SVTs:
-preventative therapy:
-pharmacological treatment-- AV node blocking agents eg. beta blockers, verapamil. If AV node not involved, anti-arrhythmic agents used.
radiofrequency ablation-- catheter placed inside heart via veins, and electrode inserted through catheter. Electrophysiology study used first to locate abnormal electrical conduction, then mild radiofrequency energy used to destroy the aberrant electrical pathway.
-cryoablation-- RF largely replaced by cryoablation-- same concept, but using extreme cold to induce apoptosis. Preferred because unlike RF ablation, is reversible-- if desired result is achieved at -10 degrees, freezing continues till -73 degrees. If not, allowing the frozen tissue to spontaneously rewarm reverses damage.

Mechanism of a supraventricular tachycardia (SVT)
2 main causes:
A re-entrant circuit is set up by the presence of an accessory (additional) pathway
- Between the atrium and the AV node
o A complete circuit is formed within the AV node
o Most common additional pathway
o Underlies AVNRT (AV nodal re-entrant tachycardia)
- Between the atria and ventricles
o May be seen on ECG during normal sinus rhythm
o Underlies AVRT (AV re-entrant tachycardia)
o Is the result of 2 or more conducting pathways: the AV node and 1 or more bypass tracts. In the normal heart, only one conduction pathway is present.
Dx on the ECG
- Regular, narrow QRS complex
- Rate of usually 150-200bpm
- Regular P waves may be visible between the QRS complexes

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Clinical Manifestation
- Recurrent attacks of rapid palpitation which can last from a few minutes to hours or even days

Wolff-Parkinson White Syndrome
- Occurs as a result of electrical conduction between the atria and ventricles at sites other than the AV node, circumventing the usual conduction delay between the atria and ventricles
- Tachyarrhythmias result
- Shortened PR interval
- Wide QRS complex due to slurred upstroke or delta wave

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Medicine at a Glance, 2nd Edition, pg 168-169
OCHM 7th Edition Pg 112

TYPES OF ARRHYTHMIA (Gaya and Michelle)


‘Extrasystole’ aka ‘ectopic’ aka ‘premature contraction’

An early contraction of the heart independent of its normal rhythm and that arises in response to an impulse in some part of the heart other than the SA node. The extrasystole is followed by a ‘compensatory’ pause, the contraction following the pause is usually more forceful than normal (felt as palpitations)


Supraventricular extrasystoles
Atrial extrasystole
Arising from stimuli discharged in atrial wall ectopic to atrial pacemaker
Atrioventricular extrasystole aka nodal extrasystole aka junctional extrasystole
One in which the stimulus is thought to arise in the atrioventricular node

Ventricular extrasystole
One in which either a pacemaker or a re-entry site is in the ventricular structure.
Rather common and usually insignificant. However, if present early in the T wave of a preceding beat they can induce ventricular fibrillations and are thus potentially dangerous.

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1. Re-entrant signalling (an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping, occurs when conduction is abnormally part of the impulse will arrive late and potentially be treated as a new impulse.)
2. Enhanced automaticity(due to unbalanced ions?) in some ectopic focus (excitable group of cells outside the SA node).


Isolated PVCs require no treatment and in healthy individuals be resolved by restoring the balance of magnesium, calcium and potassium within the body. The most effective treatment is the elimination of triggers (particularly the cessation of the abuse of substances such as caffeine, and illegal drugs.)
  • Pharmacological agents
    • Beta blockers
    • Calcium channel blockers
  • Electrolytes replacement (Mg and K supplements)
  • Radiofrequency catheter ablation treatment
  • Lifestyle modification
    • Frequently stressed individuals should consider therapy/support groups.
    • Heart attacks can increase the likelihood of having PVCs, so exercise and a healthy diet will decrease PVCs by reducing the risk of heart attacks.


The atria depolarises faster than 150/min.
The Av node cannot conduct atrial rates of discharge greater than about 200/min. If it is faster, then you get an AV block.

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P waves can be superimposed on the T waves
The QRS complexes have the same shape as those of the sinus beats

When the atrial rate is greater than 250/min and there is no flat baseline between the P waves.

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P waves are of a saw-toothed appearance.
Ventricular activation is perfectly regular.


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If the area around tha AV node depolarises frequently, the P waves can be seen very close to the (regularly shaped)QRS complex, or not at all.
Ventricular activation is perfectly regular as the ventricles are activated via the bundle of His as in all other SVTs.


A fo​cus in the ventricular muscle depolarizes with high frequency causing in effect rapid ventricular extrasystoles.
  • Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface ECG
  • Polymorphic ventricular tachycardia, has beat-to-beat variations in morphology. This most commonly appears as a cyclical progressive change in cardiac axis, previously referred to by its French name torsades de pointes ("twisting of the points").
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QRS complexes become broad and the T waves are difficult to identify.


The morphology of the tachycardia depends on its cause.
In monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being generated from increased automaticity of a single point in either the left or right ventricle, or due to a reentry circuit within the ventricle.
Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarisation. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval.


Electrical Cardioversion / Defibrillation

A patient with pulseless VT or VF will be unconscious and given high energy (360J with a monophasic defibrillator, or 200J with a biphasic defibrillator) unsynchronised cardioversion. Patients with a stable VT are given cardioversion if the tachycardia exceeds 150bpm.
The shock may be delivered to the outside of the chest using an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted.

Antiarrhythmic Drug Therapy

Drugs such as amiodarone or procainamide may be used in addition to defibrillation to terminate VT while the underlying cause of the VT can be determined.
As hypomagnesia is a common cause of VT, stat dose magnesium sulphate can be given for torsades or if hypomagnesemia is found/suspected.
Long term anti-arrhythmic therapy may be indicated to prevent recurrence of VT- Beta-blockers and a number of class III anti-arrhythmics (especially lidocaine) are used
For some of the rare congenital syndromes of VT, other drugs, and sometimes even cather ablation therapymay be useful.


Occurs when ventricular fibres contract independently.

No QRS complex can be identified and ECG is totally disorganised.


When the heart rhythm originating from the sinus node has a rate of less than 60bpm. This is a normal finding in atheletes and healthy fit people but can be found in increased vagal tone, hypothermia, hypothyroidism and sleep.


The sinus node does not fire its signals properly, so the heart rate slows down. Sometimes, the rate can alter between bradycardia and tachycardia. Occurs most commonly in the elderly as a result of degenerative changes to the heart's conduction pathways.This can result from taking some medications such as Ca channel blockers, B blockers and anti-arrhythmic drugs. Treated with pacemakers if symptoms persist.


When the conduction system through the AV node is disrupted, bradycardia or other heart rhythm disorders can occur. AV node dysfunction (sometimes called heart block) can be caused by medications, other medical conditions, or in combination with other cardiovascular conditions. AV node dysfunction can have various degrees of severity, depending on how many electrical signals are passing through the AV node.


Escape rhythms are not primary disroders but are the response to problems higher in the conducting pathway. Commonly seen in the acute phase of heart attack when they may be associated with sinus bradycardia.
If the rate of depolarisation of the SA node slows down, a focus in the strium takes over control of the heart, the rhythm is described as 'atrial escape'.
If the region around the AV node takes over as the focus of depolarisation, the rhythm is called 'nodal' or 'junctional'.
'Ventricular escape or ventricular bradycardia' is a heart rate of less than 50 beats a minute. This a safety mechanism that arises when there is lack of electrical impulse or stimuli from the atrium.Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consist of the administration of atropine and cardiac pacing.




Treatment and Management of AF (Jess)

Short term management


Rhythm control
  • Preferred treatment, as restoring sinus rhythm minimises atrial/ventricular remodelling, improves haemodynamics and enhances quality of life
  • Sinus rhythm restored via cardioversion, and then maintained with drugs
  • Important to detect underlying disorder which may have triggered the AF
  • Drugs used in cardioversion include flecainide and amiodarone
  • Sotalol (and other Class III drugs) is used to maintain sinus rhythm, however requires close monitoring (QT interval and eletrolytes) and is contraindicated in patients with structural heart disease and heart failure

Rate control

  • Involves promptly using anti-arrhythmics, without attempting cardioversion
  • Used in older patients with CV co-morbidities, and when rhythm control fails
  • Beta blockers and calcium channel blockers are the first line therapies; digoxin is effective in sedentary patients, and amiodarone is a last resort


  • Risk of embolism greatest when AF has been present longer than 48/24
  • Patients newly diagnosed with AF, or awaiting for cardioversion, can be started on IV heparin or LMWH, as well as on warfarin
  • Clopedigril – an ADP antagonist, which inhibits platelet aggregation – acts synergistically with aspirin to reduce clotting


· Used within 7 days of AF onset to restore sinus rhythm
· Can use electronic or pharmacologic agents: pharmacological methods do not require sedation or anaesthesia, but increase the risk of VT and other arrhythmias

Long term management


· Anticoagulation
· Antiarrhythmic therapy to maintain sinus rhythm
· Experimental data suggests that RAS antagonists and statins may be useful


· Surgical compartmentalisation of the atria: atria are transected and resutured, thus reducing the critical mass required for AF – however is best used in patients also undergoing mitral valve procedures
· Catheter ablation
Recreation of surgical suture lines using radiofrequency lesions (often unsuccessful, often needs repeat surgeries, uncertainties about efficacy)
Ablation of AF triggers: removal of electrically active pulmonary vein foci (very successful in appropriately-selected patients)
AV node ablation (permanently interrupting conduction between the atria and ventricles) and PPM insertion (still requires anti-coagulation)

Post-operative applications

· Beta blockers, amiodarone and sotalol are used prophylactically in patients undergoing cardiac surgery, as post-operative AF is common


No structural heart disease: flecainide, sotalol; then amiodarone
LVH: amiodarone
CAD: sotalol; then amiodarone
Heart failure: amiodarone

Drug glossary

Class 1: Na channel blockers
Class 1a
Disapyramide: generally not used to treat AF as it has adverse anticholinergic effects and is a strongly negative inotropic agent à CHF and cardiogenic shock

Class 1c
Flecainide: blocks Na and K channels, reducing cardiac conduction; used to treat paroxysmal AF and SVT; co-administered with AV nodal blocking agents when used to treat AF

Class 2: Beta blockers
Propranolol: non-selective, reduces cardiac contractility; also has some Class 1 activity
Atenolol: blocks beta 1 receptors
Metoprolol: beta 1 receptor blocker that reduces cardiac contractility; important to monitor BP/HR/ECG during IV administration

Class 3: K channel blockers
Amiodarone: antiarrhythmic effects that overlap all 4 classes; used in patients with structural heart disease – however, is extensively tissue bound and has a long t1/2
Sotalol: delays slow outward K current as well as being a non-selective B blocker; can be used to maintain sinus rhythm

Class 4: Ca channel blockers
Verapamil: blockades L-type voltage-gated Ca channels, decreases cardiac contractility, decreases preload and afterload; used to reduce the ventricular rate provided it is not contraindicated

Digoxin: slows sinus and AV node, inhibits Na/K ATPase pump; usually only used where LV function is depressed and is often contraindicated

Sources: eMedicine, Kumar and Clark

Koch’s triangle
  • AV node is located within it
  • Formation
    • Orifice of the coronary sinus (posteroinferior corner of right atrium)
    • Eustachian valve of the inferior vena cava along with its anterior extension, the tendon of Todaro that inserts into the central fibrous body
    • Tricuspid valve
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Heart murmurs

Associated peripheral symptoms
  • Systolic
    • Pansystolic – occur when ventricle leaks to a lower pressure chamber or vessel
      • Mitral regurgitation
      • Tricuspid regurgitation
      • Ventricular-septal defect
    • Ejection (mid)systolic – turbulent flow or increased flow, crescendo-decrescendo
      • Aortic/pulmonary stenosis
      • Hypertrophic cardiomyopathy (HCM)
    • Late systolic
      • Mitral valve prolapse
      • Papillary muscle dysfunction where mitral regurgitation begins mid systole
  • Diastolic
    • Early diastolic – high pitched, decrescendo quality
      • Aortic/pulmonary regurgitation
    • Mid-diastolic - lower pitch, due to impaired flow during ventricular filling
      • Mitral/tricuspid stenosis
      • Atrial myxoma (valve narrowed due to tumor)
    • Presystolic – when atrial systole increases blood flow
      • Extension of mitral/tricuspid stenosis
      • Does not occur when atrial systole is lost in atrial fibrillation
Area of greatest intensity/radiation
  • Loudest over apex, radiating to axilla
    • Mitral regurgitation
  • 2nd right intercostal space to carotids
    • Aortic stenosis
  • 2nd right IS to 5th rib sternal edge
    • Aortic regurgitation
  • 2nd left IS to 4th rib sternal edge
    • pulmonary regurgitation
  • 5th IS, left sternal edge
    • HCM
  • low
    • turbulent flow under low pressure
  • high
    • turbulent flow under high pressure
Dynamic maneuvers
  • respiration
    • murmurs on right side are louder on inspiration due to increased venous return
    • thus, murmurs on left side are louder on expiration
  • deep expiration
    • brings base of heart closer to the chest wall
      • aortic regurgitation
      • scraping sound of pericardial friction rub
  • valsalva maneuver (decreases preload)
    • raises intrathoracic pressure, decreasing left ventricular volume and thus preload
      • most murmurs become softer
      • murmur of HCM becomes louder
      • click and murmur of mitral valve prolapse begins earlier
  • squatting (increases preload)
    • increases venous return and systemic arterial resistance
      • makes most murmurs louder
      • murmur of HCM softer due to increase in ventricular size
      • click and murmur of mitral valve prolapse is delayed
  • isometric exercise eg. Hand gip (increases aferload)
    • increases systemic vascular resistance, blood pressure and heart size
    • due to a reduction in pressure gradient, murmur or AS may be softer
    • most murmurs become louder
    • HCM is softer
    • Click and murmur or mitral valve prolapse is delayed

Ventricular Tachycardia (Lionel)
Fast, wide complex rhythm.
Associated with structural heart disease, syncope.
Structural heart disease: implantable cardioverter-defibrillator is seminal therapy.


1. >= 3 consecutive ventricular premature beats.
2. Usual rate: 160-240bpm, moderately regular but less so than atrial tachycardia.
3. Usual mechanism: re-entry.
4. Frequent complication of AMI/dilated cardiomyopathy, may occur in chronic coronary disease/HOCM/mitral valve prolapse/myocarditis/most forms of myocardial disease, can occur with structurally normal hearts.
5. Torsades de pointes (form of VT with QRS twisting around baseline) may occur spontaneously with hypokalaemia/hypomagnesaemia/QT-prolonging drug.


6. Nonacute settings: patients have known/easily detectable cardiac disease - finding of VT unfavourable prognostic sign.

Clinical findings
A. Signs and symptoms
1. Asymptomatic/syncope/milder symptoms of impaired cerebral perfusion.
B. Laboratory findings
1. VT can occur in hypokalaemia/hypomagnesaemia.
C. Differentiation of aberrantly conducted supraventricular beats from ventricular beats
1. VT: nonsustained (<30s)/sustained.
2. Difficult in patients with wide QRS.
3. Different prognostic and therapeutic implications.
4. Ventricular origin:
I. AV dissociation.
II. QRS >0.14s.
III. Capture/fusion beats.


IV. Left axis deviation + RBBB morphology.
V. monophasic (R)/biphasic (qR/QR/RS) complexes in V1.
VI. qR/QS complex in V6.
5. SVT origin:
I. Triphasic QRS.
II. Ventricular rate >170bpm.
III. 0.12< QRS <0.14s.
IV. Presence of preexcitation sndrome.
6. P wave relationship to tachycardiac complex: 1:1 = SVT origin except VT with retrograde P waves.

A. Acute VT
1. Determined by level of haemodynamic compromise + duration of arrhythmia.
2. Sustained VT in AMI: lidocaine bolus if stable, electrical cardioversion if not. If lidocaine unsuccessful, procainamide/amiodarone.
3. Hypotension/HF/myocardial ischaemia: synchronised DC cardioversion unless patient is tolerating rhythm: lidocaine/amiodarone.
4. Recurrence: amiodarone.
5. Stable: procainamide.
6. ?Mg replacement.
7. Can be terminated by ventricular overdrive pacing (useful if recurrent).
B. Chronic recurrent VT
I. Sustained VT
1. Symptomatic/sustained VT without reversible precipitating cause: high risk recurrence.
2. Significant LV dysfunction: sudden death common - implantable cardioverter-defibrillators.
3. Preserved LV function: lower mortality rate, different aetiology - amiodarone + beta-blocker.
4. Outflow tract tachycardia/fascicular ventricular tachycardia: AV nodal blockers, catheter ablation.
5. EP studies: identify candidates for radiofrequency ablation of VT focus (particularly arrhythmias generating in RV outflow tract, posterior fascicle, sustained bundle branch re-entry).
6. Palliative (recurrent VT who receive ICD shocks despite antiarrhythmic therapy): catheter ablation.
II. Non-sustained VT (NSVT)
1. Runs of 3 >= ventricular beats lasting <30s: symptomatic (light-headedness)/asymptomatic.
2. No heart disease: NSVT not clearly associated with poor prognosis.
3. Structural heart disease: increased risk symptomatic VT/sudden death.
4. Coronary disease + significant LV systolic function: beta-blockers reduce risk, implantable defibrillator if sustained VT induced during EP studies.
5. Chronic heart failure + reduced EFs: beta-blockers reduce incidence of sudden death 40-50%.
6. ?Amiodarone.

Source: McPhee & Papadakis (2010) Current Medical Diagnosis & Treatment.

Ventricular Fibrillation (Lionel)


1. Sudden cardiac death (unexpected non-traumatic death in clinically well/stable patients who die within 1h of onset of symptoms): causative rhythm most often VF.
2. Usually preceded by VT except in ischaemia/infarction.

A. Acute
1. Advanced Life Support Algorithm
B. Post-acute
1. Unless VF occurred shortly after MI/associated with ischaemia/seen with unusual correctable process, surviving patients require evaluation + intervention since recurrences are frequent.
2. Coronary arteriography to exclude coronary disease as cause.
3. VF within 24h after AMI: long-term management no different from AMI.
4. Manage conduction disturbances.
5. If not MI/ischaemia/bradyarrhythmias/conduction disturbances/other identifiable + correctable precipitating causes, implantable cardioverter-defibrillator.
6. Severe LV function, ischaemic/non-ischaemic: prophylactic implantation of cardioverter-defibrillator.

Source: McPhee & Papadakis (2010) Current Medical Diagnosis & Treatment.