Ventricular Arrhythmias in ICU

Quick Answer

Quick Answer: Ventricular arrhythmias (VT, VF, PVCs) are life-threatening rhythm disturbances originating below the bundle of His. In ICU, they occur in 10-20% of patients and carry significant mortality risk. Management depends on haemodynamic stability.

Immediate management (haemodynamically unstable VT/VF):

1. Pulseless VT/VF: Defibrillation 200J biphasic → CPR → adrenaline 1 mg every 3-5 min → amiodarone 300 mg IV bolus
2. Unstable VT with pulse: Synchronised cardioversion 120-200J biphasic
3. Stable VT with pulse: Amiodarone 150 mg IV over 10 min, then 1 mg/min infusion

Critical interventions:

• Correct K+ to 4.0-4.5 mmol/L and Mg²⁺ to ≥1.0 mmol/L
• Torsades de Pointes: Magnesium 2g IV, stop QT-prolonging drugs, overdrive pacing
• Brugada syndrome: Avoid fever (antipyretics), isoproterenol for VT storm
• Electrical storm: Deep sedation, beta-blockade, stellate ganglion block, catheter ablation

Key principle: Identify and treat the underlying cause (ischaemia, electrolytes, drugs, structural heart disease, channelopathies). All wide-complex tachycardias should be treated as VT until proven otherwise.

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CICM Exam Focus

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Key Points (10)

Key Points: 1. Ventricular tachycardia (VT) is defined as ≥3 consecutive ventricular beats at rate >100 bpm; sustained VT lasts ≥30 seconds or requires intervention for termination [1]

2. VF is the most common initial rhythm in out-of-hospital cardiac arrest (approximately 25-35% in Australia/NZ), with survival highly dependent on early defibrillation [2]
3. Three mechanisms of ventricular arrhythmogenesis: Re-entry (most common, 80% of VT in structural heart disease), triggered activity (early/delayed afterdepolarisations), and enhanced automaticity [3]
4. All wide-complex tachycardias should be treated as VT until proven otherwise - VT accounts for 80% of WCTs in patients with structural heart disease [4]
5. Electrical storm (≥3 VT/VF episodes in 24 hours) requires aggressive management: deep sedation, beta-blockade, consideration of sympathetic blockade (stellate ganglion block) and emergent catheter ablation [5]
6. Torsades de Pointes is polymorphic VT in the setting of prolonged QT interval - magnesium 2g IV is first-line treatment regardless of serum magnesium level [6]
7. Brugada syndrome presents with coved ST elevation in V1-V3 and carries 10% annual risk of SCD; fever is a known trigger and must be aggressively treated [7]
8. CAST trial (1989) demonstrated increased mortality with Class IC antiarrhythmics (flecainide, encainide) in post-MI patients - a landmark study on proarrhythmia [8]
9. ICD therapy reduces mortality in high-risk patients (AVID, MADIT-II, SCD-HeFT) but requires specific ICU considerations for shock management and deactivation discussions [9,10]
10. Electrolyte targets in ICU: K+ 4.0-4.5 mmol/L, Mg²⁺ ≥1.0 mmol/L (≥2.0 mg/dL) - essential for preventing malignant arrhythmias [11]

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Red Flags

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Definition and Classification

Definitions [1,12,13]

Ventricular tachycardia (VT):

• ≥3 consecutive beats originating from the ventricles
• Rate typically 100-250 bpm
• QRS duration ≥120 ms (usually >140 ms)

Classification by Duration:

Classification by Morphology:

Polymorphic VT Subtypes:

Ventricular Fibrillation (VF):

• Chaotic, disorganised electrical activity
• No effective cardiac output
• Rapid, irregular fibrillatory waves on ECG
• Fatal without immediate defibrillation

Premature Ventricular Complexes (PVCs):

• Early ventricular depolarisation with wide QRS
• Significant if: Frequent (>10% of beats), multifocal, R-on-T phenomenon, couplets/triplets
• Associated with cardiomyopathy when burden >10-15% [14]

VT Morphology Classification

LBBB Morphology VT (V1 rS or QS pattern):

• Origin: Right ventricle or interventricular septum
• Causes: ARVC, RV outflow tract VT, idiopathic

RBBB Morphology VT (V1 dominant R wave):

• Origin: Left ventricle
• Causes: Post-MI scar, LV cardiomyopathy, fascicular VT

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Epidemiology

ICU Incidence [2,15,16]

Australian/NZ Data [2,17]

• OOHCA incidence: 53-60 per 100,000 population per year
• VF as initial rhythm: 25-35% (declining due to increased bystander CPR and earlier EMS arrival)
• Survival to hospital discharge (VF/VT): 35-45% vs 10-15% for non-shockable rhythms
• IHCA survival: 20-25% overall, higher for shockable rhythms

Risk Factors in ICU Patients

Cardiac:

• Acute coronary syndrome (highest risk in first 24-48 hours)
• Reduced LVEF (<35%) - substrate for re-entry
• Prior VT/VF or cardiac arrest
• Cardiomyopathy (ischaemic, dilated, hypertrophic, ARVC)
• Myocarditis
• Cardiac surgery (ischaemia-reperfusion, electrolyte shifts)

Metabolic/Electrolyte:

• Hypokalaemia (<3.5 mmol/L, especially <3.0 mmol/L)
• Hypomagnesaemia (<0.7 mmol/L)
• Acidosis (pH <7.2)
• Hypoxaemia

Iatrogenic:

• QT-prolonging medications (see Torsades section)
• High-dose inotropes/vasopressors (adrenaline, noradrenaline)
• Digoxin toxicity
• Central line placement (right heart irritation)

Other:

• Channelopathies (Brugada, long QT, short QT, CPVT)
• Electrolyte shifts (rapid correction, dialysis)
• Fever (Brugada unmasking)

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Pathophysiology

Three Mechanisms of Ventricular Arrhythmogenesis [3,18,19]

1. Re-entry (80% of VT in structural heart disease)

Requirements:

1. Anatomical or functional substrate (circuit)
2. Unidirectional block in one pathway
3. Slow conduction in alternative pathway
4. Excitable tissue ahead of advancing wavefront

Substrates:

• Post-MI scar tissue (most common cause of sustained monomorphic VT)
• Dilated cardiomyopathy
• ARVC (fatty/fibrofatty replacement)
• Surgical scars

ECG Clues:

• Monomorphic VT with consistent morphology
• Often inducible with programmed stimulation
• May have late potentials on signal-averaged ECG

Clinical Implications:

• Amenable to catheter ablation (mapping the circuit)
• Substrate modification with drugs (class I, III)
• ICD for secondary prevention

2. Triggered Activity

Early Afterdepolarisations (EADs):

• Occur during Phase 2 or 3 of action potential (repolarisation)
• Mechanism: Reopening of L-type Ca²⁺ channels or late Na⁺ current
• Precipitants: QT prolongation, hypokalaemia, bradycardia, drugs
• Result: Torsades de Pointes

Delayed Afterdepolarisations (DADs):

• Occur after complete repolarisation (Phase 4)
• Mechanism: Intracellular Ca²⁺ overload → spontaneous Ca²⁺ release from SR → Na⁺/Ca²⁺ exchanger activation → depolarising current
• Precipitants: Digoxin toxicity, catecholamines, ischaemia, heart failure
• Result: Catecholaminergic polymorphic VT (CPVT), digoxin-induced VT

3. Enhanced Automaticity

Normal Automaticity (accelerated):

• Enhanced rate of Phase 4 depolarisation in normally automatic cells
• Causes: Catecholamines, hyperthyroidism, hypoxia, acidosis
• Result: Accelerated idioventricular rhythm (AIVR)

Abnormal Automaticity:

• Spontaneous depolarisation in cells normally quiescent
• Occurs in ischaemic or diseased myocardium
• Usually at -60 to -40 mV resting potential (normally -85 to -90 mV)
• Less dependent on electrolytes

Electrophysiology of VF [20,21]

Initiation:

• Usually triggered by VT degenerating to VF
• May arise from single PVC during vulnerable period (R-on-T)
• Multiple wavelet hypothesis: VF sustained by 3-6+ wandering wavelets

Perpetuation:

• Requires critical mass of tissue (larger hearts sustain VF longer)
• Fibrosis and heterogeneity promote wavelet fragmentation
• Ischaemia shortens refractory period, promotes re-entry

Termination:

• Defibrillation creates uniform depolarisation
• Eliminates excitable gaps that sustain wavelets
• Success depends on timing, waveform, and myocardial state

Action Potential Changes in Arrhythmias

Normal Ventricular Action Potential:

• Phase 0: Rapid Na⁺ influx (depolarisation)
• Phase 1: Transient K⁺ outflow
• Phase 2: Plateau (Ca²⁺ influx, K⁺ outflow balanced)
• Phase 3: Repolarisation (K⁺ outflow)
• Phase 4: Resting membrane potential (Na⁺/K⁺-ATPase)

QT Prolongation (Torsades Substrate):

• Prolonged Phase 2/3 (delayed K⁺ channels, enhanced late Na⁺)
• Creates dispersion of repolarisation (apex recovers before base)
• EAD-triggered PVC conducts preferentially → polymorphic VT

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Aetiology

Ischaemic Heart Disease [22,23]

Acute Ischaemia (first 48 hours post-MI):

• Most dangerous period for VT/VF
• Mechanisms: Abnormal automaticity, re-entry through ischaemic border zone
• Primary VF: Occurs within first hour, often idiopathic, better prognosis if survived
• Late VF (>48 hours): Usually indicates larger infarct, worse prognosis

Chronic Post-MI (scar-related VT):

• Re-entry around dense scar with slow conduction zones
• Monomorphic VT most common
• Inducible with programmed stimulation
• Risk factors: LVEF <35%, large infarct, anterior MI, LV aneurysm

Electrolyte Disturbances [11,24]

Clinical Pearl: Refractory hypokalaemia often indicates concurrent hypomagnesaemia - correct Mg²⁺ first.

Drug-Induced Arrhythmias [25,26]

QT-Prolonging Drugs (Torsades Risk):

CredibleMeds (www.crediblemeds.org) is the authoritative resource for QT risk classification.

Proarrhythmic Drugs (Non-QT):

• Class IC (flecainide, propafenone): CAST trial showed increased mortality in post-MI [8]
• Digoxin: Bidirectional VT, accelerated junctional rhythm, VF
• Cocaine: Na⁺ channel blockade, coronary spasm
• Tricyclic antidepressants: Na⁺ channel blockade, QRS widening

Structural Heart Disease [31,32]

Dilated Cardiomyopathy:

• Re-entry through patchy fibrosis
• 30% of SCD in DCM is due to VT/VF
• Lower LVEF = higher risk (threshold <35%)

Hypertrophic Cardiomyopathy (HCM):

• Leading cause of SCD in young athletes
• Risk factors: Family history SCD, unexplained syncope, NSVT, maximal LV thickness >30 mm, abnormal BP response to exercise

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC):

• Fibrofatty replacement of RV myocardium
• VT with LBBB morphology (RV origin)
• Task Force Criteria for diagnosis (2010)
• High risk of exercise-induced VT

Channelopathies [7,33,34,35]

Long QT Syndrome (LQTS):

• QTc >470 ms (males) or >480 ms (females)
• Congenital (ion channel mutations: KCNQ1, KCNH2, SCN5A)
• Acquired (drugs, electrolytes)
• Risk: Torsades de Pointes, SCD

Short QT Syndrome (SQTS):

• QTc <340 ms
• Very rare, high SCD risk
• ICD is primary prevention

Brugada Syndrome: (See dedicated section below)

Catecholaminergic Polymorphic VT (CPVT):

• Adrenergic-triggered polymorphic/bidirectional VT
• RyR2 or CASQ2 mutations (SR calcium handling)
• Treatment: Beta-blockers (nadolol preferred), flecainide, ICD
• Avoid digoxin, catecholamines

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Torsades de Pointes

Definition and Recognition [6,36,37]

Torsades de Pointes ("twisting of the points"):

• Polymorphic VT in setting of prolonged QT interval
• QRS complexes "twist" around isoelectric line
• Rate typically 200-250 bpm
• Self-terminating or degenerates to VF

ECG Features:

• Preceding prolonged QTc (>500 ms high risk)
• Polymorphic ventricular rhythm
• Undulating QRS axis (appears to rotate around baseline)
• Often initiated by "short-long-short" sequence

Distinguishing from Other Polymorphic VT:

Causes of Acquired Long QT [26,38]

Mnemonic: "SHOCKED"

• Sotalol, other antiarrhythmics
• Hypokalaemia, hypomagnesaemia, hypocalcaemia
• Ondansetron, other QT drugs
• Cerebral injury (stroke, SAH - ECG changes with prolonged QT)
• Kidney disease (electrolytes, drug accumulation)
• Electrolyte disturbances
• Drugs (see table above)

Management of Torsades de Pointes [6,36,39]

Immediate Steps:

1. Discontinue all QT-prolonging drugs - review entire medication list
2. Magnesium sulfate 2g IV over 2-5 minutes - even if Mg²⁺ normal
   • Can repeat once if no effect
   • Infusion 2-4 mg/min if recurrent
3. Correct electrolytes:
   • K+ target 4.5-5.0 mmol/L (higher than usual due to QT)
   • Mg²⁺ target ≥1.0 mmol/L
4. If refractory or haemodynamically unstable:
   • Overdrive pacing (transcutaneous initially, then transvenous)
   • Target heart rate 90-110 bpm (shortens QT, prevents pauses)
   • Alternative: Isoprenaline (isoproterenol) 2-10 mcg/min (increases HR)

If VF/Pulseless VT:

• Defibrillation 200J biphasic, CPR per ALS protocol
• Magnesium 2g IV as soon as IV access
• Consider amiodarone 300 mg cautiously (can prolong QT but may stabilise)

Post-Episode Management:

• Telemetry/continuous ECG monitoring
• Daily electrolytes (K+, Mg²⁺, Ca²⁺)
• Review all medications for QT effects
• Consider temporary pacing if significant bradycardia
• Cardiology/EP consultation for recurrent episodes

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Brugada Syndrome

Definition and ECG Patterns [7,40,41]

Brugada Syndrome:

• Inherited sodium channelopathy (SCN5A mutation in 20-30%)
• Characteristic ECG pattern in right precordial leads (V1-V3)
• Risk of VF and sudden cardiac death
• Male predominance (8:1), Southeast Asian ethnicity higher prevalence

ECG Patterns:

Only Type 1 pattern is diagnostic for Brugada syndrome. Types 2 and 3 may warrant provocative testing (ajmaline, flecainide, procainamide).

Clinical Presentation

• Syncope (often nocturnal, during sleep/fever)
• Cardiac arrest/SCD (typically in 3rd-4th decade)
• Palpitations
• Nocturnal agonal respiration (reported by bed partner)
• May be completely asymptomatic (incidental ECG finding)

Triggers for Arrhythmia [7,42]

ICU Management of Brugada [7,43,44]

Acute VT/VF Episode:

1. Defibrillation per standard ALS protocol
2. Avoid flecainide, procainamide, propafenone (worsen Na⁺ channel block)
3. Isoproterenol (isoprenaline) 2-5 mcg/min for VT storm
   • Increases heart rate, enhances calcium current, suppresses VF
4. Quinidine (if available) - can suppress VF inducibility
5. Consider temporary pacing if significant bradycardia

Fever in Brugada:

• Recognise that fever can unmask or worsen Brugada pattern
• Aggressive antipyretics (paracetamol, ibuprofen)
• Physical cooling measures
• Continuous ECG monitoring
• Lower threshold for ICU admission

Long-Term:

• ICD for secondary prevention (post-arrest) or high-risk primary prevention
• Risk stratification remains controversial (EP study utility debated)
• Avoid drugs on Brugada Drug List (www.brugadadrugs.org)

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VT in Structural Heart Disease

Scar-Related Re-entrant VT [45,46,47]

Pathophysiology:

• Dense scar provides area of block
• Border zone with slow conduction provides circuit
• Critical isthmus: narrow channel where ablation terminates VT
• Typically post-MI, but also DCM, ARVC, surgical scars

ECG Characteristics:

• Monomorphic (consistent morphology beat-to-beat)
• Axis and bundle branch morphology suggest origin
• Often multiple VT morphologies (multiple circuits)

Diagnosis:

• 12-lead ECG during VT (if haemodynamically tolerated)
• Echocardiography (LVEF, regional wall motion)
• Cardiac MRI with late gadolinium enhancement (scar characterisation)
• EP study with voltage mapping and entrainment

Management in ICU [45,48]

Acute Episode (Haemodynamically Stable):

1. 12-lead ECG - document morphology for later ablation planning
2. Amiodarone 150 mg IV over 10 min, then 1 mg/min infusion
3. Correct electrolytes (K+ 4.0-4.5, Mg²⁺ ≥1.0 mmol/L)
4. Treat underlying cause (ischaemia, heart failure)
5. Cardioversion if pharmacological failure or deterioration

Haemodynamically Unstable:

• Synchronised cardioversion 120-200J biphasic
• Post-cardioversion: amiodarone infusion for suppression
• Consider intra-aortic balloon pump if cardiogenic shock

Recurrent/Incessant VT:

• This is electrical storm - see section below
• Urgent cardiology/EP consultation
• Consider emergent catheter ablation

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Ventricular Fibrillation Management

ANZCOR Guidelines [2,49,50]

VF/Pulseless VT Algorithm:

1. Confirm cardiac arrest - unresponsive, no breathing, no pulse (<10 seconds)
2. Call for help, activate emergency response
3. Begin CPR - 30 compressions: 2 ventilations (or 100-120 compressions/min if ventilated)
4. Defibrillation - 200J biphasic (360J monophasic) as soon as available
5. Resume CPR immediately - 2 minutes (5 cycles of 30:2)
6. Rhythm check at 2-minute intervals
7. Adrenaline 1 mg IV - after 2nd shock, then every 3-5 minutes (alternate cycles)
8. Amiodarone 300 mg IV - after 3rd shock (can repeat 150 mg after 5th shock)
9. Consider reversible causes (4Hs and 4Ts)
10. Continue until ROSC, decision to cease, or handover

4Hs and 4Ts (Reversible Causes):

• Hypoxia, Hypovolaemia, Hypo/hyperkalaemia, Hypothermia
• Thrombosis (coronary/pulmonary), Tamponade, Toxins, Tension pneumothorax

Defibrillation Principles [51,52]

Energy Levels:

• Biphasic waveforms: 120-200J (device-specific, usually 200J)
• Monophasic waveforms: 360J
• Paediatric: 4 J/kg (escalate if refractory)

Optimal Technique:

• Anterior-lateral (apex-sternum) or anterior-posterior pad placement
• Minimise hands-off time ("peri-shock pause" <10 seconds)
• Ensure good pad contact, avoid air pockets
• Defibrillate during compressions if double sequential possible

Refractory VF:

• Change pad position (anterior-posterior)
• Consider double sequential defibrillation (2 defibrillators)
• Ensure adequate CPR quality
• Address reversible causes
• Early ECMO consideration (E-CPR) for selected patients

Post-ROSC Care [53,54,55]

Immediate (0-2 hours):

• Airway management (ETT if not already)
• Target SpO₂ 94-98%, PaCO₂ 35-45 mmHg (avoid hyperoxia, hypocapnia)
• Haemodynamic stabilisation (MAP >65-70 mmHg)
• 12-lead ECG - emergent coronary angiography if STEMI

First 24-72 hours (ICU):

• Targeted Temperature Management (TTM): 32-36°C for 24+ hours (TTM2 trial)
• Glucose control (avoid hypoglycaemia <4 mmol/L)
• Seizure prevention/treatment (EEG monitoring if available)
• Avoid hyperthermia
• Continue haemodynamic support

Neuroprognostication:

• Wait ≥72 hours after return to normothermia
• Multimodal approach: clinical examination, EEG, SSEP, imaging, biomarkers
• Avoid premature withdrawal of life-sustaining treatment

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Antiarrhythmic Therapy

Vaughan Williams Classification [56,57]

Amiodarone [58,59,60]

The most commonly used antiarrhythmic in ICU for VT.

Mechanism:

• Blocks K⁺ channels (dominant effect - prolongs APD)
• Also blocks Na⁺, Ca²⁺ channels and beta-receptors
• Non-competitive alpha and beta antagonism
• Prolongs QT interval but low Torsades risk (unlike sotalol, dofetilide)

Dosing (IV):

• Cardiac arrest (VF/pulseless VT): 300 mg bolus, can repeat 150 mg
• Haemodynamically stable VT: 150 mg over 10 min, then 1 mg/min × 6 hours, then 0.5 mg/min × 18 hours
• Maintenance: 400-600 mg/day PO (after loading), reduce to 200-400 mg/day long-term

Adverse Effects (ICU-relevant):

• Hypotension (IV formulation, due to vasodilation and polysorbate 80)
• Bradycardia (beta-blocking effect)
• QT prolongation (but lower Torsades risk than other Class III)
• Phlebitis (use central line for prolonged infusion)
• Drug interactions (CYP3A4 inhibition - warfarin, digoxin)

Long-term toxicity (less relevant to acute ICU):

• Thyroid dysfunction (hyper- and hypothyroidism)
• Pulmonary toxicity (pneumonitis, fibrosis)
• Hepatotoxicity
• Corneal deposits
• Skin photosensitivity

Lignocaine (Lidocaine) [61,62]

Mechanism:

• Fast Na⁺ channel block (Class Ib)
• Preferential binding to ischaemic/depolarised tissue
• Shortens action potential duration
• Does not prolong QT

Dosing (IV):

• Loading: 1-1.5 mg/kg IV bolus (maximum 3 mg/kg in first hour)
• Infusion: 1-4 mg/min (reduce in hepatic dysfunction, shock)

Indications:

• Alternative to amiodarone in VF/pulseless VT (ANZCOR recognises both)
• VT in acute ischaemia (preferred by some due to no QT effect)
• Refractory VF when amiodarone contraindicated

Advantages:

• No hypotension (unlike IV amiodarone)
• No QT prolongation
• Faster onset (immediate)
• Shorter half-life (easy to titrate)

Disadvantages:

• Narrow therapeutic index
• CNS toxicity (perioral numbness, confusion, seizures)
• Less effective than amiodarone in non-ischaemic VT

Procainamide [63,64]

Mechanism:

• Intermediate Na⁺ channel block (Class Ia)
• Also K⁺ channel block (prolongs QT)
• Slows conduction, prolongs refractory period

Dosing (IV):

• Loading: 20-50 mg/min (max 17 mg/kg or until hypotension/QRS widening >50%)
• Infusion: 1-4 mg/min

Indications:

• Haemodynamically stable monomorphic VT (especially in preserved LV function)
• Pre-excited AF (WPW with AF)
• May be superior to amiodarone for haemodynamically stable VT (PROCAMIO trial, PMID: 28405017)

Cautions:

• Hypotension (negative inotropy)
• QT/QRS prolongation (stop if QRS >50% widening)
• Contraindicated in heart failure (negative inotropy)
• Contraindicated in Torsades de Pointes (prolongs QT)

Beta-Blockers [65,66]

Role in Ventricular Arrhythmias:

• First-line chronic therapy for VT/VF prevention
• Reduce catecholamine-mediated triggered activity
• Reduce mortality in post-MI and heart failure (independent of antiarrhythmic effect)
• Essential in LQTS (LQT1, LQT2), CPVT

ICU Considerations:

• Esmolol: Ultra-short acting (t½ 9 min), titratable, useful in VT storm
  • "Dose: 500 mcg/kg bolus, then 50-300 mcg/kg/min"
• Metoprolol: 5 mg IV bolus, repeat q5min to max 15 mg
• Propranolol: Non-selective, useful in LQTS and VT storm

Cautions:

• Hypotension, bradycardia
• Bronchospasm (avoid in severe asthma)
• Cardiogenic shock (relative contraindication, but consider if VT is the cause)

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Electrical Storm

Definition and Recognition [5,67,68]

Electrical Storm (VT/VF Storm):

• ≥3 distinct VT/VF episodes within 24 hours, each requiring intervention (cardioversion/defibrillation)
• OR ≥3 ICD therapies (shocks or ATP) in 24 hours
• OR incessant VT lasting >12 hours

Clinical Features:

• Multiple defibrillator discharges
• Haemodynamic instability between episodes
• Often associated with underlying acute trigger (ischaemia, electrolytes, drugs)
• High mortality (10-30% in-hospital) without aggressive intervention

Aetiology [5,69]

Management [5,67,70,71]

Tier 1: Immediate Resuscitation

1. Standard ALS for each VT/VF episode
2. Correct electrolytes urgently (K+ 4.5-5.0, Mg²⁺ ≥1.0 mmol/L)
3. Discontinue QT-prolonging/proarrhythmic drugs
4. 12-lead ECG if VT recurs (document morphology)
5. Treat acute ischaemia (urgent angiography if suspected)

Tier 2: Pharmacological Suppression

1. Amiodarone 150 mg IV bolus, then 1 mg/min infusion
2. Beta-blockade - ESSENTIAL in VT storm:
   • Esmolol 500 mcg/kg bolus, then 50-200 mcg/kg/min
   • OR Propranolol 0.15 mg/kg IV (divided doses)
   • OR Metoprolol 5 mg IV q5min (max 15 mg)
3. Lignocaine if amiodarone ineffective (1-1.5 mg/kg bolus, 1-4 mg/min infusion)

Tier 3: Sympathetic Blockade and Sedation

1. Deep sedation - Reduces sympathetic drive
   • Propofol and/or benzodiazepines
   • Consider intubation if not already ventilated
2. Stellate Ganglion Block (SGB):
   • Left or bilateral percutaneous stellate ganglion block with local anaesthetic
   • Reduces cardiac sympathetic innervation
   • Evidence: Multiple case series showing efficacy [72]
3. Neuraxial anaesthesia:
   • Thoracic epidural (T1-T4)
   • Provides sympathetic blockade

Tier 4: Emergent Catheter Ablation

• Indications: Failure of medical therapy, recurrent VT/VF despite Tier 1-3
• Best outcomes when performed early in storm
• Can be performed with haemodynamic support (IABP, ECMO)
• Targets: VT isthmus in scar-related VT, PVC triggers in polymorphic VT

Tier 5: Mechanical Circulatory Support

• VA-ECMO for refractory VT/VF storm with haemodynamic collapse
• IABP for ischaemic VT with cardiogenic shock
• Supports patient during ablation or as bridge to transplant/LVAD

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ICD Management in ICU

ICD Basics for Intensivists [73,74,75]

ICD Function:

• Continuous monitoring for VT/VF
• Tiered therapy: Anti-tachycardia pacing (ATP) → Shocks
• Also provides bradycardia pacing

Therapy Zones:

• VT zone (usually 140-180 bpm): ATP first, then shocks
• VF zone (usually >180-200 bpm): Immediate shocks
• Monitoring zone: No therapy, just detection

ICD Shock Storms in ICU [73,76]

Definition:

• ≥3 appropriate or inappropriate ICD therapies in 24 hours

Causes of Appropriate Shocks:

• Recurrent VT/VF (electrical storm - see above)
• Acute ischaemia
• Electrolyte abnormalities
• Medication non-adherence
• Underlying cardiomyopathy progression

Causes of Inappropriate Shocks:

• Supraventricular tachycardia (especially AF with RVR)
• Sinus tachycardia
• Lead fracture/failure (electrical noise)
• Electromagnetic interference
• T-wave oversensing

Magnet Application [73,77]

Effect of Magnet Placement Over ICD:

• Suspends arrhythmia detection and therapy (shocks and ATP)
• Does NOT affect pacemaker function (continues pacing if dependent)
• Effect immediately reversible when magnet removed
• Typically used for inappropriate shocks or during surgery

Technique:

1. Place magnet directly over ICD generator
2. Confirm effect (typically audible tones)
3. Secure magnet in place if ongoing suspension needed
4. Do not leave magnet in place indefinitely - reassess frequently
5. Remove to restore arrhythmia therapies

Cautions:

• Patient becomes unprotected against VT/VF while magnet applied
• Ensure external defibrillator immediately available
• Some older or specific devices may respond differently

ICD Interrogation and Programming [73,74]

When to Request Urgent Interrogation:

• Multiple shocks (appropriate or inappropriate)
• Syncope with ICD
• Signs of lead dysfunction
• Post-cardiac surgery
• Before/after MRI (if MRI-conditional)

Programming Considerations in ICU:

• May need to raise VT detection rate (if sinus tachycardia causing false detection)
• May need to adjust shock therapies
• Consider "monitor only" mode if DNR/ceiling of care established

ICD Deactivation [78,79]

Ethical Considerations:

• ICD deactivation is ethically equivalent to withdrawal of other life-sustaining treatments
• Should be discussed as part of goals of care
• Patient/family should understand implications (death may occur rapidly from VT/VF)
• Should be performed by qualified personnel

Process:

1. Goals of care discussion (document clearly)
2. Explain that ICD shocks may cause distress if not deactivated
3. Consider magnet if urgent, programming change if planned
4. Ensure comfort measures in place (analgesia, sedation)
5. Do not deactivate pacemaker function if patient is pacing-dependent and goals include comfort

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Electrolyte Correction

Potassium Targets and Correction [11,80,81]

ICU Target in Patients at Risk of VA:

• K+ 4.0-4.5 mmol/L (higher than general ICU target of >3.5 mmol/L)
• Critical patients with arrhythmias: Consider K+ 4.5-5.0 mmol/L

Potassium Replacement:

Maximum peripheral IV concentration: 40 mmol/L (to avoid phlebitis) Maximum central IV rate: 40 mmol/hour (risk of transient hyperkalaemia)

Clinical Pearls:

• Concurrent hypomagnesaemia causes refractory hypokalaemia - correct Mg²⁺ first
• Intracellular potassium shifts occur with insulin, beta-agonists, alkalosis
• Monitor renal function during aggressive replacement

Magnesium Targets and Correction [82,83,84]

ICU Target in Patients at Risk of VA:

• Mg²⁺ ≥1.0 mmol/L (≥2.4 mg/dL or ≥2.0 mEq/L)

Magnesium Replacement:

Cautions:

• Reduce dose in renal impairment
• Rapid infusion causes flushing, hypotension
• Monitor deep tendon reflexes (loss at Mg²⁺ >4 mmol/L)
• Respiratory depression at very high levels (>6 mmol/L)

---

Wide Complex Tachycardia: VT vs SVT

Differentiation [4,85,86]

Default Position: Treat all WCT as VT until proven otherwise.

VT is more likely if:

• Structural heart disease (prior MI, cardiomyopathy)
• Older age
• Haemodynamic instability (but SVT can also be unstable)

ECG Criteria for VT

AV Dissociation:

• P waves independent of QRS complexes
• Rate of P waves slower than QRS rate
• Highly specific for VT (100%) but not always visible

Capture and Fusion Beats:

• Capture beat: Narrow QRS during WCT (sinus impulse captures ventricles)
• Fusion beat: Intermediate morphology (collision of sinus and ventricular impulses)
• Diagnostic for VT

Brugada Criteria (Step-wise algorithm):

1. Absence of RS complex in all precordial leads → VT
2. RS interval >100 ms in any precordial lead → VT
3. AV dissociation → VT
4. Morphology criteria for VT in V1-V2 and V6

RBBB Morphology VT Criteria (V1):

• R wave alone or qR or RS in V1 = VT (rSR' = SVT with aberrancy)
• R wave >30 ms or S wave nadir >60 ms in V1 = VT
• R:S ratio <1 in V6 (deep S wave) = VT

LBBB Morphology VT Criteria (V1):

• R wave >30 ms in V1 or V2 = VT
• Notch on downstroke of S wave in V1 or V2 = VT
• Onset of QRS to nadir of S wave >60-70 ms = VT
• Any Q wave in V6 = VT

Management Implications

If VT (or uncertain):

• Haemodynamically unstable → Synchronised cardioversion
• Haemodynamically stable → Amiodarone 150 mg IV over 10 min
• Do NOT give verapamil (can cause cardiovascular collapse in VT)

If definitely SVT with aberrancy:

• Adenosine may be diagnostic/therapeutic
• Appropriate SVT management

When in doubt:

• Treat as VT (safer approach)
• Amiodarone is safe for both VT and SVT

---

Australian/NZ Context

ANZCOR Guidelines [2,49,50]

Key Points:

• ANZCOR (Australian and New Zealand Committee on Resuscitation) produces guidelines
• Aligned with International Liaison Committee on Resuscitation (ILCOR) with local adaptations
• Updated regularly (most recent: 2021)

VF/Pulseless VT Differences from International:

• Energy levels: 200J biphasic (same as international)
• Adrenaline timing: After 2nd shock (same)
• Amiodarone: 300 mg after 3rd shock, 150 mg after 5th shock (same)
• Lignocaine: Alternative if amiodarone not available

Remote and Rural Considerations [87,88]

Challenges:

• Delayed access to defibrillation (no public access AEDs in remote areas)
• Limited antiarrhythmic availability
• Retrieval times: May be hours to tertiary centre
• Telemedicine consultation (RFDS, state retrieval services)

Retrieval Medicine Implications:

• Stabilise rhythm before transport if possible
• Continuous ECG monitoring during retrieval
• External pacing capability
• Adequate sedation for ICD patients

Indigenous Health Considerations [89,90,91]

Epidemiology:

• Aboriginal and Torres Strait Islander peoples have higher rates of:
  • Ischaemic heart disease (2-3× higher hospitalisation)
  • Rheumatic heart disease (significantly higher in Northern Australia)
  • Sudden cardiac death at younger age
• Māori have higher cardiovascular mortality than non-Māori NZ Europeans

Access Issues:

• Geographic barriers to ICD implantation and follow-up
• Lower rates of invasive procedures (PCI, CABG, EP procedures)
• Limited access to specialised EP services in remote areas

Cultural Considerations:

• Family/community involvement in decision-making (whānau for Māori)
• Cultural liaison officers and Aboriginal Health Workers (AHWs)
• Language and health literacy considerations
• Respect for cultural practices and beliefs

ICD-Specific Issues:

• Ensure understanding of device function and follow-up requirements
• Address concerns about device during cultural practices
• Ensure culturally safe discussions about deactivation if relevant

---

Assessment

SAQ Practice Questions

SAQ: #### SAQ 1: Electrical Storm (15 marks)

Stem: A 62-year-old man with ischaemic cardiomyopathy (LVEF 25%) and a previously implanted ICD presents to the Emergency Department after receiving 6 ICD shocks at home in the last 4 hours. He is diaphoretic and anxious but conscious. His blood pressure is 90/60 mmHg, heart rate 140 bpm. The ECG shows monomorphic wide-complex tachycardia.

Question: a) Define electrical storm and outline the immediate management priorities (5 marks) b) Discuss the pharmacological agents used in VT storm, including their mechanisms and dosing (5 marks) c) What non-pharmacological interventions may be required if medical therapy fails? (5 marks)

---

Model Answer:

a) Definition and Immediate Priorities (5 marks)

Definition of Electrical Storm:

• ≥3 distinct VT/VF episodes within 24 hours requiring intervention (cardioversion, defibrillation, or ICD therapy)
• OR ≥3 ICD therapies in 24 hours
• OR incessant VT lasting >12 hours

Immediate Management Priorities:

1. Resuscitation and Stabilisation:

   • ABC approach - may need intubation if deteriorating
   • Establish IV access, arterial line
   • Apply external defibrillator pads (in case ICD therapies exhausted)

2. Magnet Application:

   • Apply ICD magnet to suspend inappropriate therapies while evaluating
   • Ensure external defibrillator ready if VF occurs

3. Electrolyte Correction:

   • Urgent K+ and Mg²⁺ levels
   • Target K+ 4.5-5.0 mmol/L, Mg²⁺ ≥1.0 mmol/L
   • Give empiric Mg²⁺ 2g IV if in VT

4. 12-Lead ECG:

   • Document VT morphology for potential ablation planning
   • Assess for ischaemia

5. Treat Reversible Causes:

   • Urgent troponin - consider coronary angiography if ischaemia suspected
   • Review medication list for proarrhythmic drugs
   • Check electrolytes, glucose, acid-base

b) Pharmacological Management (5 marks)

Amiodarone:

• Mechanism: Class III (K⁺ channel block), also Na⁺, Ca²⁺ channel and beta-receptor blockade
• Dose: 150 mg IV over 10 min, then 1 mg/min × 6 hours, then 0.5 mg/min
• First-line agent for VT in ICU
• Caution: Hypotension with IV loading

Beta-Blockers (ESSENTIAL):

• Mechanism: Block catecholamine-mediated triggered activity and enhanced automaticity
• Esmolol: Ultra-short acting (t½ 9 min), 500 mcg/kg bolus, then 50-200 mcg/kg/min
• Propranolol: 0.15 mg/kg IV in divided doses
• Metoprolol: 5 mg IV q5min (max 15 mg)
• Critical for VT storm - sympathetic activation perpetuates VT

Lignocaine (Lidocaine):

• Mechanism: Class Ib (fast Na⁺ channel block), preferential action on ischaemic tissue
• Dose: 1-1.5 mg/kg bolus, then 1-4 mg/min infusion
• Alternative or adjunct to amiodarone
• Preferred by some in ischaemic VT (no QT prolongation)

Deep Sedation:

• Propofol, midazolam, fentanyl
• Reduces sympathetic drive
• May require intubation

c) Non-Pharmacological Interventions (5 marks)

Stellate Ganglion Block (Left or Bilateral):

• Percutaneous injection of local anaesthetic to stellate ganglion
• Mechanism: Reduces cardiac sympathetic innervation
• Evidence: Multiple case series showing efficacy in refractory VT storm
• Can be temporising while arranging ablation

Thoracic Epidural:

• Provides sympathetic blockade (T1-T4)
• Alternative to stellate ganglion block
• May provide more sustained effect

Emergent Catheter Ablation:

• Indications: Refractory to medical therapy, identifiable target
• Can be performed with haemodynamic support (IABP, ECMO)
• Map and ablate VT circuit or PVC triggers
• Best outcomes when performed early

Mechanical Circulatory Support:

• VA-ECMO: For haemodynamic collapse, as bridge to ablation or recovery
• IABP: For ischaemic VT with cardiogenic shock
• Supports patient during ablation procedure

Coronary Revascularisation:

• If ongoing ischaemia is identified as trigger
• Emergent PCI or CABG

---

SAQ: #### SAQ 2: Torsades de Pointes (15 marks)

Stem: A 58-year-old woman is admitted to ICU with pneumonia requiring mechanical ventilation. She was started on moxifloxacin and haloperidol for delirium. On day 3, she develops a wide-complex tachycardia at 220 bpm with characteristic twisting QRS morphology. Her K+ is 3.2 mmol/L and Mg²⁺ is 0.6 mmol/L.

Question: a) What is the most likely diagnosis and what ECG features would confirm this? (3 marks) b) Outline the immediate management, explaining the rationale for each intervention (7 marks) c) How would you prevent recurrence in this patient? (5 marks)

---

Model Answer:

a) Diagnosis and ECG Features (3 marks)

Diagnosis: Torsades de Pointes

Confirming ECG Features:

• Polymorphic ventricular tachycardia with QRS complexes "twisting" around the isoelectric baseline
• Undulating QRS axis appearance
• Rate typically 200-250 bpm
• Often self-terminating in short bursts
• Prolonged baseline QTc interval (>500 ms is high risk)
• "Short-long-short" initiation sequence (PVC after pause)

Risk Factors in This Patient:

• Moxifloxacin: Fluoroquinolone, known QT-prolonging drug
• Haloperidol: Antipsychotic, known QT-prolonging drug
• Hypokalaemia: K+ 3.2 mmol/L
• Hypomagnesaemia: Mg²⁺ 0.6 mmol/L
• Likely prolonged QTc from drug combination and electrolyte abnormalities

b) Immediate Management (7 marks)

1. Magnesium Sulfate 2g IV over 2-5 minutes (2 marks)

• First-line treatment for Torsades regardless of serum Mg²⁺
• Mechanism: Stabilises myocardial membrane, reduces early afterdepolarisations
• Can repeat if ineffective
• Follow with infusion 2-4 mg/min if recurrent

2. Discontinue QT-Prolonging Drugs (1 mark)

• Stop moxifloxacin immediately
• Stop haloperidol immediately
• Review entire medication list (consider metoclopramide, ondansetron if on board)

3. Correct Electrolytes Urgently (2 marks)

• Potassium: Target 4.5-5.0 mmol/L (higher than usual in Torsades)
  • IV KCl 20-40 mmol/hour via central line with continuous ECG
• Magnesium: Already giving bolus; follow with infusion

4. If Haemodynamically Unstable or Refractory (2 marks)

• Defibrillation if pulseless (unsynchronised 200J biphasic)
• Overdrive Pacing:
  • Transcutaneous initially, then transvenous
  • Target HR 90-110 bpm
  • Prevents pauses that trigger Torsades
• Isoproterenol (Isoprenaline):
  • 2-10 mcg/min IV infusion
  • Increases heart rate, shortens QT
  • Bridge to temporary pacing

c) Prevention of Recurrence (5 marks)

1. Medication Review (2 marks)

• Complete review of all medications for QT effects
• Use CredibleMeds (www.crediblemeds.org) for drug reference
• Choose alternative antibiotics (non-QT-prolonging: ceftriaxone, piperacillin-tazobactam)
• Choose alternative sedation/delirium management (dexmedetomidine, low-dose quetiapine with ECG monitoring)

2. Electrolyte Maintenance (1 mark)

• Daily K+ and Mg²⁺ monitoring (at minimum)
• Higher targets: K+ 4.0-4.5 mmol/L, Mg²⁺ ≥1.0 mmol/L
• Correct underlying causes (nutrition, diarrhoea, diuretics)

3. Continuous ECG Monitoring (1 mark)

• Daily QTc measurement
• Set telemetry alarms for prolonged QTc
• Immediate escalation if QTc >500 ms or increases >60 ms from baseline

4. Consider Temporary Pacing (1 mark)

• If significant bradycardia contributing
• Overdrive pacing maintains rate, prevents pauses
• May be required for several days until drugs eliminated and electrolytes stable

---

Hot Case Scenarios

Case Study: #### Hot Case 1: ICD Shock Storm

Setting: ICU, Day 2 post-admission

Handover: "This is a 58-year-old man with dilated cardiomyopathy and an ICD who was admitted yesterday following 8 ICD shocks at home. He was found to have hypokalaemia (K+ 2.8) which has been corrected. He is currently on amiodarone infusion at 0.5 mg/min and metoprolol 25 mg BD. Overnight he has had 2 further episodes of VT requiring ATP from his ICD. He is currently in sinus rhythm."

---

Examination Findings:

General Appearance:

• Alert, anxious, cooperative
• Lying at 30° head-up
• Not currently distressed

Monitoring:

• HR 75 bpm, sinus rhythm
• BP 105/65 mmHg
• SpO₂ 96% on 2L NC
• RR 18/min

Cardiovascular:

• JVP elevated ~6 cm
• Apex beat displaced laterally (6th ICS, anterior axillary line)
• Heart sounds: S1, S2, +S3 gallop
• No murmurs
• ICD pocket visible left infraclavicular region, no signs of infection

Respiratory:

• Bibasal fine crackles (mild)
• Air entry adequate bilaterally

Other:

• Mild bilateral pedal oedema
• No hepatomegaly

Investigations:

• ECG: Sinus rhythm, LBBB morphology, QTc 480 ms
• K+ 4.2 mmol/L, Mg²⁺ 0.9 mmol/L
• Troponin I: 25 ng/L (mildly elevated)
• Echo (recent): LVEF 20%, dilated LV, moderate mitral regurgitation

---

Examiner Questions:

Examiner: "Please summarise this case in 1 minute."

Candidate: "This is a 58-year-old man with known dilated cardiomyopathy and severely reduced LV function who presented with electrical storm, likely triggered by severe hypokalaemia. He has an ICD in situ. Despite electrolyte correction and amiodarone infusion, he continues to have VT episodes overnight, though currently stable in sinus rhythm. Examination shows signs of chronic heart failure with elevated JVP, S3 gallop, and mild pulmonary congestion. He remains at high risk of further VT and requires optimisation of medical therapy, consideration of beta-blocker up-titration, and electrophysiology input for possible catheter ablation."

---

Examiner: "What further investigations would you request?"

Candidate:

• "ICD interrogation - to assess VT morphology, number and type of therapies, battery status, and lead integrity"
• "Repeat electrolytes including magnesium, calcium, phosphate"
• "Renal function to ensure safe drug dosing"
• "Repeat troponin to trend - assess for ongoing ischaemia"
• "Consider coronary angiography if ischaemia suspected as trigger"
• "ECG during VT if captured - for ablation planning"
• "Check amiodarone level if on prolonged therapy"

---

Examiner: "The ICD interrogation shows 12 ATP therapies and 4 shocks in total. All episodes were monomorphic VT at 175 bpm with RBBB morphology. What does this tell you?"

Candidate: "The monomorphic VT with consistent RBBB morphology suggests a scar-based re-entrant circuit in the left ventricle, which is consistent with his dilated cardiomyopathy. This is encouraging for catheter ablation as there appears to be a single predominant VT morphology arising from an identifiable circuit. The frequency of episodes despite therapy suggests ongoing arrhythmia substrate and the need for escalation beyond medical management."

---

Examiner: "How would you optimise his medical therapy?"

Candidate:

• "Ensure electrolytes remain optimal: K+ 4.0-4.5 mmol/L, Mg²⁺ ≥1.0 mmol/L"
• "Continue amiodarone - he may need loading optimisation"
• "Increase beta-blockade - metoprolol 25 mg BD is subtherapeutic; would aim to uptitrate carefully given BP 105/65 and signs of mild congestion"
• "Consider adding ACE inhibitor/ARB and MRA if not already on - guideline-directed medical therapy reduces SCD risk"
• "SGLT2 inhibitor consideration for heart failure"
• "Consider lignocaine infusion as bridge if VT recurs"

---

Examiner: "He has another episode of VT overnight. What is your approach to further management?"

Candidate: "This represents ongoing electrical storm despite Tier 1 and 2 management. I would escalate to Tier 3 interventions:

1. Deep sedation with propofol and/or benzodiazepines to reduce sympathetic drive
2. Consider intubation if required for sedation depth
3. Uptitrate beta-blockade - consider IV esmolol or propranolol
4. Consult EP urgently for consideration of stellate ganglion block or emergent catheter ablation
5. If haemodynamically compromised, consider mechanical support with IABP or VA-ECMO as bridge to ablation"

---

Examiner: "The family asks about long-term prognosis. What do you tell them?"

Candidate: "I would explain that his condition is serious. Electrical storm is a life-threatening situation that we are managing aggressively. His underlying cardiomyopathy is advanced, and while we can often control the arrhythmia acutely, his long-term prognosis depends on the success of ablation and optimisation of heart failure therapies. If ablation is successful, it can reduce VT recurrence significantly, but he remains at risk of further episodes and sudden death, which is why the ICD remains important. I would discuss that if medical and ablation therapies are unsuccessful, options such as LVAD or cardiac transplantation might be considered, but these are complex decisions requiring further assessment."

---

Case Study: #### Hot Case 2: Long QT and Torsades de Pointes

Setting: ICU, Day 2 post-admission

Handover: "This is a 45-year-old woman admitted with community-acquired pneumonia complicated by sepsis. She was initially treated with moxifloxacin and required ICU admission for hypotension requiring noradrenaline. She developed agitation and was given haloperidol 5 mg IV. Four hours later she had a cardiac arrest with polymorphic VT/VF requiring 3 shocks. She had ROSC after 8 minutes. She is now intubated and ventilated."

---

Examination Findings:

General:

• Intubated, sedated (propofol/fentanyl)
• RASS -4

Monitoring:

• HR 95 bpm, sinus rhythm
• BP 110/70 mmHg (noradrenaline 5 mcg/min)
• SpO₂ 97% on FiO₂ 0.4

Cardiovascular:

• Heart sounds normal
• No murmurs
• Extremities warm

Respiratory:

• Bilateral coarse breath sounds
• Adequate air entry

Lines:

• Right IJ CVC
• Right radial arterial line
• IDC in situ

Investigations:

• ECG post-arrest: Sinus rhythm, QTc 580 ms, no ischaemic changes
• K+ 3.4 mmol/L, Mg²⁺ 0.7 mmol/L
• Troponin I: 85 ng/L
• Lactate: 2.1 mmol/L (down from 5.2 on admission)

---

Examiner Questions:

Examiner: "Please summarise this case."

Candidate: "This 45-year-old woman with septic pneumonia suffered a cardiac arrest due to Torsades de Pointes in the setting of drug-induced QT prolongation. Contributing factors include moxifloxacin (fluoroquinolone QT prolongation), haloperidol (antipsychotic QT prolongation), hypokalaemia (K+ 3.4), and hypomagnesaemia (Mg²⁺ 0.7). She has had successful resuscitation and is now intubated with post-arrest care underway. The markedly prolonged QTc of 580 ms confirms the mechanism. Immediate priorities are electrolyte correction, discontinuation of QT-prolonging drugs, and consideration of temporary pacing to prevent recurrence."

---

Examiner: "What is the mechanism of Torsades de Pointes?"

Candidate: "Torsades de Pointes is a form of polymorphic VT occurring in the context of prolonged QT interval. The mechanism involves:

1. Prolonged repolarisation creating dispersion - different parts of the ventricle recover at different times
2. Early afterdepolarisations (EADs) - during Phase 2/3 of the action potential, L-type calcium channels or late sodium channels can reactivate
3. A triggered PVC typically after a short-long-short sequence (a pause followed by another PVC)
4. The triggered beat conducts preferentially through recovered tissue, initiating a re-entrant circuit
5. The twisting morphology reflects the rotating axis of depolarisation through tissue with heterogeneous refractoriness"

---

Examiner: "How would you manage this patient to prevent recurrence?"

Candidate:

1. Immediately:

   • "Discontinue moxifloxacin - switch to non-QT-prolonging antibiotic (ceftriaxone, piperacillin-tazobactam)"
   • "Do not give further haloperidol - use alternative sedation if needed (dexmedetomidine)"
   • "IV Magnesium 2g bolus then 2-4 mg/min infusion"
   • "IV Potassium to target K+ 4.5-5.0 mmol/L"

2. If QTc remains prolonged or further episodes:

   • "Temporary transvenous pacing at rate 90-100 bpm (overdrive pacing)"
   • "Alternative: Isoproterenol infusion 2-5 mcg/min to increase heart rate"

3. Monitoring:

   • "Continuous ECG with QTc trending"
   • "Serial electrolytes (at least q6h initially)"
   • "Complete medication review via CredibleMeds"

---

Examiner: "She develops another episode of Torsades. Your K+ is now 4.3, Mg²⁺ is 1.2. What do you do?"

Candidate:

1. "If pulseless - defibrillate 200J biphasic immediately"
2. "If with pulse but unstable - synchronised cardioversion"
3. "Give another bolus of magnesium 2g IV"
4. "Initiate overdrive pacing - transcutaneous immediately, then transvenous"
5. "If pacing not immediately available, start isoproterenol 2-5 mcg/min"
6. "Re-check for any remaining QT-prolonging medications"
7. "Consider if congenital LQTS could be contributing (family history, ECG review)"

---

Examiner: "The patient's Aboriginal family are concerned. How do you communicate with them?"

Candidate: "I would approach communication sensitively:

1. Introduce myself and ask if there is a family spokesperson or if they prefer to hear information together
2. Ask if they would like an Aboriginal Health Worker (AHW) or Aboriginal Liaison Officer (ALO) present
3. Explain in clear, simple language what has happened - 'The heart developed a dangerous rhythm because of the medications and low levels of potassium and magnesium in the blood'
4. Explain what we are doing to fix it and prevent recurrence
5. Provide realistic information about prognosis while maintaining hope
6. Ask if they have questions and allow time for discussion
7. Offer to meet again after they have had time to talk amongst themselves
8. Document the conversation and any expressed wishes"

---

Viva Scenarios

Viva: #### Viva 1: Mechanisms of Ventricular Arrhythmias

Examiner: "Tell me about the three mechanisms of ventricular arrhythmogenesis."

Candidate: "The three mechanisms are re-entry, triggered activity, and enhanced automaticity.

Re-entry is the most common mechanism in structural heart disease, accounting for approximately 80% of ventricular tachycardia. It requires:

1. A circuit with two pathways
2. Unidirectional block in one pathway
3. Slow conduction in the alternative pathway
4. Excitable tissue ahead of the advancing wavefront

The classic substrate is post-MI scar tissue, where dense scar provides an area of block and the border zone provides slow conduction for the circuit.

Triggered activity involves afterdepolarisations. Early afterdepolarisations (EADs) occur during Phase 2 or 3 of repolarisation, are promoted by QT prolongation, and cause Torsades de Pointes. Delayed afterdepolarisations (DADs) occur after complete repolarisation, are caused by intracellular calcium overload, and are seen in digoxin toxicity and catecholaminergic polymorphic VT.

Enhanced automaticity involves increased rate of Phase 4 depolarisation. It can be normal automaticity (enhanced) as in catecholamine-driven sinus tachycardia, or abnormal automaticity in diseased tissue that normally would not depolarise spontaneously."

---

Examiner: "A patient has QTc of 520 ms and develops Torsades. Walk me through the cellular mechanism."

Candidate: "The prolonged QT represents prolonged repolarisation at the cellular level. This is usually due to:

1. Reduced outward potassium currents (IKr blocked by drugs like sotalol, moxifloxacin)
2. Enhanced inward late sodium current
3. Hypokalaemia, which reduces IKr function

The prolonged repolarisation creates dispersion of refractoriness - different regions of the ventricle recover at different times. This heterogeneity is the substrate for re-entry.

During the prolonged plateau phase (Phase 2), L-type calcium channels can reopen, or late sodium current can cause further depolarisation. This creates an early afterdepolarisation (EAD), which if it reaches threshold, triggers a premature ventricular complex.

The typical triggering pattern is short-long-short: an initial PVC creates a compensatory pause, during which the next sinus beat has even longer repolarisation, and then another PVC occurs that conducts preferentially through recovered tissue while other areas are still refractory. This initiates the polymorphic ventricular tachycardia with the characteristic twisting morphology."

---

Examiner: "Why does magnesium work in Torsades, even when the serum level is normal?"

Candidate: "Magnesium works through several mechanisms independent of replacing a deficiency:

1. Calcium channel modulation - Magnesium blocks L-type calcium channels, which reduces the calcium current that can trigger EADs
2. Stabilisation of cell membrane - Reduces membrane excitability
3. Suppression of EADs directly - Reduces the triggered activity that initiates Torsades
4. Potassium channel effects - May enhance potassium current function

It's important to note that serum magnesium levels may not reflect intracellular or myocardial magnesium levels, so a 'normal' serum level doesn't exclude functional hypomagnesaemia at the cellular level."

---

Viva: #### Viva 2: Antiarrhythmic Drug Therapy and CAST Trial

Examiner: "Tell me about the CAST trial and why it changed practice."

Candidate: "The Cardiac Arrhythmia Suppression Trial (CAST) was a landmark study published in 1989 that fundamentally changed our approach to antiarrhythmic therapy.

Background: The hypothesis was that suppressing PVCs with antiarrhythmic drugs in post-MI patients would reduce sudden cardiac death. Class IC antiarrhythmics (encainide, flecainide) were effective at suppressing PVCs.

Study Design: Post-MI patients with frequent PVCs (≥6/hour) were randomised to encainide, flecainide, moricizine, or placebo if their PVCs were suppressed during an open-label run-in.

Results: The trial was stopped early due to excess mortality in the active treatment groups. There were 56 deaths in the encainide/flecainide group compared to 22 in placebo (relative risk 2.5). This was primarily due to arrhythmic death.

Mechanism of Harm: Class IC drugs have slow unbinding kinetics from sodium channels. In ischaemic tissue with already slowed conduction, they further slow conduction enough to promote re-entry. They also have negative inotropic effects.

Implications:

1. PVC suppression does not equal mortality reduction
2. Class IC drugs are contraindicated in structural heart disease
3. Proarrhythmia is a real and lethal phenomenon
4. Surrogate endpoints (PVC suppression) don't predict clinical outcomes
5. All new antiarrhythmics now require mortality endpoint trials"

---

Examiner: "So when can we use Class IC drugs?"

Candidate: "Class IC drugs like flecainide and propafenone are still used, but only in patients without structural heart disease:

Appropriate indications:

1. Atrial fibrillation in patients with structurally normal hearts ('lone AF')
2. Supraventricular tachycardias (AVNRT, AVRT, atrial flutter)
3. WPW syndrome (short refractory accessory pathways)
4. Catecholaminergic polymorphic VT (flecainide has specific use here)

Absolute contraindications:

1. Ischaemic heart disease (current or prior MI)
2. Heart failure or reduced LVEF
3. Significant left ventricular hypertrophy
4. Brugada syndrome (can unmask or worsen the ECG pattern)

Before initiating Class IC drugs, patients should have an echocardiogram to exclude structural heart disease and an exercise test to exclude inducible ischaemia."

---

Examiner: "Compare amiodarone and sotalol for VT suppression."

Candidate: "Both are used for VT suppression but have important differences:

Amiodarone:

• Multi-channel blocker (K+, Na+, Ca2+, beta-receptors)
• Very long half-life (40-55 days)
• Low proarrhythmic risk despite QT prolongation (due to multi-channel effects)
• Most effective antiarrhythmic for VT suppression
• Significant long-term toxicities (thyroid, pulmonary, hepatic, skin)
• Can be used safely in structural heart disease and heart failure

Sotalol:

• Class III (K+ channel block) plus beta-blocker (Class II)
• Half-life 12 hours, renally cleared
• Higher Torsades risk than amiodarone (pure QT prolongation)
• Contraindicated in severe renal impairment
• Less effective than amiodarone but better tolerated short-term
• Must be initiated in hospital with telemetry monitoring

In ICU for acute VT, amiodarone is preferred due to IV formulation and effectiveness. Sotalol is used more for chronic prevention in patients who cannot tolerate amiodarone.

The SWORD trial (1996) showed increased mortality with d-sotalol (the pure Class III enantiomer without beta-blocking activity) in post-MI patients, reinforcing the CAST lessons about proarrhythmia."

---

ZCOR? A: Amiodarone 300 mg IV bolus

12. Q: What is the amiodarone dose for haemodynamically stable VT? A: 150 mg IV over 10 minutes, then 1 mg/min for 6 hours, then 0.5 mg/min

13. Q: What effect does magnet placement have on an ICD? A: Suspends arrhythmia detection and therapy (shocks and ATP); does NOT affect pacemaker function

14. Q: What trial demonstrated increased mortality with Class IC antiarrhythmics in post-MI patients? A: CAST trial (1989) - encainide and flecainide

15. Q: Name three landmark ICD trials that showed mortality benefit. A: AVID (1997), MADIT-II (2002), SCD-HeFT (2005)

16. Q: What is the lignocaine loading dose for VT? A: 1-1.5 mg/kg IV bolus (maximum 3 mg/kg in first hour)

17. Q: What drug is used for VT storm in Brugada syndrome? A: Isoproterenol (isoprenaline) 2-5 mcg/min IV

18. Q: What ECG finding is highly specific (100%) for VT in a wide complex tachycardia? A: AV dissociation (independent P waves)

19. Q: What is the target heart rate for overdrive pacing in Torsades de Pointes? A: 90-110 bpm (prevents pauses that trigger Torsades)

20. Q: What genetic syndrome causes bidirectional VT triggered by catecholamines? A: Catecholaminergic Polymorphic VT (CPVT)

Clinical Reasoning (20 cards)

21. Q: A patient with wide complex tachycardia and previous MI - what should you assume? A: VT until proven otherwise (VT accounts for 80% of WCT in patients with structural heart disease)

22. Q: Post-intubation hypotension in a patient with severe asthma or COPD presenting with VT - most likely cause? A: Dynamic hyperinflation/auto-PEEP reducing venous return; disconnect from ventilator for 20-30 seconds

23. Q: Patient on moxifloxacin and haloperidol develops polymorphic VT with QTc 550 ms - diagnosis? A: Drug-induced Torsades de Pointes

24. Q: Refractory hypokalaemia despite aggressive replacement - what should you check? A: Magnesium level (hypomagnesaemia causes refractory hypokalaemia)

25. Q: ICD patient with multiple shocks, sinus tachycardia on monitor - likely cause? A: Inappropriate shocks due to SVT (sinus tachycardia, atrial fibrillation) being misclassified as VT

26. Q: What immediate action if patient with ICD has inappropriate shocks? A: Apply magnet over ICD to suspend therapies; ensure external defibrillator available

27. Q: Patient with fever develops Type 1 Brugada ECG pattern - management priority? A: Aggressive antipyretics, physical cooling, continuous ECG monitoring; fever is a known VF trigger in Brugada

28. Q: VT storm despite amiodarone and beta-blockers - next escalation step? A: Deep sedation, stellate ganglion block, emergent catheter ablation

29. Q: Why is verapamil contraindicated in wide complex tachycardia of uncertain origin? A: Can cause cardiovascular collapse if the rhythm is VT (negative inotropy with hypotension)

30. Q: Patient with LVEF 20% on flecainide - is this appropriate? A: NO - Class IC drugs are contraindicated in structural heart disease (CAST trial)

31. Q: What is the "short-long-short" sequence in Torsades initiation? A: PVC → compensatory pause → sinus beat with prolonged QT → PVC triggers Torsades

32. Q: Monomorphic VT with RBBB morphology - where is the VT likely originating? A: Left ventricle (RBBB morphology = LV origin; LBBB morphology = RV origin)

33. Q: Patient in electrical storm - why is beta-blockade essential? A: Sympathetic activation perpetuates VT; beta-blockade interrupts the catecholamine surge

34. Q: When should you NOT defibrillate in VT? A: When the patient has a pulse and is haemodynamically stable - use synchronised cardioversion or pharmacological treatment

35. Q: Capture beats during wide complex tachycardia - what do they diagnose? A: VT (capture beats are narrow complexes proving AV dissociation and ventricular origin)

36. Q: Why does amiodarone have lower Torsades risk than sotalol despite prolonging QT? A: Amiodarone blocks multiple channels (Na+, K+, Ca2+) creating more homogeneous repolarisation; sotalol only blocks K+ channels

37. Q: What is the mechanism of VT in digoxin toxicity? A: Delayed afterdepolarisations (DADs) from intracellular calcium overload (inhibited Na+/K+-ATPase)

38. Q: Stellate ganglion block mechanism in VT storm? A: Blocks cardiac sympathetic innervation, reducing catecholamine-driven arrhythmogenesis

39. Q: Why avoid amiodarone in Torsades de Pointes if possible? A: Further prolongs QT; however, may stabilise rhythm - use with caution alongside magnesium and pacing

40. Q: Primary VF in first hour of MI vs late VF (>48 hours) - which has worse prognosis? A: Late VF has worse prognosis (indicates larger infarct, more myocardial damage)

Guidelines and Evidence (15 cards)

41. Q: What ANZCOR guideline covers VT/VF management? A: ANZCOR Guideline 11.2 - Management of Cardiac Arrest

42. Q: When is adrenaline first given in VF per ANZCOR? A: After the 2nd shock, then every 3-5 minutes (alternate cycles)

43. Q: What is the key finding of the AVID trial (1997)? A: ICD superior to antiarrhythmic drugs (mainly amiodarone) for secondary prevention of VT/VF - 31% relative mortality reduction

44. Q: MADIT-II inclusion criteria and finding? A: Post-MI with LVEF ≤30%; ICD reduced all-cause mortality by 31% for primary prevention

45. Q: SCD-HeFT key finding? A: ICD reduced mortality 23% in ischaemic and non-ischaemic cardiomyopathy with LVEF ≤35% and NYHA II-III

46. Q: What is the PROCAMIO trial finding? A: Procainamide may be superior to amiodarone for haemodynamically stable monomorphic VT (2017)

47. Q: SWORD trial key finding? A: d-Sotalol (pure Class III) increased mortality in post-MI patients - reinforced CAST lessons about proarrhythmia

48. Q: TTM2 trial finding for post-arrest temperature management? A: Target 36°C was non-inferior to 33°C; avoid fever; focus is on avoiding hyperthermia

49. Q: What website is the authoritative reference for QT-prolonging drugs? A: CredibleMeds (www.crediblemeds.org)

50. Q: What website lists drugs to avoid in Brugada syndrome? A: www.brugadadrugs.org

51. Q: According to Australian guidelines, what K+ target reduces VT/VF risk? A: K+ 4.0-4.5 mmol/L (higher than general medical target of >3.5 mmol/L)

52. Q: What is the LVEF threshold that generally qualifies for primary prevention ICD? A: LVEF ≤35% (with optimal medical therapy for ≥3 months)

53. Q: What is the 4Hs and 4Ts mnemonic for reversible causes of cardiac arrest? A: Hypoxia, Hypovolaemia, Hypo/hyperkalaemia, Hypothermia; Thrombosis (coronary/pulmonary), Tamponade, Toxins, Tension pneumothorax

54. Q: What is the recommended approach to neuroprognostication after cardiac arrest? A: Multimodal assessment at ≥72 hours after return to normothermia (clinical, EEG, SSEP, imaging, biomarkers)

55. Q: Indigenous Australians have how much higher rate of ischaemic heart disease hospitalisation? A: 2-3 times higher than non-Indigenous Australians

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References

References

Key Citations (PMID format)

1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2018;138(13):e272-e391. PMID: 29084731

2. ANZCOR Guideline 11.2 - Management of Cardiac Arrest. 2021. Available: resus.org.au

3. Antzelevitch C, Burashnikov A. Overview of Basic Mechanisms of Cardiac Arrhythmia. Card Electrophysiol Clin. 2011;3(1):23-45. PMID: 21892379

4. Vereckei A, Duray G, Szénási G, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. 2008;5(1):89-98. PMID: 18082472

5. Eifling M, Razavi M, Massumi A. The evaluation and management of electrical storm. Tex Heart Inst J. 2011;38(2):111-121. PMID: 21494515

6. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of Torsade de Pointes in Hospital Settings. Circulation. 2010;121(8):1047-1060. PMID: 20185054

7. Brugada J, Campuzano O, Arbelo E, et al. Present Status of Brugada Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018;72(9):1046-1059. PMID: 30139433

8. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324(12):781-788. PMID: 1900101

9. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997;337(22):1576-1583. PMID: 9382893

10. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346(12):877-883. PMID: 11907286

11. Kraft MD, Btaiche IF, Sacks GS, Kudsk KA. Treatment of electrolyte disorders in adult patients in the intensive care unit. Am J Health Syst Pharm. 2005;62(16):1663-1682. PMID: 16085929

12. Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures. Circulation. 2006;114(23):2534-2570. PMID: 17130345

13. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2015;36(41):2793-2867. PMID: 26320108

14. Baman TS, Lange DC, Ilg KJ, et al. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm. 2010;7(7):865-869. PMID: 20348027

15. Reinelt P, Karth GD, Gerner C, et al. Incidence and type of cardiac arrhythmias in critically ill patients: a single center experience in a medical-cardiological ICU. Intensive Care Med. 2001;27(9):1466-1473. PMID: 11685338

16. Chan PS, McNally B, Tang F, Kellermann A; CARES Surveillance Group. Recent trends in survival from out-of-hospital cardiac arrest in the United States. Circulation. 2014;130(21):1876-1882. PMID: 25399396

17. Beck B, Bray J, Cameron P, et al. Regional variation in the characteristics, incidence and outcomes of out-of-hospital cardiac arrest in Australia and New Zealand. Resuscitation. 2018;126:49-57. PMID: 29470974

18. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998;98(21):2334-2351. PMID: 9826323

19. Wit AL, Janse MJ. Experimental models of ventricular tachycardia and fibrillation caused by ischemia and infarction. Circulation. 1992;85(1 Suppl):I32-42. PMID: 1728503

20. Jalife J. Ventricular fibrillation: mechanisms of initiation and maintenance. Annu Rev Physiol. 2000;62:25-50. PMID: 10845083

21. Weiss JN, Qu Z, Chen PS, et al. The dynamics of cardiac fibrillation. Circulation. 2005;112(8):1232-1240. PMID: 16116073

22. Henkel DM, Witt BJ, Gersh BJ, et al. Ventricular arrhythmias after acute myocardial infarction: a 20-year community study. Am Heart J. 2006;151(4):806-812. PMID: 16569539

23. Adabag AS, Therneau TM, Gersh BJ, et al. Sudden death after myocardial infarction. JAMA. 2008;300(17):2022-2029. PMID: 18984889

24. Schulman SP, Lakatta EG, Fleg JL, et al. Age-related decline in left ventricular filling at rest and exercise. Am J Physiol. 1992;263(6 Pt 2):H1932-8. PMID: 1481919

25. Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022. PMID: 14999113

26. Tisdale JE, Chung MK, Campbell KB, et al. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. Circulation. 2020;142(15):e214-e233. PMID: 32929996

27. Owens RC Jr, Nolin TD. Antimicrobial-associated QT interval prolongation: pointes of interest. Clin Infect Dis. 2006;43(12):1603-1611. PMID: 17109296

28. Beach SR, Celano CM, Noseworthy PA, et al. QTc prolongation, torsades de pointes, and psychotropic medications. Psychosomatics. 2013;54(1):1-13. PMID: 23295003

29. Hafermann MJ, Namdar R, Ginter D, et al. Effect of Intravenous Ondansetron on QT Interval Prolongation in Patients with Cardiovascular Disease and Additional Risk Factors for Torsades. Drug Saf. 2011;34(12):1201-1215. PMID: 22077506

30. Kao DP, Haigney MC, Mehler PS, Krantz MJ. Arrhythmia associated with buprenorphine and methadone reported to the Food and Drug Administration. Addiction. 2015;110(9):1468-1475. PMID: 25879534

31. Stevenson WG, Stevenson LW. Prevention of sudden death in heart failure. J Cardiovasc Electrophysiol. 2001;12(1):112-114. PMID: 11204075

32. Basso C, Corrado D, Marcus FI, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet. 2009;373(9671):1289-1300. PMID: 19362677

33. Schwartz PJ, Crotti L, Insolia R. Long-QT syndrome: from genetics to management. Circ Arrhythm Electrophysiol. 2012;5(4):868-877. PMID: 22895603

34. Antzelevitch C, Yan GX, Ackerman MJ, et al. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge. Heart Rhythm. 2016;13(10):e295-324. PMID: 27423412

35. Wlodarska EK, Wozniak O, Konka M, et al. Catecholaminergic Polymorphic Ventricular Tachycardia. Heart Fail Rev. 2021;26(3):559-566. PMID: 33237512

36. Chockalingam P, Crotti L, Girardengo G, et al. Not all beta-blockers are equal in the management of long QT syndrome types 1 and 2: higher recurrence of events under metoprolol. J Am Coll Cardiol. 2012;60(20):2092-2099. PMID: 23083782

37. Viskin S. Long QT syndromes and torsade de pointes. Lancet. 1999;354(9190):1625-1633. PMID: 10560690

38. Priori SG, Wilde AA, Horie M, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes. Heart Rhythm. 2013;10(12):1932-1963. PMID: 24011539

39. Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation. 1988;77(2):392-397. PMID: 3338130

40. Probst V, Veltmann C, Eckardt L, et al. Long-term prognosis of patients diagnosed with Brugada syndrome: Results from the FINGER Brugada Syndrome Registry. Circulation. 2010;121(5):635-643. PMID: 20100972

41. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference. Circulation. 2005;111(5):659-670. PMID: 15655131

42. Adler A, Topaz G, Heller K, et al. Fever-induced Brugada pattern: How common is it and what does it mean? Heart Rhythm. 2013;10(9):1375-1382. PMID: 23787371

43. Amin AS, Meregalli PG, Bardai A, et al. Fever increases the risk for cardiac arrest in the Brugada syndrome. Ann Intern Med. 2008;149(3):216-218. PMID: 18678859

44. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol. 1992;20(6):1391-1396. PMID: 1309182

45. Pedersen CT, Kay GN, Kalman J, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm. 2014;11(10):e166-196. PMID: 25179489

46. Stevenson WG. Ventricular scars and ventricular tachycardia. Trans Am Clin Climatol Assoc. 2009;120:403-412. PMID: 19768192

47. Sapp JL, Wells GA, Parkash R, et al. Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. N Engl J Med. 2016;375(2):111-121. PMID: 27149033

48. Santangeli P, Muser D, Maeda S, et al. Comparative effectiveness of antiarrhythmic drugs and catheter ablation for the prevention of recurrent ventricular tachycardia in patients with implantable cardioverter-defibrillators. Heart Rhythm. 2016;13(2):539-546. PMID: 26654920

49. Perkins GD, Graesner JT, Semeraro F, et al. European Resuscitation Council Guidelines 2021: Executive summary. Resuscitation. 2021;161:1-60. PMID: 33773824

50. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced Cardiovascular Life Support. Circulation. 2015;132(18 Suppl 2):S444-S464. PMID: 26472995

51. Soar J, Nolan JP, Böttiger BW, et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation. 2015;95:100-147. PMID: 26477410

52. Kerber RE. Transthoracic cardioversion of atrial fibrillation and flutter: standard techniques and new advances. Am J Cardiol. 1996;78(8A):22-26. PMID: 8903272

53. Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation care. Resuscitation. 2021;161:220-269. PMID: 33773827

54. Dankiewicz J, Cronberg T, Lilja G, et al. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med. 2021;384(24):2283-2294. PMID: 34133859

55. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197-2206. PMID: 24237006

56. Vaughan Williams EM. A classification of antiarrhythmic actions reassessed after a decade of new drugs. J Clin Pharmacol. 1984;24(4):129-147. PMID: 6144698

57. Nattel S, Singh BN. Evolution, mechanisms, and classification of antiarrhythmic drugs: focus on class III actions. Am J Cardiol. 1999;84(9A):11R-19R. PMID: 10568856

58. Vassallo P, Trohman RG. Prescribing amiodarone: an evidence-based review of clinical indications. JAMA. 2007;298(11):1312-1322. PMID: 17878423

59. Goldschlager N, Epstein AE, Naccarelli GV, et al. A practical guide for clinicians who treat patients with amiodarone: 2007. Heart Rhythm. 2007;4(9):1250-1259. PMID: 17765631

60. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2016;374(18):1711-1722. PMID: 27043165

61. Dorian P, Cass D, Schwartz B, et al. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346(12):884-890. PMID: 11907287

62. Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol. 2002;90(8):853-859. PMID: 12372572

63. Gorgels AP, van den Dool A, Hofs A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol. 1996;78(1):43-46. PMID: 8712117

64. Ortiz M, Martín A, Arribas F, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017;38(17):1329-1335. PMID: 28405017

65. Exner DV, Reiffel JA, Epstein AE, et al. Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic ventricular tachycardia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial. J Am Coll Cardiol. 1999;34(2):325-333. PMID: 10440141

66. Nademanee K, Taylor R, Bailey WE, et al. Treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000;102(7):742-747. PMID: 10942741

67. Conti S, Pala S, Biagioli V, et al. Electrical storm: A clinical and electrophysiological overview. World J Cardiol. 2015;7(9):555-561. PMID: 26413230

68. Sesselberg HW, Moss AJ, McNitt S, et al. Ventricular arrhythmia storms in postinfarction patients with implantable defibrillators for primary prevention indications: a MADIT-II substudy. Heart Rhythm. 2007;4(11):1395-1402. PMID: 17954396

69. Gao D, Sapp JL. Electrical storm: definitions, clinical importance, and treatment. Curr Opin Cardiol. 2013;28(1):72-79. PMID: 23196774

70. Pedersen CT, Kay GN, Kalman J, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Europace. 2014;16(9):1257-1283. PMID: 25172618

71. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators: short- and long-term outcomes in a prospective single-center study. Circulation. 2008;117(4):462-469. PMID: 18172038

72. Ajijola OA, Lellouche N, Bourke T, et al. Bilateral cardiac sympathetic denervation for the management of electrical storm. J Am Coll Cardiol. 2012;59(1):91-92. PMID: 22192676

73. Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. J Am Coll Cardiol. 2013;61(3):e6-75. PMID: 23265327

74. Patel B, Guzman JA. Implantable cardioverter-defibrillator therapy for shock-refractory ventricular tachycardia/ventricular fibrillation. Crit Care Med. 2016;44(8):1619-1624. PMID: 27065079

75. Moss AJ, Schuger C, Beck CA, et al. Reduction in inappropriate therapy and mortality through ICD programming. N Engl J Med. 2012;367(24):2275-2283. PMID: 23131066

76. Swerdlow CD. Implantable cardioverter defibrillator shocks: a troubleshooting guide. Rev Cardiovasc Med. 2006;7(2):61-70. PMID: 16845455

77. Jacob S, Panaich SS, Maheshwari R, et al. Clinical applications of magnets on cardiac rhythm management devices. Europace. 2011;13(9):1222-1230. PMID: 21511793

78. Lampert R, Hayes DL, Annas GJ, et al. HRS Expert Consensus Statement on the Management of Cardiovascular Implantable Electronic Devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm. 2010;7(7):1008-1026. PMID: 20471915

79. Padeletti L, Arnar DO, Boncinelli L, et al. EHRA Expert Consensus Statement on the management of cardiovascular implantable electronic devices in patients nearing end of life or requesting withdrawal of therapy. Europace. 2010;12(10):1480-1489. PMID: 20675674

80. Crop MJ, Hoorn EJ, Lindemans J, Zietse R. Hypokalaemia and subsequent hyperkalaemia in hospitalized patients. Nephrol Dial Transplant. 2007;22(12):3471-3477. PMID: 17890253

81. Ahmed A, Zannad F, Love TE, et al. A propensity-matched study of the association of low serum potassium levels and mortality in chronic heart failure. Eur Heart J. 2007;28(11):1334-1343. PMID: 17449877

82. Reinhart RA, Desbiens NA. Hypomagnesemia in patients entering the ICU. Crit Care Med. 1985;13(6):506-507. PMID: 3995996

83. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. 2005;20(1):3-17. PMID: 15665255

84. Oster JR, Epstein M. Management of magnesium depletion. Am J Nephrol. 1988;8(5):349-354. PMID: 3223958

85. Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659. PMID: 2022022

86. Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579-585. PMID: 11602560

87. Gardiner FW, Bishop L, Gale L, et al. Rural and remote cardiac rehabilitation: A systematic review. Aust J Rural Health. 2016;24(3):156-163. PMID: 27334379

88. Ting HH, Rihal CS, Gersh BJ, et al. Regional systems of care to optimize timeliness of reperfusion therapy for ST-elevation myocardial infarction: the Mayo Clinic STEMI Protocol. Circulation. 2007;116(7):729-736. PMID: 17673459

89. Brown A, O'Shea RL, Mott K, et al. A strategy for translating evidence into policy and practice to close the gap--developing national research priorities to address cardiovascular disease in Aboriginal and Torres Strait Islander peoples. Heart Lung Circ. 2010;19(8):431-438. PMID: 20605760

90. Katzenellenbogen JM, Sanfilippo FM, Hobbs MS, et al. Aboriginal to non-Aboriginal differentials in 2-year outcomes following non-fatal first-ever acute MI persist after morbidity and treatment. Heart Lung Circ. 2012;21(5):295-302. PMID: 22153685

91. Tham EB, Yeung AC, Seto AH, et al. Disparities in Cardiovascular Disease and Stroke in Asian-Americans. Curr Cardiol Rep. 2020;22(4):21. PMID: 32030485

92. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225-237. PMID: 15659722

93. Waldo AL, Camm AJ, deRuyter H, et al. Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol. Lancet. 1996;348(9019):7-12. PMID: 8691967

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