Ventricular tachycardia

Overview and definitions

VT is defined by where the rhythm starts and how fast it runs: at least 3 consecutive ventricular beats faster than 100 b.p.m., arising independently of atrial and AV nodal conduction. Its ESC subtypes are defined by duration (or the need for an intervention to terminate it), QRS morphology and, for TdP, QT prolongation; the table below also gives the ESC definitions of VF, electrical storm and incessant VT.^[1]

^{[1] [1]}

Epidemiology and risk factors

^[1]

Sudden cardiac death (SCD) accounts for approximately 50% of all cardiovascular deaths, and up to 50% of these are the first manifestation of cardiac disease. The incidence rises markedly with age. It is very low in infancy and childhood (1 per 100 000 person-years), approximately 50 per 100 000 person-years in the fifth to sixth decades, and at least 200 per 100 000 person-years in the eighth decade. At any age, males have higher SCD rates than females, even after adjustment for CAD risk factors.^[1]

Cardiac diseases associated with SCD vary with the individual's age. In the young, primary electrical diseases and cardiomyopathies predominate, as do myocarditis and coronary anomalies. In older populations, chronic structural diseases predominate, while potentially inherited electrical diseases or structural non-ischaemic diseases may cause more than 50% of SCD under the age of 50 years.^[1]

Pathophysiology

The majority of patients presenting with SMVT have underlying structural heart disease (SHD). In SHD, SMVT is mainly due to scar-related re-entry and only occasionally due to re-entry involving a diseased conduction system or due to focal sources. The critical part of a re-entrant circuit, the 'protected VT isthmus', is the primary target for ablation.^[1]

Where the circuit sits depends on the disease. Post-infarct VTs are mainly related to an endocardial circuit, whereas circuit location is more variable in cardiomyopathies, where intramural and/or epicardial involvement is more common. The ESC states that this significantly contributes to better ablation outcomes in CAD than in non-ischaemic aetiologies.^[1]

^[1]

Idiopathic VT is the other half of the story. The term covers VTs that are not associated with SHD or a genetic arrhythmic syndrome. Most are mediated by triggered activity, but a re-entrant mechanism involving the LV Purkinje network explains verapamil-sensitive fascicular VT. Intravenous adenosine may terminate specific VT subtypes, and such a response supports cyclic AMP-mediated triggered activity as an underlying mechanism.^[1]

^[1]

Bundle branch re-entrant VT (BBR-VT) resembles a BBB configuration on the ECG and is a feature of conduction impairment, e.g. in dilated cardiomyopathy (DCM), myotonic dystrophy and after cardiac valve surgery. Catheter ablation of BBR-VT has been very successful since the early 1990s and is considered first-line therapy.^[1]

Triggers matter because some are reversible. Electrolyte imbalances such as hypokalaemia may trigger VA. Bradycardia, ischaemia, coronary spasm, thrombosis, fever, acute starvation and dieting may also contribute. Reversible causes may account for up to 50% of sudden cardiac arrest (SCA).^[1]

Clinical presentation

The first question is whether the tachycardia is haemodynamically tolerated. The ESC says patients presenting with SMVT should be treated according to symptoms and aetiology, and haemodynamic instability requires immediate synchronised cardioversion. Even when SMVT is tolerated, prompt termination is recommended, as rapid haemodynamic deterioration may occur.^[1]

The history should focus on red flags, including features of arrhythmic syncope (e.g. absence of a vagal prodrome) and a family history of premature or sudden cardiac death. Drowning or a car accident in the family can point to long QT syndrome (LQTS) or CPVT. Subtler inherited clues include a family history of epilepsy, sudden infant death syndrome, deafness (LQTS), heart failure, or pacemaker implantation at under 50 years old.^[1]

Examination features of pro-arrhythmic conditions include a mid-systolic click in mitral valve prolapse and outflow tract murmurs with Valsalva in hypertrophic cardiomyopathy (HCM). Arrhythmic syncope is syncope that remains unexplained after conventional work-up but is highly suspicious for intermittent bradycardia, rapid SVT or VA.^[1]

Electrical storm can range from recurrent asymptomatic VT episodes terminated by anti-tachycardia pacing (ATP) to life-threatening electrical instability with VA recurring frequently after multiple shocks. Patients who experience it are prone to psychological disorders, heart failure decompensation and increased mortality.^[1]

Differential diagnosis: the wide QRS tachycardia

Wide QRS tachycardias can be VT, SVT conducting with BBB aberration, or antegrade conduction over an accessory pathway (AP), with reported proportions of 80, 15 and 5%. Misdiagnosis and administration of drugs usually used for SVT can be harmful for patients in VT. The 2019 ESC SVT guideline therefore states that the default diagnosis should be VT until proven otherwise.^[2]

The 2019 ESC SVT guideline says the differential diagnosis includes:^[2]

1. SVT with BBB, from pre-existing BBB or aberrancy developing during tachycardia (phase 3 block), more commonly, although not invariably, a right BBB (RBBB) pattern.
2. SVT with antegrade conduction over an AP ('pre-excited SVT'), as part of the circuit (antidromic AV re-entrant tachycardia [AVRT]) or as a bystander during AF, focal atrial tachycardia/atrial flutter, or AV nodal re-entrant tachycardia.
3. SVT with QRS widening induced by drugs or electrolyte disturbances; class IA, IC and III drugs can result in atypical BBB morphologies that mimic VT.
4. Pacemaker-related endless loop tachycardia and artefacts, which can also mimic VT.

^[2]

The differential diagnosis of an irregular wide QRS tachycardia is either pre-excited AF or polymorphic VT, or atrial tachycardia with variable block in the context of aberrancy. Pre-excited AF shows irregularity, a varying QRS morphology and a rapid ventricular rate.^[2] The 2022 ESC guideline describes it as the 'FBI' (fast, broad, irregular) pattern, which may mimic VT; intravenous drugs that slow AV conduction, such as adenosine, beta-blockers and amiodarone, should be avoided.^[1]

Bedside assessment: reading the ECG

Record any haemodynamically tolerated wide QRS tachycardia on a 12-lead ECG.^[1] If a sinus-rhythm ECG is available and the QRS morphology is identical in sinus rhythm and tachycardia, the arrhythmia is most likely not VT, although BBR-VT and high septal VTs exiting close to the conduction system can have a morphology similar to sinus rhythm. A contralateral BBB pattern in sinus rhythm is more indicative of VT.^[2]

AV dissociation or capture/fusion beats during tachycardia are key diagnostic features of VT. AV dissociation may be difficult to recognise because P waves are often hidden by the wide QRS and T waves; they are usually more prominent in the inferior leads and with a modified chest lead (Lewis lead). Ventriculoatrial conduction can be found in up to 50% of patients with VT and a 1:1 relationship is possible, but most VTs have more QRS complexes than P waves.^[2]

^[2]

Three further clues come from the same guideline. A QRS duration above 140 ms with RBBB or above 160 ms with LBBB suggests VT, but these criteria do not help separate VT from SVT in some settings, such as pre-excited SVT or when class IC or IA drugs are given. In SVT with aberrancy the axis is confined between −60 and +120°, and extreme axis deviation (−90 to ±180°) is strongly indicative of VT.^[2]

Negative chest lead concordance is almost diagnostic of VT, with a specificity above 90%, but is present in only 20% of VTs. Positive concordance can indicate VT or an antidromic tachycardia using a left posterior or left lateral AP.^[2]

Named algorithms

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Know the limits. Independent studies found that ECG-based methods have specificities of 40–80% and accuracies of about 75%, and a similar accuracy would be achieved by calling every wide QRS tachycardia VT, because only 25–30% are SVTs. Conditions such as BBR-VT, fascicular VT, VT exiting close to the His–Purkinje system and tachycardia during AAD treatment are difficult to diagnose with morphological criteria.^[2]

Investigations

^[1]

For a first episode of SMVT, initial evaluation includes a comprehensive clinical and family history, 12-lead ECG and echocardiography, and recording the 12-lead VT ECG is indicated because it gives important information on the site of origin. Specific VT morphologies (e.g. RVOT or fascicular origin), without a family history of cardiomyopathy or evidence of SHD, suggest idiopathic VT. Atypical ECG morphologies and uncommon presentations should raise suspicion of SHD even with a normal ECG and echo, and CMR should then be considered.^[1]

If initial evaluation raises suspicion of CAD, coronary angiography can exclude significant CAD; if ECG and echo suggest cardiomyopathy, CMR gives information on scar distribution and tissue characteristics. When non-invasive evaluation is inconclusive, electroanatomical mapping and programmed electrical stimulation (PES) may be considered to separate idiopathic VT from early arrhythmogenic right ventricular cardiomyopathy (ARVC). In suspected inflammatory disease, PET-CT, autoimmune serology and biopsies of affected tissue are part of the evaluation.^[1]

In a patient presenting with a first SMVT episode, electrophysiological study, electroanatomical mapping and mapping-guided biopsies may be considered for aetiological evaluation (ESC Class IIb, level C). A negative imaging study supports primary electrical disease in a patient with VA. There is not sufficient evidence to use B-type natriuretic peptide to select the need for an ICD.^[1]

Ambulatory monitoring should match how often events happen. Monitoring over 24–48 h (typically Holter recording) suits daily arrhythmias, intermittent longer monitoring should be preferred for infrequent events, and implantable loop recorders can help when symptoms are potentially life-threatening, such as unexplained syncope.^[1]

Reversible causes

^[1]

Suspect a drug cause in patients on agents that alter cardiac electrical properties (e.g. QRS and/or QT prolongation) or cause electrolyte abnormalities (e.g. thiazide and loop diuretics). In a large observational study of SCA survivors with a reversible and correctable cause, subsequent ICD implantation was associated with lower all-cause mortality, except for arrest occurring with acute myocardial infarction (MI).^[1]

After resuscitated cardiac arrest

^[1]

Management: acute termination

^{[1] [3]}

Haemodynamically not tolerated

DC cardioversion is the ESC first-line treatment for patients with haemodynamically not-tolerated SMVT (Class I, level B). Patients presenting with haemodynamic instability need immediate synchronised cardioversion, and an unsynchronised shock should be used if synchronisation is not possible. Cardioversion is not indicated for repetitive runs of NSVT.^[1]

Haemodynamically tolerated

Termination can be achieved with electrical cardioversion, AADs or pacing techniques. All AADs may lead to hypotension, but the individual risk of the anaesthesia or sedation needed for cardioversion must also be considered.^[1]

^[1]

Adenosine or vagal manoeuvres, with continuous 12-lead ECG recording, should be considered if SVT is likely. For drug termination of a tolerated VT of unknown aetiology, intravenous procainamide or amiodarone can be used. Intravenous procainamide should not be used in patients with severe heart failure, acute MI or end-stage renal disease.^[1]

Availability shapes the choice: procainamide is not available in many European countries. Ajmaline, sotalol and flecainide may be considered in patients without significant heart disease, but the risk of adverse events should be carefully weighed. In patients with an ICD, manual overdrive pacing may terminate VTs with a cycle length under the programmed detection rate.^[1]

^{[4] [1]}

In PROCAMIO, adverse events in the following 24 h occurred in 18% with procainamide and 31% with amiodarone (OR 0.49; P=0.24). Among the 49 patients with structural heart disease, the primary endpoint was less common with procainamide (11% vs 43%; OR 0.17).^[4]

Intravenous drug doses (ESC 2022 Table 8)

ESC Table 8 gives the intravenous dose in brackets after the oral daily dose. The doses below are selected intravenous regimens (landiolol and isoproterenol are given under electrical storm and torsades de pointes); check each against the contraindications column.^[1]

^[1]

For drugs marked with QT prolongation in Table 8, take precautions with concomitant QT-prolonging conditions or drugs, and stop the drug if the QTc exceeds 500 ms. For sotalol, the pro-arrhythmic side effects require a strong indication in patients without an ICD.^[1]

Torsades de pointes

Hypomagnesaemia and/or hypokalaemia may be associated with TdP, and intravenous magnesium is effective even in the absence of hypomagnesaemia. When drug-induced arrhythmia is presumed, the offending drug is withdrawn and QT-prolonging substances (e.g. sotalol) are avoided. In refractory recurrent TdP with acquired long QT, raising the heart rate with isoproterenol (isoprenaline) or transvenous pacing can suppress the arrhythmia.^[1]

The two ESC TdP rows sit in Recommendation Table 9 under the heading "Management of electrical storm".^[1]

• Intravenous magnesium with supplementation of potassium is recommended in patients with TdP (Class I, level C).^[1]
• Isoproterenol or transvenous pacing to increase heart rate is recommended in acquired LQT syndrome with recurrent TdP despite correction of precipitating conditions and magnesium (Class I, level C).^[1]
• ESC Table 8 gives isoproterenol 0.5–10 µg/min intravenously, listing TdP and acquired LQTS among its indications; the same row lists ACS and LQTS as contraindications.^[1]

Electrical storm and incessant VT

The ESC text defines electrical storm as 3 or more episodes of sustained VA within 24 h requiring ATP or cardioversion/defibrillation, with each event separated by at least 5 min. The most common arrhythmia underlying storm is SMVT associated with SHD that is amenable to catheter ablation.^[1]

^[1]

In case of haemodynamic instability at initial evaluation, advanced life support is recommended. Management is often multifaceted: ICD reprogramming when appropriate, AAD therapy, sedation, catheter ablation, autonomic modulation and mechanical circulatory support. For inappropriate ICD shocks (e.g. due to SVT or lead defects) or unnecessary ICD therapy (e.g. for NSVT), disabling of ICD therapies is recommended. If an electrophysiology specialist or programmer is not available, the ICD can be disabled by placing a magnet over the device.^[1]

For patients with recurrent ICD shocks, sedation is indicated to alleviate psychological distress and decrease pro-arrhythmogenic sympathetic tone. In electrical storm, initial treatment with beta-blockers, preferably non-selective such as propranolol (superior to metoprolol in one study), combined with amiodarone is most commonly used. In recurrent haemodynamically not-tolerated VT resistant to amiodarone, landiolol was effective for arrhythmia suppression in two smaller studies. ESC Table 8 gives intravenous landiolol (no oral use) as a 100 µg/kg bolus in 1 min, then an infusion of 10–40 µg/kg/min (maximum 80 µg/kg/min; maximum 24 h total dose 57.6 mg/kg/day), with limited experience beyond 24 h.^[1]

Successful ablation was associated with a significant reduction in VT and storm recurrence and improved long-term survival in retrospective analyses. In incessant slow monomorphic VT, ablation is preferred over AAD therapy, which may only further slow the VT. Overdrive pacing at a slightly higher rate than the baseline rhythm can temporarily suppress slow recurrent or incessant VT. Rescue mechanical circulatory support during ablation was associated with a high mortality rate.^[1]

VT and VF in acute coronary syndromes

Electrical cardioversion or defibrillation is the intervention of choice to terminate VA acutely in ACS. Recurrent sustained VT, especially when polymorphic, or recurrent VF can indicate incomplete reperfusion or recurrence of acute ischaemia, and immediate coronary angiography is then indicated. For VA in the context of relative bradycardia or pauses, pacing may prevent re-initiation.^[1]

^[1]

Management: long-term

Drugs

Optimal medical treatment including ACE-I/ARB/ARNI, MRA, beta-blockers and SGLT2 inhibitors is indicated in all heart failure patients with reduced EF (ESC Class I, level A). AADs have an important role as adjunctive therapy, especially in symptomatic patients, but no AAD except beta-blockers has shown a reduction in all-cause mortality. Each drug has significant potential for adverse events, including pro-arrhythmia.^[1]

In SHD, the choice of anti-arrhythmic agents is mostly limited to beta-blockers, sotalol and amiodarone to help control VT/VF recurrences, and this treatment is frequently hampered by side effects. In chronic CAD, the ESC says frequent, symptomatic VT in ICD recipients should be treated medically with either amiodarone or sotalol. The amiodarone row of ESC Table 8 lists bradycardia and (infrequent) TdP as cardiac side effects, and photosensitivity, corneal deposits, hypothyroidism, hyperthyroidism, pulmonary toxicity, hepatotoxicity, polyneuropathy and skin discoloration as extracardiac side effects.^[1]

The ICD

ICDs do not prevent VA, and many patients have symptomatic VT/VF recurrences with syncope or ICD shocks that may need additional treatment.^[1]

^[1]

Recommendation Table 12 covers general secondary prevention; the ESC directs readers to its Section 7 for primary prevention and specific aspects of secondary prevention.^[1]

^[5]

A patient-level meta-analysis of AVID, CASH and CIDS showed an ICD-versus-amiodarone hazard ratio of 0.72 for death from any cause and 0.50 for arrhythmic death. Survival was extended by a mean of 4.4 months over 6 years of follow-up. Patients with LVEF of 35% or less derived significantly more benefit than those with better preserved LV function.^[6] The ESC adds that around 80% of these trial patients had CAD, that patients with well-tolerated SMVT were excluded, and that the trials failed to show a survival benefit with an LVEF of 35% or more.^[1]

Primary prevention ICD by substrate

^[1]

Forty days after STEMI, approximately 5% of patients have an LVEF ≤35%. Early revascularisation and modern heart failure medication have reduced the overall risk of SCD in heart failure patients. Although total mortality has fallen, the ESC states that the relative reduction by the ICD is a consistent 27%, corroborated in the EU-CERT-ICD and SwedeHF registries. There are no data supporting a primary prophylactic ICD in post-infarct patients with preserved or mildly reduced LVEF.^[1]

^{[7] [8] [9]}

Catheter ablation in structural heart disease

^{[1] [1]}

Before ablation, collect all available information about the arrhythmogenic substrate, especially to identify scar (using CMR or CT), and 12-lead ECG documentation of the clinical VTs or of the PVCs that induce PVT/VF to help determine the VA exit site. In post-MI patients with haemodynamically tolerated SMVT and preserved or mildly reduced EF, the ESC notes that SMVT is rarely caused by ischaemia and revascularisation alone does not prevent VT recurrence, but excluding or treating significant CAD before ablation is reasonable. Mean long-term ablation success is 30–70%, depending on the underlying SHD, and stroke, cardiac tamponade or death may occur.^[1]

^{[10] [1] [11] [1]}

In VANISH2, adverse events within 30 days of ablation included 2 deaths (1.0%) and nonfatal events in 23 patients (11.3%); in the drug arm, 1 death from pulmonary toxic effects (0.5%) and nonfatal events in 46 patients (21.6%) were attributed to AADs.^[11]

^{[14] [15] [12] [13]}

The ESC summarises that three randomised trials in CAD found ablation, compared with conventional treatment, decreases the likelihood of subsequent ICD shocks and prevents recurrent VT episodes. Preventive ablation after a first SMVT followed by an ICD reduced neither mortality nor hospitalisations for arrhythmia or worsening heart failure, compared with ablation deferred until after the third ICD shock. Even so, when an ICD is indicated after a first VT, ablation immediately before or shortly after implantation may be considered to decrease subsequent VT and shocks.^[1]

Idiopathic VT and PVC-induced cardiomyopathy

PVCs/VT in patients without SHD are defined as idiopathic; in presumed idiopathic PVCs/VT with a negative history and normal examination, 12-lead ECG and transthoracic echocardiography are important first diagnostic steps to exclude underlying SHD. Patients need treatment when the PVCs/VT are symptomatic or associated with deterioration of cardiac function. When drug therapy is used, beta-blockers and calcium channel blockers are the most-studied drugs, and a calcium channel blocker should be the drug of choice for fascicular PVC/VT; catheter ablation remains the first-line treatment for symptomatic RVOT and left fascicular VT/PVCs (table below).^[1]

^[1]

A PVC burden of 10% seems to be the minimal threshold for LV dysfunction, with higher risk above 20%. Only a minority of patients with more than 1000 PVCs per day develop ventricular dysfunction after 5 years. Amiodarone is associated with severe systemic toxicity and should be used only if ablation or other drugs fail or cannot be used. In a randomised study of RVOT PVCs, ablation was superior to AAD therapy for arrhythmia suppression with no difference in complications.^[1]

PVC-induced cardiomyopathy is a secondary and reversible cause of LV dysfunction in patients without SHD, and PVC burden is its strongest independent predictor in several studies. In patients with frequent PVCs, factors predicting adverse LV remodelling include superior PVC axis, epicardial origin, NSVT, shorter coupling interval and male gender. LGE suggests SHD with frequent PVCs rather than PVC-induced cardiomyopathy, in which LGE is mostly absent. PVC-induced (versus PVC-aggravated) cardiomyopathy can be confirmed only after LVEF improvement or normalisation following suppression of the PVCs.^[1]

^[1]

Catheter ablation of the PVCs has reported success rates of 75–90% and is considered first-line treatment for PVC-induced cardiomyopathy.^[1]

Specific subtypes and scenarios

Dilated cardiomyopathy. DCM is characterised by LV dilatation and systolic dysfunction unexplained by CAD or abnormal loading conditions. SCD occurs in up to 12% of patients with DCM and accounts for 25–35% of all deaths. CMR with LGE should be considered in DCM/HNDCM for aetiology and VA/SCD risk (ESC Class IIa, level B).^[1]

Bundle branch re-entry. BBR-VT resembles BBB on the ECG, occurs with conduction impairment (e.g. DCM, myotonic dystrophy, after valve surgery), and its catheter ablation is considered first-line therapy.^[1]

Channelopathy pointers. These rows are examples from the ESC disease-specific tables; see the dedicated topics for full management.^[1]

• LQTS: beta-blockers, ideally non-selective (nadolol or propranolol), are recommended in patients with documented QT prolongation, to reduce the risk of arrhythmic events (Class I, level B). An ICD in addition to beta-blockers is recommended in LQTS patients with cardiac arrest (Class I, level B).^[1]
• Brugada syndrome: an ICD is recommended in survivors of an aborted cardiac arrest and/or those with documented spontaneous sustained VT (Class I, level C).^[1]
• CPVT: diagnosed with a structurally normal heart, normal ECG and exercise- or emotion-induced bidirectional VT or PVT (Class I, level C); beta-blockers, ideally non-selective (nadolol or propranolol), are recommended in all patients with a clinical diagnosis of CPVT (Class I, level C).^[1]

Complications and pitfalls

• Giving SVT drugs to VT: misdiagnosis and administration of drugs usually used for SVT can harm patients in VT.^[2]
• Intravenous verapamil in broad QRS tachycardia of unknown mechanism: ESC Class III, level B.^[1]
• Intravenous drugs that slow AV conduction (e.g. adenosine, beta-blockers, amiodarone) in pre-excited AF: avoid.^[1]
• Intravenous procainamide in severe heart failure, acute MI or end-stage renal disease: should not be used.^[1]
• Implanting an ICD in incessant VA before it is controlled: ESC Class III, level C.^[1]
• Ablation complications: stroke, cardiac tamponade or death may occur.^[1]
• Rescue mechanical circulatory support during ablation in electrical storm: associated with a high mortality rate.^[1]

Prognosis and disposition

Early VA, defined as VT/VF within 48 h of STEMI, almost all occur within the first 24 h in the PCI era. They have been associated with an up to six-fold increase in in-hospital mortality, whereas long-term prognosis seems not to be significantly affected. Early monomorphic VT, by contrast, was associated with more ICD interventions than early VF and independently predicted death during long-term follow-up.^[1]

Haemodynamic instability, cardiogenic shock, LVEF under 40% and the sum of ST-segment deviations in all leads independently predict VA in both STEMI and non-STEMI. Patients who experience an electrical storm are prone to psychological disorders, heart failure decompensation and increased mortality. Idiopathic VTs have a benign prognosis.^[1]

A comprehensive evaluation of patients presenting with SMVT is mandatory if the underlying cardiac disease is unknown or disease progression is suspected.^[1]

Special populations

^[1]

Children. Catheter ablation of idiopathic VT/PVCs is not recommended in children under 5 years of age or under 10 kg, except when previous medical therapy fails or the VT is not haemodynamically tolerated (ESC Class III, level C). Verapamil is not recommended in children under 1 year of age with PVC/VT, particularly with signs of heart failure or concurrent use of other AADs (Class III, level C).^[1]

Older patients. In elderly patients in whom no benefit from the defibrillator is expected because of age and comorbidities, omission of a primary prevention ICD may be considered (ESC Class IIb, level B).^[1]

Evidence, guidelines and regional differences

This topic follows the 2022 ESC ventricular arrhythmia guideline for European recommendations.^[1] No North American ventricular arrhythmia guideline text was available to this build, so no ACC/AHA/HRS class or level is stated. VANISH2 (N Engl J Med 2025) post-dates the ESC guideline, which listed it as ongoing.^[11][1]

In Australia and New Zealand

The Australian and New Zealand Committee on Resuscitation (ANZCOR) Guideline 11.9, Managing Acute Dysrhythmias, gives the following acute approach.^[3]

• Adverse features that suggest a need for immediate treatment: systolic BP under 90 mmHg, heart rate over 150/min, chest pain, heart failure, or drowsiness or confusion.^[3]
• A pulseless patient with a tachyarrhythmia is managed with the cardiac arrest algorithm (ANZCOR Guideline 11.2).^[3]
• In the peri-arrest setting, if unstable and deteriorating with adverse features caused by the tachyarrhythmia: immediate synchronised cardioversion, with sedation as required. If unsuccessful, give amiodarone 300 mg intravenously over 10–20 min, repeat cardioversion, then infuse amiodarone 900 mg over 24 h.^[3]
• Without adverse features, decide whether the QRS is narrow or broad (0.12 s or longer); in the peri-arrest setting, assume broad-complex tachycardia is ventricular, because treating SVT as VT is less likely to lead to deterioration than treating VT as SVT.^[3]
• Regular broad-complex tachycardia without adverse features: amiodarone 300 mg intravenously over 20–60 min, then an infusion of 900 mg over 24 h; monitor, seek expert help, and be ready to cardiovert if adverse signs develop or the arrhythmia persists for several hours.^[3]
• ANZCOR summary recommendations: presume a wide-QRS tachycardia is VT if the diagnosis is unclear; DC cardioversion with appropriate sedation at any point for suspected sustained monomorphic VT with haemodynamic compromise.^[3]
• Intravenous lignocaine is reasonable for the initial treatment of stable sustained monomorphic VT specifically associated with acute myocardial ischaemia or infarction. Calcium channel blockers such as verapamil and diltiazem should not be used to terminate wide-QRS tachycardia of unknown origin, especially with a history of myocardial dysfunction.^[3]
• Torsades: stop all QT-prolonging drugs and correct electrolyte abnormalities (especially hypokalaemia) and other causes (e.g. ischaemia). Give a 5 mmol bolus of magnesium intravenously over 10 min, which may be repeated once, followed by an infusion of 20 mmol over four hours. ANZCOR advises avoiding amiodarone in torsades, as it can make the situation worse.^[3]

The two documents frame the stable patient differently. For regular broad-complex tachycardia without adverse features, ANZCOR advises amiodarone, with cardioversion if adverse signs develop or the arrhythmia persists for several hours.^[3] ESC 2022 recommends DC cardioversion as first-line treatment for tolerated SMVT provided that the anaesthetic/sedation risk is low (Class I, level C).^[1]

High-yield summary

• Definitions: VT is 3 or more consecutive beats above 100 b.p.m. originating from the ventricles, independent from atrial and AV nodal conduction; NSVT persists for 3 beats to 30 s; sustained VT continues for at least 30 s or requires an intervention for termination.^[1]
• Wide QRS tachycardia: reported proportions VT 80%, SVT with BBB aberration 15%, antegrade AP conduction 5%; the default diagnosis should be VT until proven otherwise.^[2]
• ECG clues: AV dissociation, capture/fusion beats, negative concordance (specificity above 90%), extreme axis, initial R in aVR.^[2]
• Acute ESC rows: DC cardioversion first-line for haemodynamically not-tolerated SMVT, I B, and for tolerated SMVT provided that the anaesthetic/sedation risk is low, I C; IV procainamide for haemodynamically tolerated SMVT with known or suspected SHD, IIa B; IV amiodarone for haemodynamically tolerated SMVT in the absence of an established diagnosis, IIb B; IV verapamil not recommended in broad QRS tachycardia of unknown mechanism, III B.^[1]
• TdP: intravenous magnesium with supplementation of potassium in patients with TdP, Class I, level C (Recommendation Table 9, electrical storm group).^[1]
• Storm: mild to moderate sedation in electrical storm, to alleviate psychological distress and reduce sympathetic tone, I C; beta-blocker (non-selective preferred) plus intravenous amiodarone in SHD and electrical storm, unless contraindicated, I B; catheter ablation for incessant VT or electrical storm due to SMVT refractory to AADs, I B.^[1]
• ICD: documented VF or haemodynamically not-tolerated VT in the absence of reversible causes, I A; CAD with symptomatic heart failure (NYHA II–III) and LVEF ≤35% despite 3 months or more of OMT, I A; DCM/HNDCM with symptomatic heart failure (NYHA II–III) and LVEF ≤35% after 3 months or more of OMT, IIa A.^[1]
• Ablation: recommended in preference to escalating AADs in CAD with recurrent, symptomatic SMVT, or ICD shocks for SMVT, despite chronic amiodarone therapy (I B); first-line for symptomatic idiopathic VT/PVCs from the RVOT or the left fascicles (I B; level C for the left fascicles).^[1]

References17ShowHide

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2. [2]Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J, 2020.PMID 31504425
3. [3]Australian and New Zealand Committee on Resuscitation Guideline 11.9 – Managing Acute Dysrhythmias ANZCOR, 2026.Source
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6. [6]Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg . Canadian Implantable Defibrillator Study. Eur Heart J, 2000.PMID 11102258
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8. [8]Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med, 2005.PMID 15659722
9. [9]Køber L, Thune JJ, Nielsen JC, et al. Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure. N Engl J Med, 2016.PMID 27571011
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