VT / VF

See Cardiac Implantable Electronic Devices for ICD indications, Cardiac Arrest for the acute management of VF/pulseless VT, and Prolonged QT / Torsades de Pointes for polymorphic VT on a long QT.

Definitions

Ventricular tachycardia is a wide-complex tachycardia of three or more consecutive beats above 100/min, arising below the AV bundle. Monomorphic VT comes from a single focus and has uniform QRS complexes; polymorphic VT has QRS complexes of varying shape and duration.

• Non-sustained VT: 3 or more beats, lasting under 30 seconds.
• Sustained VT: longer than 30 seconds, or terminated earlier by intervention.
• VT storm: 3 or more sustained episodes in 24 hours needing intervention.
• Ventricular fibrillation: disorganised ventricular activity with no coordinated contraction and no cardiac output.

Causes

Most VT occurs on a background of structural heart disease, from myocardial scar or fibrosis. Reentry around scar is the usual mechanism, which is why VT in this setting is typically monomorphic and reproducible.

• Ischaemic scar from prior myocardial infarction — the commonest substrate.
• Non-ischaemic cardiomyopathy, hypertension, prior cardiac surgery.
• Acute ischaemia, hypoxia, sepsis.

Around 10% of VT occurs with no structural heart disease at all. In this group think idiopathic outflow tract VT and inherited channelopathies.

• Idiopathic outflow tract VT is the commonest form in a structurally normal heart.
• Long QT syndrome is the commonest inherited channelopathy; others are Brugada syndrome, CPVT and short QT syndrome.
• Channelopathies are more prevalent in younger patients — take a three-generation family history.

Reversible triggers to look for in every case:

• Hypokalaemia, hypocalcaemia, hypomagnesaemia.
• Stimulants — cocaine, methamphetamine.
• Digoxin and other prescribed arrhythmogenic drugs; QT-prolonging medications.

Presentation

• Palpitations, lightheadedness, syncope, dyspnoea, chest pain, sudden cardiac death.
• VT in a patient with LV systolic dysfunction is poorly tolerated and causes marked haemodynamic compromise.
• Idiopathic VT typically presents as palpitations during exercise or emotional stress.
• A patient with an ICD may present having had device shocks.
• Examination may show tachycardia, hypotension, altered conscious state, cannon jugular venous waves and pulmonary congestion.

In VF there is immediate collapse. Pulses are absent, blood pressure falls precipitously, and respiratory effort ceases.

Assessment

Decide haemodynamic stability first — responsiveness, heart rate, blood pressure. An unstable patient is stabilised before any further history-taking.

Get a 12-lead ECG. A wide-complex tachycardia is VT in roughly 80% of cases. The main alternatives are SVT with aberrancy, AF with aberrant conduction, a paced rhythm, and QRS widening from drug toxicity or electrolyte disturbance (particularly hyperkalaemia). The Brugada and Vereckei algorithms help differentiate.

In a rural or GP setting, treat a wide-complex tachycardia as VT until proven otherwise. Do not give verapamil or adenosine on an assumption of SVT with aberrancy.

Investigations after an episode:

• Potassium, magnesium and calcium — essential to both diagnosis and management.
• High-sensitivity troponin if infarction is possible.
• A 12-lead ECG in sinus rhythm, looking for infarct pattern, long QT, HCM, Brugada or ARVC.
• Transthoracic echocardiography, the first-line test of cardiac structure and function.
• Coronary angiography where ischaemia is presumed to be the cause.
• Genetic testing and family screening where a channelopathy is suspected.

Non-sustained VT

Evaluate for structural heart disease and refer to a cardiologist. Correct ischaemia and electrolyte disturbance. Treat only when there are prolonged episodes with haemodynamic compromise, or significant symptoms.

An asymptomatic patient with non-sustained VT and no structural heart disease may need no treatment at all.

Drug options when treatment is warranted:

• Atenolol 25mg daily, increasing if required to 100mg daily; or metoprolol tartrate 25mg BD, increasing if required to 100mg BD.
• If beta-blockers are contraindicated or not tolerated, and there is no LV dysfunction: flecainide 50mg BD (up to 150mg BD), or verapamil MR 180mg daily (up to 360mg daily). Avoid flecainide in coronary disease.
• If symptoms persist, or VT-induced cardiomyopathy is suspected: amiodarone 200–400mg orally TDS for 1 week, then BD for 1 week, then once daily.
• Consider catheter ablation for significant symptoms uncontrolled by drug therapy, or suspected cardiomyopathy.

Sustained VT — acute

Unstable: DC cardioversion. Pulseless: defibrillate and run the ACLS algorithm. If VT recurs after successful cardioversion, IV amiodarone is used to hold sinus rhythm.

Stable, with structural heart disease: IV procainamide, amiodarone or sotalol, depending on what is available. IV lidocaine is the alternative if none of those are. Where ischaemia is driving it, an IV beta-blocker may be considered.

Stable idiopathic VT: IV beta-blockers and non-dihydropyridine calcium channel blockers are first-line. DC cardioversion is used if drug therapy fails.

Doses in local use: amiodarone 300mg IV over 10–20 minutes, then 900mg IV over 24 hours if required; or lidocaine 1mg/kg (usually 75–100mg) IV over 1–2 minutes, then 4mg/min IV for 1 hour, reducing to 1–3mg/min.

Optimise potassium, magnesium and calcium in every patient. Any patient with unstable VT on a background of infarction or ischaemia needs angiography and revascularisation.

Sustained VT — ongoing management

Evaluate thoroughly for structural heart disease, particularly coronary ischaemia and LV dysfunction. Everyone with structural heart disease and LV systolic dysfunction should be on guideline-directed heart failure therapy.

With structural heart disease:

• Refer for an ICD. A survivor of sudden cardiac death or of sustained VT with ischaemic cardiomyopathy warrants one if meaningful survival beyond a year is expected.
• ICDs prevent sudden death but do not prevent VT recurring.
• Long-term beta-blockade reduces recurrence and sudden cardiac death risk in ischaemic cardiomyopathy.
• Amiodarone or sotalol for recurrent VT or ICD shocks despite optimal beta-blockade, under specialist supervision. Amiodarone is more effective and less proarrhythmic than sotalol, but its systemic adverse effects often force early discontinuation.
• Catheter ablation for drug-refractory VT. Ablation reduces recurrence, VT storm and ICD shocks compared with drug therapy, without improving survival.

Without structural heart disease: prognosis is generally good and an ICD is not usually required. Refer to cardiology. Beta-blockers and verapamil control most idiopathic VT, and catheter ablation is effective in the drug-refractory minority.

Ventricular fibrillation

Sustained VT and VF are a medical emergency — call an ambulance and start advanced life support. Both are shockable rhythms — see Cardiac Arrest for the full ALS algorithm.

VF is treatable precisely because it is shockable, and shockable rhythms carry higher survival than non-shockable ones. Time to first defibrillation is the critical determinant of outcome in any setting. Outcomes still depend on finding and treating the precipitant, not just on the shock.

Practical implications for a GP or rural practice:

• Know where the nearest AED is, and check the practice defibrillator regularly.
• Only about 10% of out-of-hospital cardiac arrests survive to hospital discharge; survival approaches 30% when the VF arrest is witnessed.
• After ROSC, correct electrolytes, acidosis and hypoxia, and arrange urgent transfer.
• Every VF survivor needs a family history of unexplained cardiac death taken and their medication list reviewed for arrhythmogenic agents.

Prognosis

Prognosis follows the underlying disease. Ischaemic cardiomyopathy carries the worst outlook, with two-year mortality reaching 30% in untreated patients. Idiopathic VT in an otherwise well patient has an excellent prognosis, with near-normal life expectancy.

Tachycardia-induced cardiomyopathy and heart failure are the usual complications of incessant VT.