Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

adult: undifferentiated supraventricular tachycardia

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adenosine

Causes AV node blockade with slowing of the ventricular response rate or cessation of the atrial tachycardia.[13] Effects are transient, and can be misleading when trying to differentiate from other forms of supraventricular tachycardia, if the focal AT terminates with adenosine.[Figure caption and citation for the preceding image starts]: Response to adenosine 6 mg intravenouslyFrom the collection of Sarah Stahmer, MD [Citation ends].com.bmj.content.model.Caption@452d421e

Transient slowing of the ventricular response rate with sustained atrial activity indicates flutter or focal AT. Flutter will have the characteristic saw-tooth pattern of an atrial macro-re-entrant circuit. Focal AT will show discrete P waves with an isoelectric baseline.

Lack of response to adenosine suggests either sinus tachycardia or focal AT, and strongly suggests that the rhythm is not re-entrant supraventricular tachycardia or atrial flutter.

Some forms of atrial tachycardia will break in response to adenosine.[17]

Primary options

adenosine: adults: 6 mg/dose intravenously initially, followed by 12 mg/dose in 1-2 minutes if no effect, may repeat 12 mg/dose once more in 1-2 minutes if no effect, maximum 30 mg/total dose

ACUTE

adult: focal AT; digoxin excess not suspected

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beta-blocker or calcium-channel blocker

Calcium-channel blockers or beta-blockers may be helpful in controlling the ventricular response rate or breaking the tachycardia.[1]

Catecholamine excess should be suspected if there is a history or suspicion of recent use of exogenous catecholamines, cocaine, or alcohol with clinical features of catecholamine excess (agitation, diaphoresis, hypertension).

Supportive care and withdrawal of any offending agent are first-line therapy. Supportive care includes intravenous fluids for any haemodynamic instability without overt congestive heart failure, as well as correction of any associated electrolyte imbalance.

Beta-blockers should be used with caution if there is a suspicion that the dysrhythmia was triggered by cocaine.[1][Figure caption and citation for the preceding image starts]: Focal atrial tachycardia in a 35-year-old with history of recent cocaine useFrom the collection of Sarah Stahmer, MD [Citation ends].com.bmj.content.model.Caption@1b5bd824

Blocking the beta receptors leaves the circulating noradrenaline (norepinephrine) free to activate the alpha receptors with no opposing beta effects. This may induce hypertensive crisis and vasospasm.

Beta-blockers are generally reserved for patients who are not suspected to have taken cocaine, and who are refractory to supportive care, show evidence of cardiac ischaemia, or are haemodynamically unstable.

The effects of any pharmacological intervention for focal AT are often unpredictable given the multitude of causes and underlying mechanisms. For this reason, if there are any concerns about the potential risks of giving an agent to a stable patient, choose agents that are short acting and can be stopped if there are adverse effects.

Beta-blockers and calcium-channel blockers should be avoided in patients with decompensated heart failure or haemodynamic instability. Beta-blockers should also be avoided in patients with active pulmonary disease.

Primary options

diltiazem: adults: 0.25 mg/kg intravenously initially, followed by 10 mg/hour infusion, consult specialist for further guidance on dose

OR

esmolol: adults: 500 micrograms/kg/dose intravenously initially, followed by 50 micrograms/kg/minute infusion for 4 minutes, if no response after 5 minutes repeat loading dose and increase infusion, consult specialist for further guidance on dose

Secondary options

verapamil: adults: 5-10 mg intravenously initially, followed by 10 mg 30 minutes later if no effect, consult specialist for further guidance on dose

OR

metoprolol: adults: 5 mg/dose intravenously initially, may repeat every 5 minutes, maximum 3 doses

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catheter ablation

Electrophysiological study involving ablation may aid in diagnosing the mechanism of the tachycardia; it can be curative and may be offered as first-line therapy to select patients.[1]

The need to confirm the mechanism of SVT and preference for an alternative to long-term pharmacological therapy are factors that may support the use of catheter ablation.

Catheter ablation is a specialised intervention undertaken by electrophysiologists and may be dependent on availability of an electrophysiologist.

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amiodarone or ibutilide

Patients who are refractory or have contraindications to adenosine, beta-blockers, or calcium-channel blockers may benefit from these second-line medications.

Amiodarone is a highly effective agent in the management of a wide range of supraventricular and ventricular tachycardias.[1]​ It prolongs the duration of the action potential and the refractory period in atrial and ventricular tissues, slows automaticity in pacemaker cells, and slows AV nodal conduction. Patients should, therefore, be closely monitored when this treatment is started.

Ibutilide has been reported to be effective in some cases of focal AT, but its mechanism of action is not clear.[1][16] Continuous ECG monitoring is recommended and caution should be used in patients with QT prolongation.

Primary options

amiodarone: adults: 150 mg intravenously over 10 minutes, followed by 1 mg/minute infusion over 6 hours (total dose 360 mg), then 0.5 mg/minute infusion over 18 hours (total dose 540 mg)

OR

ibutilide: adults body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

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third-line pharmacotherapy or direct current (DC) cardioversion + cardiology consult

Patients who are refractory to second-line pharmacotherapy should be referred for a cardiology consult. Cardioversion may be effective in some cases; usually if re-entry is the mechanism. Other forms of focal AT are often resistant to electrical disruption. Medications that may be effective are in the Ic class of anti-arrhythmics. Because of the risk of untoward side effects with these medications, cardiology consultation is advised when considering these therapies.

Primary options

flecainide: adults: 50 mg orally every 12 hours initially, increase gradually according to response, maximum 300 mg/day

OR

propafenone: adults: 150 mg orally (immediate-release) every 8 hours initially, increase gradually according to response, maximum 900 mg/day; 225 mg orally (extended-release) every 12 hours initially, increase gradually according to response, maximum 850 mg/day

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direct current (DC) cardioversion

Electrical disruption may be effective in some cases of focal AT. When a patient has become unstable, it is reasonable to attempt DC cardioversion when it is clear that the tachyarrhythmia is non-sinus and is responsible for the haemodynamic compromise.

Electrical disruption is usually only effective if re-entry is the mechanism; other forms of focal AT are typically resistant to electrical disruption.

If an underlying cause is identified, this should be treated.

adult: focal AT; digoxin toxicity suspected

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supportive care

Digoxin toxicity should be suspected if there is a history of congestive heart failure, the patient is taking digoxin, and the rhythm is atrial tachycardia with evidence of atrio-ventricular blockade.

When atrial tachycardia is a manifestation of digoxin toxicity, treatment is aimed at supportive care, withholding digoxin, optimising volume status, and replacing potassium if there is a deficit.[Figure caption and citation for the preceding image starts]: Focal atrial tachycardia in an 88-year-old woman with 2:1 AV nodal block in the setting of digoxin therapy and potassium 2.8 mmol/L (2.8 mEq/L)From the collection of Sarah Stahmer, MD [Citation ends].com.bmj.content.model.Caption@5872ae06

This approach is usually sufficient for restoring sinus rhythm.

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digoxin immune Fab

Additional treatment recommended for SOME patients in selected patient group

Patients with evidence of refractory arrhythmias, particularly ventricular, or haemodynamically compromising AV block may benefit from digoxin-specific antibody fragments (Fab) therapy to bind digoxin.[19]

Primary options

digoxin immune Fab: adults: consult specialist for guidance on dose

child

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anti-arrhythmic medication ± catheter ablation

Paediatric atrial tachycardias are uncommon. Atrial tachycardia in children is often incessant and refractory to typical treatments used for atrioventricular nodal re-entrant tachycardia; tachycardia-induced cardiomyopathy is commonly observed.

The treatment of paediatric patients with atrial tachycardia includes medications to suppress the arrhythmia and/or control the ventricular response and catheter ablation. Beta-blockers, digoxin, and antiarrhythmics such as amiodarone are often effective as first-line pharmacological interventions to achieve rate control. Many children will have spontaneous resolution of the arrhythmia.

Amiodarone should not be used in babies aged <1 month because of the additive benzyl alcohol, which may precipitate metabolic acidosis and gasping syndrome.[20]

Patients with incessant tachycardias will usually require catheter ablation, which is associated with a high degree of success, a low complication rate, and a low recurrence rate.

Selection of drug therapy in children should be under specialist guidance.

ONGOING

adult: sustained or recurrent focal AT

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catheter ablation

Many patients with sustained and/or recurrent atrial tachycardias are referred for catheter ablative therapy. The success of this treatment depends on the site of origin and underlying mechanism.[1]​ The presence of recurring symptoms, persistent tachycardia leading to heart failure, and unsuccessful medical treatment, are factors that may support the use of catheter ablation for focal atrial tachycardia.​

Catheter ablation is a specialised intervention undertaken by electrophysiologists and may be dependent on availability of an electrophysiologist.

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antiarrhythmic medication

There is limited evidence that these drugs are moderately effective for the long-term pharmacological therapy of focal AT. Most of the evidence for the long-term use of these drugs in the management of focal AT come from studies in children. Due to the risk of pro-arrhythmia and other potential complications it is important to consider individual benefit versus harm.[1]​ Class Ic or class III antiarrhythmics are typically used in this setting. Consult a specialist for guidance on selection and dose of antiarrhythmics.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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