Approach
Treatment of acute presentations is based on the nature of the arrhythmia. Ongoing treatment is decided according to the symptoms of the patient as well as risk stratification for sudden cardiac death.
Acute management
Acute management follows a path by whether the patient is stable or unstable; and if stable, by whether they are in orthodromic atrioventricular (AV) reciprocating tachycardia (narrow complex with short RP tachycardia), antidromic AV reciprocating tachycardia (wide complex tachycardia), or whether they have atrial fibrillation, flutter, or tachycardia.[3][20]
Patients with an acute tachycardia and who are haemodynamically unstable (BP <90/60 mmHg, with signs of systemic hypoperfusion) or who have atrial fibrillation with >250 bpm, or in whom the atrial fibrillation has degenerated to ventricular fibrillation, require immediate direct-current (DC) cardioversion.
AV reciprocating tachycardia
Narrow complex (orthodromic AV reciprocating) tachycardia:
Because orthodromic reciprocating tachycardia involves the AV node as one limb of the circus movement tachycardia, any manoeuvre or drug that slows or interrupts conduction in the AV node can terminate the tachycardia. In a haemodynamically stable patient, vagal manoeuvres such as carotid sinus massage should be performed at the bedside, or, alternatively, patients can be instructed to perform a Valsalva manoeuvre to terminate the arrhythmia. If this fails, pharmacotherapy with intravenous adenosine, AV nodal blocking drugs, or anti-arrhythmic agents is indicated.
Adenosine is preferred because of its ultra-short half-life (<18 seconds). It should be given as a rapid intravenous injection in a central vein or in the antecubital vein, followed by 10 to 20 mL of rapid normal saline flush. It can be used a second time if there is no response. Adenosine injection may cause chest pain, chest tightness, bronchospasm, dizziness, and a short run of atrial fibrillation (1% to 15%). Although atrial fibrillation is usually transient, it can cause rapid conduction to the ventricle via the accessory pathway (AP), and if the conduction is rapid then it can potentially result in ventricular fibrillation. Therefore, resuscitation equipment should be available as a standby. Adenosine should be avoided in patients with severe asthma and in patients with a known hypersensitivity to the drug. In addition, adenosine injection is associated with a higher risk of heart block in patients on carbamazepine therapy.
AV nodal blocking drugs (diltiazem, verapamil, metoprolol) can be used when there is no response or a recurrence after carotid sinus massage and adenosine. Anti-arrhythmic drugs (procainamide, ibutilide, amiodarone, flecainide) can be used when there is no response or a recurrence after carotid sinus massage, adenosine, and AV nodal blocking drugs.
Rapid atrial pacing using a temporary pacemaker for overdrive suppression of the tachycardia can be used if previous drug treatments fail. DC cardioversion can then be used when symptoms persist in patients or if the patient becomes haemodynamically unstable.
Wide complex (antidromic AV reciprocating) tachycardia:
If the tachycardia is haemodynamically stable, then management of antidromic reciprocating tachycardia is with intravenous adenosine or anti-arrhythmic drugs.
Adenosine is preferred because of its ultra-short half life (<18 seconds). It can be used a second time if there is no response.
Anti-arrhythmic drugs (procainamide, ibutilide, amiodarone) can also be used when there is no response or a recurrence after adenosine.
Calcium-channel blockers, digoxin, and beta-blockers are contraindicated in this population, because these drugs slow the conduction via the AV node but do not have any effect on the AP. This may result in a rapid conduction via the AP, which may cause ventricular tachycardia and ventricular fibrillation leading to sudden cardiac death.
Rapid atrial pacing using a temporary pacemaker for overdrive suppression of the tachycardia can be used if previous drug treatments fail. DC cardioversion can then be used when symptoms persist in patients or if the patient becomes haemodynamically unstable.
Atrial fibrillation, atrial flutter, and atrial tachycardia
Pre-excited tachycardia results in a rapid irregular wide complex tachycardia with varying duration and amplitude of QRS complexes depending upon the degree of pre-excitation. Intravenous infusions of anti-arrhythmic drugs such as procainamide, ibutilide, or flecainide, which prevent rapid conduction through the AP, are used, even though they may not be able to terminate the atrial arrhythmia.[3][20]
Anticoagulation should be considered in atrial fibrillation and atrial flutter depending on the presence of comorbid cardiological abnormalities and duration of onset.
Rapid atrial pacing using a temporary pacemaker for overdrive suppression of atrial flutter or atrial tachycardia can be used if the previous drug treatments fail. Rapid atrial pacing has no role in atrial fibrillation.
DC cardioversion can be used when symptoms persist in patients or if the patient becomes haemodynamically unstable. However, the recurrence of atrial arrhythmia after DC cardioversion may be higher in atrial tachycardia, compared with atrial fibrillation/flutter, depending on the mechanism. If the atrial tachycardia is related to abnormal automaticity, DC cardioversion may not be effective at all, such as in multifocal atrial tachycardia.[Figure caption and citation for the preceding image starts]: Atrial fibrillation in a patient with WPW syndrome with rapid ventricular rate; resulted in aborted sudden cardiac deathFrom the collection of Dr Mithilesh K. Das [Citation ends].
Asymptomatic
While controversy exists, most experts recommend that all patients with ventricular pre-excitation undergo risk stratification to determine their risk of sudden cardiac death, regardless of the presence of symptoms.[4][15][16][21] The risk of sudden cardiac death is determined by the anterograde refractory period of the AP during an isoproterenol infusion.[3] The presence of multiple APs and inducible tachycardia have also been identified as risk markers.
If the refractory period is very short, there are multiple APs, or tachycardia is induced, patients are at risk for developing ventricular fibrillation in the setting of atrial fibrillation conducting rapidly over the AP. Shorter anterograde refractory periods are associated with an increased risk for sudden cardiac death because the AP can conduct impulses more rapidly to the ventricles. This is particularly important if the patient develops atrial fibrillation. Normally, the ventricles are 'protected' from rapid depolarisation due to the decremental properties of the AV node. However, in patients with an AP with a short anterograde refractory period, rapid conduction over the AP can lead to rapid ventricular rates that can deteriorate to ventricular fibrillation.
If ventricular pre-excitation is intermittent at rest, this suggests the anterograde refractory period is relatively long, and the AP is low risk for causing sudden cardiac death.
If ventricular pre-excitation is always present at rest, patients should undergo exercise treadmill testing looking for abrupt loss of pre-excitation, again indicative of an AP incapable of dangerously rapid conduction from the atrium to the ventricle. If pre-excitation does not abruptly disappear with exercise, invasive risk stratification with an electrophysiology study should be considered. APs capable of rapid anterograde conduction should be ablated to reduce the risk of sudden cardiac death, regardless of whether or not they cause supraventricular tachycardia. Asymptomatic patients in specialised jobs with particular safety issues (e.g., airline pilot, school bus driver) can also be considered for catheter ablation. Catheter ablation is generally not performed in pregnant patients and should be deferred until after delivery.
Symptomatic patients
Symptomatic patients usually undergo catheter ablation as a first-line therapy.[3][4]
Anti-arrhythmic drugs are one of the therapeutic options for the management of symptomatic WPW syndrome, but they have been increasingly replaced by catheter ablation.
AV nodal blocking drugs are generally avoided in patients with WPW syndrome or WPW pattern because they theoretically can speed conduction through the AP. If anti-arrhythmic drug therapy is chosen, a class 1C anti-arrhythmic medication (flecainide or propafenone) or amiodarone is generally preferred. Class I anti-arrhythmic agents (flecainide or propafenone) are suitable for patients with no additional cardiac disease but cannot be used in people with coronary artery disease or structural heart disease. In patients with coronary artery disease or structural heart disease, class III anti-arrhythmic agents (sotalol, amiodarone, or dofetilide) may be used. QT interval must be determined prior to starting therapy with dofetilide as it is contraindicated if corrective QT interval (QTc) is >440 milliseconds (>500 milliseconds in patients with ventricular conduction abnormalities).
The incidence of symptomatic tachycardia is reported to be higher during pregnancy, which may be refractory to drugs that are safe to use in such circumstances. Therefore, a radiofrequency ablation should be considered prior to the next planned pregnancy. Catheter ablation is generally not performed in pregnant patients and should be deferred until after delivery. In the event a patient with WPW syndrome becomes pregnant prior to ablation of their AP, and if frequent recurrences of supraventricular tachycardia are observed during pregnancy, it is reasonable to treat the patients with flecainide or propafenone.[3]
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