Medical Care: The primary treatment during a bout of atrial tachycardia is considered to be rate control using beta-blockers or calcium channel blockers. However, great caution is required. Numerous reports describe cardiovascular collapse and even deaths following the assumption that an SVT is AV junctional dependent and that a calcium channel blocker such as verapamil will terminate this tachycardia. Remember that beta-blockers and especially verapamil frequently do not terminate reentrant atrial tachycardias, but they cause peripheral vasodilation (in the case of calcium channel blockers) and myocardial depression. Thus, in the setting of patients with symptoms of hypotension and in patients with structural heart disease, the administration of a calcium channel blocker, which may fail to terminate the SVT, may cause deterioration of the hemodynamic status and collapse.
In the setting of hemodynamic compromise due to SVT or known atrial tachycardia in which a drug may be therapeutic, the ultra-short acting adenosine or short-acting beta-blocker esmolol may be tried. In the setting of structural heart disease or previous cardiac surgery (repair or corrective surgery for congenital or valvular heart disease), particularly if there is hemodynamic instability, proceeding directly to electrical cardioversion is safest.
Determining the etiology or cause of the atrial tachycardia is important because this tachycardia can also be observed in patients with underlying structural heart disease, acute pulmonary embolus, acute noncardiac illness, or thyroid disease, or it can be due to drugs, especially sympathomimetics or bronchodilators. The rhythm often self-terminates and may be nonsustained if the cause is addressed. Beta-blockers often help decrease the frequency of episodes and may reduce symptoms by decreasing AV nodal conduction to the ventricles.
The rhythm itself is generally not life threatening, and long-term management depends on the underlying cause, the frequency and severity of the episodes, and comorbidities that may determine the type of medical therapy. Antiarrhythmic drugs of various classes have been used in refractory cases.
The rhythm can be life threatening in children with complex congenital heart disease, especially after a Fontan procedure. In this case, urgent cardioversion may be required.
For any patient in whom the rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective or contraindicated, cardioversion should be considered. However, if the rhythm has persisted for longer than 48 hours, cardioversion may be associated with the theoretically increased risk of thromboembolic complications if the tachycardia is associated with absence of organized atrial mechanical contraction, as during atrial fibrillation and atrial flutter. In this case, anticoagulation may be recommended as in atrial fibrillation before attempting to cardiovert.
Remember that some atrial tachycardias cannot be cardioverted. Automatic atrial tachycardias and MATs do not respond to electrical cardioversion. However, electrical cardioversion may be attempted in unifocal atrial tachycardia because, unlike MAT which can be distinguished from the ECG, it is usually impossible to be certain if the atrial tachycardia is focal or not.
Antiarrhythmic drugs can prevent recurrences and may be required. A calcium channel blocker or beta-blocker also may be required.
" Electrophysiology studies help identify the subset of patients with atrial tachycardia due to triggered activity. This form of tachycardia is sensitive to verapamil, beta-blockers, and adenosine. In this case, verapamil alone or in combination with a beta-blocker may be effective for controlling the tachycardia. Triggered activity-related atrial tachycardia is most frequently found in the setting of digitalis toxicity. The treatment is withdrawal of digitalis and careful observation in hospital without the use of the above-mentioned drugs.
" Beta-blockers may be used to suppress atrial tachycardia due to enhanced automaticity, but overall success rates are low.
" For refractory recurrent (particularly recurrence after electrical cardioversion) atrial tachycardias causing symptoms, antiarrhythmic drugs such as quinidine or procainamide have been tried. These drugs prolong the atrial refractoriness and slow the conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia. The adverse effects of class IA drugs are significant. Therefore, the use of class IA drugs is limited. These drugs are effective only approximately 50% of the time. Class IC drugs (ie, flecainide, propafenone) may slow the conduction and stop the tachycardia. These drugs can be proarrhythmic when used in patients with structural heart disease or even in those without disease. These drugs should be administered with AV node-blocking drugs such as beta-blockers or calcium channel blockers.
" Class III antiarrhythmic drugs such as amiodarone and sotalol are not always effective in terminating the atrial tachycardia, but they may be highly effective for maintaining sinus rhythm after conversion to a normal sinus rhythm. Ibutilide and dofetilide can terminate some atrial tachycardias.
" Atrial tachycardia due to digitalis intoxication often manifests with AV conduction block and/or ventricular arrhythmias. Recognizing this at an early stage is crucial because it may be a harbinger of more lethal ventricular tachyarrhythmias. Treatment often includes prompt discontinuation of digoxin and correction of electrolyte disturbances. The administration of antidigoxin antibodies is usually indicated in patients with conduction block, severe bradycardia, ventricular arrhythmias, and congestive heart failure. Electrical cardioversion is contraindicated because it may provoke a ventricular tachyarrhythmia.
" Ablation can cure macroreentrant and focal forms of atrial tachycardia.
o Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and effective treatment option for symptomatic, medically refractory patients. However, the success rates are not as high as those for AV nodal reentrant tachycardia or AV reentrant tachycardia using an accessory pathway.
o After activation mapping, the origin of the tachycardia can be localized. Focal application of radiofrequency energy via an ablation catheter to the origin of the tachycardia results in termination of the tachycardia.
o Focal atrial tachycardia originating from the pulmonary veins has been associated with atrial fibrillation. Radiofrequency ablation abolishing the focal triggering activity within the orifices of the pulmonary vein can be curative in patients with atrial fibrillation of this mechanism.
o Of note, complex ablation procedures primarily for atrial fibrillation that isolate pulmonary veins or make circumferential left atrial ablations lines have been associated with new reentrant atrial tachycardias or left-sided atypical atrial flutter. These tachycardias usually require a further ablation procedure.
Surgical Care: For patients with complex congenital heart disease, surgical ablation may occasionally be useful. However, this is generally supplanted by radiofrequency ablation approaches.
At surgery, particularly for congenital heart disease and particularly if complex, such as the Fontan procedure, incisions should be situated or extended to lines of natural conduction block in order to prevent subsequent incisional or scar-related atrial reentrant tachycardias.
Consultations: Consultation with a cardiologist or electrophysiologist is recommended for patients with recurrent atrial tachycardia and when structural heart disease is diagnosed or considered.
DRUG TREATMENT :
1. BETA BLOCKERS :
- ATENOLOL
- ACEBUTOLOL
- ESMOLOL
2. CLASS III ANTIARRHYTHMIC AGENTS :
- AMIODARONE
- SOTALOL
3. CLASS IA ANTIARRHYTHMIC AGENTS
- PROCAINAMIDE
4. CLASS IC ANTIARRHYTHMIC AGENTS
- FLECAINIDE
- PROPAFENONE
5. CALCIUM CHANNEL BLOCKERS
- DILTIAZEM
- VERAPAMIL
6. MISCELLANEOUS ANTIARRHYTHMIC AGENTS
- DIGOXIN