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whereas microreentrant ATs from other locations generally will not be terminated by these drugs. Sinus node reentrant tachycardia is an uncommon type of focal AT that involves a microreentrant circuit in the region of the sinoatrial node, causing a P-wave morphology that is identical to that of sinus tachycardia (although this is not sinus tachycardia). Characteristics that distinguish sinus node reentry from sinus tachycardia are an abrupt onset and termination and often a longer RP interval than that observed during normal sinus rhythm. Sinus node reentry is characterized by paroxysmal episodes of tachycardia, generally 100 bpm to 150 bpm.201–203 Confirmation of the reentrant mechanism requires an EP study. Induction of sinus node reentrant tachycardia during programmed stimulation, demonstration of entrainment, and localization of the tachycardia origin in the region of the sinus node are necessary to confirm the diagnosis.

4.1.1 Acute Treatment: Recommendations

RCTs of drug therapy for comparative effectiveness in patients with focal AT in the acute setting are not available. Many of the clinical outcomes are reported from small observational studies that included infants or pediatric patients.204,205 The design or execution of these studies is frequently suboptimal because of the poorly defined inclusion criteria or variable clinical settings. Several studies included a mix of patients with congenital or postoperative AT, and some of these patients likely had macroreentrant AT. In many reports, the response to intravenous drug therapy was evaluated by EP study rather than in the clinical environment.123,200,204–207 In the clinical setting, if the diagnosis is uncertain, vagal maneuvers may be attempted to better identify the mechanism of SVT.

Digoxin has not been well studied for focal AT. Intravenous class Ic drugs (eg, flecainide, propafenone) may be moderately effective in treating focal AT in the acute setting, as reported in earlier, small observational studies, although intravenous forms of IC drugs are not available in the United States. In patients with an implanted cardiac pacing device, it may be possible to perform overdrive pacing through the device, although close monitoring is required to prevent any significant adverse effect, such as pacing-induced AF or other atrial arrhythmias. Equipment should be available to provide support for cardioversion of AF if needed.

Ibutilide Contraindicated when QTc >440 ms‡; 1 mg over 10 min (if ≥60 kg); if <60 kg, then 0.01 mg/kg Can repeat 1 mg once, if the arrhythmia does not terminate within 10 min§ QT prolongation, torsades de pointes, AV block •  Prolonged QT interval •  History of torsades de pointes •  Avoid other QT interval–prolonging drugs •  Concurrent administration of high-dose magnesium has been associated with enhanced efficacy and safety119,120 Note: For this reference table, drugs are presented in alphabetical order within the drug classes, not by COR and LOE. *When 1 drug is used in combination with other drugs, appropriate dosing adjustments should be made with consideration of at least additive effects during dosage titration. All potential drug–drug interactions are not included in this list. For a more detailed list of drug–drug interactions, clinicians should consult additional resources. †If hypotension is a consideration, a slow infusion of diltiazem (2.5 mg/min) or verapamil (1 mg/min) for up to 20 minutes may lessen the potential for hypotension.92 ‡QTc calculation used the Bazett’s Formula in most clinical studies. Patients should be observed with continuous ECG monitoring for at least 4 h after infusion or until QTc has returned to baseline. §The infusion should be stopped as soon as the arrhythmia is terminated or in the event of sustained or nonsustained ventricular tachycardia or marked prolongation of QT or corrected QT interval. AF indicates atrial fibrillation; AV, atrioventricular; BID, twice daily; COR, Class of Recommendation; HF, heart failure; INR, international normalized ratio; IV, intravenous; LOE, Level of Evidence; LV, left ventricular; PVC, premature ventricular contraction; QTc, corrected QT interval; SA, sinoatrial; SVT, supraventricular tachycardia; and WPW, Wolff-Parkinson-White.

Table 6.  Continued

Drug Initial Dose Subsequent or Maintenance Dose Potential Adverse

Effects Precautions (Exclude or Use With

Caution) and Interactions

Recommendations for Acute Treatment of Suspected Focal Atrial Tachycardia COR LOE Recommendations

I C-LD 1.  Intravenous beta blockers, diltiazem, or verapamil is useful for acute treatment in hemodynamically stable patients with focal AT.123,204,205,207

See Online Data Supplement 6. Intravenous beta blockers, diltiazem, or verapamil is recommended to treat focal AT. During EP study, propranolol or verapamil is moderately effective in either terminating the focal AT or slowing the ventricular rate in approximately 30% to 50% of the patients.204,205 Although these agents are relatively safe, close monitoring is recommended during intravenous drug therapy to evaluate for hypotension or bradycardia.

I C-LD 2.  Synchronized cardioversion is recommended for acute treatment in patients with hemodynamically unstable focal AT.94,208

See Online Data Supplement 6. Although minimum data are available on cardioversion of focal AT, synchronized cardioversion is a consideration in patients with drugresistant arrhythmias associated with signs and symptoms of compromised hemodynamics. Termination of tachycardia is expected when a focal AT is of a microreentrant mechanism. Response of a triggered focal AT to cardioversion can be variable, whereas electrical cardioversion is not likely to be effective in focal AT with an automatic mechanism. In this latter case, antiarrhythmic drug therapy is usually required.

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