a. Adenosine. Ectopic atrial tachycardia and atrial flutter or fibrillation do not use AV node as a critical part of their circuit and generally are not responsive to treatment with adenosine. However, adenosine can have a role in management of these tachycardias. Some ectopic atrial foci and flutter circuits use specialized conduction tissue that is adenosine sensitive and will be terminated with administration of adenosine. Adenosine can be used diagnostically to demonstrate that atrial tachycardia persists despite block of AV node. This phenomenon can be observed on a rhythm strip performed with administration of adenosine. P waves will march along at tachycardia rate with loss of AV conduction (atrial rate constant with slowed ventricular rate).
b. AV-nodal blocking agents. Short-term goal is to control ventricular rate with administration of AV-nodal blocking drugs such as calcium channel blockers (verapamil, dilti-azem), 0-blockers (esmolol), or digoxin.
c. Cardioversion. Patients who do not respond to medications or who are hemodynamically unstable should undergo synchronized DC cardioversion. Once rhythm is controlled, more potent oral antiarrhythmic medications can be instituted.
3. Ventricular tachycardia. Most wide-complex tachycardias are ventricular in origin, especially if AV dissociation is present.
a. Adenosine. If patient is hemodynamically stable and QRS complexes are associated with P waves, adenosine should be considered due to possibility of terminating SVT with aberrancy. This is especially true in patients with baseline bundle branch block who now have SVT. If the rhythm is ventricular tachycardia, adenosine will produce AV-nodal block and dissociate the P wave from the QRS complex (ventricular rate remains same and atrial rate slows).
b. Lidocaine. May be used in hemodynamically stable patients. Administer IV bolus of 1 mg/kg, followed by infusion of 20-50 mcg/kg/min.
c. Amiodarone. May also be used to treat stable patients. Initial dose is 5 mg/kg over 20 minutes, repeated up to 3 times; with infusion of 7 mcg/kg/min after conversion. Most significant side effect involves a-blockade (hypotension, bradycardia). Be prepared to treat these effects (with volume expanders, temporary pacing) should they occur.
d. DC cardioversion. Use in treatment of hemodynamically unstable VT (synchronized if pulse is present).
4. Torsades de pointes. Treatment is directed at electrolyte imbalance if present or withdrawing offending medication. Infusion of magnesium can terminate tachycardia or prevent recurrence even in patients with normal magnesium levels. Unstable patients should undergo DC cardioversion and magnesium therapy. Patients with known long QT syndrome may benefit from infusion of esmolol. Ventricular pacing may also prevent recurrence, because induction of tachycardia usually involves a prolonged pause.
VI. Problem Case Diagnosis. The 12-lead ECG in this 6-year-old boy demonstrated a wide-complex tachycardia with no discernible P waves. Patient was awake and talking with no hemodynamic instability. Clinician suspected ventricular tachycardia rather than SVT with aberrancy. (For further discussion, see VII and VIII, below.)
VII. Teaching Pearl: Question. Given this patient's current hemody-namic stability, what could be done to both diagnose and possibly treat his rhythm disturbance?
VIII. Teaching Pearl: Answer. Administration of adenosine while obtaining a multilead rhythm strip should allow clinician to discriminate ventricular tachycardia from SVT with aberrancy and also treat supraventricular arrhythmia. Children frequently have retrograde AV-nodal conduction during ventricular tachycardia, with activation of atrium and production of P waves within or following the QRS complex. This is also true for AV node reentry tachycardia, because it is the mechanism of tachycardia. These P waves may not be discernible
■ during arrhythmia or, if they are seen, will be associated with the QRS complex. Therefore, in a hemodynamically stable patient, adenosine can be used to block conduction in the AV node and dissociate the P wave from QRS, in the case of ventricular tachycardia, or terminate SVT, at least temporarily. It is of utmost importance that this maneuver be performed during recording of a multilead rhythm strip, because P waves that are demonstrated in other leads may be missed in a single lead. Dissociation of P wave from QRS with no change in tachycardia is diagnostic for ventricular tachycardia. Hemodynamic stability or instability should not be used to differentiate ventricular tachycardia from supraventricular tachycardia with aberrancy.
Was this article helpful?