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Over the last 10 years adenosine has become the initial drug administered for narrow complex tachycardia, or for broad complex tachycardia where a diagnosis other than ventricular tachycardia is suspected. The response to adenosine depends on the tachycardia mechanism. Atrial arrhythmias usually do not terminate, but unmasking the atrial rhythm by temporarily increasing atrioventricular block (AV) is diagnostically helpful. Arrhythmias utilising the AV node (AV nodal re-entrant tachycardia and AV reciprocating tachycardia) terminate if AV block is achieved. Finally, ventricular tachycardia usually shows no response, although occasional ventricular (and atrial) tachycardias are adenosine sensitive. Occasionally a subtherapeutic dose of adenosine may provide very precise diagnostic information.
A 52 year old man attended casualty with his first prolonged bout of palpitations. The initial ECG showed a left bundle branch block (LBBB) morphology broad complex tachycardia with a rate of 170 beats per minute (bpm). Intravenous adenosine 3 mg changed this into a narrow complex tachycardia at 210 bpm (A, top). A further 6 mg bolus of adenosine restored sinus rhythm. The patient's resting ECG was within normal limits with no evidence of pre-excitation.
The diagnosis is orthodromic AV reciprocating tachycardia utilising a left sided accessory pathway. During the LBBB tachycardia, the tachycardia circuit conducted anterogradely over the right bundle, and retrograde invasion of the left bundle maintained the LBBB (B, bottom). Slight slowing of AV nodal conduction by the adenosine allowed recovery of excitability, and since the impulse could now reach the accessory pathway via the left bundle, the circuit became shorter and the tachycardia rate faster.