Supraventricular tachycardia (SVT) is a common cardiac arrhythmia characterized by rapid heart rates originating above the ventricles. Adenosine, a potent pharmacological agent, is frequently employed in the acute management of SVT. This article elucidates the mechanism of action, efficacy, dosing considerations, and clinical implications of adenosine administration for SVT.
Adenosine acts primarily by activating adenosine A1 receptors in the atrioventricular (AV) node, thereby inhibiting calcium influx and slowing conduction through the AV node. This transient AV nodal block interrupts reentrant tachycardias, such as AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT), terminating the arrhythmia.
Adenosine is highly effective in terminating SVT, with success rates exceeding 90% in most cases. It rapidly converts narrow-complex SVT to sinus rhythm within seconds of administration, making it a first-line agent for acute SVT management in emergency settings.
The standard dosing regimen for adenosine in SVT is an initial intravenous bolus of 6 mg administered rapidly followed by a saline flush to ensure delivery to the central circulation. If there is no response within 1-2 minutes, a second bolus dose of 12 mg can be administered in a similar manner. Higher doses may be required in some cases, particularly in patients with refractory SVT or delayed response to initial therapy.
Several clinical factors should be considered when using adenosine for SVT:
Adenosine administration may be associated with transient adverse effects, including:
Adenosine is a highly effective and rapidly acting pharmacological agent for terminating SVT by interrupting reentrant tachycardias involving the AV node. With proper dosing, careful patient monitoring, and attention to clinical considerations, adenosine administration is safe and can restore sinus rhythm promptly in patients with SVT.
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