Adenosine Mechanism and Clinical Applications

Primary Mechanisms

The American College of Cardiology recommends adenosine for terminating AV nodal re-entrant tachyarrhythmias (PSVT) due to its ability to block AV nodal conduction through activation of specific purine receptors, particularly A1 receptors in cardiac tissue and A2 receptors in vascular tissue 1, 2, 3
A1 receptor activation causes direct negative chronotropic effect by suppressing cardiac pacemaker automaticity and produces negative dromotropic effect by inhibiting AV nodal conduction 1, 2, 4

Adenosine can transiently slow ventricular rate in other SVTs (such as atrial fibrillation or flutter), which helps in diagnosis but does not typically terminate these arrhythmias 2, 5
In PSVT, adenosine is administered as a 6 mg rapid IV push through a large vein followed by a 20 mL saline flush; if no response within 1-2 minutes, a 12 mg dose can be given 2, 4

The American Heart Association notes that adenosine has important drug interactions that affect dosing, including larger doses required with theophylline, caffeine, or theobromine due to competitive antagonism 1, 2
Initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine, those with transplanted hearts, or when given by central venous access 2, 4
Common side effects are transient and include flushing, dyspnea, and chest discomfort, with a potential for transient complete heart block (must be given in monitored environment) 1, 2, 5
Contraindications include asthma (risk of bronchospasm) and caution in patients with Wolff-Parkinson-White syndrome due to risk of initiating atrial fibrillation with rapid ventricular rates 1, 2, 4

Adenosine causes transient atrioventricular (AV) nodal block, making it highly effective for terminating supraventricular tachycardias (SVT) involving the AV node, with success rates ranging from 78% to 96% 6
Adenosine causes vasodilation primarily in the microcirculation with minimal effect on epicardial conduit arteries, acting through A2 receptors to increase cytosolic cyclic adenosine monophosphate 7
In pulmonary circulation, adenosine causes relaxation of pulmonary arterial smooth muscle, making it useful for vasoreactivity testing in pulmonary hypertension 8, 9

Adenosine is the preferred agent for acute termination of SVT due to AVNRT or AVRT, administered as a rapid IV bolus followed by saline flush 6
Adenosine can be used diagnostically to unmask atrial flutter or atrial tachycardia, though it rarely terminates these arrhythmias 6
Continuous ECG recording during adenosine administration helps distinguish drug failure from successful termination with immediate arrhythmia reinitiation 6
Adenosine is used to achieve maximal coronary hyperemia for fractional flow reserve (FFR) measurement to assess the functional significance of coronary stenoses 7
Patients commonly experience transient chest discomfort, shortness of breath, flushing, headache, throat/neck/jaw discomfort, gastrointestinal discomfort, and dizziness 6
Patients should avoid Valsalva maneuvers during intravenous infusion as this can interrupt continuous drug delivery 7