Major side effects of adenosine

INTRODUCTION

Since the half-life of adenosine is brief (less than 5 to 10 seconds), both its intended and unintended effects are short-lived. Nevertheless, adverse effects occur in 40 to 60 percent of patients. Caffeine or theophylline should be at the bedside if an untoward effect is considered likely, since these drugs competitively antagonize the actions of adenosine.

CARDIAC

The most common cardiovascular side effects of adenosine are facial flushing (18 percent), palpitations, chest pain, and hypotension. Both tachyarrhythmias and bradyarrhythmias also occur.

The primary mechanism of action of adenosine is to decrease conduction through the atrioventricular (AV) node; it can therefore produce a transient first, second, or even higher degree of AV block [1]. While bradyarrhythmias and AV nodal prolongation are common, transient asystole is rare.

AV block is also common when adenosine infusions are given during cardiac stress testing. In one study in 600 patients, adenosine infusion (140 mg/kg/min for six minutes) produced first, second, and third degree AV block in 13, 10, and 2 percent of patients [2]. The frequency of AV block depended upon age group, being least frequent among patients aged 50 to 65 and most common among patients over 75. The conduction block was of short duration and did not require discontinuation of adenosine administration. However, use of adenosine for nuclear stress testing in patients with evidence of underlying conduction system disease may result in serious complications such as sustained second-degree AV block requiring permanent pacemaker implantation [3].

A few patients develop atrial fibrillation after adenosine injection. As an example, in one study of 200 patients with supraventricular tachycardia (SVT) undergoing electrophysiologic testing, the incidence of atrial fibrillation after the administration of 12 mg of adenosine was 12 percent [4]. In a second series of 229 patients with SVT, the occurrence of atrial fibrillation was related to the mechanism of the tachycardia; it occurred in 15 percent of those with atrioventricular reentrant tachycardia, 11 percent with atrial tachycardia, and 17 percent of those with a junctional reciprocating tachycardia, while atrial fibrillation did not occur in patients with an atrioventricular nodal reentrant tachycardia [5]. Adenosine-induced shortening of the atrial action potential and the atrial refractory period (due to activation of outward potassium current) and the induction of frequent ectopic complexes are predisposing factors for the development of atrial fibrillation [6].