OzEMedicine - Wiki for Australian Emergency Medicine Doctors

see also:

• pharmacology main index
• autacoids
• methylxanthines - adenosine receptor antagonists

• adenosine is a naturally occurring endogenous nucleoside
• adenosine is rapidly taken up by RBC's & endothelial cells such that almost completely eliminated from circulation after 1st pass → plasma T1/2 < 10secs;
• hence can expect exaggerated response in anaemic patients, & reduced response if infusion in peripheral vein rather than IV bolus into central vein;

• only use with full resuscitative facilities on hand
• avoid in severe coronary artery disease as risk of vasodilatation of normal vessels may produce ischaemia in vulnerable territory
• avoid in severe asthma
• patients on theophylline may require higher doses
• dipyridamole potentiates effects of adenosine
• carbamazepine increases risk of prolonged AV block

• see also SVT
• give half these doses if administering via a central venous catheter (CVC).
• Insert cannulae into a large proximal peripheral vein (the cubital fossa is ideal) with three way tap attached
• Draw up starting dose of adenosine 0.1-0.2 mg/kg (6 or 12mg for an adult). If necessary dilute to 1 ml with normal saline.
• Draw up 10 ml saline flush & warn patient they will feel awful!
• Turn on the ECG trace recorder
• Administer adenosine as a rapid IV push followed by the saline flush
• Repeat procedure at 2 minutely intervals, until tachycardia terminated, increasing the dose of adenosine by 0.05mg/kg (6mg for an adult) each time up to a maximum of 0.5 mg/kg (max dose 18mg).
  • adenosine success rates in adults with Rx SVT:
    • 1 dose 43%; 2nd dose 34%; 23% require a 3rd dose although a third of these will fail (ie. 8% of all patients and 23% of those with PH SVT)
    • failure risk score = (age/heart rate on admission) + number of past paroxysmal SVT episodes
      • if score > 1.18 then sens. 96% and spec. 71% for failure of adenosine protocol
      • ref: Am J Emerg Med 2008; 26:304-9.

• usually last < 2 min. due to short half life
• facial flushing -18% if IV bolus;
• SOB -12% if IV bolus;
• chest pain/pressure - 11% if IV bolus;
• hypotension
• occasionally, more prolonged AV block or sinus arrest after IV bolus
• dose dependent decreased renal blood flow, GFR & urine flow if infusion
• myocardial ischaemia presumably via coronary steal;
• AV block - 2nd/3rd degree occurred in 6% with infusion @ 140ug/kg/min for 6min;
• adenosine used to Rx SVT is said to result in atrial fibrillation in up to 12% of patients (Strickberger et al. Ann.Intern.Med. 1997)
• adenosine used to unmask flutter waves in atrial flutter has been reported to result in 1:1 conduction with haemodynamic compromise.

• Effects mediated by adenosine receptors on outer surface of cell membrane:
  • Type A1:
    • activate K channels & inhib. c-AMP accumulation;
    • predominate in myocardium;
  • Type A2:
    • stimulate release of EDRF & the accum. of i/cell. c-AMP;
    • esp. in coronary arteries;
  • Type A3:
  • Type A4:
• Adenosine may play a key role in the production of, & mediation of anginal PIC;
• Electrophysiologic effects (mediated by A1):
  • -ve chronotropic effect on sinus node automaticity;
  • -ve dromotropic effect on AV nodal conduction;
  • In supraventricular tissues (sinus node, AV node):
    • activates K outward current in a distinct K channel
      • ⇒ tissue hyperpolarisation;
  • In ventricular tissue:
    • acts primarily by attenuation of catecholamine-stimulated Ca fluxes;
  • Summary:
    • when given as a bolus dose IV, it directly inhibits AV nodal conduction and increases AV nodal refractory period, but has only mild effects on SA nodal function.
• Cardioprotective effects:
  • Adenosine is released from myocardium when O2 supply:demand ratio falls →:
    • coronary vasodilatation
    • antiadrenergic via:
      • decr. release NA from cardiac symp. Ns;
      • attenuates stimulating effects of catecholamines on heart;
    • antiarrhythmic:
      • exog. adenosine → decr. severity of ischaemia-induced vent. arrhthm.
    • metabolic effects:
      • delays myocardial ATP depletion;
      • incr. myocardial glucose uptake;
      • incr. glycolytic fluxes;
    • attenuation of microvascular injury:
      • ? prevention of neutrophil/platelet aggreg.
      • ? inhib. of free O2 radical release from activated neutrophils;