ABNORMAL MYOCARDIAL REPOLARIZATION IN RESPONSE TO HYPOXEMIA AND FENOTEROL

Background - Prolongation of the QTc interval has been associated with cardiac dysrhythmias and sudden death. QTc dispersion (interlead vari ability in QTc interval) has recently been proposed as being a more se nsitive marker of repolarisation abnormalities and shown to be a more specific index of arrhythmia risk. Although hypoxaemia and fenoterol h ave previously been shown to prolong the QTc interval, this does not r eflect regional myocardial repolarisation abnormalities. Methods - Ele ctrophysiological effects were measured at baseline and after 30 minut es steady state hypoxaemia at an arterial oxygen saturation (SaO(2)) o f 75-80% (study 1) and at baseline then 30 minutes after inhaled fenot erol 2.4 mg (study 2). From the EGG, lead II corrected QT interval (QT c) and overall corrected QT dispersion were measured using a computer linked digitising tablet according to standard criteria. Results - QTc dispersion was increased during hypoxia compared with baseline values (mean (SE) 69 (6) ms v 50 (5) ms) and after fenoterol compared with b aseline (79 (13) v 46 (4) ms), respectively. There was also an increas e in QTc interval and heart rate after fenoterol (493 (23) v 420 (6) m s and 98 (3) v 71 (6) bpm, respectively). The heart rate was increased during hypoxaemia compared with baseline (78 (3) v 64 (2) bpm), but n o change occurred in the QTc interval. Conclusions - Both hypoxaemia a nd fenoterol cause myocardial repolarisation abnormalities in man in t erms of increased QTc dispersion, but only fenoterol increased the QTc interval. This may be relevant in the aetiology of arrhythmias in pat ients with acute severe asthma where beta agonist therapy and hypoxaem ia coexist.