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An Unusual Effect of Atropine on Overdrive Suppression
Author(s) -
Tali T. Bashour,
R Hemb,
Rajasekaran Wickramesekaran
Publication year - 1973
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.48.4.911
Subject(s) - medicine , atropine , bradycardia , sinus bradycardia , sinus (botany) , heart rate , anesthesia , cardiology , blood pressure , botany , biology , genus
To the Editor: By their elegant assessment of sinoatrial conduction during premature atrial stimulation, Strauss et al. (CIRCULATION 47: 86, 1973) have uncovered one major limitation of the rapid atrial pacing as a method of evaluating sinoatrial node automaticity by post drive suppression. This and probably other yet undiscovered facts may account for the inconsistent results obtained by this technique including those from our center.1 During the past year we have been repeating the studies after the administration of 1 mg atropine intravenously. On several occasions we have noticed an apparent paradoxical prolongation after atropine of a previously normal post overdrive sinoatrial recovery time in patients who had the classical clinical picture of the sick sinus node syndrome.2 Most recently, we have evaluated a 64-year-old woman with sinus bradyeardia, frequent sinus arrest, congestive heart failure, palpitations, and two previous episodes of near syncope occurring after usual activity. Premature atrial stimulation indicated high grade sinoatrial entrance block as outlined by Strauss et al. Sinus post overdrive recovery time was normal at rates 80, 100, 110/min for pacing durations of 30 see, 60 see, and 180 sec each time. Only after pacing at a rate of 120 for one minute, did recovery time increase to 2.92 sec (fig. 1). Following 1 mg atropine intravenously, pacing at a rate of 120/mim for one minute resulted in marked post drive suppression and an escape junctional rhythm with retrograde atrial capture of 4.9 sec. Sinus activity was apparent only after 18.3 sec (fig. 2). Although actual sinus recovery may have occurred anytime between 4.9 and 18.3 sec and was suppressed by the retrograde junctional activity, nevertheless, this still represents marked delay. We postulate that sinoatrial entrance block was reversed or significantly reduced by atropine, thus allowing more constant discharge of the sinoatrial node during atrial pacing which has unmasked its profound post drive suppression. We are currently in the process of evaluating this phenomenon in other patients; meanwhile we believe atropine should be given and recovery time reassessed whenever rapid atrial pacing fails to elicit a prolongation of sinoatrial recovery time in patients with the sick sinus node syndrome. TALI BASHOUR, M.D. RAUL HEMB, M.D. RAJASEKARAN WICKRAMESEKARAN, M.D.

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