Ion channels and ElectrophysiologyP314Pathphysiological significance of the medicamentous autonomous blockades for the assessment of sinoatrial node function in patients with heart rhythm disturbances

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To differentiate structural and functional impairments of sinus node (SN) from secondary autonomous insufficiencies pts (aged 18-65 years) with paroxysmal supraventricular tachycardia, atrial fibrillation, sinus bradicardia and sinoatrial block were investigated. Medicamentous autonomous blockade (MAB)- total SN denervation with atropine and propranolol or cholinergic blockade with atropine were performed in each case. Under MAB Tran esophageal left atrial stimulation (TLAS) was performed and sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT) and sinoatrial conduction time (SACT) were determined. The SN was denervated with i.v. propranolol (0,2 mg/kg during 3 min) and 10 min later with atropine (0,04mg/kg during 2min). To assess the value of chronotrope influence of autonomous nervous system (ANS) on intrinsic heart rate (IHR) and percent of deviation of heart rate at rest (HRR) from IHR were determined. During isolated atropine tests (AT) max percent of HR increase and background heart rate recovery time (BHRRT) were evaluated. HR deviation from intrinsic above 15% was detected in 22,9 ± 1,6% of pts with secondary (autonomous) SN dysfunction and in 25,4 ± 0,6% of pts with intact function of SN. HR deviation from IHR below 15% was shown in 12,5 ± 1,8% of pts with primary (organic) SND. At HRR deviation from IHR below 15% the administration of AT for the identification of secondary SND is recommended. Under AT the percent of HRR increase below 35% and BHRRT below 45 min are the indicators of primary SND. 35 to 60% increase of HRR deviation above 60% is the indicator of intact function of SN. Under total MAB in pts with primary and secondary SND the prolonged CSNRT and CSSNRT were reduced. We conclude that coupled with TLAT the total MAB and AT facilitate SND diagnosis and its path physiological mechanism determination.

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