Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/61534
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Type: Journal article
Title: Atrial electrophysiology is altered by acute hypercapnia but not hypoxemia: Implications for promotion of atrial fibrillation in pulmonary disease and sleep apnea
Author: Stevenson, I.
Roberts-Thomson, K.
Kistler, P.
Edwards, G.
Spence, S.
Sanders, P.
Kalman, J.
Citation: Heart Rhythm, 2010; 7(9):1263-1270
Publisher: Elsevier Inc.
Issue Date: 2010
ISSN: 1547-5271
1556-3871
Statement of
Responsibility: 
Irene H. Stevenson, Kurt C. Roberts-Thomson, Peter M. Kistler, Glenn A. Edwards, Steven Spence, Prashanthan Sanders, Jonathan M. Kalman
Abstract: Background: Chronic pulmonary disease and sleep apnea have been associated with the development of atrial fibrillation (AF). Objective: The purpose of this study was to characterize the atrial electrical changes that occur with hypercapnia and hypoxemia and to determine their role in AF development. Methods: Seventeen sheep (6 control, 5 hypercapnia, 6 hypoxemia) underwent open chest electrophysiologic evaluation under autonomic blockade. A 64-electrode endocardial basket catheter was positioned in the right atrium, and 2 × 128 electrode epicardial plaques were sutured to the right atrial and left atrial appendages to determine atrial refractoriness (effective refractory period [ERP]) at 9 sites and 5 cycle lengths, conduction time to fixed points on each plaque, and AF vulnerability. Results: Hypercapnia was associated with a 152% lengthening of ERP from baseline and increased conduction time. ERPs rapidly returned to baseline, but recovery of conduction was delayed at least 117 ± 24 minutes following resolution of hypercapnia. AF vulnerability was reduced during hypercapnia (with increased ERP) but increased significantly with subsequent return to eucapnia (when ERP normalized but conduction time remained prolonged). No significant changes in ERP, atrial conduction time, or AF vulnerability occurred in hypoxemic or control groups. Conclusion: Differential recovery of ERP and conduction that occurs following hypercapnia might account for the increased vulnerability to AF observed in the phase after return to eucapnia. This may explain in part the increased prevalence of AF in pulmonary disease and sleep apnea.
Keywords: Atrial fibrillation; Electrophysiology; Hypercapnia; Hypoxemia; Sleep apnea
Rights: © 2010 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.
RMID: 0020097503
DOI: 10.1016/j.hrthm.2010.03.020
Appears in Collections:General Practice publications

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