Increased propensity for apnea in response to acute elevations in left atrial pressure during sleep in the dog

• Published in: Journal of applied physiology (1985) 2006-07, Vol.101 (1), p.76-83
• Main Authors: Chenuel, Bruno J, Smith, Curtis A, Skatrud, James B, Henderson, Kathleen S, Dempsey, Jerome A
• Format: Article
• Language: English
• Subjects: Animals; Apnea - etiology; Apnea - physiopathology; Atrial Function, Left - physiology; Biological and medical sciences; Blood pressure; Blood Pressure - physiology; Carbon Dioxide - analysis; Cardiac arrhythmia; Cardiac Output - physiology; Chemoreceptor Cells - physiology; Dogs; Expiratory Reserve Volume - physiology; Female; Fundamental and applied biological sciences. Psychology; Heart failure; Heart Failure - complications; Heart Rate - physiology; Hypertension, Pulmonary - complications; Hypertension, Pulmonary - physiopathology; Hyperventilation - etiology; Hyperventilation - physiopathology; Pulmonary Ventilation - physiology; Respiratory Mechanics - physiology; Sleep - physiology; Sleep apnea; Sleep Wake Disorders - etiology; Sleep Wake Disorders - physiopathology; Studies; Wakefulness - physiology
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.01617.2005

1 Laboratoire de Physiologie, Faculté de Médecine de Nancy, Université Henri Poincaré, Nancy, France; and 2 John Rankin Laboratory of Pulmonary Medicine, Departments of Population Health Sciences and Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin Submitted 22 December 2005 ; accepted in final form 14 March 2006 Periodic breathing is commonly observed in chronic heart failure (CHF) when pulmonary capillary wedge pressure is abnormally high and there is usually concomitant tachypneic hyperventilation. We hypothesized that acute pulmonary hypertension at pressures encountered in CHF and involving all of the lungs and pulmonary vessels would predispose to apnea/unstable breathing during sleep. We tested this in a chronically instrumented, unanesthetized dog model during non-rapid eye movement (NREM) sleep. Pulmonary hypertension was created by partial occlusion of the left atrium by means of an implanted balloon catheter in the atrial lumen. Raising mean left atrial pressure by 5.7 ± 1.1 Torr resulted immediately in tachypneic hyperventilation [breathing frequency increased significantly from 13.8 to 19.9 breaths/min; end-tidal P CO 2 (P ET CO 2 ) fell significantly from 38.5 to 35.9 Torr]. This tachypneic hyperventilation was present during wakefulness, NREM sleep, and rapid eye movement sleep. In NREM sleep, this increase in left atrial pressure increased the gain of the ventilatory response to CO 2 below eupnea (1.3 to 2.2 l·min –1 ·Torr –1 ) and thereby narrowed the CO 2 reserve [P ET CO 2 (apneic threshold) – P ET CO 2 (eupnea)], despite the decreased plant gain resulting from the hyperventilation. We conclude that acute pulmonary hypertension during sleep results in a narrowed CO 2 reserve and thus predisposes toward apnea/unstable breathing and may, therefore, contribute to the breathing instability observed in CHF. heart failure; pulmonary hypertension; tachypnea; apneic threshold Address for reprint requests and other correspondence: C. A. Smith, John Rankin Laboratory of Pulmonary Medicine, Dept. of Population Health Sciences, Univ. of Wisconsin School of Medicine and Public Health, Rm. 4245 MSC, 1300 Univ. Ave., Madison, WI 53706 (e-mail: casmith4{at}wisc.edu )