Baroreceptor unloading in postural tachycardia syndrome augments peripheral chemoreceptor sensitivity and decreases central chemoreceptor sensitivity

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 301; no. 1; pp. H173 - H179
• Main Authors: Taneja, Indu, Medow, Marvin S., Clarke, Debbie A., Ocon, Anthony J., Stewart, Julian M.
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.07.2011
• Subjects: Adolescent; Adult; Blood Pressure - physiology; Carbon dioxide; Cardiovascular Neurohormonal Regulation; Central Nervous System - physiopathology; Chemoreceptor Cells - physiology; Data Interpretation, Statistical; Female; Heart Rate - physiology; Humans; Hypercapnia - physiopathology; Hyperoxia; Hyperventilation - etiology; Hyperventilation - physiopathology; Hypoxia; Hypoxia - physiopathology; Male; Oxygen; Peripheral Nervous System - physiopathology; Postural Orthostatic Tachycardia Syndrome - complications; Postural Orthostatic Tachycardia Syndrome - physiopathology; Pressoreceptors - physiology; Ventilation; Young Adult
• ISSN: 0363-6135; 1522-1539; 1522-1539
• DOI: 10.1152/ajpheart.01211.2010

While orthostatic tachycardia is the hallmark of postural tachycardia syndrome (POTS), orthostasis also initiates increased minute ventilation (V̇e) and decreased end-tidal CO 2 in many patients. We hypothesized that chemoreflex sensitivity would be increased in patients with POTS. We therefore measured chemoreceptor sensitivity in 20 POTS (16 women and 4 men) and 14 healthy controls (10 women and 4 men), 16–35 yr old by exposing them to eucapneic hyperoxia (30% O 2 ), eucapneic hypoxia (10% O 2 ), and hypercapnic hyperoxia (30% O 2 + 5% CO 2 ) while supine and during 70° head-upright tilt. Heart rate, mean arterial pressure, O 2 saturation, end-tidal CO 2 , and V̇e were measured. Peripheral chemoreflex sensitivity was calculated as the difference in V̇e during hypoxia compared with room air divided by the change in O 2 saturation. Central chemoreflex sensitivity was determined by the difference in V̇e during hypercapnia divided by the change in CO 2 . POTS subjects had an increased peripheral chemoreflex sensitivity (in l·min −1 ·%oxygen −1 ) in response to hypoxia (0.42 ± 0.38 vs. 0.19 ± 0.17) but a decreased central chemoreflex sensitivity (l·min −1 ·Torr −1 ) CO 2 response (0.49 ± 0.38 vs. 1.04 ± 0.18) compared with controls. CO 2 sensitivity was also reduced in POTS subjects when supine. POTS patients are markedly sensitized to hypoxia when upright but desensitized to CO 2 while upright or supine. The interactions between orthostatic baroreflex unloading and altered chemoreflex sensitivities may explain the hyperventilation in POTS patients.