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Tidal volume and breathing frequency responses to poikilocapnic and isocapnic hypoxia in humans
Author(s) -
Steinback Craig D,
Poulin Marc J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a376-c
Subject(s) - tidal volume , chemistry , ventilation (architecture) , hypoxia (environmental) , hypoxic ventilatory response , respiration , anesthesia , torr , respiratory frequency , medicine , zoology , oxygen , respiratory system , biology , anatomy , mechanical engineering , physics , engineering , thermodynamics , organic chemistry
The acute response to hypoxia in humans has been reported to arise predominately from increases in tidal volume (V T ) with negligible changes in breathing frequency (f B ). The effect of arterial CO 2 on this response has not been described. We examined the ventilatory contributions of V T and f B to the hypoxic response under both poikilocapnic (PH) and isocapnic (IH) conditions in 10 normal adults (26 ± 4 yrs, mean ± SD). During IH, PETCO 2 was held constant at 37 ± 2.0 Torr (1 Torr above resting values) while PETO 2 was reduced stepwise to 45 Torr using the technique of dynamic end‐tidal gas forcing. During PH, PETO 2 was reduced stepwise to 45 Torr while PETCO 2 was uncontrolled (i.e. zero inspired CO 2 ). Hypoxia was maintained for 20 minutes, and tests were separated by 1 hour. Peak ventilation (V E ), was significantly higher during IH (49.8 ± 14.3 L·min −1 ) compared to PH (24.1 ± 7.7 L·min −1 , P < 0.001). During IH, peak V E was mediated by increases in both V T (1.0 ± 0.4 to 2.2 ± 0.5 L, P < 0.001) and f B (14.7 ± 4.6 to 19.2 ± 4.5 breaths·min −1 , P < 0.05), while during PH peak V E was mediated by increased V T (0.8 ± 0.2 to 1.5 ± 0.4 L, P < 0.01) with no change observed in f B . At the termination of both IH and PH, a significant frequency undershoot was observed (20 ± 23 %, P < 0.05 and 22 ± 22 %, P < 0.01 respectively), previously documented only in animals. These data demonstrate a role of arterial CO 2 in the development of a f B response to hypoxia, though whether this is due to CO 2 per se or the magnitude of peak V E remains unknown. We have also documented a significant post hypoxic frequency decline not previously reported in humans occurring during both conditions. This study was approved by the local Ethics board and supported by AHFMR, HSFA and CIHR.