TY - JOUR
T1 - Hypocapnia and increased ventilatory responsiveness in patients with idiopathic central sleep apnea
AU - Xie, Ailiang
AU - Rutherford, Ruth
AU - Rankin, Fiona
AU - Wong, Brian
AU - Bradley, T. Douglas
PY - 1995/12
Y1 - 1995/12
N2 - We previously demonstrated that central apneas during sleep in patients with idiopathic central sleep apnea (ICSA) are triggered by abrupt hyperventilation. In addition, baseline P(CO2) at the time of augmented breaths which triggered central apneas was lower than for augmented breaths which did not trigger apneas. These observations led us to hypothesize that patients with ICSA chronically hyperventilate maintaining their P(CO2) close to the threshold for apnea during sleep owing to increased chemical respiratory drive. To test these hypotheses, we recorded transcutaneous P(CO2) (Ptc(CO2)) during overnight sleep studies on nine consecutive patients with ICSA and nine sex-, age-, and body-mass-index-matched control subjects. Daytime Pa(CO2) as well as rebreathing and single breath ventilator/responses to CO2 were also measured. Compared with the control subjects, the patients had significantly lower mean Ptc(CO2) during sleep (37.8 ± 1.2 versus 42.7 ± 10.9 mm Hg, p < 0.01) and lower Pa(CO2) while awake (35.1 ± 1.3 versus 38.8 ± 0.9 mm Hg, p < 0.05). Furthermore, patients with ICSA had significantly higher ventilatory responses to CO2 for both the rebreathing (3.14 ± 0.34 versus 1.60 ± 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 ± 0.10 versus 0.25 ± 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1) patients with ICSA chronically hyperventilate awake and asleep and (2) chronic hyperventilation is probably related to augmented central and peripheral respiratory drive which predisposes to respiratory control system instability.
AB - We previously demonstrated that central apneas during sleep in patients with idiopathic central sleep apnea (ICSA) are triggered by abrupt hyperventilation. In addition, baseline P(CO2) at the time of augmented breaths which triggered central apneas was lower than for augmented breaths which did not trigger apneas. These observations led us to hypothesize that patients with ICSA chronically hyperventilate maintaining their P(CO2) close to the threshold for apnea during sleep owing to increased chemical respiratory drive. To test these hypotheses, we recorded transcutaneous P(CO2) (Ptc(CO2)) during overnight sleep studies on nine consecutive patients with ICSA and nine sex-, age-, and body-mass-index-matched control subjects. Daytime Pa(CO2) as well as rebreathing and single breath ventilator/responses to CO2 were also measured. Compared with the control subjects, the patients had significantly lower mean Ptc(CO2) during sleep (37.8 ± 1.2 versus 42.7 ± 10.9 mm Hg, p < 0.01) and lower Pa(CO2) while awake (35.1 ± 1.3 versus 38.8 ± 0.9 mm Hg, p < 0.05). Furthermore, patients with ICSA had significantly higher ventilatory responses to CO2 for both the rebreathing (3.14 ± 0.34 versus 1.60 ± 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 ± 0.10 versus 0.25 ± 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1) patients with ICSA chronically hyperventilate awake and asleep and (2) chronic hyperventilation is probably related to augmented central and peripheral respiratory drive which predisposes to respiratory control system instability.
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U2 - 10.1164/ajrccm.152.6.8520761
DO - 10.1164/ajrccm.152.6.8520761
M3 - Article
C2 - 8520761
AN - SCOPUS:0028867009
SN - 1073-449X
VL - 152
SP - 1950
EP - 1955
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 6 I
ER -