SUSCEPTIBILITY TO PERIODIC BREATHING WITH ASSISTED VENTILATION DURINGSLEEP IN NORMAL SUBJECTS

Citation
S. Meza et al., SUSCEPTIBILITY TO PERIODIC BREATHING WITH ASSISTED VENTILATION DURINGSLEEP IN NORMAL SUBJECTS, Journal of applied physiology (1985), 85(5), 1998, pp. 1929-1940
Citations number
34
Categorie Soggetti
Physiology,"Sport Sciences
ISSN journal
87507587
Volume
85
Issue
5
Year of publication
1998
Pages
1929 - 1940
Database
ISI
SICI code
8750-7587(1998)85:5<1929:STPBWA>2.0.ZU;2-Q
Abstract
Assisted ventilation with pressure support (PSV) or proportional assis t (PAV) ventilation has the potential to produce periodic breathing (P B) during sleep. We hypothesized that PB will develop when PSV level e xceeds the product of spontaneous tidal volume (VT) and elastance (VTs p.E) but that the actual level at which PB will develop [PSV(PB)] will be influenced by the Delta PCO2 (difference between eupneic PCO2 and CO2 apneic threshold) and by Delta RR [response of respiratory rate (R R) to PSV]. We also wished to determine the PAV level at which PB deve lops to assess inherent ventilatory stability in normal subjects. Twel ve normal subjects underwent polysomnography while connected to a PSV/ PAV ventilator prototype. Level of assist with either mode was increas ed in small steps (2-5 min each) until PB developed or the subject awa kened. End-tidal PCO2, VT, RR, and airway pressure (Paw) were continuo usly monitored, and the pressure generated by respiratory muscle (Pmus ) was calculated. The pressure amplification factor (PAF) at the highe st PAV level was calculated from [(Delta Paw + Pmus)/Pmus], where Delt a Paw is peak Paw - continuous positive airway pressure. PB with centr al apneas developed in 11 of 12 subjects on PSV. Delta PCO2 ranged fro m 1.5 to 5.8 Torr Changes in RR with PSV were small and bidirectional (+1.1 to -3.5 min-l). With use of stepwise regression, PSV(PB) was sig nificantly correlated with VTsp (P = 0.001), E (P = 0.00009), Delta PC O2 (P = 0.007), and Delta RR (P = 0.006). The final regression model w as as follows: PSV(PB) = 11.1 VTsp + 0.3E - 0.4 Delta PCO2 - 0.34 Delt a RR - 3.4 (r = 0.98). PB developed in five subjects on PAV at amplifi cation factors of 1.5-3.4. It failed to occur in seven subjects, despi te PAF of up to 7.6. We conclude that I) a PCO2 apneic threshold exist s during sleep at 1.5-5.8 Torr below eupneic PCO2, 2) the development of PB during PSV is entirely predictable during sleep, and 3) the inhe rent susceptibility to PB varies considerably among normal subjects.