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What are the mechanisms producing increased ventilation in dead space studies in neonates?
Author(s) -
Upton C. J.,
Milner A. D.,
Stokes G. M.,
Carman P. G. T.
Publication year - 1990
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950090303
Subject(s) - dead space , ventilation (architecture) , medicine , pco2 , respiratory minute volume , anesthesia , tidal volume , artificial ventilation , respiration , respiratory system , mechanical ventilation , lung , respiratory disease , anatomy , meteorology , physics
In 21 studies on 15 infants an additional dead space tube produced a significant rise in end‐tidal P CO 2and fall in end‐tidal P O 2, associated with a rise in minute ventilation (228 ± 77 mL/kg/min at zero, 348 ± 85 mL/kg/min at one, and 437 ± 128 mL/kg/min at two anatomical dead spaces). The differences between end‐inspiratory and end‐expiratory P CO 2and P O 2did not change significantly, suggesting an increase in dead space, but not in alveolar ventilation. In a further 9 babies the rise in ventilation was unchanged when measurements were repeated in 30% oxygen (361 ± 65 vs. 340 ± 54 mL/kg/min at one anatomical dead space). Studies on 8 babies, with the added tube ventilated by a fan, showed that a mean 28% of the rise in minute ventilation was due to increased resistance. Although the response to tube breathing in neonates is complex, carbon dioxide appears to be the major factor producing increased ventilation. Pediatr Pulmonal 1990; 9:136–139 .