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End‐expiratory lung volume remains stable during N 2 MBW in healthy sleeping infants
Author(s) -
Gustafsson Per M.,
Kadar Laszlo,
Kjellberg Sanna,
Andersson Lena,
Lindblad Anders,
Robinson Paul D.
Publication year - 2020
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14477
Subject(s) - functional residual capacity , washout , nitrogen washout , lung volumes , plethysmograph , respiratory system , tidal volume , medicine , anesthesia , ventilation (architecture) , cardiology , lung , chemistry , mechanical engineering , engineering
We have previously shown that functional residual capacity (FRC) and lung clearance index were significantly greater in sleeping healthy infants when measured by N 2 (nitrogen) washout using 100% O 2 (oxygen) versus 4% SF 6 (sulfur hexafluoride) washout using air. Following 100% O 2 exposure, tidal volumes decreased by over 30%, while end‐expiratory lung volume (EELV, i.e., FRC) rose markedly based on ultrasonic flow meter assessments. In the present study to investigate the mechanism behind the observed changes, N 2 MBW was performed in 10 separate healthy full‐term spontaneously sleeping infants, mean (range) 26 (18–31) weeks, with simultaneous EELV monitoring (respiratory inductance plethysmography, RIP) and oxygen uptake (V´O 2 ) assessment during prephase air breathing, during N 2 washout by exposure to 100% O 2 , and subsequently during air breathing. While flow meter signals suggested a rise in ELLV by mean ( SD ) 26 (9) ml over the washout period, RIP signals demonstrated no EELV change. V'O 2 /FRC ratio during air breathing was mean ( SD ) 0.43 (0.08)/min, approximately seven times higher than that calculated from adult data. We propose that our previously reported flow meter‐based overestimation of EELV was in fact a physiological artifact caused by rapid and marked movement of O 2 across the alveolar capillary membrane into the blood and tissue during 100% O 2 exposure, without concomitant transfer of N 2 to the same degree in the opposite direction. This may be driven by the high observed O 2 consumption and resulting cardiac output encountered in infancy. Furthermore, the low resting lung volume in infancy may make this error in lung volume determination by N 2 washout relatively large.

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