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Indices of acceleration atelectasis and the effect of hypergravity duration on its development: Acceleration atelectasis measurements

Research output: Contribution to journalArticle

Ross Pollock, S Gates, Jessica Storey, Jeremy Radcliffe, Alec Stevenson

Original languageEnglish
JournalExperimental Physiology
Published3 Apr 2020


King's Authors


New Findings: What is the central question of the study? The aim was to determine the effects of duration of acceleration in the cranial–caudal direction (+Gz) on acceleration atelectasis and identify measurement techniques that can be used to assess it. What is the main finding and its importance? Non-invasive measurement of acceleration atelectasis using electrical impedance tomography and estimates of pulmonary shunt provide more detailed assessment of acceleration atelectasis than traditional forced vital capacity measures. Using these techniques, it was found that as little as 30 s of exposure to +Gz acceleration can cause acceleration atelectasis. The results of the present study will allow a more accurate and detailed assessment of acceleration atelectasis in the future. Abstract: Recently, there have been reports of acceleration atelectasis during fast jet flight despite the use of systems designed to minimize this. Before further investigation of this, indices suitable for use in applied settings and identification of acceleration durations that elicit it are required. Fifteen non-aircrew subjects underwented five centrifuge exposures lasting 15, 30, 60 and 2 × 90 s with a plateau of +5 Gz (acceleration in the cranial-caudal direction) while breathing 94% O 2 during all but one control exposure (21% O 2). Lung volumes and gas exchange limitation were assessed after each exposure. Regional lung impedance and compliance were measured after Gz exposure using electrical impedance tomography and the forced oscillatory technique, respectively. The presence of acceleration atelectasis was confirmed by reductions of 10–17% in vital and inspiratory capacity after 60 and 90 s Gz exposures (P < 0.05) and resulted in reduced regional lung impedance and a gas exchange limitation of 8.1 and 12.5%, respectively (P < 0.05). There was also a small but significant decrease in regional lung impedance after 30 s exposures. Functional residual capacity and lung compliance were unchanged in atelectatic lungs (P > 0.05). In the majority of individuals, >60 s of Gz exposure while breathing 94% O 2 causes acceleration atelectasis. Electrical impedance tomography and the measurement of gas exchange limitation provide useful indicators of acceleration atelectasis. Acceleration atelectasis exerts its effects primarily through basal lung closure and reflex inspiratory limitation, both of which can be reversed by performing three maximal inspiratory breathing manoeuvres.

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