Respiratory oscillations in alveolar oxygen tension measured in arterial blood

Federico Formenti,Clive E W Hahn,Nikhil Bommakanti,John N Cronin,Anders Larsson,Hanne Mcpeak,Goran Hedenstierna,Rongsheng Chen,Delphine Holopherne-Doran,Andrew D Farmery

doi:10.1038/s41598-017-06975-6

Abstract

Arterial oxygen partial pressure can increase during inspiration and decrease during expiration in the presence of a variable shunt fraction, such as with cyclical atelectasis, but it is generally presumed to remain constant within a respiratory cycle in the healthy lung. We measured arterial oxygen partial pressure continuously with a fast intra-vascular sensor in the carotid artery of anaesthetized, mechanically ventilated pigs, without lung injury. Here we demonstrate that arterial oxygen partial pressure shows respiratory oscillations in the uninjured pig lung, in the absence of cyclical atelectasis (as determined with dynamic computed tomography), with oscillation amplitudes that exceeded 50 mmHg, depending on the conditions of mechanical ventilation. These arterial oxygen partial pressure respiratory oscillations can be modelled from a single alveolar compartment and a constant oxygen uptake, without the requirement for an increased shunt fraction during expiration. Our results are likely to contribute to the interpretation of arterial oxygen respiratory oscillations observed during mechanical ventilation in the acute respiratory distress syndrome.

Highlights

In the healthy lung, arterial partial pressure of oxygen (PaO2) is thought to remain almost constant within the respiratory cycle during spontaneous breathing, via a physiological PO2 gradient between the alveoli and the pulmonary circulation[1]
PaO2 oscillations with an amplitude of about 10 mmHg and the same frequency as breathing were observed at a Respiratory rates (RR) of 12 breaths per minute, inspired-to-expired ratio (I:E) of 1:1, tidal volume (VT) of about 10 ml kg−1, and at mean PaO2 near 130 mmHg
The rate of PaO2 decline during breath holding depends on lung volume and metabolic rate, and is not associated with atelectasis in the uninjured lung

Summary

Introduction

Arterial partial pressure of oxygen (PaO2) is thought to remain almost constant within the respiratory cycle during spontaneous breathing, via a physiological PO2 gradient between the alveoli and the pulmonary circulation[1]. Respiratory PaO2 oscillations smaller than 16 mmHg have been detected with slow response time sensors[2] in animals with uninjured lungs when abnormally large tidal volumes (VT) greater than 20 ml kg−1 or even 30 ml kg−1 were delivered during mechanical ventilation[3, 4]. A significant limitation of the above mentioned studies is that the PaO2 oscillations observed in animal models of ARDS mostly appeared in association with a high average VT of 20 ml kg−1 7, 13, 30 ml kg−1 6, 14, or greater[10] These large VT were delivered in experiments without application of positive end-expiratory pressure (PEEP), and imposing elevated peak end-expiratory pressures in order to provoke cyclical atelectasis in the injured lung. We developed a fibre optic oxygen sensor[16], optimized its response time and linearity[17,18,19,20], tested it in vitro[21], showed it to be resistant to clotting, and demonstrated it to be capable of detecting rapid PaO2 changes in an www.nature.com/scientificreports/

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