Non‐Invasive Pulmonary Gas Exchange Measurements Following Deep Breath‐Hold Diving
Authors: Patrician Alexander , Drvis Ivan , Dawkins Tony , Otto Barak , Coombs Geoff , Howe Connor , Caldwell Hannah , Janjic Nebojsa , Spajic Boris , Stembridge Michael , Dujic Zeljko , Ainslie Philip 
Published: June 2021

Breath‐hold diving is a ubiquitous activity, with recreational, fishing, military and competitive divers. During a dive, immersion and the increasing hydrostatic pressure of descent facilitate cardiovascular adjustments that promote a blood volume shift into the heart and chest vasculature, further augmenting autonomic responses (i.e. diving bradycardia, peripheral vasoconstriction, and splenic contraction) to conserve O2. Exceeding the compliant capacity of the lung and associated tissues can result in pulmonary injury called squeeze, which is characterized by post‐dive coughing, wheezing and hemoptysis. To provide insight into the consequences of such lung squeeze, our objective was to evaluate the time‐course of a maximal deep dive on pulmonary gas exchange, pulmonary artery systolic pressures (PASP), and ultrasound lung comets (ULCs). Ten healthy trained breath‐hold divers (33±9 yr; 80±15 kg; 185±9 cm) performed a maximal effort dive (55±12 m; range 40–76 m). Pulmonary gas exchange and PASP were performed at baseline, and repeated at 10 and 60 min post dive. Pulmonary gas exchange was non‐invasively measured by collecting end‐tidal PO2 and PCO2 during steady‐state breathing, and derived arterial PO2 via pulse oximetry. O2 deficit was defined as the difference between end‐tidal and calculated arterial PO2; consistent with the Bohr effect by utilizing end‐tidal PCO2. The ULCs were collected bilaterally, parasternal to mid‐axillary, at baseline and again 2.5 h post dive. Following the dive, although there was an impairment of pulmonary gas exchange, evident by an increase in O2 deficit from 10.9±4.5 mmHg at baseline to 22.9±5.1 mmHg 10‐min post dive (p=0.02), this deficit had normalized by 60‐min post. There was persistent hyperventilation up to 60 min post dive, reflected by reductions in end‐tidal PCO2 (p=0.02). PASP was unaltered post‐dive. Although ULCs trended to increase from baseline to 2.5 h post dive (3.7±3 to 10.4±13.2 comets; p=0.09), the delta change in ULC from baseline to post‐dive was positively correlated with depth (r=0.67, p=0.04) and, to a lesser extent, with both change in SpO2 (r=−0.62, p=0.06) and O2 deficit (r=0.58, p=0.08). The findings of this novel study suggest impairment in pulmonary gas exchange is present following diving to depth, even up to 10 min after surfacing. The mechanism(s) driving the slight hyperventilation are unclear, but potentially could be mediated via mild pulmonary edema and/or stimulation of juxtapulmonary capillary receptors. Together, there is transient impairment in gas exchange and associations with ULC during ‘modest’ dives. The development of pathological pulmonary edema, and severe and sustained impairment in pulmonary gas exchange, would seem likely at the forefront of breath‐hold diving performances (e.g, >100 m). There remains little data regarding safe return‐to‐dive practices following a squeeze, and non‐invasive pulmonary gas exchange monitoring could provide valuable utility.Support or Funding InformationCanada Research Chair, NSERCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.