Immersion Pulmonary Edema

Emmanuel Gouin1,2, Emmanuel Dugrenot1,2,3
1: Divers Alert Network (DAN), Durham, NC, USA
2: Univ Brest, ORPHY Laboratory, Brest, France
3: Department of Biomedical Engineering, University of North Carolina at Chapel Hill and NC State, Chapel Hill, NC, USA

Acknowledgments: Dr. Jim Chimiak and Dr. Matias Nochetto (DAN Medical Services, USA) as well as Dr. Sébastien De Maistre (Service de Santé des Armées, France) for their review and comments.

During a dive, the cardio-pulmonary changes may provoke an immersion pulmonary edema (IPE/IPO) and increase drowning risk (Castagna et al, 2017). The increase in capillary transmural pressure, influenced by hemodynamic and breathing dynamics, is considered a key factor in the mechanism of IPE (MacIver and Clark, 2015). A combination of stressors and adaptive mechanisms, such as blood shift associated with right to left ventricle imbalance, gas density, hyperoxia, thermal strain, exercise, etc. challenges the respiratory system (Tetzlaff and Thomas, 2017).

Extravascular Lung Water as an IPE Risk Marker
In humans, ultrasonic lung comets (ULC) or B-Lines (Figure 1) have been evidenced after scuba diving and might be related to impaired ventilation related with an accumulation of extravascular lung water (EVLW). Most studies have shown an accumulation of ULC in repetitive deep Open Circuit (OC) dives to 60–80 meters of seawater (msw or 200-260 fsw – feet of sea water), which is not observed at 33 msw (110 fsw) depth (Ljubkovic et al, 2010; Marinovic et al, 2010; Dujic et al, 2011). Conversely, with Closed Circuit Rebreathers (CCR), the lung aeration loss was detected, even in shallow water, between 1 and 10 msw (3.3 and 33 fsw) and was amplified by a moderate fin swimming exercise (Castagna et al, 2017; 2018; Martinez-Villar et al, 2022). The ULC appeared to be transient with a return to the baseline at 24 hours (Gouin et al, 2022).

Figure 1: Example of B-lines on pulmonary echography. A B-line is defined as an echogenic, coherent, wedge-shaped signal with a narrow origin arising from the hyperechogenic pleural line and extending to the far edge of the viewing area.

Rebreathers’ Impact on Pulmonary Function and IPE Risk
The breathing apparatus by itself may add constraints that influence the static lung load and the work of breathing (WOB). In CCR, the static lung breathing stems from the pressure gradient between the counter lungs and the diver’s lung centroid (i.e., the point of confluence of the forces exerted by the respiratory system). Indeed, in prone position, a back-mounted counter lungs CCR induces a negative pressure breathing (NPB) while the anterior position induces positive pressure breathing (PPB). Castagna has showed that the WOB during immersed activities and the development of interstitial pulmonary edema were more amplified with NPB in comparison to PPB, when the divers are in prone position (Castagna et al, 2018).

To the best of our knowledge, no studies are focusing on the effect of the CCR diver’s position. This position might influence the transpulmonary hydrostatic difference by influencing the pressure gradient (Wilmshurst, 2019), so we hypothesize that a trim position at 30° maximum (as it is usually taught to CCR divers) can reduce the in-water breathing constraints and the negative impact of equipment on the lung during CCR dives. Thus, this trim position might reduce the risk of IPE occurrence and could be encouraged in CCR community while open-circuit divers promote the prone position (Figure 2). Therefore, more studies are needed on this topic.

Figure 2: A) Back mounted CCR in a prone position; B) back mounted CCR in a modified trim position.

As previously mentioned, Gouin et al, (2022) study on CCR divers evaluated the cardiopulmonary impact of repeated back mounted CCR dives. During that study, they followed 8 CCR divers on a one-week diving trip in the Baltic Sea, and measured, among other things, spirometry parameters, oxygen saturation (SpO2), Heart Rate Variability (HRV), and lung ultrasonography score (LUS), which reflects possible extravascular lung water.

Interestingly, if they did observe transient increased LUS after diving combined with a slight non-pathological decrease in oxygen saturation (SpO2), it did not seem to correlate with depth, while the dives were up to 230 fsw or 70 msw (Figure 3).

Figure 3: Evolution of individual lung ultrasound score (LUS) throughout the repetition of day dives. All divers developed B-lines after several days and returned to baseline after the last dive.

In that study, the lung aeration disorders observed seem to be transient and not associated with functional alteration. This implies the impact of these impairments is unknown and should not be neglected until we better understand IPE physiopathology and the decrease in Forced Vital Capacity (FVC, which is a pulmonary function marker) observed during deeper CCR dives (Dugrenot et al, 2021). Further studies are needed on these two topics.

Besides these cardiopulmonary parameters, Gouin et al (2022) also collaborated in another study focused on the inflammatory pathway related to decompression sickness (DCS), more precisely on circulating microparticles, which are known to initiate a systemic inflammatory response. These microparticles were indeed increased after a deep CCR dive or after repetitive shallow CCR dives, highlighting that inflammatory events are decorrelated from the depth of diving, and might also impact lung function (Arya et al, 2023).

IPE Risk Factors
Well supported risk factors of IPE are: being over 50 years old, being a female, non-steroidal anti-inflammatory drug (NSAID) intake before diving, physical exertion prior to or during the dive, increased work of breathing (which will be affected by gas density), tight suit/equipment, cold water and arterial hypertension (Henckes et al, 2019; Wilmshurst, 2019). Some other factors, like overhydration, have also been cited (Edmonds et al, 2019). However, none of the statistics from the studies cited above have been able to confirm this.

Before drawing any conclusions, it is important to remember that even exercise itself can cause the appearance of B-lines, even on healthy subjects (Simonovic et al, 2018). Pressure variations could also impact B-line formation (Debevec et al, 2022). Moreover, negative pressure itself can trigger IPE (Bhattacharya et al, 2016) and even laryngospasm can draw fluids from pulmonary capillaries and trigger pulmonary edema (Andersen et al, 1988). Similarly, an increased inspiratory resistance caused by a poorly calibrated regulator may cause a transient sub-ambient pressure (negative pressure breathing) that could play a role in it the pathogenesis of IPE. This highlights the importance of a well set ADV (Automatic or Added Diluent Valve) and proper Optimal Loop Volume management, and even raises the question of a mandatory use of the ADV for training and exploration.

CCR: Closed Circuit Rebreathers
EVLW: extravascular lung water
Fsw: feet of salt water
FVC: Forced Vital Capacity
HRV: Heart Rate Variability
IPE/IPO: Immersed Pulmonary O(E)dema
LUS: lung ultrasonography score
Msw: meters of sea water
NPB: negative pressure breathing
NSAID: non-steroidal anti-inflammatory drug
OC: Open Circuit
PPB: positive pressure breathing
SpO2: oxygen saturation
ULC: ultrasonic lung comets
WOB: work of breathing

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