Immersion pulmonary edema is potentially a catastrophic condition; however, the pathophysiological mechanisms are ill-defined. This study assessed the individual and combined effects of exertion and negative pressure breathing on the cardiovascular system during the development of pulmonary edema in SCUBA divers. Sixteen male professional SCUBA divers performed four SCUBA dives in a freshwater pool at 1 m depth while breathing air at either a positive or negative pressure both at rest or with exercise. Echocardiography and lung ultrasound were used to assess the cardiovascular changes and lung comet score (a measure of interstitial pulmonary edema). The ultrasound lung comet score was 0 following both the dives at rest regardless of breathing pressure. Following exercise, the mean comet score rose to 4.2 with positive pressure breathing and increased to 15.1 with negative pressure breathing. The development of interstitial pulmonary edema was significantly related to inferior vena cava diameter, right atrial area, tricuspid annular plane systolic excursion, right ventricular fractional area change, and pulmonary artery pressure. Exercise combined with negative pressure breathing induced the greatest changes in these cardiovascular indices and lung comet score. A diver using negative pressure breathing while exercising is at greatest risk of developing interstitial pulmonary edema. The development of immersion pulmonary edema is closely related to hemodynamic changes in the right but not the left ventricle. Our findings have important implications for divers and understanding the mechanisms of pulmonary edema in other clinical settings.

Background: Pulmonary immersion oedema is a frequent diving accident. Although its outcome is generally favourable within 72 h, it can nonetheless lead to heart failure or sudden death. Cases of transient myocardial dysfunction have been reported in the literature. This phenomenon is similar to Takotsubo syndrome in many ways. It is characterised by transient myocardial hypokinesia, without associated coronary lesions. Methods: We report on 20 cases of patients who showed transient alteration of left ventricular kinetics with normal coronary angiography over the course of an immersion pulmonary oedema. Results: The echocardiographic localisation of the myocardial damage was generally focal and not centred on the apex with an average left ventricular ejection fraction of 45%. The main anomalies in the electrocardiographic repolarisation were T wave inversion with corrected QT interval prolongation. We also observed a moderate increase in troponin levels, with discordance between the enzymatic peak and the severity of the left ventricle segmental dysfunction. Conclusion: These cases suggest the incidence of a clinical entity strongly reminiscent of Takotsubo phenomenon of atypical topography as a consequence of diving accidents.

In healthy divers, the occurrence of immersion pulmonary oedema (IPE) is commonly caused by contributory factors including strenuous exercise, cold water and negative-pressure breathing. Contrary to this established paradigm, this case reports on a 26-year-old, well-trained combat swimmer who succumbed to acute IPE during static immersion in temperate (21°C) water, while using a front-mounted counterlung rebreather. The incident occurred during repeated depth-controlled ascent practice at the French military diving school. It was discovered that the diver had attempted to stop any gas leakage into the system by over-tightening the automatic diluent valve (ADV) (25th notch of 27) during the dive, thus causing a high resistance to inspiratory flow. The ventilatory constraints imposed by this ADV setting were assessed as a 3.2 Joules∙L-1 inspiratory work of breathing and -5 kPa (-50 mbar) transpulmonary pressure. This report confirms the key role of negative pressure breathing in the development of interstitial pulmonary oedema. Such a breathing pattern can cause a lowering of thoracic, airway and interstitial lung pressure, leading to high capillary pressure during each inspiration. Repetition of the diving drills resulted in an accumulation of interstitial lung water extravasation, causing pathological decompensation and proven symptoms.

Head-out water immersion alters respiratory compliance which underpins defining pressure at a “Lung centroid” and the breathing “Static Lung Load”. In diving medicine as in designing dive-breathing devices a single value of lung centroid pressure is presumed as everyone’s standard. On the contrary, we considered that immersed respiratory compliance is disparate among a homogenous adult group (young, healthy, sporty). We wanted to substantiate this ample scattering for two reasons: (i) it may question the European standard used in designing dive-breathing devices; (ii) it may contribute to understand the diverse individual figures of immersed work of breathing. Resting spirometric measurements of lung volumes and the pressure–volume curve of the respiratory system were assessed for 18 subjects in two body positions (upright Up, and supine Sup). Measurements were taken in air (Air) and with subjects immersed up to the sternal notch (Imm). Compliance of the respiratory system (Crs) was calculated from pressure–volume curves for each condition. A median 60.45% reduction in Crs was recorded between Up-Air and Up-Imm (1.68 vs 0.66 L/kPa), with individual reductions ranging from 16.8 to 82.7%. We hypothesize that the previously disregarded scattering of immersion-reduced respiratory compliance might participate to substantial differences in immersed work of breathing.