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.

Objective We investigated the role of right-to-left shunt with standardized transcranial Doppler ultrasonography in a large population of divers referred for symptoms of decompression illness. Design Case series compared with a control group. Setting Military teaching hospital, hyperbaric unit. Patients Patients were 101 consecutive divers with clinical evidence of decompression illness and a control group of 101 healthy divers. Intervention Specification of the type of decompression illness involved and detection/evaluation of right-to-left shunt by standardized transcranial Doppler. The degree of right-to-left shunt was defined as major if the number of high-intensity transient signals in the middle cerebral artery was >20. Measurements and Main Results We evaluated the odds ratios by logistic regression analysis with vs. without right-to-left shunt for subjects with cochleovestibular symptoms, cerebral decompression illness, spinal decompression illness, and Caisson sickness. Of the 101 divers presenting with decompression illness, transcranial Doppler detected a right-to-left shunt in 59 (58.4%), whereas control subjects demonstrated a right-to-left shunt in 25 cases (24.8%; odds ratio, 4.3; 95% confidence interval, 2.3–7.8;p = .09). When a right-to-left shunt was detected, the right-to-left shunt was major in 12 of 25 patients in the control group and in 49 of 59 patients in the decompression illness group (odds ratio, 8.7; 95% confidence interval, 4.2–18.0;p < .001). Within the decompression illness group, the proportion of major right-to-left shunt was 24 of 34 (odds ratio, 29.7; 95% confidence interval, 10.0–87.2;p < .0001) in the cochleovestibular subgroup, 13 of 21 (odds ratio, 24.1, 95% confidence interval, 6.8–86.0, p < 0.0001) in the cerebral decompression illness subgroup, ten of 31 (odds ratio, 3.9; 95% confidence interval, 1.5–10.3;p < .01) in the spinal decompression illness subgroup, and two of two (odds ratio, 1.1; 95% confidence interval, 0.2–5.7;p = .9) in the subgroup of divers with Caisson sickness. Conclusion Based on our results, we conclude that major right-to-left shunt was associated with an increased incidence of cochleovestibular and cerebral decompression illness, suggesting paradoxical embolism as a potential mechanism.

Objective: To investigate whether prehydration 90 min before a dive could decrease bubble formation, and to evaluate the consequent adjustments in plasma volume (PV), water balance and plasma surface tension (ST). Methods: Eight military divers participated in a crossover trial of pre-dive hydration using saline–glucose beverage (protocol 1) and a control dive with no prehydration (protocol 2). Drink volume was 1300 ml (osmolality 324 mOsm/l) and drinking time was 50–60 min. The diving protocol consisted of an open sea field air dive at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Haemodynamic parameters, body weight measurements, urine volume and blood samples were taken before/after fluid intake and after the dive. Decompression bubbles were examined by a precordial pulsed Doppler. Results: Bubble activity was significantly lower for protocol 1 than for protocol 2. PV increased after fluid ingestion by 3.5% and returned toward baseline after diving for protocol 1, whereas it decreased by 2.2% after diving for protocol 2. Differences in post-dive PV between the two conditions were highly significant. Body weight loss before/after diving and post-dive urine volume after diving were significant in both protocols, but the relative decline in weight remained lower for protocol 1 than for protocol 2, with reduction of negative water balance due to higher fluid retention. There were no differences in ST after fluid intake and after diving for the two protocols. Conclusion: Pre-dive oral hydration decreases circulatory bubbles, thus offering a relatively easy means of reducing decompression sickness risk. The prehydration condition allowed attenuation of dehydration and prevention of hypovolaemia induced by the diving session. Hydration and diving did not change plasma surface tension in this study.