Cardiovascular effects of breath-hold diving at altitude.

Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.

B-type natriuretic peptide secretion following scuba diving.

AIM: To examine the neurohormonal effects of a scuba dive, focusing on the acute changes in the plasma concentrations of the different peptide fragments from the B-type natriuretic peptide (BNP) precursor. MATERIALS & METHODS: We studied 12 healthy scuba divers (mean age ± standard deviation: 44 ± 7 years; range: 34-55 years; BMI: 24.8 ± 2.8 kg/m(2)), who performed a 15-m depth dive in salt water, with a bottom time of 30 min. Blood samples for BNPs (pro-B-type natriuretic peptide [pro-BNP], BNP and aminoterminal pro-BNP) and catecholamines were measured in plasma before immersion, and after the dive. A continuous electrocardiographic recording was obtained during the entire protocol. RESULTS: BNP, aminoterminal pro-BNP and pro-BNP plasma concentrations slightly, but significantly, increased after the scuba dive (18 ± 15 to 21 ± 11 ng/l, p = 0.020; 32 ± 19 to 38 ± 21 ng/l, p = 0.008; and 7.8 ± 1.6 to 10.3 ± 3.6 ng/l, p = 0.028, respectively) in parallel with norepinephrine concentration (743 ± 323 to 1163 ± 656 ng/l, p = 0.014), with no variations in total plasma proteins, hematocrit or osmolality. A persistent sinus tachycardia was observed during all phases of the dive. CONCLUSIONS: A 15-m depth scuba dive induces an acute slight release of the different peptide fragments from the BNP precursor, likely through the stimulation of a constitutive secretory pathway promoted by adrenergic activation and cardiac chamber dilation.