Decompression illnesses (DCI), or as they are called more scientifically: dysbaric disorders, represent a complex spectrum of pathophysiological conditions with a wide variety of signs and symptoms related to dissolved gas and its subsequent phase change.1,2 Any significant organic or functional dysfunction in individuals who have recently been exposed to a reduction in environmental pressure (i.e., decompression) must be considered as possibly being caused by DCI until proven otherwise.

Infrequently, healthy individuals can develop acute pulmonary oedema when exposed to an extreme or unusual environment (ie, deep dives or high altitudes), especially during physical exertion. High-altitude pulmonary oedema (HAPO) has been reported in 0·5–7·0% of individuals who climb to altitudes higher than 4000 m (according to ascent speed), whereas swimming-induced pulmonary oedema (SIPO) has been reported in a different proportion of individuals engaged in aquatic activities.

Introduction: Heart rate variability (HRV) during underwater diving has been infrequently investigated because of environment limitations and technical challenges. This study aims to analyze HRV changes while diving at variable hyperoxia when using open circuit (OC) air diving apparatus or at constant hyperoxia using a closed-circuit rebreather (CCR).

The metabolism of nitric oxide plays an increasingly interesting role in the physiological response of the human body to extreme environmental conditions, such as underwater, in an extremely cold climate, and at low oxygen concentrations.

SCUBA diving exposes divers to decompression sickness (DCS). There has been considerable debate whether divers with a Patent Foramen Ovale of the heart have a higher risk of DCS because of the possible right-to-left shunt of venous decompression bubbles into the arterial circulation.