In breath-hold diving as in ordinary scuba diving, there are reported incidents of serious neurological symptoms, mimicking cerebral insults. The etiology for the symptoms in breath-hold diving is uncertain. It has been speculated that it may be due to decompression sickness, provided that there is enough nitrogen in tissue to cause supersaturation. However, as far as we are aware of, such venous gas bubbles have not been demonstrated. Neurological symptoms during breath-hold diving may also be consistent with arterial gas embolism (AGE) caused by gas entering the arterial circulation due to pulmonary barotrauma. The divers often use a special respiratory maneuver to hyperinflate the lungs before diving, termed glossopharyngeal insufflation (GI). After a maximal inspiration the diver opens the glottis and uses the glossopharyngeal musculature to force air into the lungs repeatedly. We hypothesized that this maneuver may increase pulmonary pressure to a degree which overdistends the lungs and causes rupture of the alveoli, thereby being a substrate for AGE.
Six competitive breath-hold divers were examined for pneumomediastinum and AGE, by performing computer tomography thorax and transthoracic echocardiography during ongoing GI. Massive amounts of pneumomediastinum were present in four out of six divers. The CVP increased from 0 to a maximum of 28 mmHg, with a mean of 21 at 120seconds apneatime. We conclude that the GI maneuver itself may elevate pulmonary pressures to an extent that may cause pulmonary barotraumas and alveolar rupture. This is a plausible substrate for AGE and subsequent development of neurological symptoms in breath-hold diving.