Pulmonary decompression sickness is the result of sudden, massive blocking the pulmonary arterial circulation by bubbles. Ordinarily, the lungs act as a filter and protect the arterial circulation from circulating bubbles (except when there is a PFO). The chokes is a rare condition in diving, usually occurring with very rapid ascents from deep dives, often from failure of buoyancy control.
Hypobaric decompression, or sudden change of ambient pressure applied to a subject saturated with inert gas has been reported to produce pulmonary decompression sickness in 6% of cases. The onset of the chokes is usually heralded by a midchest discomfort that commences within minutes of reaching the surface. The pain may be accompanied by a cough and is accentuated by deep breathing which worsens the discomfort and may provoke paroxysms of unproductive coughing. The breathing pattern becomes rapid and shallow, and cyanosis may develop as the disorder rapidly progresses to right-side heart failure and cardiovascular collapse. Oxygen, fluid resuscitation, and pressors may be helpful, but immediate recompression and hyperbaric oxygen are essential for survival.
In experimental animals, pressure in the vessels going into the lung and right ventricular pressure rise, and heart function and arterial blood oxygen fall after a severe decompression stress. These changes occur in concert with the detection of bubbles in the pulmonary artery and are identical to the changes produced by deliberate infusions of gas into the pulmonary artery. White blood cells attach to the bubbles, and the activation of leukocytes contributes to the rapid development of increased leakiness of blood vessels and lung edema. Pulmonary decompression sickness resembles ARDS, the adult respiratory distress syndrome, which has been reported to be a consequence of accidental venous air embolism in the operating room.