Pulmonary Decompression Sickness ('Chokes')
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, butimmediate 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.
What kills in pulmonary DCS or 'chokes'?
What is happening is quite simple. When the body has sufficient inert gas
super-saturation, it forms bubbles in the small veins. These bubbles are carried
to the heart by the circulation and pumped out to the lungs where they are
trapped. This of course assumes no holes in the heart (PFO, ASD, or VSD) and no
bypass shunts in the lungs. The bubbles trapped in the lungs disappear after
minutes and are almost always totally assymptomatic.
So why is this? At rest, the heart is pumping about 5 liters of blood per
minute. This blood is traveling through only 10% of the capillaries in the
lungs. The other 90% are empty. So what happens when you throw enough
bubbles at the lungs to block 10% of the circulation? Absolutely nothing;
now 10% of the circulation is blocked by bubbles, 10% is carrying the blood from
the heart and 80% is sitting empty. The action only starts after 90% of the
circulation to the lungs is blocked. Then the heart has difficulty pumping
blood through the lungs, the pressure in the pulmonary artery rises, the
arterioles leak, the lungs fill up with fluid, the systemic blood pressure
falls, the person goes into DCS shock, and DIES. This all happens VERY
QUICKLY, after the first 90% of the circulation to the lungs is blocked.