When Barotrauma Occurs
The presumed mechanism of pulmonary barotrauma is as follows.
With ascent, if the expanding air cannot be properly vented, the
lungs (or some portion of them) expand in response to the increase
in pressure; if they expand too much, individual alveoli are prone to
rupture. If the lungs are structurally normal, i.e., there are no
blebs,
bullae, or areas of abnormal tissue (which are more prone to
rupture), barotrauma should not occur until a transpulmonary
pressure of around 80 mm Hg is reached (Schaefer 1958). Above 80
mm Hg the alveoli are prone to tear and vent air into the
surrounding space (called the interstitial space). This
transpulmonary pressure should not occur in healthy lungs unless
breath is held on ascent.
From the interstitial space, escaped air can take one of three paths
(Figure 4): between the two lungs (mediastinal air), around one of
the lungs (pneumothorax), or into the blood stream (air embolism)
(Macklin 1944).
1) Escaped air can dissect along tissue layers into the area known as
the mediastinum, the large space between the two lungs. Once in
the
mediastinum, the air can go into spaces around the heart (but not
in
it), into the neck, and into spaces around the abdominal organs.
2) Escaped air can rupture through the visceral pleura (thin
membrane that lines the lungs), resulting in a pneumothorax,
which
is an abnormal air collection between the chest wall and the lung.
This air collection can compress or collapse the lung.
3) Escaped air can enter the pulmonary veins, from where it can
travel to the arterial circulation as an air embolism (traveling air
bubbles). This is by far the most serious complication of a ruptured
lung, since the air embolism can block blood vessels to the brain or
heart and be fatal.
Figure 4. Three pathways air can take once there is a rupture of lung
tissue.
WHY DOES PULMONARY BAROTRAUMA OCCUR?
There is no doubt that pulmonary barotrauma results from unequal
air pressures across the lung. But why does it occur in some people
and not others. Is it always from a breath-hold ascent?
Although breath-hold ascents account for some cases, there are also
cases of barotrauma where the divers are certain they never held
their
breath.
There are two explanations for this latter group. First, some divers
probably have abnormal lungs and don't know it. Such changes as
sub pleural blebs and bullae (abnormal air pockets in the lungs) can
often be demonstrated by chest CT scanning or even a plain chest
x-ray in people with no respiratory symptoms or problems.
After one diver suffered major barotrauma, a chest x-ray that was
done before the dive was reviewed; it showed a large bulla, or
abnormal air space with thin walls. Probably a certain percentage of
people have such "weak lungs" (for want of a better term); these
weak
lungs may cause them no difficulty except when exposed to slight
pressure changes that would not affect normal lungs.
Still, there are apparently other divers with completely normal
lungs,
who are confident breath was not held, yet who still suffered
pulmonary barotrauma. These events are difficult to explain, and are
fortunately rare (as is pulmonary barotrauma in general).
Pulmonary barotrauma remains a definite, albeit small, risk of scuba
diving.
A hyperbaric chamber is not used for pulmonary barotrauma unless
there is suspicion of air embolism. Chest tube placement for
pneumothorax follows the same guidelines as without diving.
Pneumothorax is particularly dangerous if the patient is to be
transported by air or receive hyperbaric therapy (which might be
needed for decompression sickness or air embolism, not the
pneumothorax).
The decreased barometric pressure of altitude, as well as the
decompression phase of hyperbaric therapy, will further expand the
pneumothorax space and increase the risk of compressing the lung
(and, if very severe, the heart).
The presumed mechanism of pulmonary barotrauma is as follows.
With ascent, if the expanding air cannot be properly vented, the
lungs (or some portion of them) expand in response to the increase
in pressure; if they expand too much, individual alveoli are prone to
rupture. If the lungs are structurally normal, i.e., there are no
blebs,
bullae, or areas of abnormal tissue (which are more prone to
rupture), barotrauma should not occur until a transpulmonary
pressure of around 80 mm Hg is reached (Schaefer 1958). Above 80
mm Hg the alveoli are prone to tear and vent air into the
surrounding space (called the interstitial space). This
transpulmonary pressure should not occur in healthy lungs unless
breath is held on ascent.
From the interstitial space, escaped air can take one of three paths
(Figure 4): between the two lungs (mediastinal air), around one of
the lungs (pneumothorax), or into the blood stream (air embolism)
(Macklin 1944).
1) Escaped air can dissect along tissue layers into the area known as
the mediastinum, the large space between the two lungs. Once in
the
mediastinum, the air can go into spaces around the heart (but not
in
it), into the neck, and into spaces around the abdominal organs.
2) Escaped air can rupture through the visceral pleura (thin
membrane that lines the lungs), resulting in a pneumothorax,
which
is an abnormal air collection between the chest wall and the lung.
This air collection can compress or collapse the lung.
3) Escaped air can enter the pulmonary veins, from where it can
travel to the arterial circulation as an air embolism (traveling air
bubbles). This is by far the most serious complication of a ruptured
lung, since the air embolism can block blood vessels to the brain or
heart and be fatal.
Figure 4. Three pathways air can take once there is a rupture of lung
tissue.
WHY DOES PULMONARY BAROTRAUMA OCCUR?
There is no doubt that pulmonary barotrauma results from unequal
air pressures across the lung. But why does it occur in some people
and not others. Is it always from a breath-hold ascent?
Although breath-hold ascents account for some cases, there are also
cases of barotrauma where the divers are certain they never held
their
breath.
There are two explanations for this latter group. First, some divers
probably have abnormal lungs and don't know it. Such changes as
sub pleural blebs and bullae (abnormal air pockets in the lungs) can
often be demonstrated by chest CT scanning or even a plain chest
x-ray in people with no respiratory symptoms or problems.
After one diver suffered major barotrauma, a chest x-ray that was
done before the dive was reviewed; it showed a large bulla, or
abnormal air space with thin walls. Probably a certain percentage of
people have such "weak lungs" (for want of a better term); these
weak
lungs may cause them no difficulty except when exposed to slight
pressure changes that would not affect normal lungs.
Still, there are apparently other divers with completely normal
lungs,
who are confident breath was not held, yet who still suffered
pulmonary barotrauma. These events are difficult to explain, and are
fortunately rare (as is pulmonary barotrauma in general).
Pulmonary barotrauma remains a definite, albeit small, risk of scuba
diving.
A hyperbaric chamber is not used for pulmonary barotrauma unless
there is suspicion of air embolism. Chest tube placement for
pneumothorax follows the same guidelines as without diving.
Pneumothorax is particularly dangerous if the patient is to be
transported by air or receive hyperbaric therapy (which might be
needed for decompression sickness or air embolism, not the
pneumothorax).
The decreased barometric pressure of altitude, as well as the
decompression phase of hyperbaric therapy, will further expand the
pneumothorax space and increase the risk of compressing the lung
(and, if very severe, the heart).
 |  |  |  |
Adventure Dominica
| The Eustachian tube was first identified by Bartolomeo Eustachio (Latin: Eustachius), an Italian anatomist who died in the 1500's. In the United States the Eustachian tube is usually pronounced "yoo-sta-shan", but some pronounce it "yoo-sta-ke-an" in honor of the anatomist as it more closely approximates the original Latin pronunciation of the name. The tube is approximately 1.5" long and is located in the back of the nasopharynx at approximately nostril level. The tube is normally closed and has a highly variable patency. This means that some individuals will virtually never have problems with middle ear equalization while diving. Others with narrow or partially obstructed Eustachian Tubes may have trouble equalizing their middle ears in airplanes or elevators. These later individuals can dive safely, but for them middle ear pressurization requires meticulous attention to detail and much practice. Thanks to the comments of Francisco Javier Orellana Ramos, a Diving Medical Officer from Spain, I am reminded that there are several factors that influence tubal patency and tolerance to pressure changes. The Eustachian Tube angle and the shape of the tube can affect ones ability to pressurize the middle ear. Individuals with a relatively large volume of air in the mastoid sinuses will be less tolerant to pressure changes as the actual volume change in the middle ear will be greater for a given amount of descent. Allergies, trauma, infection and Thyroid disorders are other possible causes of disruption in normal tubal function. |