"Hyperventilation
before doing a
breath-hold
dive is one
cause of shallow
water blackout."

Shallow Water Blackout

In cases of pulminary overpressure, the onset of symptoms is always during ascent or within a few minutes of reaching the surface. Symptoms of Decompression Sickness (DCS) usually do not start until several minutes or even hours after surfacing.

In the January/February issue I started a discussion on the problems divers can experience with their lungs while diving. We looked at the possibility of lung squeeze and decided that while breath-hold diving or normal scuba diving, lung squeeze was highly unlikely. In this column we will look at a much more common and serious problem-shallow water blackout, and then start our discussion on the various lung problems divers can experience during ascent.

In the USA there are approximately 7000 deaths per year due to drowning (500 in Canada), some of them because the swimmer lost consciousness while under water. Interviews with swimmers who lost consciousness but survived have revealed that all of them hyperventilated before doing a breath-hold dive. Hyperventilation before doing a breath-hold dive is one cause of shallow water blackout.

The primary stimulus to breathe is the partial pressure of carbon dioxide (pCO2) in the blood and pCO2 is controlled by ventilation (breathing). Therefore, by voluntarily hyperventilating (breathing more than is required by the body) a diver can reduce the level of CO2 in their body (they blow it off) so that the pCO2 can be as low as 30 mm Hg (a normal resting pCO2 is around 40 mm Hg). If the person then holds their breath, because they started with less CO2 than normal, it will take longer for the pCO2 to increase to the level where they must breathe (a pCO2 of about 50 mm Hg) and they will be able to hold their breath longer. Hemoglobin (the molecule that carries oxygen in the blood) is 97% saturated with oxygen during normal respiration and therefore hyperventilating does not increase the quantity of oxygen in the body. As breath-hold time is increased, the amount of oxygen used is increased. The partial pressure of oxygen (pO2) in the blood is a very weak stimulus for respiration and easily ignored by the diver. Therefore, the pO2 can fall to a point where the diver loses consciousness before the pCO2 rises to a level that forces the diver to surface and breathe. As can be seen from the following table, pO2 becomes very low when a person hyperventilates and exercises while holding their breath (typical of breath-hold diving).

A diver who loses consciousness underwater will usually drown and therefore a person should not hyperventilate before doing a breath-hold dive.

A second problem during breath-hold diving is that as the diver goes deeper, the pO2 is increased as a result of compression. The pO2 in the blood is usually around 100 mm Hg on the surface. If the diver does a breath-hold dive and quickly descends to 66 fsw, the pO2 will be almost 300 mm Hg (total pressure of 1 ATA on the surface and 3 ATA at 66 fsw). The diver therefore has a high pO2 on the bottom. If the diver has hyperventilated before diving and stays at 66 fsw until the desire to breathe becomes very strong, they will have used up most of the oxygen in their bodies, even though the pO2 might still be quite high at 90 mm Hg. As they ascend, the pO2 will drop precipitously and they might lose consciousness before reaching the surface. In our example, the pO2 would be less than 30 mm Hg by the time the diver surfaced. Diving very deep during a breath-hold dive, especially after hyperventilating, is a second cause of shallow water blackout. The combination of hyperventilation before and diving deep during a breath-hold dive will cause loss of consciousness in most divers.

Those of you who have been following my columns closely and understanding them will see a way to get around the problem. The diver simply has to breathe 100% oxygen for several minutes before the dive. They will get rid of a lot of CO2 and probably be able to hold their breath for several minutes. By diving with their lungs full of oxygen, they will not risk passing out. Great idea, as long as they stay at less than 20 fsw depth. If they dive deep with lungs full of 100% O2, they risk having an oxygen conclusion! No matter how you look at it, breath-hold diving can be quite a dangerous activity.

Lung Problems During Ascent

When a diver takes a breath of compressed gas at depth and ascends, the gas must expand with reducing pressure in accordance with Boyles' Law (P1V1=P2V2). Damage to the lungs is normally prevented by exhalation during ascent. If the diver does not exhale, the gas in the lungs will expand until the lungs are completely full. With continued ascent, the pressure in the alveoli increases and at an over pressure of 70-90 mm Hg, the alveoli will rupture. This pressure differential (over pressure) is equal to a change in depth of three to four fsw and documented cases of lung damage have occurred in six foot deep swimming pools. The most dangerous depth is the first 10 feet from the surface because this is where the largest volume changes occur. The same pressure changes occur deeper but the volume changes are so small that it is almost impossible to fully expand the lungs and thus get into an over pressure situation.

As the lungs stretch and tear, there are three places the gas can go. It can rupture through the pleura (a strong layer of skin on the surface of the lungs) and enter the pleural space (the potential space between the lungs and the chest wall) resulting in a pneumothorax. It can track back along the pulmonary vessels (the arteries and veins of the lungs) and enter the mediastinum (the space around the heart) and cause mediastinal emphysema. The gas can then move up beside the great vessels in the mediastinum (aorta and superior vena cava) into the neck and under the skin (subcutaneous emphysema). Or it can enter the pulmonary capillaries and get carried to the pulmonary veins, the left heart and get pumped into the aorta causing arterial gas embolism (AGE). The first major branches off the aorta are the carotid arteries (the primary supply of blood to the brain) and therefore AGE usually results in a shower of arterial bubbles to the brain (cerebral arterial gas embolism, CAGE)

Precipitating factors include breath-holding on ascent (panic, buddy-breathing, laryngospasm) and air trapping in the lungs. One possible cause of air trapping in normal lungs is vigorous exhalation to low lung volumes during ascent. This results in small airway closure and localized gas trapping and has been implicated in several diving accidents. Most commonly, air trapping in the lungs is secondary to pathological causes including: previous spontaneous pneumothorax, cyst and blebs (Tuberculosis), asthma, bronchospasm, infection, inflammation, mucous plugs, sarcoidosis, tumors, pleural adhesions, reduced pulmonary compliance and fibrosis. These abnormalities may result in airway obstruction or altered local lung compliance.

Prevention of this problem centres around medical screening of diving students and training to reduce the likelihood of panic. The initial medical before taking a basic scuba course should include a complete history (looking for conditions incompatible with diving), chest X-rays at full inspiration and expiration, pulmonary function tests if indicated, and psychological screening. Commercial/military divers require an annual medical to ensure continued fitness to dive. One of the purposes of training is stress reduction. Emergency procedures are practised so that when a real emergency happens the diver is able to handle the situation without panic. Most training takes practise but free ascents and buddy-breathing while ascending should not be practiced as more people have been killed practising these manoeuvres than performing them in real emergencies. Other dangerous practices that should be avoided to reduce the risk of pulmonary barotrauma are skip breathing (breath-holding), deep diving (narcosis and panic) and fast ascents.

In cases of pulmonary overpressure, the onset of symptoms is almost always during ascent or within a few minutes of reaching the surface. This is distinctly different from Decompression Sickness (DCS) where symptoms usually do not start until several minutes or even hours after surfacing. In pulmonary overpressure, the diver may surface with a sudden high pitched cry from the release of compressed gas, have cyanosis (blue colour), cough, hemoptysis (coughing blood) and dyspnea (shortness of breath).

We are out of room in this column. Next time we will start to look at where the air can go when the alveoli rupture; pneumothorax, mediastinal and subcutaneous emphysema and arterial gas embolism.