Chapter 1: Introduction

This course is designed to equip the candidate to deal with medical crises, which may occur under pressure and at sea level.

In order to pursue the underwater perspective a short resume of underwater physiology is given below.

1. Vision

In underwater diving a facemask is worn. In the air most of the refraction (bending) of light takes place by the cornea, which is the front part of the eye. Underwater this refraction is lost, resulting in blurred vision and most of the focusing ability of the eye is lost. The facemask traps a pocket of air in front of the eye, improving the situation but light is refracted at the faceplate, which makes objects, appear larger and closer than they actually are.

2. Pressure Changes

Gas varies its volume according to pressure, water does not. For example, if the pressure in a given volume of gas is increased, the volume decreases (Boyle's Law). If the pressure in a given amount of gas is doubled the volume is reduced by half but if the pressure in a given volume of water is increased the volume remains virtually the same.

At sea level (barometric pressure of 760mmHg) the weight of air produces a pressure of 14.7 psi - referred to as one Ata of pressure. If the water pressure on a diver is taken to be one Ata absolute (1Ata) at the surface, it has been shown that water pressure increases by 1 Ata for every 10 metres that the diver descends. The following table demonstrates the effect of water depth on Ata and volume mass of gas.

It is important to stress that the body has pockets of air e.g. airway and lungs, gastro-intestinal tract (oesophagus, stomach and bowels), middle ears, sinuses and behind fillings in teeth. As the depth increases, so does the pressure within these gas pockets. However inequalities in pressure can result in symptoms related to these areas - both during ascent and descent.

3. Ears & Sinuses

During a descent the eardrums bend resulting in pain unless pressure is equalised through the Eustachian tubes. This equalisation does not happen automatically. It can be achieved by using the valsalva manoeuvre. "Squeezing" of the sinuses of the head may cause facial pain.

4. Breath Hold Diving

Hyperventilation before diving can result in loss of consciousness by causing a delay in the urge to breathe which is normally caused by an increase in the level of arterial CO₂. Hyperventilation "blows off" some of the CO₂ and this reduction in CO₂ prolongs the time the breath can be held. There is no significant increase in the amount of O₂ stored in the body by hyperventilation. Oxygen is consumed during the dive but low levels do not cause much urge to breath but may result in unconsciousness before the CO₂ level is high enough to compel the diver to breath and thus the diver will have no insight or warning of the risk.

5. Effects of Changes in Pressure on Air Spaces

If a diver takes a deep breath at 4Ata below the surface and proceeds to the surface without exhaling. Trapped gas within the chest will expand the lung beyond normal size and cause rupture of the alveoli, which are the smallest and most vulnerable air spaces in the lung. Severe rupture results in shattering of lung tissues, capillaries and veins and propels gas into the circulation where it can cause further damage. The injury to the lung can result in it collapsing (Pneumothorax - pneumo - air, thorax - chest) and the passage of air along the circulation can result in brain damage or death (air embolism).

6. Air Embolus

In an air embolism, air bubbles are forced by the above mechanism into torn blood vessels in the lung and subsequently travel along the circulation to the heart, where they can impair its pumping action and/or be pumped to any part of the body, resulting in circulatory blockage, causing paralysis, coma and death. The presence of gas in the blood triggers mechanisms, which damage and derange the blood.

7. Pneumothorax

(Entry of air into the chest cavity)

Following the rupture of lung tissue (alveoli) there may be an accumulation of air in the chest cavity (pneumothorax). As the diver continues his/her ascent, the air in the pleural cavity will expand further resulting in a collapsed lung. A continuous expansion of the air will result in a collapsed lung and the heart being pushed to the opposite side of the chest (tension pneumothorax). This constitutes a life threatening crises where the pumping action of the heart will be severely impaired to the point that the diver will become unconscious and the heart will eventually arrest (stop beating effectively - cardiac arrest). This situation can be remedied by draining the entrapped gas in the chest. Passing a tube into the affected side of the chest does this.

8. Decompression Sickness

Helium and Nitrogen are inert gases (the body does not naturally consume it unlike oxygen). As the diver descends the pressure around the diver increases, forcing the inert gases into the solution within the blood and tissues. The greater the depth, the longer the time of the dive, the higher the exercise intensity and the warmer the diver the more inert gas will go into solution in the tissues. Helium and Nitrogen dissolves quite rapidly in the blood. The inert gas in the tissues is not a problem until the diver ascends towards the surface. The decrease in pressure may lead to bubble formation in the blood or tissues and cause circulatory blockage and tissue damage. A very fast ascent by the diver has been compared to the removal of a cap of soda bottle in that the dissolved gas is liberated and forms the bubbles. A diver can reach the surface from 30 metres (4Ata) in 2 or 3 minutes, the diver will breath air at atmospheric pressure on the surface but will have inert gas dissolved in his blood and tissues at a pressure equivalent to his dive depth of 4 Ata. Another complication includes bubbles reaching the heart and brain, cutting off the blood supply to these organs, triggering a heart attack or causing brain or nerve damage. Paralysis of the legs can result from bubble formation in the spinal cord. By and large the sooner symptoms occur after a dive the more serious the decompression illness, but there can be a delay. (For these reasons any discomfort and illness after a dive must be presumed to be decompression illness until proven otherwise.)

Prevention of Decompression Sickness

1. The dive is restricted in depth (10m or 2 Ata). Although most tables allow unrestricted diving to shallower depths, it should be remembered that repeated descents and ascents would result in the accumulation of inert gas within the tissues, thereby resulting in the possibility of DCI.

2. Divers who descend more than 2 Ata but limit their time at depth based on established guidelines.

3. Beyond certain limits of depth and time the accumulation of inert gas requires a decompression period i.e. the return to the surface must be slowed to permit elimination of inert gas through the lungs to avoid large bubble formation which can cause damage. If this has been omitted or cannot be arranged then rescue treatment is by use of recompression i.e. - the DDC pressure is raised to a level, which controls symptoms. The increased pressure results in the inert gas being forced back into solution. With slow decompression the inert gas is allowed to come slowly from the solution without bubble formation and be exhaled. Oxygen breathing at safe pressures (1.6 Ata or less) will speed up this process.

9. Nitrogen Narcosis

Nitrogen in the air at high pressure acts like an anaesthetic gas. That is to say it impairs the action of the brain and nerves. The greater the depth, the worse the effect. CNS, the central nervous system is affected by nitrogen narcosis. The symptoms include dizziness, impaired judgement and euphoria. While nitrogen narcosis is not in itself fatal, it can impair judgement and ability at depth, which may lead, to serious accidents. The greater depth, the more nitrogen is forced into solution in the body. It should be noted that the effects are individualistic. The depth at which divers are affected varies, and there is marked variation in the severity of symptoms.

10. High Pressure Neurological Syndrome

This was described in 1965 following some Royal Navy experiments as a condition found in depths in excess of 160 metres. The developments of symptoms are related to the rate of compression at great depths. The serious symptoms include in order of progression - course tremor, inco-ordination, and disorientation, leading to poor judgement, apathy and confusion. These effects are minimised by the use of Tri-mix i.e. oxygen, nitrogen and helium. Other means of avoiding this syndrome are slow compression to saturation depth from which short excursions may be carried out at greater depths with fairly rapid compression rates, which would otherwise not be tolerable.

When subjects are exposed to extreme depth for prolonged periods a condition known as hydrostatic pressure syndrome can occur. This is not related to the rate of compression but to the duration of it. Treatment for both these conditions is gradual decompression until symptoms disappear.