During ascent through the atmosphere there is a fall in density of air and a reduction in the molecular concentration of oxygen. This in turn leads to a fall in the partial pressure of oxygen within the lung, and hence the blood. At 8000 feet (2400 m), atmospheric pressure is reduced by 25%, from 101 kPa to 75 kPa. The alveolar partial pressure of oxygen (PAo2) drops from 14kPa to 8.5 kPa. There is minimal effect on the physiology of fit individuals, other than some minor reversible deterioration in mental performance for novel tasks, detected on psychometric tests. The patient's susceptibility to hypoxia depends on the underlying cardiopulmonary function, intercurrent dis ease, physical activity and metabolic rate. The drop in partial pressure of oxygen at cabin altitudes of 8000 feet (2400 m) is sufficient to cause tissue hypoxia and the development of symptoms in patients with reduced car-diopulmonary reserve. The physiological response to this hypoxia is to increase ventilation, which leads to a reduction in alveolar carbon dioxide and a rise in alveolar oxygen tension. This is explained by the simplified alveolar gas equation:
where PAo2 is the alveolar oxygen tension, P,o2 is the tracheal oxygen tension, PAco2 is the alveolar carbon dioxide tension and RQ is the respiratory quotient. In extreme cases, the degree of hyperventilation and hypo-capnia can itself induce a separate group of symptoms.
Boyle's law states that the volume of a gas is inversely proportional to its absolute pressure; therefore, as atmospheric pressure falls with ascent, gas expands (Table 19.3). In the pressurised aircraft, cabin ascent to an altitude of 8000 feet (2400 m) leads to gas volume increasing by 35%. This gas expansion can affect the gas-filled body cavities, depending on the degree with which they communicate with the external environment. The lungs, middle ear, paranasal sinuses and the gastrointestinal tract are all potential problem areas. In a fit individual there are few problems with this degree of gas expansion, other than mild middle-ear discomfort. However, certain conditions may become significantly worse and even life threatening with this change in volume. Patients with pneumothora-cies, pneumocephalus, severe bowel distension or obstructed middle ears should be taken to altitude with caution.
During take off and landing, patients laying flat maybe exposed to forces of acceleration in the longitudinal (Gz) plane of the body. Acceleration describes the rate of change of velocity of an object and can be positive ( + Gz) or negative, sometimes described as deceleration ( — Gz). In aviation, acceleration is expressed as multiples of the force of acceleration exerted on a body by gravity (g) which is equal to 9.8ms"2:
G = applied acceleration/g
The effects of G on the body depend on duration and direction. Short or intermediate duration forces are those associated with an abrupt deceleration, such as vehicle crashes. Long duration accelerations of more than 2 s occur mainly in military aircraft. In commercial aircraft, linear acceleration seldom reach magnitudes of any sig nificance, especially in the seated patient. The horizontal patient is unlikely to experience forces greater than 1-2 + Gz on take off in a small subsonic jet. In the fit volunteer, a force of 4-6 + Gz is required to experience grey-out (loss of peripheral vision), black-out (total loss of vision) and G-LOC (G-related loss of consciousness). These are manifestations of reduced perfusion of the retina and brain as a result of the effects of hydrostatic forces on the cardiovascular system. There is also a progressive fall in mean arterial pressure at the level of the heart over 6-12 s, due to a decrease in peripheral vascular resistance and reduction cardiac return. A compensatory reflex tachycardia and vasoconstriction then occurs in response to reduced pressure in the carotid sinus.
The critically ill patient may be volume depleted, vasodilated, possess a poor myocardium and have a depressed sympathetic response due to drugs or pathology. In such cases even the relatively small acceleration forces experienced combined with the 45° head-up tilt of take off may be enough to cause a deterioration in cardiovascular function. This is easily prevented by adequate monitoring and volume loading before take off.
Deceleration forces may cause increased blood flow to the head and neck, leading to carotid sinus distension. Reflex bradycardias and other arrhythmias have been reported in experimental situations with high G forces. Once again, it is unlikely that the forces experienced in commercial aircraft are great enough to cause these problems.
Cabin decompression is a rare event that can occur rapidly or slowly. A rapid decompression can be explosive in nature when a major defect occurs in the aircraft frame. It results in a near normal environment being quickly converted to an extreme environment, with lack of oxygen, cold and the effects of gas expansion putting the lives of patient and crew at risk. The effects of gas expansion depend on the cabin differential pressure, the altitude of the aircraft and the size of the defect in the aircraft frame in relation to the cabin volume. The medical risks from decompression are: rapid loss of consciousness from hy-poxia, barotrauma to the middle ear or sinuses, inducement of a pneumothorax and altitude decompression sickness. In the event of a cabin decompression, oxygen masks are automatically released and the aircraft is brought to a lower altitude. Aircrew are advised to place their own oxygen mask on before helping others because of the risk of becoming incapacitated by hypoxia.
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