TP 13312

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Hypoxia and Hyperventilation

• Respiratory Physiology
• Hemoglobin Dissociation
• Figure 6 - Oxyhemoglobin Dissociation Curves for Human Blood
• Hyperventilation
• Pressurization and Depressurization
• Figure 7 - Cabin Pressurization
• Figure 8 - Times of Useful Consciousness
• For Those of Mathematical Bent 

The hazards of high altitude became evident as soon as men set out in balloons, although the dangers had been suspected by missionaries in mountainous areas long before. In 1590 the Jesuit Priest Acosta noted “... I am convinced that the element of the air is in this place so thin and so delicate that it is not proportioned to human breathing which requires extensive and more temperate air”. 

In 1862 Glaisher and Coxwell made an ascent by balloon to almost 29,000 ft. and became unconscious. Fortunately one of them, his hands frozen, was able to raise his head sufficiently to grab the valve cord of the balloon in his teeth before passing out, thus releasing hydrogen and bringing the balloon back down. Paul Bert in the late 1860’s built an altitude chamber and reached the conclusion that, regardless of barometric pressure, air could not supply life when the partial pressure of oxygen reached 45 mm. Hg. In April of 1875 Crocé-Spinelli, Sivel and Tissandier made the first flight in a balloon using oxygen although Bert had warned them the supply was far too small. Only one of the three survived, the other two dying of hypoxia.

Respiratory Physiology

To maintain life, oxygen has to be inhaled, diffused across the alveolar-capillary membrane, carried by hemoglobin to the tissues and then transferred to the individual cells for aerobic metabolism. Dalton’s Law states that the partial pressure of a gas in a gas mixture is equal to the pressure which the gas would exert if it alone occupied the space taken up by the mixture. Each of the gas components in the mixture therefore exerts pressure proportional to the fraction which it represents. Oxygen, being present as 20.9%, (21%) of the gases in our atmosphere exerts a partial pressure of 160 mm. Hg in dry air at sea level. However this changes when it is inspired. In the nasopharynx air is exposed to water vapor and becomes saturated at body temperature (37°C). Water vapour pressure is 47 mm. Hg. In the trachea therefore the partial pressure of oxygen will be (760 - 47) x 0.21 or approximately 150 mm. Hg. Passing from the trachea to the alveolus, oxygen becomes mixed with carbon dioxide. It is also diffusing into the tissues from the respiratory bronchioles down, so by the time the alveolus is reached, the partial pressure of oxygen is much lower. The partial pressure of carbon dioxide is about 40 mm. Hg so the alveolar partial pressure of oxygen at ground level, when the respiratory quotient is taken into account, is 103 mm. Hg (For those mathematically inclined relevant formulas are given at the end of this chapter). This steadily dropping partial pressure is known as the respiratory cascade. 

The diffusion of oxygen (and of carbon dioxide in the opposite direction) takes place at the level of the respiratory bronchioles and below. The majority of the diffusion takes place at the alveolus which is virtually surrounded by capillary blood. The area of the alveolar-capillary interface is astonishingly large, between 90 and 100 sq. metres. If spread out the alveoli would cover a double tennis court. Diffusion at the alveolus takes place along the pressure gradient with most of the oxygen being picked up by hemoglobin for transfer to the tissues. The rate of diffusion of a gas is proportional to its solubility and to the pressure gradient. Carbon dioxide, being more soluble than oxygen, diffuses at a faster rate. In the tissues the pressure of oxygen falls with increasing distance from the capillary, with the lowest level being found midway between two capillaries. If the partial pressure of oxygen falls below 3 mm. Hg in the tissues anaerobic metabolism develops. Under normal conditions a rise in PC02 and the formation of tissue lactic acid causes capillaries to dilate. In muscle the number of open capillaries can increase by 200 times but in the brain most of the capillaries are open, even at rest, so even in the face of imminent hypoxia the number of cerebral capillaries can increase only by a factor of four. This is why hypoxia affects the brain first. 

Hemoglobin Dissociation

Oxy-hemoglobin (Hb02) dissociation describes an S-shaped curve (See Figure 6) when saturation is plotted against oxygen partial pressures. The characteristics of this curve are important. Down to a partial pressure of 60 mm., saturation remains above 90%. Below this point saturation drops off rapidly being less than 80% by the time the partial pressure has dropped to 45 mm. The sharp drop-off of the curve enables oxy-hemoglobin to unload rapidly in the relatively hypoxic tissues and equally allows reduced Hb to pick up oxygen rapidly at normal diffusion gradients. Under hypoxic conditions lactic acid is formed in the tissues causing a relative acidosis which moves the curve to the right, increasing the uptake and release of oxygen. In alkalosis, as in hyperventilation, the curve moves left, lessening tissue availability. (Fig.6)

At 10,000 ft. the PAO2 has reached 60 mm., which is the beginning of the rapid drop in hemoglobin saturation. Above this altitude significant tissue hypoxia develops and it is for this reason that oxygen is required while flying above 10,000 ft. If the pilot is breathing 100% oxygen however the partial pressure of oxygen at any level will be much higher. The critical level of 60 mm. at the alveolus for example will not be reached until 40,000 ft. This is referred to as an “equivalent oxygen level”.

Figure 6

Hypoxia

Hypoxia is an insidious killer. There is a tendency for euphoria to develop while motor skills and reasoning abilities deteriorate. The result is that in many cases the pilot may become seriously hypoxic without appreciating that there is a problem. To the observer tachypnea, cyanosis, mental confusion and loss of muscle coordination are obvious. To the pilot however, the only symptoms may be slight dyspnea, dizziness, fatigue, decreasing vision and finally loss of muscular control. Night vision can be impaired at as low as 5000 ft. Tolerance to hypoxia varies from individual to individual and from time to time.  Tolerance can be increased by continual exposure to high altitudes and varies with the level of the hemoglobin and the oxygen carrying capacity of the blood. It is decreased by fatigue, cold and poor physical conditioning. Even at 5,000 ft. night vision is decreased.

Types

Hypoxia is generally divided into four types. 

Hypoxic hypoxia is due to a decrease in the oxygen available to the body such as typically occurs with altitude. 

Hypemic hypoxia is caused by a reduction in the oxygen carrying capacity of the blood for any reason. It also occurs when hemoglobin is saturated by gases for which it has a higher affinity, the most common of which is carbon monoxide. This is not only produced by exhaust leaks into the cockpit but also by cigarette smoking. Carbon monoxide is a product of incomplete combustion and may be present at levels of 6-8% in the blood of a heavy smoker and such individuals may become significantly hypoxic at levels below 10,000 ft. 

Stagnant hypoxia is a less common problem caused by a reduction in total cardiac output, pooling of the blood or restriction of blood flow. Heart failure, shock, continuous positive pressure breathing and Gforces in flight can create stagnant hypoxia. Local stagnant hypoxia can occur with tight and restrictive clothing or, in the cerebral circulation, in association with vasoconstriction due to respiratory alkalosis provoked by hyperventilation.

Histotoxic hypoxia refers to poisoning of the respiratory cytochrome system by chemicals such as cyanide or carbon monoxide but it can also be caused by the effects of alcohol. Needless to say a pilot in poor physical condition, recovering from a hangover and smoking while in flight can quickly become an unfortunate statistic!

Gravity and Atelectasis

In the seated position the lungs, due to the pull of gravity, are stretched at the apices and condensed at the bases. At the same time, the blood supply is least at the apices and greatest at the bases. Thus in the area where the alveolar ventilation is best, perfusion is least and at the bases the opposite is true. Only in the mid section of the lung is there an ideal ventilation – perfusion ratio. Under positive G, the situation is exaggerated and if it is of long duration in crews breathing oxygen, rapid absorption from the alveoli tends to cause basilar atelectasis. 

Hyperventilation

Hyperventilation may be described as a respiratory rate excessive for the body’s oxygen requirements. It may be voluntary or involuntary and can occur in relation to many different activities. In the pilot the most common precipitating causes are anxiety, fear, excessive concentration on a flight procedure and as a reaction to pain or illness. Hyperventilation may be obvious, as in the case of children preparing to compete in underwater swimming, or it may be covert as for example when the respiratory rate increases from a required 12 per minute to an excessive 15 per minute and remains elevated for a prolonged time.

Whatever the cause the results are the same. Carbon dioxide, the most potent stimulus to respiration, is blown off in excessive amounts. The PACO2 falls and respiratory alkalosis develops. The cerebral vessels become constricted and subjectively the pilot often notices a feeling of dizziness, a coldness and tingling around the lips and a feeling as though there was a band around the head. Nausea may be present. Peripherally there is vasodilatation and stimulation of sensory nerves causing a sensation of pins and needles in the hands and in the feet. If hyperventilation continues carpopedal spasm develops and the subject may become unconscious and develop frank tetany. With the breath held the carbon dioxide levels build up once more and the symptoms disappear in reverse order.

Obviously such a chain of events can lead to an accident. This has been documented in some incidents in young fighter pilots or untrained private pilots who have inadvertently flown into bad weather and have kept the microphone button depressed, broadcasting their breath patterns up to their final moment. Hyperventilation is often suspected in unexplained accidents. If one considers the symptoms of hypoxia and hyperventilation it will be seen that they are very similar. As it is imperative in the air that no mistake be made, the treatment for both is to breathe 100% oxygen and to reduce the rate and depth of respiration.

Pressurization and Depressurization

Although it is usually in military pilots that problems arise with hypoxia at levels above 30,000 ft., it must be remembered that more and more commercial aircraft are now cruising at extreme altitudes and flight above 40,000 ft. is common. The Concorde, for example, cruises above 60,000 ft. Cabin pressurization in these aircraft ensures that the partial pressure of oxygen is adequate and it is rare for the cabin pressure to be above 7,000 ft. (See Fig. 7). However, it is wise to remember that passengers with chronic lung diseases or serious anemia, particularly those who are smokers, may be significantly hypoxic even at this altitude.

Figure 7 - Cabin Pressurization

More dangerous however is the situation which develops when cabin pressure suddenly fails, usually due to the loss of a window or door. The result is rapid decompression with a sudden increase in the cabin altitude to match the ambient altitude. In aircraft such as the Concorde the windows have been made particularly small to lessen this effect but in older aircraft more serious problems have occurred. The immediate effect of decompression is a loud noise, condensation of water vapour causing a mist and a shower of dust and small particles. The temperature falls dramatically. The resultant cabin pressure may actually fall below that of the ambient pressure due to “aerodynamic suck”. This refers to the Venturi effect created by the speed of the aircraft through the air.

The initial hazard to aircraft safety is hypoxia. The crew are unlikely to be wearing oxygen masks at the time of the incident and, if the final cabin altitude is high, the time of useful consciousness may be very short (see Figure 8). It may actually be lower than would be anticipated because of the sudden escape of expanding gas from the lungs due to the reduced ambient pressure. This causes reversal of the oxygen diffusion gradient across the alveolar membrane and
oxygen passes back into the lung from the blood. At 35,000 ft. the time of useful consciousness is generally quoted as 30 – 60 seconds but at altitudes of above 40,000 ft. this may be reduced to 12 – 15 seconds, the normal circulation time. Airlines make provision for this eventually by providing pilots with “quick-donning” oxygen masks, which can be donned in 5 seconds or less.

Figure 8 - Times of Useful Consciousness
(Effective performance time)

For Those of Mathematical Bent

In Dry Air:

PIO2 = AP x FIO2 where PIO2 is the partial pressure of oxygen, AP is atmospheric pressure and FIO2 is the fraction of oxygen in the inspired air. 

In the Trachea:

PIO2 = (AP – WVP) x FIO2 where WVP is water vapour pressure. At sea level this is (760 – 47) x 0.21 = 150 mmHg.

In the Alveolus:

PAO2= PIO2 – PAC O2 [FIO2+ (1 – FIO2/R)] where PACO2 is the partial pressure of carbon dioxide and R is the respiratory quotient.

Therefore at sea level PAO2 = 150 – 40 [0.21 + (1 – 0.21/0.82)] = 103 mmHg.

Or at 18,000 ft. = (380 - 47) x 0.21 - 30 (0.21 + 1 – 0.21/0.82) = 35 mmHg.

The respiratory quotient (R) on a pure carbohydrate diet is 1.00, on a protein diet 0.81 and on an animal fat diet 0.71. On a balanced diet of carbohydrate, protein and fat, R is generally about 0.83.