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The term altitude means �the height of an object in relation to a given point i.e. sea level,’ Tulloch (1999). For the purpose of this essay though, I will consider the effects of high altitude on the body and the subsequent adaptations to its exposure. High altitude generally refers to terrestrial elevations which are between 10,000-18,000 feet above sea level, (McArdle Katch and Katch pg 603).

Adaptations to a change in altitude work towards acclimatisation. Acclimatisation means to �come accustom to a new set of conditions’, i.e. altitude, Tulloch (1999). This requires maintenance of homeostasis by increasing oxygen delivery to cells and the efficiency of oxygen utilisation, (Miasnikov, 2007). If homeostasis is not maintained then serious illnesses can onset which could result in hospitalisation and/or death. Such instances will be discussed later.

Upon ascent to high altitude the most obvious and known consequence is the decreased partial arterial pressure of oxygen (PaO2) which is related to the drop in barometric pressure. At sea level the normal barometric pressure is 760mmHg. However, on ascending to high altitude the pressure drops to approximately 510mmHg by 10,000ft and then dramatically to 380mmHg by 18,000 ft. A lower partial pressure of oxygen in the air decreases the percentage of oxygen that is saturated into the blood. This therefore results in arterial hypoxia, (McArdle Katch and Katch p603). Hypoxia is therefore the most well known consequence of high altitude exposure.

The reason that a decrease in barometric pressure causes a decrease in PaO2 is that at sea level barometric pressure of 740mmHg there is a huge gradient between the pressure in the air and in the arteries but when the gradient drops significantly there is less pressure to force the oxygen into the bloodstream. This can be demonstrated by a shift to the right in the oxygen dissociation curve, (see figure one).

Figure 1.

The Oxygen Dissociation Curve

Insert reference

Aircrafts overcome this problem by having airtight cabins that can cope with huge pressure gradient differences. They also have the ability to slowly decrease pressure up until 8,000ft and then slowly increase it to sea level during decline using their compressors, (Readers Digest 1991).

One immediate physiological adaptation to a lowered partial pressure and thus decreased oxygen saturation is an increase in the effected individual’s respiratory rate and depth, (Miasnikov 2007). A decrease in oxygen in the blood results in an increase in the acidity of the blood; this is detected by the chemoreceptors and fed back to the brain. From here, the medulla sends messages to the intercostal muscles and diagphram initiating the increase in breathing rate and depth.

An increase in respiratory rate increases the volume of carbon dioxide lost, whilst at the same time it increases the amount of oxygen which is delivered to alveoli of the lungs, (Miasnikov 2007). One consequence of an increased respiratory rate is an increased rate of water loss. This means dehydration is another possible consequence of ascending to high altitude where water is not readily available.

Figure 2.

Hyperventilation and Alveolar PCO2

(Frisancho 1993)

Alongside the increase in respiratory rate is an increase in heart rate due to an increased demand for oxygen to be delivered to the hypoxic tissues, (Miasnikov 2007). This increased HR contributes to an increase in cardiac output as (cardiac output = HR x SV) and stroke volume remains constant at altitude. Heart rate and cardiac output can increase by as much as 50% of that at sea level values, (McArdle Katch and Katch p608), to increase perfusion to the tissues.

The other immediate response to exposure to altitude is an increase in the individual’s blood flow both at rest and during exercise. Blood flow to the brain, lungs and extremities increases. In contrast to this, blood flow to the non essential organs (splanchnic and renal system) decreases, McArdle Katch and Katch p475).

The change in blood flow is to ensure that the oxygen demands of the brain at sea level are still met at altitude. Blood flow to the lungs increases to increase the perfusion of oxygen and carbon dioxide. The increase in blood flow to the periphery is important in constriction due to ischemia.

If these adaptations do not occur homeostasis is lost and an individual will encounter altitude illness. This may be due to; an inadequate perfusion of oxygen to the tissues or because of the consequences of a sudden increase in blood flow to the brain/lungs.

Acute mountain sickness (AMS) as the name suggests is quick in onset. The symptoms of AMS occur 6-72 hours after an individual is exposed to high altitude. The cause of acute mountain sickness is believed to be a lack of oxygen to the brain to maintain normal functioning, (Miasnikov 2007).

Lung/brain edemas have also been reported. HAPE or high altitude pulmonary edemas occur due to accumulation of fluid in the lungs due to the extra pressure created by the increase blood flow to the area. The high volume of fluid in the lungs impairs gaseous exchange of both oxygen and carbon dioxide at the alveoli.

HACE or high altitude cerebral edema is a result of damage to brain tissue. The increase in the blood flow to the brain may cause brain swelling and a high cranial pressure, (Miasnikov 2007).

Figure 3.


(Dietz 2000)

The treatment for both conditions is obvious. Hypoxia is causing the conditions so in order to counteract this problem the symptomatic individual should be descended slowly and or given oxygen by means of a cylinder, (Yusi 2007).

There are a number of reasons why adaptation is inadequate and thus altitude illness is suffered, these include; the rate of ascent, total altitude reached, length of time at a given altitude, hydration, diet and exertion levels, (Yusi 2007). Therefore if an individual climbs slowly, does not go to extreme heights, stays for a short duration, keeps well hydrated,



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