Acclimatisation can be termed as changes in metabolism and physiology in order to withstand the new conditions (McArdle et al., 1996).
(Sonna, 2002).
As can be seen from figure 2 the number of people who contract AMS is high with a mean value of 49.5 % ± 14.6 %, however the number of people who then develop HAPE is relatively low at 2.5 % ± 1.9 %.
High altitude pulmonary oedema (HAPE) is a subject that has grown in interest in the past 15 years as more people are getting into situations where they may develop HAPE and better scientific techniques such radiographic images, which can specify between other pulmonary oedemas and HAPE (Gluecker et al., 1999) are allowing gradual understanding of the aetiology and pathophysiology of this condition.
The pulmonary circulation main function is to move a good supply of blood from the right ventricle to the alveolar capillaries (blood gas barrier) so gas exchange can occur (Cotes, 1993; West, 2000). This system is disrupted when HAPE occurs as the rise in pulmonary capillary pressure causing interstitial oedema, which disrupts the ventilatory perfusion ratio, the congestion caused by the oedema results in reduced lung compliance and maximum ventilation, hence many patients continually hyperventilate (Cotes, 1993; Maggiorini et al., 2001). Symptoms include those that are similar to AMS, dyspnea, chest congestion, nausea, tachycardia, fever, weakness, coughing, chest infections, sputum upbringing on coughing and even cyanosis; unlike AMS the death rate can be as high as 50 % without treatment, fortunately treatment can reduce this down to 3 – 4 % (Hultgren et al., 1996; Lumb, 2000).
Sufferers of HAPE are most likely those people who are at acute altitudes (over 3000m) not allowing for effective acclimatisation often following a rapid ascent and those who partake in strenuous exercise at altitude. Therefore the most common sufferers of HAPE are usually inexperienced overambitious climbers, although people who live at altitude and return to altitude after a period at lower altitudes are among the most at risk group. This last point is mainly unexplainable to scientist at the current moment in time (Bradbury, 2001; Lumb, 2000). According to a large recent study of 150 people of a variety of sexes staying at a ski resort in the Colorado Rocky Mountains, men seemed to be most susceptible to HAPE although no apparent explain could be found for this finding (Hultgren et al., 1996). Other studies have looked at HAPE and susceptibility due to age. In 1995, at Vail Colorado in the Rocky Mountains USA at an elevation of 2500m, 97 older age participants (59 – 83 years) with a range of diseases associated with people of that age, including, hypertension, lung disease and coronary artery disease participated in a study for (Roach) Results showed that an AMS of 16 % was actually lower than the average value for younger age groups and despite the pulmonary and cardiovascular diseases no other serious clinical signs or symptoms of HAPE developed. This study showed that elderly people at a moderate altitude (under 3000m) are less susceptible to HAPE (Duer, 1998; Roach et al., 1995). The study also shows that pulmonary and cardiovascular diseases do not increase the risk of contracting HAPE (Roach et al., 1995). What can increase incidence of HAPE is if a person as already had HAPE in the past or is venerable to oedema. Values for development of HAPE rise from 2 – 4 % of people at 4000m to over 60 % in previous HAPE sufferers (Maggiorini et al., 2001).
The aetiology of HAPE is complex and two possible ideas about its occurrence have stood firm for several years. (1) The pulmonary capillaries become leaky as a result of inflammation. (2) The high altitude cause pulmonary hypertension leading to oedema (Bradbury, 2001). In the past couple of years experimental evidence has started to support explanation (2). Maggiorini’s laboratory study in 2001 compared the results of a 16-subject group all who had previously suffered from HAPE and a 14-subject control group who have never suffered from HAPE despite regularly climbing to high altitudes. The recommended rate of ascent is 400m a day between 2000m and 3000m and then 300m a day above 3000m (Bradbury, 2001; Lumb, 2000), in Maggiorini’s study after being at a low altitude (490 m) a rise to high altitude (4559m) after 48 hours can be described as a rapid ascent as there is an increase of 2034m per day. The HAPE susceptible group had significantly higher pulmonary artery and pulmonary capillary pressure; 7 of the group also developed HAPE, leading to the conclusion that the initial cause of HAPE is an increase in pulmonary artery and capillary pressure at the precapillary arterioles brought about by hypertension due to hypoxia (Maggiorini et al., 2001). Chest radiographs of patients with HAPE show patchy lungs indicating the pulmonary vasoconstriction is not uniform, meaning some parts of the lungs have increased blood flow, while others have decreased blood flow. The high capillary blood flow in some places then causes excess stress on the capillary walls leading to oedema in the lungs. This theory would explain why a pre-curser of HAPE is high exertion, as this would increase cardiac blood flow and the chance of oedema due to more blood flowing through the lungs (Gluecker et al., 1999; Lumb, 2000).
HAPE is a life threatening condition with a 50 % death rate of the untreated, with treatment this decreases to 3 – 4 %. There are several steps that can be taken in the treatment of HAPE, firstly a decent with as little exertion as possible followed by the inhalation of a gas with a high oxygen concentration (Taylor et al., 1989). Secondly the administration of a vasodilator such as Prophylactic nifedipine recommended by several leading HAPE associated scientists (Bärtsch and Maggiorini), (Bradbury, 2001). Recent studies have also shown that inhalation of nitric oxide can produce a greater amount of vasodilatation in subjects who are susceptible to HAPE (Scherrer et al., 1996). Decreased altitude and increased oxygen inhalation reduces hypoxia and causes the patient to feel more at ease, the use of vasodilators decrease the capillary pressure and reduce the risk of oedema.
HAPE is a dangerous condition that can kill, however as long as precautions like a safe ascent rate, proper acclimatisation and climbing sensibly within you own limits and in an experienced group the development of HAPE is rare and resultant death after treatment is even lower.
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