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LIVING IN THIN AIR 

Why is there less oxygen at high altitude?

We all live underneath a huge ocean of air that is several miles deep: the atmosphere. The pressure on our bodies is about the same as ten metres of sea water pressing down on us all the time. At sea level, because air is compressible, the weight of all that air above us compresses the air around us, making it denser. As you go up a mountain, the air becomes less compressed and is therefore thinner.

The important effect of this decrease in pressure is this: in a given volume of air, there are fewer molecules present. This is really just another way of saying that the pressure is lower (this is called Boyle's law). The percentage of those molecules that are oxygen is exactly the same: 21%. The problem is that there are fewer molecules of everything present, including oxygen.

So although the percentage of oxygen in the atmosphere is the same, the thinner air means there is less oxygen to breathe.

Try using our barometric pressure calculator to see how air pressure changes at high altitudes. Or use the altitude oxygen graph to see how much less oxygen is available at any altitude.

The pictures above demonstrate the effect of altitude on barometric pressure. I sealed a plastic bottle like this one in La Paz, Bolivia, at an altitude of 3600m (about 12000ft). I then brought it home with me to Edinburgh (which is pretty much at sea level). As you can see, the pressure of the atmosphere pushing down on the bottle has caused it to collapse.

The same thing happens in reverse to sealed objects when you take them up to high altitudes. Above is a photograph of a roll-on deodourant that I sealed in London, then opened in La Paz. It exploded across my hotel room.

The body makes a wide range of changes in order to cope better with the lack of oxygen at high altitude. This process is called acclimatisation. If you don’t acclimatise properly, you greatly increase your chance of developing altitude sickness, or even worse, HAPE (high altitude pulmonary oedema)or HACE (high altitude cerebral oedema).

by Kenneth Baillie

 

ACCLIMATISATION

Acclimatisation to altitude involves breathing faster & more deeply, and the heart pumping more blood to the brain & muscles

If you go to high altitude quickly, your body has to adapt to the thinner air and the lack of oxygen. Two important things happen almost immediately:

you breathe faster and more deeply to maximise the amount of oxygen that can get into the blood from the lungs, and your heart pumps more blood to increase the supply of oxygen to your brain and muscles.

You can demonstrate how important breathing harder is by using our high altitude oxygen calculator. Some people include breathlessness during exercise as a component of altitude sickness, but this is misleading. Breathing harder is a normal response to the shortage of oxygen, but it does have other effects on the body: click to learn more about breathing at altitude.

The sensation of breathlessness usually indicates that the lungs are having difficulty in supplying the body’s demand for oxygen. Therefore, if a climber is walking too fast for his lungs to keep up, he feels breathless and slows down. However, breathlessness at rest indicates that the lungs are having difficulty in supplying even the small amount of oxygen that the body needs when it is resting. This is an ominous sign at high altitude and may indicate the development of high altitude pulmonary oedema (HAPE). Any climber who is breathless at rest at high altitude should descend to a safer altitude as soon as possible. If you have had HAPE, please register with the online HAPE database.

 

by Kenneth Baillie

 

BREATHING AT HIGH ALTITUDE

Everyone breathes faster and deeper (hyperventilates) at high altitude – it is necessary to do this in order to survive. The function of the lungs is to expose blood to fresh air, and breathing faster essentially increases the flow of fresh air past the blood. This means that whenever an oxygen molecule is taken away by the blood, it is quickly replaced by a fresh one. This means that there is always more oxygen available to be taken up into the blood. (Click to read more about the carriage of oxygen in the blood.)

Carbon dioxide (CO2) is constantly produced by the body and the lungs remove it by allowing it to diffuse into the fresh air in the lungs. Increasing the flow of fresh air through the lungs, by hyperventilating, increases the rate at which CO2 is lost. This happens for the same reason that wet laundry dries faster in a strong wind: the wind blows away the water vapour, so there is space for more water to evaporate. You can see how hyperventilating changes the level of carbon dioxide in the blood using the altitude oxygen calculator. Simply increase the number of breaths taken per minute, and watch what happens to the CO2.

Because CO2 is an acid gas, losing more of it from the blood leaves the blood relatively alkaline. At altitudes up to about 6000m, the kidneys correct the alkalinity of the blood over a few days by removing alkali (in the form of bicarbonate ions, HCO3-) from the blood. Our oxygen calculator will allow you to remove bicarbonate ions; watch the effect on the alkalinity of the blood.

These processes have important effects on the binding of oxygen to haemoglobin in the blood. You can read more about this in our tutorial on oxygen transport.

Shunt

The diagrams on this page show what happens if there is a blockage to an air space in the lungs. The simplest example is a peanut stuck in one of the air passages in the lungs, but the same process happens in pneumonia, or pulmonary edema. Blood still flows past the air spaces, but because there is no fresh air getting to the blood, it can’t take up any more oxygen. That means that a lot of de-oxygenated blood makes its way straight past the lungs. When it mixes with the blood from all the other parts of the lungs, the total amount of oxygen is less. This causes hypoxia – a shortage of oxygen getting to where it is needed.

Physiological Shunt

Even in completely healthy people, there is always some blood that makes its way past the lungs without encountering any fresh air. This blood passes through the bronchial circulation, and the thebesian veins in the heart. This is called physiological shunt. You can calculate the effect of different amounts of shunt by downloading our oxygen delivery model in microsoft excel (but beware – this is a very large file).

How do the lungs cope with shunt?

We have evolved a clever mechanism to reduce the effect of shunt. When the blood passing through an area of lung isn’t picking up enough oxygen, the blood vessels carrying that blood tighten, so that less deoxygenated blood can get through the lungs. This is called hypoxic pulmonary vasoconstriction. The diagram to the right shows how this means that less deoxygenated blood gets through, so there is more oxygen in the mixture of blood leaving the lungs.

At high altitude, there is less oxygen in the air that you breathe. (Click for an explanation of why there is less oxygen at high altitude.) This means that all of the blood from all areas of the lungs, is relatively short on oxygen or hypoxic.

Physiological Shunt

Even in completely healthy people, there is always some blood that makes its way past the lungs without encountering any fresh air. This blood passes through the bronchial circulation, and the thebesian veins in the heart. This is called physiological shunt. 

How do the lungs cope with shunt?

We have evolved a clever mechanism to reduce the effect of shunt. When the blood passing through an area of lung isn’t picking up enough oxygen, the blood vessels carrying that blood tighten, so that less deoxygenated blood can get through the lungs. This is called hypoxic pulmonary vasoconstriction. The diagram to the right shows how this means that less deoxygenated blood gets through, so there is more oxygen in the mixture of blood leaving the lungs.

 

At high altitude, there is less oxygen in the air that you breathe. This means that all of the blood from all areas of the lungs, is relatively short on oxygen or hypoxic.

Unfortunately, the lungs still respond to the shortage of oxygen in the same way: by tightening the blood vessels. But because all areas of the lung are lacking in oxygen, all of the blood vessels in the lungs constrict.

The heart still pumps the same amount of blood through the lungs, but because all of the blood vessels are tightly constricted, the pressure needed to force blood through them is much greater. In fact the pressures get so high that some of the tiniest blood vessels break open, and this is thought to be part of the cause of HAPE (high altitude pulmonary edema).

by Kenneth Baillie

 

PARTIAL PRESSURE 

Partial pressure is a way of describing how much of a gas is present. All gases exert pressure on the walls of their container. This is because the molecules of gas constantly bounce off the walls. Partial pressure is used to describe a mixture of gases. It is defined as the pressure that any one gas would exert on the walls of the container if it were the only gas present.

This is defined more formally under Dalton’s law, which states that the sum of the partial pressures of all of the gases in a mixture will be equal to the total pressure of that mixture.

Confusingly, partial pressure is also used to describe dissolved gases, particularly in blood. In this case, the partial pressure of a gas dissolved in blood is the partial pressure that the gas would have, if the blood were allowed to equilibrate with a volume of gas. Why do we use this counter-intuitive system? The main reason is that when blood is exposed to fresh air in the lungs, it equilibrates completely so that the partial pressure of oxygen in the air spaces in the lungs is equal to the partial pressure of oxygen in the blood. This is demonstrated by the altitude oxygen calculator. You will notice that the partial pressure of oxygen in arterial blood is slightly less than the partial pressure of oxygen in the lungs: this is because there is always a little bit of blood that passes through the lungs without encountering an air space. This is called physiological shunt.

by Kenneth Baillie

 
 

OXYGEN CARRIAGE IN THE BLOOD 

Haemoglobin carries oxygen in the blood.

Oxygen in inhaled air diffuses into the blood in the lungs. Blood has a massive capacity to dissolve oxygen – much more oxygen can dissolve in blood than could dissolve in the same amount of water. This is because blood contains haemoglobin – a specialised protein that binds to oxygen in the lungs so that the oxygen can be transported to the rest of the body.

The amount of haemoglobin in blood increases at high altitude. This is one of the best-known features of acclimatisation (acclimation) to high altitude. Increasing the amount of haemoglobin in the blood increases the amount of oxygen that can be carried. However, there is a downside: when there is too much haemoglobin, blood becomes sticky and viscous and it is harder for the heart to pump the blood around the body. This happens in chronic mountain sickness.

Haemoglobin consists of four subunits joined together. When an oxygen molecule binds to one subunit, the other subunits become more likely to bind oxygen. This feature of haemoglobin gives the haemoglobin saturation curve (the graph opposite) its characteristic S shape. Interestingly, the curve shifts a little in some conditions, such as on ascent to high altitude. This is important because a shift to the right indicates that oxygen is bound less tightly, so that less is taken up in the lungs, but it is more easily released in the tissues.

The following physiological variables decrease the affinity of haemoglobin for oxygen, so they cause the curve to shift to the right: H+, temperature, CO2, and a substance called 2,3 DPG. A decrease in any of these variables has the opposite effect - the curve shifts to the left.

For example, in the graph opposite, the green line shows a normal curve. The blue line shows the curve for a patient with very acidic blood (H+=80nM, pH 7.1). In contrast, the red line shows a patient who is hypothermic, with a body temperature of only 30ºC.

When you ascend to high altitude, the curve initially shifts to the right at moderate altitudes, under the influence of 2,3 DPG. At extreme altitude, it shifts to the left because there is much less CO2 in the blood (see acclimatisation to find out why). You can explore these changes in any combination using the interactive oxygen saturation graph.

by Kenneth Baillie

 

OXYGEN CARRIAGE IN THE BLOOD 

Haemoglobin carries oxygen in the blood.

Oxygen in inhaled air diffuses into the blood in the lungs. Blood has a massive capacity to dissolve oxygen – much more oxygen can dissolve in blood than could dissolve in the same amount of water. This is because blood contains haemoglobin – a specialised protein that binds to oxygen in the lungs so that the oxygen can be transported to the rest of the body.

The amount of haemoglobin in blood increases at high altitude. This is one of the best-known features of acclimatisation (acclimation) to high altitude. Increasing the amount of haemoglobin in the blood increases the amount of oxygen that can be carried. However, there is a downside: when there is too much haemoglobin, blood becomes sticky and viscous and it is harder for the heart to pump the blood around the body. This happens in chronic mountain sickness.

Haemoglobin consists of four subunits joined together. When an oxygen molecule binds to one subunit, the other subunits become more likely to bind oxygen. This feature of haemoglobin gives the haemoglobin saturation curve (the graph opposite) its characteristic S shape. Interestingly, the curve shifts a little in some conditions, such as on ascent to high altitude. This is important because a shift to the right indicates that oxygen is bound less tightly, so that less is taken up in the lungs, but it is more easily released in the tissues.

The following physiological variables decrease the affinity of haemoglobin for oxygen, so they cause the curve to shift to the right: H+, temperature, CO2, and a substance called 2,3 DPG. A decrease in any of these variables has the opposite effect - the curve shifts to the left.

For example, in the graph opposite, the green line shows a normal curve. The blue line shows the curve for a patient with very acidic blood (H+=80nM, pH 7.1). In contrast, the red line shows a patient who is hypothermic, with a body temperature of only 30ºC.

When you ascend to high altitude, the curve initially shifts to the right at moderate altitudes, under the influence of 2,3 DPG. At extreme altitude, it shifts to the left because there is much less CO2 in the blood (see acclimatisation to find out why). 

by Kenneth Baillie

ALTITUDE TRAINING 

Training at altitude may help athletes gain a competitive edge at sea level; altitude exposure also presents problems to athletes, and these could possibly cancel out benefit.

All athletes seek a competitive advantage. Although the benefits of some interventions (like training, for example) are clear, most strategies are less well proven. Altitude is no exception to this. Training at high altitude has been used by competitive athletes as a means of improving their potential. However, despite a good deal of research into the topic, its true effects and a recommended approach are still not well established. Additionally, altitude training is usually expensive and fraught with logistical problems.

Benefits of Altitude Exposure

Exposure to high altitude could theoretically improve an athlete’s capacity to exercise. Exposing the body to high altitude causes it to acclimatise to the lower level of oxygen available in the atmosphere. Many of the changes that occur with acclimatisation improve the delivery of oxygen to the muscles -the theory being that more oxygen will lead to better performance.

For any type of exercise lasting longer than a few minutes, the body must use oxygen to generate energy. Without it, muscles simply seize up and can become damaged. This type of exercise is called aerobic exercise, meaning with oxygen.

The body naturally produces a hormone called erythropoetin (EPO) which stimulates the production of red blood cells which carry oxygen to the muscles. Up to a point, the more blood cells you have, the more oxygen you can deliver to your muscles. There are also a number of other changes that happen during acclimatisation which may help athletic performance, including an increase in the number of small blood vessels, an increase in buffering capacity (ability to manage the build up of waste acid) and changes in the microscopic structure and function of the muscles themselves.

Problems of Altitude Exposure

However, acclimatisation to high altitude is not simple, and there are a number of other effects that could cancel out the above benefits. For example the increase in red blood cells comes at a cost - having too many blood cells makes the blood thicker and can make blood flow sluggish. This makes it harder for your heart to pump round the body, and can actually decrease the amount of oxygen getting to where it is needed.

At very high altitudes (>5000m), weight loss is unavoidable because your body actually consumes your muscles in order to provide energy. There is even a risk that the body’s immune system will become weakened, leading to an increased risk of infections, and there may be adverse changes in the chemical make-up of the muscles. Additionally, the body cannot exercise as intensely at altitude. This results in reduced training intensity, which can reduce performance in some sports. At very high altitudes, further problems are encountered: loss of appetite, inhibition of muscle repair processes and excessive work of breathing. On top of this, there is the problem of altitude illnesses, which can dramatically reduce the capacity to be active at altitude, or foreshorten the exposure to high altitude altogether.

Altitude Exposure Techniques

Taking some of the information about altitude training into consideration, various techniques have been devised in order to expose the athlete to the beneficial effects of high altitude whilst not reducing their ability to train effectively. These have been labelled ‘Live High – Train High, ‘Live Low – Train High’ and ‘Live High – Train Low’. The typical altitudes used are around 2000-2500m, which in itself reduces the risk of some of the unhelpful effects of altitude exposure. The ‘low’ altitudes may not actually be at sea level, but could be 1250m, for example. However, the difference between the two altitudes is significant enough to have an effect on training [see the difference in oxygen and pressure at these altitudes with our high altitude calculator].

Live High – Train High

Maximum exposure to altitude. Evidence of a positive effect at sea level is controversial, and there is less support for this method amongst experts.

Live Low – Train High

The idea behind this regime is that the athlete is exercising in a low oxygen environment, whilst resting in a normal oxygen environment. There have been some interesting findings suggesting that this technique might work, but there are no good studies showing that the technique makes any difference to the ultimate competitive performance of the athlete at sea-level. Additionally, training intensity is reduced so some athletes may find that they actually lose fitness using this regime.

Live High – Train Low

The theory behind this regime is that the body will acclimatise to altitude by living there, whilst training intensity can be maintained by training at (or near) sea level. Hence, the beneficial effects of altitude exposure are harnessed whilst some of the negative ones are avoided. However, residence at altitude must be for more than 12 hours per day and for at least 3 weeks. With this technique, improvements in sea-level performance have been shown in events lasting between 8 and 20 minutes. And interestingly, athletes of all abilities are thought to benefit.

 
 

DIVING AT ALTITUDE 

Elevated altitudes produce unique challenges for the diver. The  reduced atmospheric pressure at the surface of any mountain lake affects the divers’ depth gauges, as does the fresh water which is less dense than in the sea (Wienke, 1993). Then, when the diver ascends from depth, the rate of change as the ambient pressure drops is far greater than when ascending from a dive in the sea (Smith, 1976). These factors need to be compensated for, otherwise dives considered relatively safe in the sea might generate copious bubbles of inert gas within a diver’s bodily tissues, causing a disease called Decompression Sickness (DCS), popularly known as “the bends”. The bends may range from a mild skin rash, through increasing severity to paralysis and death. According to Gribble (1960), the first mention of a possible altitude bend was by von Schrotter in 1906, though the quotation attributed to Boycott and Haldane regarding this has not been found by this author (Boycott, Damant, & Haldane, 1908; Gribble, 1960; Schrotter, 1906). Regardless, it appears that “altitude bends” are a modern disease, meaning we probably have much more to learn yet before we fully understand the mechanisms involved.

Fizzyology

As a diver descends the pressure surrounding the diver increases. This increase does not affect divers wearing rigid “atmospheric” suits but, for the majority of us who wear flexible diving dress, we compensate for the increased pressure by increasing the pressure of the gas we breath. Ignoring minor variations due to the weather, at sea-level the ambient air pressure approximates one atmosphere of pressure, at a depth of ten metres in the sea the pressure should be two atmospheres, and another atmosphere of pressure is added for each additional ten metres of depth. Thanks to the development of the SCUBA regulator by Emile Gagnan and Jacques Cousteau, when a diver breathes compressed gas at depth then the gas is delivered at a pressure equivalent to the surrounding pressure. In this way the diver does not have to “suck” his gas from a much lower pressure down to a higher pressure, (and this is why we cannot simply use a long snorkel). The pressure is “regulated” by the SCUBA unit, which senses what the ambient pressure is.

Inhaling gas at increased pressure solves one problem (of delivering gas to the lungs), but as the blood transports this gas around the body the diver’s tissues naturally move towards equilibrium with the new ambient pressure by absorbing the gas. When the diver later ascends to a much lower pressure, such as at the surface, these tissues now have a greater pressure of gas dissolved within them than the surrounding air pressure, and this gas moves towards equilibrium once again, this time by leaving the tissues (Lenihan & Morgan, 1975). It is generally accepted that the rate of this move towards equilibrium, that is, the size of the difference between the tissue pressure and the ambient pressure, is largely responsible for the generation of bubbles within a diver’s tissues. The principle is akin to opening a can of soda: if you open the can suddenly then the soda will fizz, due to the sudden difference between the dissolved pressure and the ambient pressure. If you open the can slowly then the soda will not fizz as much, because the change is more gradual. If you have flown in a commercial jet, which usually has a much lower ambient air pressure in the cabin than on the ground, then did you notice that your soda was unusually fizzy? That would have probably been due to the even greater difference between the dissolved gas pressure in the soda (usually around 1.5 atmospheres) and the ambient pressure in the cabin. This is equivalent to one of the main concerns of a diver at high altitude: the increased difference between the pressure of the gas dissolved within his tissues after a dive and the (much lower) ambient pressure at the surface of the mountain lake. These increased differences first become a cause for concern at altitudes of just 300m or higher (NOAA, 2001).

Popularity of diving at altitude.

There are many reasons people dive at high altitude: searching for particular objects such as WWII aircraft, training when the sea is inhospitable or too distant to be practical, for scientific research, even just for the plain fun of it. At last count, in 2008 there were 30 dive businesses above 1,500m advertising in the Johannesburg business telephone directories, and 53 above 1,500m advertising in Colorado telephone directories (Buzzacott & Ruehle, 2009). The University of California conduct scientific diver training in Lake Tahoe, at an altitude of 6,200ft (1,890m)(Bell & Borgwardt, 1976), and the Bolivian Navy maintain a school of diving on the shores of Tiquina, at 12,500ft (3,810m).

For some, the challenge of diving at altitude is the purpose. In 1968 a team led by Jacques Cousteau established the record for altitude diving in Lake Titicaca, at an altitude of 12,500ft (3,810m). In the 1980’s an American team made a series of dives in the South American Andes, at 19, 450ft (5,928m) (Leach, 1986). In 1988 a team from the Indian Navy Diving Training School in Cochin, Southern India, made many training dives in Pykara Dam in the Nilgiri Hills at 7,000ft (2134m) before making 22 dives at Lake Manasbal (7,000ft, 2134m), 16 dives at Leh (11,000ft, 3,353m) and finally diving at 14,200ft (4,328m), in Lake Pangong Tso in the north of Ladakh state in the Himalayas (Sahni, John, Dhall, & Chatterjee, 1991). In true expedition fashion, some of the troop suffered hypothermia, headaches or unconsciousness. No such troubles for the British expedition to the Khumbu Glacier in the Everest region of the Himalayas in 1989, when they made 18 ice-dives in Gokyo Tsho at 15,700ft (4,785m) and eight ice-dives in Donag Tscho at 16,000ft (4,877m), cutting through 1.2m thick ice to reach almost 30m depth (Leach, McLean, & Mee, 1994). The record at Lago Lincancabur has been equalled a number of times since the 1980’s (Morris, Berthold, & Cabrol, 2007) but currently stands, and these days the Bolivian Navy dive there every few years (H. Crespo, personal communication, 2010). The school at Tequina have recently taken delivery of a new hyperbaric chamber, have goals to substantially increase their mixed-gas diving capabilities and, in this authors opinion, they are poised to reach new depths in Lake Titicaca, to map uncharted caves, to recover artefacts from pre-Inca civilisations that will revise our understanding of pre-Columbian history, to monitor human physiology in environments not previously endured and to record fauna that is currently unknown to science.

Methods of compensation

Dive tables are a tabular matrix of depths and times that relate to post-dive estimates of the resulting pressures within a range of theoretical tissues. If a diver stays too deep for too long then his tissues will have so much pressure within them that he will not be able to safely ascend to the surface. He will need to “decompress” on the way up or, else, too many bubbles will form. Of course, remembering the can of soda analogy: it is not just the amount of gas in the tissues that needs to be limited, it is the rate of change when the ambient pressure drops that is the second key factor to account for. The faster the rate of change then the lower the limits (shorter times and/or shallower depths). Therefore, each table is designed with a maximum rate of ascent in mind and this rate of ascent is dependent upon altitude. Modern divers rely on personal dive computers to generate real-time limits and these computers utilise a governing algorithm to estimate how many minutes might be allowably left at whatever depth the diver is at. These algorithms, as with the algorithms used to generate dive tables, vary between dive computer manufacturers. Not only do the algorithms differ, (and they are often proprietary information which hinders comparison), dive computers differ in other ways too, such as in the frequency a diver’s time limits are computed. One model may estimate the remaining allowable time once every second whereas another model may estimate the remaining allowable time every ten seconds. Other safety mechanisms differ between models too, such as ascent-rate alarms, which emit a regular beep if the maximum ascent rate, (allowed by the individual dive computer’s algorithm), is exceeded. Many dive computers utilise a variable ascent rate too, allowing faster ascents at deeper depths, then requiring the diver to slow his ascent nearer the surface, as the rate of change increases exponentially. The debate between proponents of the constant ascent rate, originally recommended by a scientist called Hill, and the variable ascent rate, originally recommended by Haldane, is known as the “Hill vs. Haldane controversy” (Marroni, 2002).

Of course, remember that the underlying causes of decompression sickness are still unproven. The evidence is convincingly supportive but the scientifically proven link remains elusive. We think we understand the mechanisms of bubble generation and the causes of decompression sickness but many of the assumptions used to predict our limits are based on empirical trial-and-error, where limits have been predicted and then revised downwards after in-water use. Accordingly, there are a variety of algorithms in use today that rely on different physiological and physical assumptions about human tissues, bubbles and gas kinetic theory. For recreational dives in the sea these various algorithms usually result in similar predictions of time limits for each depth, give or take a small proportion of the total allowable time. For example, most dive computers and tables allow a diver to make his first dive of the day to 30m for between 16-25 minutes, (most allow around 20 minutes). Some then assume the inert gas is washed out more quickly during a surface interval between dives, and others impose higher time penalties for dives made when divers already have residual gas left over from previous dives. The upshot of all this is that algorithms vary in many ways, and the ways they compensate for dives at high altitude also vary (Egi & Brubank, 1995).

Compensation mechanisms

Possibly the most common method of adapting tables for use at high altitude is to convert the maximum depth a diver is planning to reach into an “equivalent sea dive” depth (Paulev & Zubieta-Calleja Jr, 2007), which is a way of reducing the time allowed by using the time limit from a deeper depth. This method is known as the “Haldane method” (Hennessy, 1977), later referred to by the US Navy as the “Cross Correction”, after E.R. Cross promoted the method in 1967 and again in 1970 (Egi & Brubank, 1995). The higher the altitude, the more a diver adds to his planned actual depth when searching for his limit. For example, a diver may be planning to go to 18m depth. To find his limit he will look at the 18m time limit at sea level, the 21m limit at 5000ft and the 27m limit at 10,000ft altitude (Bell & Borgwardt, 1976). But, there are a number of other theoretical ways to adapt sea-level dive tables for use at altitude, and even more ways being utilised by personal dive computers. In one recent study (Buzzacott & Ruehle, 2009) the order of a series of dive computers when ranked according to how conservative they were at sea-level was reversed at 10,000 feet, so that the most conservative at sea-level became the most generous at altitude, and the most generous at sea-level became the most conservative at altitude.

 

Conclusion

Recreational diving at altitude carries risks that are additional to diving at sea-level and additional training is required by recreational divers. For decompression diving the jury is still out concerning which method is best for adapting existing decompression schedules for use at altitude. Accordingly, any team planning significant exposure to decompression stress at altitude are well advised to consult a diving physiologist with experience in altitude diving. Furthermore, all divers should accept that whatever dive schedule is adopted, the assumptions underpinning that model may be untested or unproven and that many decompression dives at high altitude could even be considered experimental in nature. Some tables, for example, have been tested in water up to a certain altitude and remain unproven beyond that height (Boni, Schibli, Nussberger, & Buhlmann, 1976). To minimise risk of the bends additional prophylactic measures should be taken when possible, such as engaging in a suitable pre-dive exercise regime, the introduction of additional oxygen into the breathing mix, removal of inert gas from the breathing mix, warmth during decompression to promote peripheral circulation, an ascent-rate rate reference such as a weighted line or suspended trapeze, a horizontal pose to have the natural buoyancy of the lungs promote maximal surface area for gas exchange, and immediate post-dive assistance to reduce diver workload.

Diving at altitude can be a lot of fun, a challenge, and there are many worthy reasons to dive in mountain lakes. Take care though – diving at altitude is a lot less forgiving if you get it wrong. A simple matter like a stuck buoyancy jacket inflator button might bring you up quickly and you’d be more likely to get away with it in the sea than you will in the mountains. Add complications like having to cross a mountain pass to get to the hospital and a relatively minor bend could turn really nasty very quickly, and no-one wants to end-up paralysed from the neck down.

References

Bell, R. L., & Borgwardt, R. E. (1976). The theory of high-altitude corrections to the U.S. Navy standard decompression tables. The cross corrections. Undersea Biomed Res, 3(1), 1-23.

Boni, M., Schibli, R., Nussberger, P., & Buhlmann, A. A. (1976). Diving at diminished atmospheric pressure: air decompression tables for different altitudes. Undersea Biomed Res, 3(3), 189-204.

Boycott, A. E., Damant, G. C. C., & Haldane, J. S. (1908). The prevention of compressed air illness. J. Hyg. (Lond.)(8), 342-443.

Buzzacott, P., & Ruehle, A. (2009). The effects of high altitude on relative performance of dive decompression computers. International Journal of the Society for Underwater Technology, 28(2), 51-55.

Egi, S. M., & Brubank, A. O. (1995). Diving at altitude: a review of decompression strategies. Undersea Hyperb Med, 22(3), 281-300.

Gribble, M. d. G. (1960). A comparison of the 'high altitude' and 'high pressure' syndromes of decompression sickness. British Journal of Industrial Medicine, 17, 181-186.

Hennessy, T. R. (1977). Converting standard air decompression tables for no-stop diving from altitude or habitat. Undersea Biomed Res, 4(1), 39-53.

Leach, J. (1986). Andean high altitude diving expedition. Journal of Underwater Technology, 12, 27-31.

Leach, J., McLean, A., & Mee, F. B. (1994). High altitude dives in the Nepali Himalaya. Undersea Hyperb Med, 21(4), 459-466.

Lenihan, D., & Morgan, K. (1975). High Altitude Diving. Santa Fe, New Mexico: U.S. Department of the Interior. National Parks Service.

Marroni, A. (2002). What ascent profile for the prevention of decompression sickness? II - A field model comparing Hill and Haldane ascent modalities, with an eye to the development of a bubble-safe decompression algorithm. DAN Europe DSL special project 'Haldane Vs Hill'. Eur. J. Underwater Hyperb. Med., 3(3).

Morris, R., Berthold, R., & Cabrol, N. (2007). Diving at extreme altitude: Dive planning and execution during the 2006 High Lakes Science Expedition. Paper presented at the American Academy of Underwater Sciences 26th Symposium, Dauphin Island, AL.

NOAA. (2001). NOAA Diving Manual. Diving for science and technology (4th ed.): U.S. Department of Commerce. National Oceanic and Atmospheric Administration.

Paulev, P., & Zubieta-Calleja Jr, G. (2007). High altitude diving depths. Research in sports medicine, 15, 213-223.

Sahni, T. K., John, M. J., Dhall, A., & Chatterjee, A. K. (1991). High altitude dives from 7000 to 14,200 feet in the Himalayas. Undersea Biomed Res, 18(4), 303-316.

Schrotter, H. v. (1906). Der sauerstoff in der prophylaxie und therapie der luftdruckerkrankungen (2nd ed.).

Smith, C. L. (1976). Altitude procedures for the ocean diver (pp. 46): National Association of Underwater Instructors.

Wienke, B. R. (1993). Diving above sea level. Flagstaff, AZ: Best Publishing Company.

by Peter Buzzacott

HYPOTHERMIA 

Hypothermia is one of the biggest risks to your life at high altitude

Hypothermia is defined as a core temperature below 35 degrees. It is broadly categorised into:

  • Mild hypothermia (32-35 degrees C)

  • Moderate hypothermia (30-32 degrees C)

  • Severe hypothermia (<30 degrees C)
     

It is estimated that up to 25% of people brought off the hill by Mountain Rescue in the UK may have some form of hypothermia. Onset of hypothermia in an individual depends on multiple factors both individual and environmental. Individual factors include fitness, food intake, clothing, injury and illness. It is important to remember it can occur at modest temperatures when there is prolonged exposure to water, driving rain or wind chill. (1)The two most common causes of hypothermia on the hill are exhaustion and injury (2).

Hypothermia, dehydration, low blood sugar and altitude sickness share common symptoms and signs. If an individual develops one condition the others should be sought and if one member of a group develops hypothermia the whole group should be checked.

 

Thermoregulation

Normally thermoregulation within the body balances heat loss into the environment with heat production by the body organs and muscles. This is important as the body's enzyme systems only function within a narrow range of temperature around 37degrees C. In mild hypothermia this process is still active producing voluntary and involuntary responses. Involuntary responses include skin vasoconstriction and shivering. Unfortunately shivering is an extremely inefficient way of producing heat, significantly increasing utilisation of energy stores. Voluntary responses include seeking shelter, putting on clothes, exercise and eating. These are much more effective, especially eating and exercise, which increases heat production by a factor of 10-15 and eating.

Once the core temperature goes below 32, shivering stops as thermoregulation fails. The body then gets stuck in a vicious cycle as dropping core temperature itself reduces body metabolism which in turn reduces the body temperature more. The victim's body systems, particularly the heart and brain function, gradually slow down.

 

Classification

The temperature at which any individual displays the various signs and symptoms of hypothermia varies as it depends on the factors mentioned above. It is also unusual to be able to accurately measure core body temperature in the pre-hospital environment. Oral, rectal or tympanic/inner ear temperatures are all inaccurate. Therefore diagnosis must be made on clinical signs and symptoms alone.

There are a number of different classifications of hypothermia. These have been developed in seperate areas of the world in response to their differing geography, rescue services and medical back-up. The Swiss Society of Mountain Medicine grade hypothermia from one to five whereas the UK Lake District Search and Mountain Rescue Association simply classify hypothermia as mild (alert and shivering) or severe (no longer shivering and/or reduced level of consciousness) which is safe and adequate for rescuers without additional equipment. For the purposes of this article severe hypothermia is subdivided into moderate hypothermia, where the victim has stopped shivering but is not completely unconscious and severe hypothermia, where the victim is unconscious and signs of life are difficult to detect.

Ability to estimate which stage of hypothermia the victim has reached is important as this then allows treatment and possible evacuation to be planned.

Symptoms
















 



Death from hypothermia 

This is a very difficult situation in the wilderness. Technically only trained health care staff can actually pronounce death however in some circumstances it is recognised that attempts at resuscitation are futile. According to the Alaskan Guidelines these include obvious fatal injury, a core temperature of less than 10degrees C, an airway blocked by snow or ice, incompressible chest or eyeballs (on gentle pressure - compare with live persons eyeball) or finally not coming back to life once re-warmed.

Treatment

Below simple and effective treatments that can be given by non healthcare personnel in a wilderness environment are described.

Mild hypothermia can be reversed relatively easily. The key is to recognise it early and act swiftly. Shelter, warm clothes and warm food and drink will raise core temperature. Remember to insulate them from the ground. A thick plastic survival bag helps them retain any heat they are producing (these have been shown to be more efficient than 'space blankets'). To add heat, body warmth can be used, for example putting the victim in a sleeping bag with someone else or using manoeuvres like a penguin huddle. Once re-warmed victims can generally then get themselves to a place of safety but should be watched carefully.

Moderate hypothermia: The patient will no longer be shivering and may have reduced level of consciousness. This is a life-threatening situation. Their heart will already be at risk of arrhythmias. Good shelter needs to be found rapidly and the group should be prepared for a prolonged stop.

The victim should be nursed lying down and insulated from the ground. If the conscious level is significantly reduced they should be placed in the recovery position to protect their airway. Any movement should be slow and gentle - a good policy is to treat them as if they have a spinal injury. Start re-warming as soon as possible:

  • Removing wet clothing and gently patting dry.

  • Place them in a pre-warmed sleeping bag (another person or hot water bottles can be used for this).

  • Add heat by using chemical heat packs or hot water bottles (wrapped in cloth to prevent burns) placed against armpits, upper abdomen, neck and groin. Heat sources should not be placed on limbs, the person should not be immersed in hot water and limbs should not be massaged as all these produce peripheral blood vessel dilatation which can cause paradoxical core cooling.

  • Warm the tent/bivvy (taking care not to cause Carbon Monoxide poisoning).

  • If/once awake enough to swallow give hot sweet drinks and energy foods.

Generally these patients should be evacuated as they can need ongoing medical care following an episode of hypothermia. Only evacuate by stretcher if the victim is re-warmed, stable and you are sure they won't get cold again during evacuation

Severe hypothermia.

The victim will be unconscious. Concerns are: 

  1. Their airway is at risk of compromise. 

  2. They may also be on the cusp of a fatal cardiac dsyrythmia.

  3. The pulse and breathing may be so slow that the rescuer has to look, listen and feel for at least a minute to detect them.
     

If there are no detectable signs of life then key decisions need to be made. The following recommendations are based on the State of Alaska cold Injuries Guidelines. (3)

  1. Are they salvageable? I.e. should re-warming be attempted - this being both an energy and time consuming process in the wilderness. If the signs discussed above in the death from hypothermia section are present then the only thing to do is organise appropriate evacuation . Other factors that should be taken into account are if the rescuers are exhausted or the rescue will put more people in danger.

  2. If there are no signs of life then rescue breaths (as per basic life support) should be given for 3 minutes and then cardiac activity reassessed, as this simple manoeuvre can improve previously undetectable cardiac activity.

  3. If the victim still has no signs of life then continued treatment depends on whether it is possible to evacuate to an appropriate medical facility which has a cardiac monitor and can give definitive care, within three hours.
     

If evacuation to a medical facility is possible within three hours then the victim should be protected from further cooling (by drying and insulation) whilst rescue ventilation should be continued throughout the evacuation. Chest compressions should NOT be started. The reason for this is that the patient may be in a very slow, undetectable heart rhythm which is maintaining their life and commencing chest compressions could actually tip the irritable heart into VF/cardiac arrest as discussed above. For this reason CPR is only recommended if swift evacuation to a medical facility is possible as once it is commenced it must be continued until the patient's heart can be monitored with an ECG.

If evacuation cannot happen within three hours then rescue breaths should be continued and chest compressions should be commenced. Oxygen should be given if available. This basic life support should be continued for 60 minutes (30 minutes for medical staff using ALS protocols ) whilst all the above active warming measures are instituted. If after 60 minutes the patient has been warmed up but there is still no pulse or breathing effort to be seen then life support should be stopped and the victim evacuated as appropriate. If possible this decision should be made in conjunction with the expedition/base camp health care professional.

Other problems

Two physiological phenomena that are useful to know about in severe hypothermia are:

  1. Afterdrop: this is defined as a continued fall in the core temperature, after removal from the cold stress, which may even occur during rewarming. It is due to heat redistribution within the body. The importance of this is that even when re-warming has started the patient may be at risk of cardiac arrest.

  2. Circum-rescue collapse: this is when a hypothermic victim is found with stable vital signs but then collapses during or soon after rescue. It is thought to be caused by a massive drop in blood pressure or precipitation of VF (as above) on handling of the victim. This phenomenon was initially described in maritime rescue but it has also been seen with rescue of hypothermic victims in the mountain environment.

 

Prevention is better than cure

The old adage that prevention is better than cure counts for double when dealing with illness in the wilderness. Although it is important to know the steps of treatment the take home message should be that anyone in the mountains should be able to recognise the symptoms of hypothermia in themselves and those around them and act upon the diagnosis.

  • Remember high altitude makes hypothermia (and frostbite) more likely.

  • Avoid sweating and/or exchange damp clothes for dry ones.

  • Adequate food and drink gives your body fuel to sustain exercise.

  • Always be prepared to stop and shelter. Multi-person both/bivvy bags are available that are light and compact enough to be carried in a personal pack. These are very efficient at maintaining heat and allow you to gain shelter from the wind anywhere.

  • Keep an eye on other members of your party to watch for the early signs of hypothermia and be prepared to change your route, or go back, if necessary. A buddy system for this works well.

 

 

References

1.Casualty Care in Mountain Rescue. Ellerton J. 2nd. Edition 2006.

2.Mountaineering Council of Scotland Information Leaflet 'Freezing to Death'. 1997.

3.State of Alaska Cold Injuries Guidelines: Alaska Multi-level 2003 (Rev. 2005) Prepared by: Department of Health and Social Services, Division of Public Health, Section of Community Health and EMS.

by Kitty Duncan

MODERATE

The moderately hypothermic victim has slurred speech, is apathetic, confused, irrational, and clumsy. Lips may turn blue and consciousness may be reduced. The pulse first slows down and then the heart becomes more irritable as temperature reduces further, often leading to an irregular pulse (atrial fibrillation) at core temperatures below 32 degrees C.

SEVERE

As temperature drops below 30degrees C the victim will become unresponsive. The breathing and pulse will be faint or even undetectable and they may look dead. Below 30 there is a high risk of the heart going into Ventricular Fibrillation (VF - a form of cardiac arrest) with any kind of rough handling. This includes large limb movements or rapid changes in body position i.e. sitting them up from horizontal position.

MILD

As described above, in mild hypothermia the victim will be shivering with cold white peripheries. There is loss of manual dexterity. They may become quiet and feel cold to touch, be mildly confused or be disorientated and irritable. They may also lose insight - denying having any problem - and reject help, which can make it quite difficult to treat them.

 

KILIMANJARO

A safe and successful ascent of Mount Kilimanjaro: don't die of acute mountain sickness

Acute mountain sickness (AMS) is a common illness that affects a significant proportion of people that ascend to high altitude. The symptoms are headache and fatigue, sleep disturbance, problems with the digestive system and dizziness.

For the majority of sufferers AMS remains no more than an inconvenience. However, for a significant minority AMS can develop into one of two potentially fatal conditions: High Altitude Pulmonary Edema (HAPE) or High Altitude Cerebral Edema (HACE). These conditions both require immediate attention.

Sufferers of HAPE develop breathlessness at rest and may develop blue lips and a raised body temperature. HACE often presents initially with severe headache, vomiting and lethargy. These potentially fatal conditions can be prevented if a pragmatic golden rules approach is taken.

Mount Kilimanjaro is an extremely popular climb amongst inexperienced climbers. As a result of expensive park fees and the abundance of alternative tourist attractions nearby, the rushed round trip to the 5895m summit is often attempted in as little as 5 days. It is therefore perhaps not surprising that many of the climbers attempting the summit suffer altitude sickness. Only one formal investigation into the incidence of HACE has been performed on the mountain, in which 18% of climbers were found to be suffering from HACE. Although no studies into the incidence of HAPE have been performed on the mountain it would not be surprising if the incidence of HAPE mirrored the high incidence of AMS and HACE.

Acclimatisation treks are the only thing that has been proven to protect against AMS on Kilimanjaro. Climbers looking for the best chance of avoiding altitude sickness can acclimatise on the conveniently located Mount Meru (4566m). This approach also gives you the best chance of success on the summit attempt of Mount Kilimanjaro. Climbers are often reassured by locals that the slower ascent rates offered by several of the ascent routes provides protection from AMS development. However, there is no evidence that any of these routes are slow enough to confer protection. In addition, the ascent of Mount Kilimanjaro is so rapid that climbers should not assume that acetazolamide (Diamox) can protect them from developing Acute Mountain Sickness.

by Stewart Jackson, Kenneth Baillie

 

SURVIVAL AT EXTREME ALTITUDE

There have been several reports of people surviving at altitudes greater than 9000m

Is it possible to survive above the summit of Everest? Although it would almost certainly not be possible to climb any higher than an altitude of about 9000m (Everest is 8848m), there are several reports of people surviving unpressurised flights at higher altitudes. At least ten people have stowed away in the wheel bays of long-haul aircraft, which generally fly at altitudes well over 9000m.

This is almost certainly only possible because of the combined effects of extreme cold and unconsciousness, both of which greatly reduces the body's demand for oxygen. The condition could be described as being analogous to hibernation. Sadly, estimates suggest that between 50% and 80% of wheel-bay stowaways do not survive. Perhaps the most compelling account of such a journey is given by Armando Socarras Ramirez, who escaped from Fidel Castro's Cuba in 1969:

The jet engines of the Iberia Airlines DC-8 thundered in ear-splitting crescendo as the big plane taxied toward where we huddled in the tall grass just off the end of the runway at Havana’s Jose Marti Airport. For months my friend Jorge Perez Blanco and I had been planning to stow away in a wheel-well on this flight, No. 904 — Iberia’s once weekly, nonstop run from Havana to Madrid! Now, in the late afternoon of last June 3, 1970, our moment had come.

We realized that we were pretty young to be taking such a big gamble; I was seventeen, Jorge sixteen. But we were both determined to escape from Cuba, and our plans had been carefully made. We knew that departing airliners taxied to the end of the 11,500-foot runway, stopped momentarily after turning around, then roared at full throttle down the runway to take off. We wore rubber-soled shoes to aid us in crawling up the wheels and carried ropes to secure ourselves inside the wheel well. We had also stuffed cotton in our ears as protection against the shriek of the four jet engines. Now we lay sweating with fear as the massive craft swung into its about-face, the jet blast flattening the grass all around us. Let’s run! I shouted to Jorge.

We dashed onto the runway and sprinted toward the left-hand wheels of the momentarily stationary plane. As Jorge began to scramble up the 42-inchhigh tires, I saw there was not room for us both in the single well. I’ll try the other side! I shouted. Quickly I climbed onto the right wheels, grabbed a strut, and, twisting and wriggling, pulled myself into the semidark well. The plane began rolling immediately, and I grabbed some machinery to keep from falling out. The roar of the engines nearly deafened me. As we became airborne, the huge double wheels, scorching hot from takeoff, began folding into the compartment. I tried to flatten myself against the overhead as they came closer and closer; then, in desperation, I pushed at them with my feet. But they pressed powerfully upward, squeezing me, terrifyingly, against the roof of the well.

Just when I felt that I would be crushed, the wheels locked in place and the bay doors beneath them closed, plunging me into darkness. So there I was, my 5 foot 4 inch, 140 pound frame literally wedged in amid a spaghettilike maze of conduits and machinery. I could not move enough to tie myself to anything, so I stuck my rope behind a pipe.

Then, before I had time to catch my breath, the bay doors suddenly dropped open again and the wheels stretched out into their landing position. I held on for dear life, swinging over the abyss, wondering if I had been spotted, if even now the plane was turning back to hand me over to Castro’s police. By the time the wheels began retracting in, I had seen a bit of extra space among the machinery where I could safely squeeze. Now I knew there was room for me even though I could scarcely breathe. After a few minutes, I touched one of the wheels and found that it had cooled off. I swallowed some aspirin tablets against the headsplitting noise and began to wish that I had worn something warmer than my light sport shirt and green fatigues. Up in the cockpit of flight 904, Captain Valentin Vara del Rey, 44, had settled into the routine of the overnight flight, which would last 8 hours and 20 minutes. Takeoff had been normal, with the aircraft and its 147 passengers, plus a crew of 10, lifting off at 170 mph. But, right after lift-off, something unusual had happened. One of three red lights on the instrument panel had remained lighted, indicating improper retraction of the landing gear.

Are you having difficulty? the control tower asked.

Yes replied Vara del Rey. There is an indication that the right wheel hasn’t closed properly. I’ll repeat the procedure. The captain relowered the landing gear, then raised it again. This time the red light blinked out.

Dismissing the incident as a minor malfunction, the captain turned his attention to climbing to the designated cruising altitude. On leveling out, he observed that the temperature outside was 241°F. Inside, the pretty stewardesses began serving dinner to the passengers.

Shivering uncontrollably from the bitter cold, I wondered if Jorge had made it into the other wheel well and began thinking about what had brought me to this desperate situation...

The sun rose over the Atlantic like a great golden globe, its rays glinting off the silver and gold fuselage of Iberia’s DC-8 as it crossed the European coast high over Portugal. With the end of the 4636-mile flight in sight, Captain Vara del Rey began his descent toward Madrid’s Bara Airport. Arrival would be at 8 A.M. local, the captain told his passengers over the intercom, and the weather in Madrid was sunny and pleasant. Shortly after passing over Toledo, Vara del Rey let down his landing gear. As always, the maneuver was accompanied by a buffeting as the wheels hit the slipstream and a 200mph turbulence swirled through the wheel wells. Now the plane went into its final approach; a spurt of flame and smoke from the tires as the DC-8 touched down at about 140 mph.

It was a perfect landing—no bumps. After a brief postflight check, Vara del Rey walked down the ramp steps and stood by the nose of the plane waiting for a car to pick him up, along with his copilot. Nearby, there was a sudden, soft plop as the frozen body of Armando Socarras fell to the concrete apron beneath the plane. Jose Rocha Lorenzana, a security guard, was the first to reach the crumpled figure. When I touched his clothes, they were frozen as stiff as wood Rocha said. All he did was make a strange sound, kind of moan.

I couldn’t believe it at first Vara del Rey said when told of Armando. But then I went over to him. He had ice over his nose and mouth. And his color... As he watched the unconscious boy being bundled into a truck, the captain kept exclaiming to himself, Impossible! Impossible! The first thing I remember after losing consciousness was hitting the ground at the Madrid airport. Then I blacked out again and woke up later at the Gran Hospital de la Beneficencia in downtown Madrid, more dead than alive. When they took my temperature, it was so low that it did not even register on the thermometer. Am I in Spain? was my first question. And then, Where’s Jorge? (Jorge is believed to have been knocked down by the jet blast while trying to climb into the other wheel well and to be in prison in Cuba.)

Doctors said later that my condition was comparable to that of a patient undergoing 'deep-freeze' surgery, a delicate process performed only under carefully controlled conditions. Dr. Jose Maria Pajares, who cared for me, called my survival a 'medical miracle,' and, in truth, I feel lucky to be alive. A few days after my escape, I was up and around the hospital, playing cards with my police guard and reading stacks of letters from all over the world. I especially liked one from a girl in California. You are a hero, she wrote, but not very wise. My uncle, Elo Fernandez, who lives in New Jersey, telephoned and invited me to come to the United States to live with him. The International Rescue Committee arranged my passage and has continued to help me. I am fine now. I live with my uncle and go to school to learn English. I still hope to study to be an artist. I want to be a good citizen and contribute something to this country, for I love it here...

Armando Socarras Ramirez