Altitude Sickness, Part 3

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gregw822
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Altitude Sickness, Part 3

Post by gregw822 »

Altitude Sickness, Part 3
HACE and HAPE

First, a disclaimer: I am not an expert on the details of altitude sickness. I am a chemist, not an MD or a physiologist, or even a mountaineer. I understand some of the chemistry of altitude sickness, and in writing these pieces I am trying to stay out of places where my knowledge is limited. If you are interested in the medical, symptomatic or preventive aspects of altitude sickness, please look elsewhere. My coverage here is limited to some of the chemical features of altitude sickness that can be explained in common language.

Acute Mountain Sickness is an “entry level” form of altitude sickness, the least aggressive of the three forms. Nevertheless, AMS is not a condition that should underestimated. It can be dangerous in its own right and can be an indicator of more threatening stages of altitude sickness.

Climbing to altitude without proper acclimatization can result in the accumulation of water in the lungs, a form of altitude sickness known as High Altitude Pulmonary Edema (HAPE). Water collects in the lungs by seeping across a thin membrane that separates the air-filled alveoli from the blood-filled capillaries. That lower atmospheric pressure described in Part 2 goes all the way down to the alveoli. Fewer molecules per lungful of air translates to lower pressure in the alveoli. It’s the pressure differential across the capillary-alveoli membrane that matters. Lower pressure in the alveoli “pulls” water across the membrane from the higher-pressure capillaries. There’s a lot more to this, of course. For example, hypoxia also triggers a constriction of the capillaries, presumably to increase the rate of blood flow and hasten the collection of oxygen. This higher pressure in the capillaries “pushes” water molecules from the higher-pressure capillaries to the lower-pressure alveoli. These effects, and others, lead to the same outcome: Gradually, the alveoli fill with water. High Altitude Pulmonary Edema is the leading cause of death from altitude sickness. Onset usually doesn’t occur below 8,000’, but cases down to 5,000’ are known. Fortunately, the symptoms of HAPE are obvious and graduated. The clearest indicator is a rasping cough on top of AMS symptoms. Again, this is not meant to be a complete coverage of HAPE. Readers are urged to consult other sources.

The third form of altitude sickness is High Altitude Cerebral Edema (HACE). I don't have much to say here. HACE is similar to HAPE in that the condition is about the accumulation of water. In this case, water collects in the brain rather than the lungs. HACE is an uncommon form of altitude sickness. The condition is observed is less than 1% of climbers who ascend to 13,000’. While rare, however, HACE is very dangerous. I am not familiar with the mechanism of HACE, but it appears to involve similar capillary-tissue pressure differentials characteristic of HAPE. Water is forced from the capillaries into the cranial tissue.

For further information, I recommend "Medicine for Mountaineering" by James Wilkerson, Mountaineers Books. My older edition has an excellent chapter on the effects of altitude. I did learn one very interesting thing here about very high-altitude mountaineering. In the death zone, climbers cannot acquire enough oxygen to survive. In fact, they barely collect enough oxygen to sustain their breathing. Breathing takes work, of course, and way high up there, so much breathing has to be done that the amount of work involved in that breathing is barely covered by the oxygen taken in by all that breathing. There isn't enough O2 left over to energize anything else. Life is unsustainable in the death zone because (at least in part) virtually all the oxygen taken in by breathing is used up to fuel even more breathing. It's a death spiral

Next up: Acclimatization
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Re: Altitude Sickness, Part 3

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I thought I had read in the past that altitude sickness is also a matter of staying in the zone of aerobic respiration as oxygen concentrations drop. In one study they found that the slower people actually did better. The gung-ho strong fellows fell the first. You can minimize anaerobic respiration by slow and rhythmic breathing, never getting out of breath. How does anaerobic respiration fit into your chemistry equations?
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Re: Altitude Sickness, Part 3

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That's a question about systems, and I know about molecules, but I'll try.

Higher organisms don't do true anaerobic respiration. We do fermentation, but the difference isn't important here. Lactate fermentation takes place in muscle tissue, separated from the oxygen that will eventually be needed to fully oxidize glucose. That's the difference, I guess: Fermentation is anaerobic, but its products (lactic acid in this case) are oxidized elsewhere, aerobically.

Aerobic respiration takes glucose all the way to carbon dioxide and water: C6H12O6 ––> 6 CO2 + 6 H2O. You can see that doesn't balance, however. We're short 12 oxygen atoms on the left. You can't get all the way to carbon dioxide and water without a source of oxygen atoms: C6H12O6 + 6 O2 ––> 6 CO2 + 6 H2O
It's a very fast process that produces a lot of energy.

Fermentation of glucose to lactic acid happens any time the need for oxygen outpaces its production. We can heave air in and out of the lungs and process lots of O2, but out in the extremities, hard-working muscle tissue can quickly exhaust the "local O2". Ongoing work by O2-deficient muscle tissue triggers fermentation. The lactic acid produced is what causes sore muscles, because there's no O2 around to flush the lactic acid out of the tissue and move it on to carbon dioxide and water.

Anaerobic fermentation cannot take glucose all the way to carbon dioxide and water. The process stops at lactic acid:
C6H12O6 ––> 2 C3H6O3
This is a slow reaction compared to aerobic respiration, and it's not very efficient. There's a lot of energy that can be extracted from lactic acid. It's still a long way downhill from lactic acid to carbon dioxide and water, but you won't get there without oxygen.

What all this has to do with altitude sickness is beyond my scope. I'm sure there's a link, but it will be complex and involve multiple biochemical systems. At no point, however, will either anaerobic respiration or fermentation produce enough energy to keep an organism going for long (natural anaerobes excepted, of course.) It makes perfect sense that if you go slow enough to avoid more than minor oxygen deficiency, you're unlikely to suffer from altitude sickness. However, when it comes to comparing a hypoxic gung-ho with a hypoxic wanderer, there may be a correlation, but it's no sure thing. As I understand it (which could be poorly), while there are leading indicators, it is still hard to predict who, when and how deeply altitude sickness will strike.

Bear in mind, a lot of this might make a biochemist shudder. I'm about out of my depth here.
Last edited by gregw822 on Mon Apr 12, 2021 10:58 am, edited 1 time in total.
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Re: Altitude Sickness, Part 3

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There is something else going on, and it is in the hemoglobin. When oxygen appears in the alveoli, it can hop across the semipermeable membrane into the blood stream, latch onto hemoglobin, and then it goes for a ride around the circulatory system where it gets used in the muscles. Then CO2 comes out of the muscles, latches onto hemoglobin, and then goes for a ride back toward the alveoli in the lungs. Normally, that is the process. When a person goes to high elevation, the blood chemistry can change somewhat. The same process operates, except that when the CO2 comes back to the alveoli, sometimes the hemoglobin is too sticky, and the CO2 does not release back into the alveoli. Instead, the CO2 goes for another ride around the circulatory system. The more that goes on, the less O2 is being carried, so the person's ability to do work becomes more and more limited. Eventually, the person collapses. For some people, that might be at 10,000 feet. For others, it might be 29,000 feet. It's hard to predict, but everybody has a ceiling. They have found a number of people that let this cycle run, and they never get into CO2 trouble, and those are the people who have been able to summit on Everest without supplementary oxygen. The secret, it seems, is being able to blow off excess CO2, not inhaling more O2.
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Re: Altitude Sickness, Part 3

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Hemoglobin (Hb) is Part 4, but the CO2 complication is deeper in the weeds than I intended to go.

Carbon dioxide binds to hemoglobin, but not at the same site or in the same way as O2. Carbon dioxide forms a carbamate with the N-terminal amino groups of the four Hb subunits. I do not think Hb becomes too sticky to release CO2. I say "think" because there are multiple and complex allosteric effects at work in Hb, and they differ between the T and R states of the complex. In addition to CO2, allosteric effects occur for "H+" and also for diphosphoglycerate. The allosteric dependence on "H+" assures that blood pH will have an effect on O2 loading and unloading. I do not believe that tighter CO2 binding is what interferes with CO2 offloading. What you're referring to here takes place in damaged alveoli. If the alveoli (is the singular "alveolus"?) is compromised by water, O2 will not be able cross the membrane into the capillaries, nor will CO2 be able to get into the alveoli. Blocked membrane gates prohibit offloading of CO2, not tighter binding to Hb. I don't think the allosteric effects of CO2 are strong enough to form a single Hb complex that hauls CO2 around until a suitable place for offloading is discovered. Hemoglobin bonds to CO2 much more weakly than it bonds to O2. Inhibited CO2 offloading becomes more important as HAPE develops, and more and more alveoli are compromised.

The reason CO2 offloading isn't important except under dire conditions is that Hb is not a major factor in CO2 transport. Carbon dioxide is far more soluble in water than O2 because of the bicarbonate buffer system. The CO2/H2CO3/("H+",HCO3) buffer system is responsible for 85% of CO2 transport, with no direct protein involved at all. A bit more CO2 moves through the plasma, either as free CO2 (not much) or complexed with other plasma proteins. Only 5-13% of the CO2 is transported by Hb. So, if a small population of the alveoli are damaged by water, the buffer system (not Hb-CO2) will quickly move CO2 off to a healthy region of alveoli. Dump enough water into the lungs, and sure, you're going have a problem, but at that point, excess retention of CO2 probably won't matter.

Finding some other way to "sweep out" excess CO2 won't do anything to remove the water that blocks the alveoli. There's still no mechanism for bringing O2 into the transport system. So, in the end, barring some very strange allosteric effects at the deadly end of HAPE, it is all about bringing in more oxygen.
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Re: Altitude Sickness, Part 3

Post by bobby49 »

Edema in the alveoli is the effect of the problem, not the cause of the problem, in my opinion.
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Re: Altitude Sickness, Part 3

Post by gregw822 »

Yes, of course. The problem is sustained hypoxia. The result is edema, in the lungs (HAPE) or the brain (HACE).
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Re: Altitude Sickness, Part 3

Post by wsp_scott »

Thanks for these three parts, I learned something today and that is always a good day :)
My trip reports: backpackandbeer.blogspot.com
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Re: Altitude Sickness, Part 3

Post by bobby49 »

A few years ago when I was on the Whitney summit, there was a medical team from Fresno State. They were doing testing on the hikers reaching the summit, so they recorded blood pressure, blood oxygen saturation, and any perceived symptoms. They asked about how much acclimatization had been done. They were trying to figure out why some hikers are consistently asymptomatic at high elevation and others suffer so dearly.

The medical researchers on the big peaks get the publicity, but even those in our own backyard, like on Whitney, are getting things done.
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Re: Altitude Sickness, Part 3

Post by Lumbergh21 »

This triggered a memory of a video I had watched about the Wim Hof Method, a breathing technique that is supposed to have all of these wonderful effects (according to Wim Hof). A doctor decided to examine and research what was going on with this breathing technique. One of the purported benefits was high altitude acclimitization, avoiding AMS at altitude. The doctors conclusion was this was a likely benefit because the WHM involves hyperventilation which allows you to expel more CO2 with the added benefit of taking in more O2. The presentation of the AMS portion begins around minute 28 if anyone is interested https://youtu.be/D6EPuUdIC1E
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