White Mountain Peak Pictures: July 2011: AMS is not fun

Below is a small sample of some of the photos and video I recorded on White Mountain Peak and a very short account of our new found experience with altitude mountain sickness (AMS).  I will be positing additional photos and video in the weeks to come as I find time to communicate our knowledge and wisdom around high-altitude climbing.  I look forward to hearing any of your comments and critiques; I further invite you to add this site to your RSS feed, to your Chrome Gadget page, or to your iGoogle page so that you can stay on top of our adventures. To add us to your feed, click on the RSS icons under the "subscribe to" heading on the right-hand bar of this page.

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Right now my head is swimming with our experience on the mountain and the value I discovered in having a portable SP02 meter with us to measure our blood hemoglobin saturation to help us adapt our breathing style on the mountain and to forecast potential problems.

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We started from Victoria, British Columbia (sea level) on Tuesday evening and drove all night to finally arrive in Bishop, California at around 7pm the next day.   Upon arrival in Bishop, we packed ourselves into a hotel room and got a good night's sleep.  The next morning, we got up and drove to the parking lot on the mountain (approximately 12000 feet) and started hiking towards the top of the mountain. Four of us began the ascent.  Two of us made it to the top. Two did not go to the top.  One person became ill and was escorted down by one of the original four.

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At altitude, with slightly reduced O2 saturation, we experienced a bit of euphoria and subtle changes in our perception of our surroundings.  While this was quite fun and interesting, this was also dangerous and we do not fully understand the long-term impact when O2 levels go "too low".  In fact, I don't believe we really know what the SPO2 number is for "too low" or how long is "too long" for "too low".  If there is one piece of wisdom to take from this blog, it is to purchase an oximeter that provides you with an indication of the percent oxygen saturation of your blood hemoglobin. You can use such a meter to learn how to breath "properly" to maximize your oxygen consumption and you can use it to decided if you are receiving enough oxygen, if you are exerting too much energy, or if you should perhaps get off the mountain.

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For reference, when I sit at my desk at my office in Victoria my SPO2 ranges between 96 and 99%.  When I  was at rest after driving to Bishop CA (roughly 18 hours later) my SP02 was approximately 92%.  My perception is of course subjective but I believe I could notice differences in my clarity of thought even at 92% in Bishop.  I could maintain a SP02 of between 86 and 92% on the mountain with the breathing technique I adopted and stuck with.  The meter was instrumental in helping me develop my breathing style and keeping my SPO2 above 80%.

I found that each movement of my body and each force that I exerted would lower the SP02 if I wasn't focusing on deep breathing. I now have first-hand experience as to why they say "pole, pole" on Kilimanjaro (step slowly).

My primary purpose for ascending high altitude and measuring how our bodies respond is to investigate brain function changes related to low air pressure and the related hypobaric anoxia.  Often people who ascend to high altitude perceive changes in their own brain function such as differences in the way things sound, a feeling of euphoria, a bit of a disconnection from our bodies, and subtle changes to our vision among other things. We noticed some of these experiences ourselves at only 12000 feet since we gave ourselves essentially no time to get used to altitude.  Our plan is to investigate brain function using EEG equipment on our forthcoming trip up Mount Kilimanjaro.

I carried the equipment that I will be using on Kilimanjaro to assess brain function to the top of White Mountain Peak so that I could try out the weight and balance of a backpack full of equipment and warm clothes for mountain survival.  However, I did not do any brain function measurements at the top of the mountain given the short time we had available and our recent encounter with AMS.  As a team, all of us were not ready to climb to an altitude of 14000 feet because only 2 days before we were at sea level.  I did however experiment with recording EEG data using the Emotiv EPOC on White Mountain peak at an altitude of 13000 feet.  The video below shows me recording ambulatory EEG data using the Emotiv EPOC while my colleague participates in a computer-based cognitive assessment task.

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Before I scare too many people into staying inside their homes this summer, there is a simple concept to digest to make you feel at ease.  This concept is acclimatization-- get used to the altitude slowly and let your body's physiology adjust to the change in air pressure.  There are various stages to this change.  The first stage I would call "conscious behavioral changes".  This is when you decide you will take it easy, move slowly, and breath hard.  The second change is a change to the characteristics of your blood (takes about a week).  The third change is a change to the capillary proliferation in your body to reduce the distance between  your blood supply and your cells (takes about a month).  There is a research station on the mountain at about 12000 feet and another one at 14000 feet on this mountain and  I assume that when people are properly acclimatized there is little problem.  People actually work at this altitude!

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I titled the previous blog posting "AMS for fun?".  The question mark was included in the blog title because I really had no first or second hand experience with AMS.  I now say that it is "not fun".  I didn't develop AMS but a friend of mine did. Having a friend develop AMS wasn't pleasant for anyone on the mountain, nor was it pleasant for the person who was sick.  In a week or two I will post some more detail of our account at high altitude and the insights we had that will help us on our ascent to the top of Kilimanjaro.

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As an afterthought to this story, I've posted additional information for people interested in data collection at high altitude.

The photograph below depicts one of us wearing an Emotive EPOC that I plan to bring on our Kilimanjaro trip to record EEG data. For information on the Emotiv EPOC, go to the Emotiv website.

For more information about blood oxygen levels and what it might feel like to be at high altitude, see the website: http://www.anesthesiaweb.org/hypoxia.php.  (I have not verified the information on the anesthesia website.)

I just found this video of John Severinghaus describing why the research stations were created on White Mountain Peak and gives some history of high altitude research.

Research: Right temporal cerebral dysfunction heralds symptoms of AMS

I just read through an article written in 2007 today that found specific features in scalp EEG data, measured at moderate altitude, might predict the occurrence of AMS. You can download the study from the web if you have access to PubMed. I have put the abstract and title of the article at the bottom of this blog entry.

In their study, the authors investigated AMS in relation to brain function, cerebral blood flow, and end-expiratory CO2 and found effects related to AMS in the right-hemisphere scalp EEG. Supportive of this EEG finding are correlated changes in expiratory CO2 and an increase in cerebral blood flow velocity in the right middle cerebral artery.

Notably, changes in the EEG that were determined to be related to AMS occurred before changes in cerebral blood flow and end-expiratory CO2. (Significant changes in the EEG occurred before changes in the cerebral blood flow and end-expiratory CO2.)  Hence, changed EEG at moderate altitude might be a good way to identify who will get AMS at high altitude.

While the study showed some encouraging results, the study also has some weaknesses that can be addressed with some replication and some data processing modification. The main weaknesses of the study are: (1) the low number of participants that participated in the study beginning to end (22, at most) and (2) the low significance threshold of 0.05 (for the number of comparisons) that was used. In addition, data plotted in the paper show that for a few participants, the effect of altitude on the EEG was in a direction that was inconsistent with the group.  This inconsistency could be artefactual in nature and could arise for a number of reasons unrelated to brain function.  A replication of this study would add weight to these findings and offer an opportunity to investigate EEG processing methods that are less susceptible to noise.

Hence, it is worthwhile to do further investigation of EEG as a predictor of AMS in various circumstances, at a variety of altitudes, and investigate how varied training regimes prior to ascent modulate the likelihood of occurrence of AMS.

The abstract and author information obtained from PubMed is given below.

J Neurol. 2007 Mar;254(3):359-63. Epub 2007 Mar 7.

Right temporal cerebral dysfunction heralds symptoms of acute mountain sickness.
Feddersen B, Ausserer H, Neupane P, Thanbichler F, Depaulis A, Waanders R, Noachtar S.

Source

Department of Neurology, Klinikum Grosshadern, University of Munich, Marchioninistr. 15, 81377, Munich, Germany. berend.feddersen@med.uni-muenchen.de

Abstract

Acute mountain sickness (AMS) can occur during climbs to high altitudes and may seriously disturb the behavioral and intellectual capacities of susceptible subjects. During a Himalayan expedition 32 mountaineers were examined with electroencephalography (EEG) and transcranial doppler sonography (TCD) to assess relative changes of middle cerebral artery velocity in relation to end-expiratory CO2 (EtCO2), peripheral saturation (SaO2), and symptoms of AMS. We tested the hypothesis that O2 desaturation and EtCO2 changes precede the development of AMS and result in brain dysfunction and compensatory mechanisms which can be measured by EEG and TCD, respectively. Contrary to our hypothesis, we found that subjects who later developed symptoms of AMS between 3,440 m and 5,050 m altitude exhibited an increase of slow cerebral activity in the right temporal region already at 3,440 m. Cerebral blood flow increased in these mountaineers in the right middle cerebral artery at 5,050 m. These findings indicate that regional brain dysfunction, which can be documented by EEG, heralds the appearance of clinical symptoms of AMS.

Research: General introduction to altitude adaptation and mountain sickness

I just read through a research paper written by Bärtsch P., Saltin, B. General introduction to altitude adaptation and mountain sickness. Scand. J. Med. Sci. Sports 2008 (Suppl. 1):1-10.

I have put a few excerpts from the paper into this blog to inform my fellow climbers.  The text below is a mixture of paraphrasing and quotes from the paper.  This is a really good paper and I highly recommend tracking it down and giving it a complete read.

Abstract

The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24–48 h to improve the oxygen carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [1000m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO2 is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10–30% of subjects at altitudes between 2500 and 3000ma.s.l. Pulmonary edema is rarely seen below 3000ma.s.l. and brain edema is not seen below 4000ma.s.l. It is possible to travel to altitudes of 2500–3000ma.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000ma.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.

Definitions:


Erythropoiesis is the process by which red blood cells (erythrocytes) are produced. It is stimulated by decreased O₂ in circulation, which is detected by the kidneys, which then secrete the hormone erythropietin. This hormone stimulates proliferation and differentiation of red cell precursors, which activates increased erythropoiesis in the hemopoietic tissues, ultimately producing red blood cells. 

Notes of Interest:

A significant increase in red blood cell mass may already occur after 3 wees at a minimum altitude of 2100 m a.s.l. (Schmitd & Prommer, 2008) and this gets more pronounced as altitude increases.

During the first 24-48 h, at even a low altitude (15000-2000 m a.s.l.), Hb concentration is elevated by 0.5-1.0g/100 mL blood, which may correspond to a loss of plasma water of 0.2-0.3 L.  At 3000 and 4000 m a.s.l., the rise in Hb concentration may amount to another 0.5-0.8g/100 mL per 1000m, indicating a decrease in plasman volume of 0.600.9 L (Saltin, 1966; Svedenhag et al., 1997; Calbet et al., 2004).

Classic high-altitude training involves living and training at altitudes between 2000 and 2800 m a.s.l. for a period of 2-4 weeks.  Living high and training low, introduced by Levine & Stray-Gundersen (1997), consists of living about 20h/day at an altitude of 2800 m a.s.l. and training at an altitude of 1200 m a.s.l., which already impairs maximum aerobic performance in well-trained subjects.

AMS (Acute Mountain Sickness)

There appears to be a threshold altitude of about 2100 m a.s.l. for significant development of AMS (acute mountain sickness) with exposure to hypobaric hypoxia at rest (Muhm et al., 2007).  At altitudes between 2500 and 300 m, the prevalence of AMS is betwen 10% and 30%, depending on the population and the definition of AMS.  At these altitudes, AMS is usually mild, transient, and does not progress to more severy symptoms of altitude illnesses, such as cerebral or pulmonary edema. [PHIL: note, they say nothing about cognitive function or neuronal damage].  At altitudes of 4000 - 4500 m a.s.l., the prevalence of AMS is 40%-60%, and in some susceptible individuals treatment with oxygen, dexamethasone, and descent ar necessary for improvement and prevention of progression to cerebral edema (Bärtsch & Roach, 2001).  When going to altitudes above 3000m, staged ascent and /or prevention of AMS by acetazolamide (2 x 250 mg/day may be necessary to avoid physical discomfort within the first few days of altitude exposure.  A low hypoxic ventilatory response (HVR) may be associated with increased susceptibility to AMS (Moor aet al., 1986; Richalet et al., 1988a), and HVR tends to be lower in endurance-trained athletes (Schoene, 1982). [PHIL: This means that if you're an endurance-trained athlete, it is a good idea to learn how to breath properly for a trip to the top of Kilimanjaro.)

The text below discussing HACE and HAPE comes directly from Bärtsch & Saltin, 2008.

HACE (High-Altitude Cerebral Edema)

HACE is usually preceded by progressive symptoms of AMS. It is characterized by progressive truncal ataxia, clouded consciousness, and variable focal neurologic symptoms. Without treatment, coma usually develops within 1–2 days, and death occurs rapidly because of brain herniation. Vasogenic edema has been demonstrated by MRI (Hackett et al., 1998). Treatment consists of administration of supplemental oxygen, dexamethasone, and descent. HACE rarely occurs below 4000ma.s.l. (Fig. 2), and the prevalence at 4000 5000ma.s.l. is 0.5–1.5%. HACE can be avoided by preventing AMS or by fast and adequate treatment of AMS.

HAPE (High-Altitude Pulmonary Edema)

HAPE is a non-cardiogenic edema that is due to a non-inflammatory capillary leak caused by an abnormally high hypoxic pulmonary vasoconstriction (Bärtsch et al., 2005). Early symptoms are dyspnoea, decreased performance, and cough. In advanced cases, dyspnoea at rest, orthopnoea, and pink frothy sputum occur (Bä rtsch, 1999). HAPE is rare below 3000ma.s.l. and is usually associated with abnormalities in the pulmonary circulation. Prevalence of HAPE after rapid ascent to 4550ma.s.l. within 24 h, including an overnight stay at 3600m a.s.l., is 6% in a general mountaineering population (Fig. 2) and 60–70% in HAPE-susceptible individuals (Bärtsch et al., 2002). Susceptible individuals are characterized by an abnormal increase in pulmonary artery pressure with exposure to hypoxia and also during normobaric exercise (Grünig et al., 2000). This abnormal response pattern of the pulmonary circulation can be found in about 10% of the population in Germany (Grünig et al., 2005). The rate of ascent, the altitude of exposure, and exertion are the major risk factors for development of HAPE, in addition to individual susceptibility based on an abnormal pulmonary hypoxic vasoconstriction. HAPE can be avoided in susceptible individuals with slow ascent (300–400 m/day above 2000ma.s.l.). If slow ascent is not possible, HAPE can also be prevented by drugs that lower pulmonary artery pressure, such as nifedipine (Baürtsch et al., 1991), sildenafil, or dexamethasone (Maggiorini et al., 2006). Treatment consists of administration of supplemental oxygen, application of pulmonary vasodilators (nifedipine or tadalafil), and descent. Mortality is estimated to be 50% if no treatment is possible (Lobenhoffer et al., 1982), while adequate treatment leads to a complete recovery without sequelae.