Blood Hemoglobin Saturation and Pressure Breathing Data

We are now posting some of the results that we found from our altitude investigation on Mount Kilimanjaro. For the purpose of explaining these results to the lay-person, a colleague of mine has given his own interpretation of the results (why the graphs below look the way they do) and his own experience at altitude intermixed with my writing below.

Phil: Some of the early results of our altitude experiment are illustrated in the following plots. Essentially, the data speak to the idea that what I would call "intense" pressure breathing and rest stepping contributes to larger SPO2 levels than moderate to no pressure breathing. Note that this assumes that all persons from whom data were collected are somewhat similar in physiology related to oxygen transport from the atmosphere into the blood. The data collected are from males between the ages of 35 and 57 years of age. (No significant correlation of hiking SPO2 with age was found (corr=-0.72 n=4; -0.95 would be required for n=4 at p=0.05). Measurements were taken so as to not distract (too much) from their hiking experience although each time a measurement was taken, that hiker was informed of their SPO2 level and heart rate and encouraged to keep their SPO2 numbers high. You will note in Figure 1 that a different number of measures were taken each day. The values in Figure 2 were calculated using a daily average (for each of days 2, 3, and 4) so as not to weight one day more than another in the statistics derived. Hiking SPO2 data were not recorded for day 1 or our final ascent on the summit (day 5).

Figure1: (click image to enlarge) SPO2 levels for various measurement taken while moving during the hike up on Kilimanjaro. SPO2 AVG indicates the average calculated across the group at each for each recorded point. SPO2 AVG2 refers to the average calculated across a subset of the participants (SB2, 3, and 4).

Figure 2: (click image to enlarge) Comparison of hiker SPO2 levels and the typical "home" SPO2 for "hiking" and "resting" conditions. In the hiking condition, persons were stepping with approximately the same weight backpacks and where moving forward at approximately the same speed (as a group). In the resting conditions, persons were seated in a chair (at the end of a day of hiking) for approximately 20 minutes before the measurement was taken while seated. Noticeably, the hiker (SB1) indicated by the blue bar of the left-side of this figure does not have standard error bars that overlap with those of the other hikers. When listening to the breathing of all hikers, SB1 was doing noticeably much more intense pressure breathing than the other 3 hikers. During the post-data collection interview, hikers SB2, 3, and 4 indicated that they were not confident in the pressure breathing process and adopted their own versions of pressure breathing that they preferred. SB1 is the youngest hiker (age 35) out of a relatively even spread of age across the group however given how the SPO2 levels fall towards those of the main group in that hiker when intense pressure breathing is not used (data not provide), it is unlikely that age is a differentiating factor. In addition, hiker SB2 is only 5 years older than SB1 and SB2. 

Comparing Figures 1 and 2, for participants SB2,3, and 4, one notices that the "resting" SPO2 levels are higher than the "hiking" SPO2 levels. (For SB1, the resting SPO2 level was comparable to the resting SPO2 of the other climbers; data not provided). Two things are noteworthy in this comparison.  First, the SPO2 levels for SB1 doing intense pressure breathing while hiking fall in the range of SPO2 levels for resting suggesting that this hiker maintained "resting" levels of SPO2 even though he was working physically to get up the mountain. Second, hikers SB2, 3, and 4, had significantly lower SPO2 levels while hiking than they did while resting. This suggests that they might have more cognitive impairment (and be facing additional physiological issues) while hiking than while resting.  That said, it isn't clear what impairment might continue into the post-hiking period (while resting) from the low SPO2 levels experienced while hiking.

There are two additional pieces of information that we do not have data for that would impact altitude health and cognitive function: tissue CO2 levels, and a measure of blood vessel dilation in the brain that is related to CO2 levels. I briefly describe why these measures are important in a post on my company website and why we should collect these data next time.

If you haven't quite figured it out yet, SB1 refers to data collected from myself. I am the one that is concerned about having my own oxygen levels fall and any subsequent lasting cognitive impairment related to altitude and mild anoxia. Bringing this into perspective, this whole investigation is about figuring out how to enjoy very high mountains safely and understanding how the tools we are presented with (in this case, pressure breathing and rest stepping) impact our altitude health and our health thereafter.

Gord: (the 57 year old member) what does SPO2 stand for Phil? That was a great hike! As a novice at altitude, I kept wondering what the teams who blasted past us on the trail were doing (if anything) about the ever-increasing effects of higher-altitude. My experience with having my SPO2 levels regularly recorded was that I variously felt like a) I'm in a scientific experiment b) I'm striving to reach a huge goal c) I'm on a team going for the top and not just doing this for myself.

While being "in an experiment" mode I really did consciously change my breathing to bring my SPO2 levels up. Two reasons - I'm a bit competitive in a team environment AND I wanted to avoid the experience of suffering AMS again. In the end I really believe that my rest-stepping and increased breathing helped get me comfortably to the summit. Those techniques helped me feel more in control of the outcome rather than wondering if I was going to one of those who arbitrarly gets dragged off the mountain.


The first graph (fig 1) moves up and down depending on the steepness of the trail (if I remember correctly) and, for me, what was going on in my head at the time. Distractions meant lower breathing rate, which is my natural tendancy. The lines heading down to lower SPO2 levels with higher altitude make sense. Our scientist's encouragement to stay above 80 finally sunk in on summit day for me. Before then I felt strong and capable on my own. On summit day I knew that any tool which increased the odds of making it to the top without getting AMS was worth adopting.


BTW I finally figured out what "pressure breathing" was (for me) on the way DOWN from the summit. Before then I was just breathing as deep as I could. I'm not yet sure how to describe it in words. I do know it sounds like what I imagine a steam engine sounds like. More to come on that later.

Phil: SPO2 stands for "Saturation (peripheral) of haemoglobin with oxygen" which is a percentage ratio compared to fully saturated haemoglobin. Basically, it is how filled your red bloods cells are with oxygen. At our home altitude (sea-level) we measure approximately 98%.  Of course, these meters often have a error of 2%.  At any rate, we're close to complete saturation at our home altitude.


On our final ascent towards the summit of Kilimanjaro I distinctly recall 2 things: some people being helped down the mountain by their guides, and every once and a while reminding the team about their oxygen levels.  On our training hike to the summit of White Mountain Peak, I recalled that SPO2 levels below 60% were definitely bad news (at least for us tourists at altitude).  Again, on that particular ascent I wanted to look after myself so I worked to maintain an SPO2 above 86%.  That said, I picked that number because I seemed to be OK there. I don't know if it is a good guideline; we will get more data on this topic.  What I have noticed for us is that levels in the 80% seem to relate to some mild cognitive changes (we joke around a little more, things are funnier, my sense of time is way off), in the 70s there is some distinct drunkenness (altitude drunk), loss of balance, and loss of body awareness, and in the 60s loss of color in the skin and look a bit ill.  After we got back to Victoria from White Mountain Peak, I found this information about SPO2 levels on the internet (http://www.anesthesiaweb.org/hypoxia.php; I have not verified the information at this link). The information on this site seems a bit arbitrary because they have put the boundaries of the altitude effects on body function in steps of 10%.  Still, it supports the idea that we want to keep our oxygen levels high.


I noticed that if I got into a conversation with someone while hiking, my oxygen levels would drop quite quickly.  I talked to one of our guides for a while in French and it seemed really easy (I speak terrible French at sea-level; presumably it was equally terrible at altitude).  It is easy and even fun to get 'distracted' from breathing.  On one of the days I borrowed a porter's radio, gave him my camera to make video recordings, and then rocked-out to Shaggy for a good 10 minutes (or something like that; remember that I seem to have poor sense of time at altitude). While I was up to these antics, I was not pressure breathing (or taking measurements). That said, I did this for a relatively short amount of time.


The descent at the end of the day as the sun was falling was 'interesting'.  I remember measuring some "too low" oxygen levels and noticing the temperature fall. I was genuinely concerned about getting back.  And we did- we did get back to our camp and crashed-out in our chairs for dinner. The guides and our support team did a fantastic job getting us down safely and supporting our recovery.

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.