Minutes

Committee Meeting

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Minutes from Meeting 15th January 2009

‘The Caudwell Xtreme Everest Expedition'


Dr Mike Grocott, Senior Lecturer and Consultant in Intensive Care Medicine, University College London

The Meeting was opened by the President of the LMI, Dr Geoff Gill, who welcomed everybody to the meeting and then handed over to Professor Hunter.

Professor Hunter firstly announced the sad news of the death of a former President of the LSA, Dr Alan Stead, who died on January 2nd and asked everyone to stand for a minute’s silence.

Professor Hunter then introduced the speaker for the evening, Dr Mike Grocott from University College London. Dr Grocott introduced his talk about the Caudwell Extreme Everest Expedition in 2007 with a video of the effects of 8848m altitude on a climber. He reminded the audience of the first successful ascent of Everest on the 29th May 1953 by Edmund Hillary and Tenzing Norgay. Almost 25 years later, on the 8th May 1978, Reinhold Messner and Peter Habeler were the first climbers to ascend Everest without the aid of oxygen. Dr Grocott then showed a graph of the effects of altitude on barometric pressure. This equated to an atmospheric pressure of approximately 50 kPa at base camp and 30 kPa at the top of Everest. He then showed the effects of acute hypoxia, in unacclimatised individuals and the time to loss of consciousness at increasing height. Dr Grocott explained the physiological changes of acclimatisation such as an increase in heart rate, respiratory rate, haemoglobin and capillary density. He then pointed out that an elite high altitude climber has a unique performance that goes beyond the physiological adaptations to high altitude. He showed a graph of measurements made during the expedition which indicated that oxygen delivery was very well maintained at an altitude of over 7000m despite a significant fall in PA02 because of compensatory mechanisms such as a rise in haemoglobin. Despite relative normality in oxygen delivery, people have great difficulty performing at this altitude and it is not entirely certain why.

Dr Grocott then looked at the work of Montgomery (Nature 1998) on the ACE intracellular enzyme system. In particular, he looked at the I and D alleles. In the average population, there is a normal distribution but in elite mountaineers there is a skew towards the I allele. Conversely in ARDS, patients with a high mortality have a skew to the D allele.

Dr Grocott then explained some of the purposes of the expedition. Firstly, extreme environments, as seen for example in ITU patients, and also at high altitude, cause derangement of homeostatic physiological systems, and the expedition may help to define the limiting factors to some of these systems. Secondly, hypoxia is a fundamental mechanism of injury in critical illness and exercise at altitude can be seen as a model for oxygen delivery and utilisation in critical illness. Changes in exercise capacity that occur with increasing altitude are not explainable by a reduction in oxygen delivery as the body adapts to altitude to maintain this. Therefore, other factors come into play such as micro-circulatory dysfunction, diffusion limitation and changes in metabolic efficiency. Consequently, utilisation of oxygen rather than its delivery may better explain the limitation of performance at altitude.

Dr Grocott looked at some of the investigations, in particular, cellular mechanisms. Muscle biopsies were taken in 20 people, initially at sea level, then at arrival at base camp at 5,300m and then again at base camp following their ascent to the summit. These biopsies will be used to try to better understand metabolic mechanisms for surviving hypoxia which may be relevant to critical illness.

Dr Grocott looked more generally at the expedition itself with its aims of safety, science and summit, in that order. The preparation for the trip had been extensive with field studies in 2005 and 2006 to the Alps and Himalayas which had been helpful with the massive logistical challenge of the Everest expedition. He explained that there were 2 subject groups, consisting of 198 trekkers who were healthy volunteers. They had physiological measurements done at sea level, on arrival at Kathmandu (1300m), Namche (3500m), Pheriche (4,250m) and then at Everest base camp (5,300m). There were also 24 investigators, 4 of whom had extensive investigation at 8,400m on the balcony of Everest. The large amount of equipment required had to be taken up by porters and then there was the challenge of computers at altitude. There were physiological laboratories at all levels and a vast amount of data was collected. Because the ascent to Everest base camp was slower than in commercial treks, there was less mountain sickness and consequently there was little loss of data due to illness. Dr Grocott then showed some of the challenges of the ascent from Everest base camp with some stunning pictures of crossing crevasses and the amount of equipment taken up to continue with physiological testing at higher altitudes.

The variables that were measured in the trekkers, included cardio-pulmonary exercise testing, muscle and brain neuro-infrared spectroscopy, neuro- cognitive testing and retinal photography. In addition, investigators had arterial blood gas analysis, skeletal muscle biopsies, cerebral doppler and other invasive tests. The data continues to be analysed.

Dr Grocott went through some of the results. These showed that there was both a reduction in oxygen content and a 35% reduction in maximum oxygen consumption at Everest base camp, although there were no differences with gender, age or level of fitness. In contrast to the trekkers, the 14 climbers showed a significant increase in oxygen content at Everest base camp although despite this, they showed a similar fall in maximum oxygen consumption. A fall in anaerobic threshold of 50% was demonstrated by the time the climbers had reached 8000m. They demonstrated the increase in ventilation at altitude and showed that the maximum voluntary ventilation could actually go up with altitude due to the lower air density. He showed on video the micro-circulatory dysfunction at altitude. Dr Grocott said that the extensive research into the muscle biopsies was still ongoing.

He then went onto describe the successful ascent of the summit of Everest. Although it had been planned to take blood gases on the summit at 8,848m, this turned out to be not possible. Samples were therefore taken on the balcony of Everest at 8,400m where barometric pressure had been measured as 33.7 kPa, with a PIO2 of 5.7 kPa. Measurements showed that PaO2 ranged from 2.5 to 3.9 with a mean of 3.2 kPa. PaCO2 ranged from 1.5 to 2.1 kPa. Dr Grocott commented that despite very low values of PaO2, individuals were still able to function adequately. The only other examples of mammalian physiology working at such low levels of oxygen are in-utero and diving seals.

Dr Grocott finished his talk by asking the question as to whether critically ill patients should have lower PaO2 targets to try and reduce the toxic effects of oxygen therapy in the critically ill.

Professor Hunter thanked Dr Grocott for his talk and opened the floor for questions. These included items on data storage, diet and the use of Diamox. Dr Neil Fergusson then gave the vote of thanks and the meeting finished at 8.30 p.m.

Ewen Forrest

Hon Sec

 

 

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Last updated: 9 November, 2011 LSA