health care. Today is a series of programs in continuing medical education and is presented by the faculty of Health sciences. McMaster University, the Ontario Medical Association mohawk College, the Ontario chapter of the Canadian College of Family Physicians, The Hambleton Academy of Medicine and Ch ch T.V. Here is dr john Sutton, assistant professor of medicine at the Faculty of Health Sciences. McMaster University. Good evening tonight. David Pengelly and I wish to discuss with you some of the important but largely unrecognized problems associated with high altitude. Now you may say high altitude seems to be the realm of the mountaineer, abominable snowman and other strange creatures that any discussion of high altitude sickness is largely irrelevant. This is untrue, high altitude can and does kill ordinary people and can seriously affect many others who each year take a ski holiday in the Rockies last year, at least pre at least four previously healthy skiers died while on a holiday in the colorado Rockies. I wish to illustrate with some clinical case histories, some of these problems. And David Pengelly will discuss with you some of the path of physiology of high altitude pulmonary edema. And finally, we'd like to bring to your attention some of the simple ways in which one can prevent and if necessary treat high altitude sickness. Let's take the example of the family of Brown's for Hamiltonian who last year went to a ski resort near aspen Colorado Jim Brown 46. The father was a businessman who golfed and curled his wife Irene 44 years old. It was a housewife and she golfed and swam. Now Bill Brown, the 22 year old student from McMaster was extremely active in hockey, football and other intramural activities. And he also was a fine athlete. His sister Kathy 21 was a secretary, but she was also active swimming and skating. None had previously been ill. And they were all relatively advanced skiers. Now they flew from Toronto Through to Colorado and arrived at a ski area near Aspen in the evening following a rather long flight. They had supper, a few drinks and then went out in the town and they retired about 12 p.m. local time. None slept particularly well and they each had mild headaches. They attributed this to being over tired and to the strange surroundings. Now the next morning they were up on the ski slopes by 10 a.m. taking the chairlift to the top at about 11,100 ft. Now the parents jim and Irene skied for the morning only and they developed mild headaches. Bill and Cathi skied all day mainly on the upper runs on the mountain. Believin cut short his lunch break to squeeze in some extra ski runs. By late afternoon, both Bill and Kathy were exhausted and both had quite marked headaches. When they came back to the hotel, they had a few drinks and supper followed by a dance Bill actually didn't feel very much like eating that night. Neither slept very well. Both had persistent headaches and Bill developed a dry hacking cough. Next morning the second day skiing, mom and dad felt better, but they thought they would only ski for the morning. Bill was tired and still had a headache. He also had a persistent cough and fell short of breath on exertion. Kathy also had a headache and didn't feel like eating breakfast. She decided she'd stay around the hotel that morning. By contrast, Bill was determined to beat the headache and was out on the slopes. By the time the lifts began operating, he felt that the rarefied mountain air would soon fix his headache. Once he began exerting himself, the headache became worse. The cough became more pronounced and he was distinctly more short of breath. During the first run he felt a little unsteady, but nevertheless he skilled all morning on the top of the mountain. At lunch time he went to the mountaintop restaurant. He was a little nauseated and felt very thirsty. He had a beer, but shortly after this he vomited several times. He remained there for about 1.5 hours, but his headache was no better. He was unsteady when leaving the restaurant and he took a side run but soon lost his balance and fell quite severely and twisted his knee. This was extremely painful. He was unable to stand and he decided to wait for help. He soon became cold. His cough worsened. He had much more difficulty breathing and he could hear rattles in his chest and he now coughed up some pink frothy sputum. When help finally arrived they found bill delirious and coughing up pink frothy sputum. He was then evacuated off the mountain to the first aid post and finally to the hospital. On examination. He was agitated. Saya knows he had audible riles had a tachycardia of 100 and 50 beats per minute. His blood pressure was 100 and 10 on 70. His jugular venous pressure was elevated on palpitation of his chest. He had a right ventricular lift and he had two heart sounds present, but the second was widely split and very loud. You also had course reputations throughout both lung fields. His fund I shed a marked retinal hemorrhage and when his chest X ray was performed, he had widespread pulmonary infiltrates indicative of pulmonary edema at that point in time. His blood gasses shade a marked arterial hypoxia mia, with a P. 02 of 35 millimeters of mercury was also hyperventilating, giving him a PCO two of 32 millimeters of mercury. And he had a slight respiratory alka Los ph being 7.4 eight. No, at that stage, he was given oxygen. He was treated with a diuretic and it was also given intravenous fluids And he actually recovered remarkably well over the next 24 hours and by 48 hours he was symptom free and his chest X ray as seen here was completely back to normal now he was actually discharged from hospital on the fourth day, virtually just in time to join his family for their return trip to Hamilton's. Now, while this drama had occurred with bill, Kathy had actually recovered from her mild altitude illness after about 48 hours and she and mother and father were able to ski for the rest of the week without any trouble whatsoever. And they enjoyed their holiday. If we were to work out and discuss precisely what was going on, we know that Bill was suffering from high altitude pulmonary and cerebral edema and even on that first night in colorado Bill and the whole family had mild symptoms related to altitude. Kathie had slightly more severe symptoms with headaches, insomnia and anorexia. But if we look at Bill, he really had life threatening altitude sickness with both the cerebral edema and the pulmonary edema. He also had retinal hemorrhages. You will remember now, at high altitude cerebral and pulmonary edema can develop hand in hand, pulmonary edema. Unlike that we find in left heart failure is not associated with left arterial left atrial hypertension. We're not really sure the exact mechanisms that produce high altitude pulmonary edema nor of the high altitude cerebral edema. However, pulmonary hypertension is always present and we anticipate and expect some sort of arterial or capillary leakage of fluid, some sort of as a mechanism associated with cerebral facilitation and increased cerebral blood flow is thought to produce the cerebral edema. and what I'd like at this point in time to do is to ask my colleague, David Pengelly to go through with us some of the possible mechanisms that may be related to the development of high altitude pulmonary edema and what actually happens in terms of lung function when high altitude pulmonary edema does develop. Thank you, john that was a rather grim story. In order to understand the problem of pulmonary edema, we must first ask two fundamental questions. The first question is what keeps the lung dry? The second question is what happens when it gets wet. To answer the first question. We must have a look at our first illustration. This takes us deep within the recesses of the lung where the inspired air finally reaches the pulmonary circulation. We have shown in schematic form, a tiny portion of this circulation, the pulmonary capillary and its neighboring valvular membrane. In the illustration, you will see four large arrows indicating forces which influence movement of fluid from the capillary toward the al villas. These arrows are shown applying forces on either side of an al gore membrane, which consists of two membranes on either side of a tissue space. The first factor that prevents fluid from moving from the capillary to the al is the membrane itself. The capillary membrane is a semi permeable membrane acting in a way like a filter and in health allows only water molecules to escape from the capillary to the the second factor in the keeping dry of the lung is the balance of forces which are applied to water molecules on either side of the membrane. The prime force, which tends to move water from the capillary to the al is the hydrostatic pressure difference. The difference between capillary pressure and pressure. Under normal conditions, the hydrostatic pressure gradient is about eight of mercury tending to push water from the capillary into the Alvin in the al villas. However, there is an additional pressure caused by the force of surface tension, which accounts for approximately three millimeters of mercury pressure, tending to draw water from the capillary. Thus there is a net hydrostatic force of about 11 millimeters of mercury, tending to move water from the capillary to the opposing. This hydrostatic force is the colloidal osmotic pressure exerted by the plasma proteins, which exert a pressure of some 25 millimeters of mercury directed inward toward the capillary, tending to absorb water from the surrounding space. Thus it is easy to see under equilibrium conditions there is a net pressure which acts to prevent the movement of water from the capillary to the the third factor, which may be brought into play is a drain mechanism to remove excess fluid before it reaches the al villas. The lymphatic system acts as a sort of storm sewer for excess fluid leaving a capillary, eventually, if the lymphatic drainage is exceeded or compromised, the fluid will appear first around the alveoli in the tissue space, then eventually on the surface. This brings us to the 2nd question. What happens if the lung gets wet? If the mechanisms referred to previously begin to fail, then a process starts which leads to the reduction in diameter of a number of channels in the lung. First of all, fluid accumulates around the pulmonary arterials, which tends to press inward on and reduce the flow in these vessels, a process called cuffing. This causes a redistribution of flow to the more dependent areas of the lung where it is already high. In addition the lymphatic themselves become partially cuffed and their function is impaired. Cuffing also occurs around the smaller airways, especially in the dependent zones of the lung, which caused air to be redirected to the upper parts of the lung and therefore away from the areas of the lung to which perfusion is increasingly directed. We see the beginning of a ventilation perfusion mismatch secondly, as the airways become closed by cuffing, the lung functionally becomes smaller as the fluid moves out into the space, the effectiveness of the pulmonary surfactant is diminished and thus the lung becomes stiffer, requiring larger pressures to achieve a given volume change. This stiffening of the lung occurs principally in the dependent areas of the lung, causing further shift of ventilation to the upper parts of the lung shown in the right hand panel of this illustration. This requires larger pressures to achieve the same title volume. In the illustration we see that to maintain the same title volume V. T. The pressure required DELTA P. Is much greater than before. The third change which occurs is as a result of the regional alterations and mechanical properties of the lung which we have seen taking place. The increase in stiffness of the lung calls for increased effort on the part of the respiratory muscles and in addition, regional mechanical distortions of the lung give rise to unusual stresses within it. The sensation of Disney arises as a result of the unusual strains and stresses within the lung tissue and in addition to the extra forces required for breathing, the result of these processes may be summarized as follows. First ventilation, perfusion mismatch giving rise to widen al villa arterial oxygen differences and ultimately hypoglycemia. Secondly, increased stiffness of the lung, leading to significantly increased work of breathing. Third increased work of breathing, increased sensations of breathing and possibly the effects of arterial de saturation give rise to a distressful state of dystonia. As dr Sutton pointed out earlier, the Hema dynamic picture of high altitude pulmonary edema differs from that of the more familiar edema of left heart failure. Here in schematic form we have the right heart, the pulmonary circulation and the left heart in left heart failure. The left heart is enlarged and the left atrial pressure, therefore elevated this pressure backs up through the pulmonary circulation and it gives rise to the hydro and increased hydrostatic force tending to push fluid out into the lung john would you like to comment on the differences in high altitude pulmonary edema? The major difference is we know it is that the left side of the heart is actually quite normal and in fact where it's been measured, the left atrial pressure seen here is also normal. However, pressures on the right side of the heart, pulmonary arterial pressure in particular is considerably elevated and so the usually implied mechanisms producing pulmonary edema that would occur in left ventricular failure do not apply. And while the fundamental mechanisms are still unknown, it is assumed that we have a trans arterial arterial or capillary leakage of fluid producing high altitude pulmonary edema. So far we've discussed the path of physiology of the high altitude pulmonary edema and we chose to illustrate some clinical stories of high altitude pulmonary and cerebral edema by going to colorado with the Brown family. Now, high altitude illness isn't really such a new entity. That's been known to various civilizations for centuries. Classic example, of course is in south America, the in the middle of the Andes. The inca civilizations here seen at Machu Picchu were well familiar with the problems of exquisite shortness of breath and headache, on climbing to high altitudes and they called it these people here we see in the capital of Cusco marching through the streets, we're able to adapt to altitude quite remarkably well and in fact the Western will only knew the problems of high altitude when in 15 69 a Jesuit called Jose de acosta across a mountain pass at nearly 16,000 ft. And there he was stricken with this dreadful sorrow. The indians were very, very familiar with this and not only that, but they knew the cure. They use cocoa leaves. And in the next illustration you'll see the Children in the streets of La paz Bolivia selling cocoa leaves, cocoa leaves when chewed, liberate cocaine. And he we have an Andean mullet ear that appears to have unilateral mumps. You can see his cheek is swollen and he has a quid of cocoa leaves on which he's chewing this, liberates cocaine and it's thought to prevent and minimize high altitude illness. Well, is this really true? And have we learned all that much about high altitude illness? We certainly don't advocate the use of cocaine to treat or even prevent high altitude illness, mainly because it doesn't work. What we think happens is that it just makes these people oblivious to the the the sickness they're really suffering at this point in time, I'd like to sum up our feelings about the causes of high altitude illness. Obviously you don't get high altitude illness if you stay at sea level, you have hypoxia. And when you breathe up Hipaa cap Niya, we also know that with both of these influences there is an increase in cerebral blood flow in the lung. We know pulmonary hypertension occurs. There is, however, a fairly large jump from the cerebral edema, from the effect of cerebral blood flow and pulmonary hypertension to the development of the cerebral edema and pulmonary edema that's associated with the illnesses. And you see the symptoms that come from the cerebral edema, the anorexia, the nausea, the vomiting, the headache, the ataxia and the disordered consciousness and sometimes death. And on the right, you see the symptoms that arise from the pulmonary oedema, namely the exquisite shortness of breath, the cough and the pink frothy sputum. Now, in fact, these two, while they go hand in hand, the cerebral edema and pulmonary edema may themselves be interrelated. It's possible that once the cerebral edema develops, the there is a neurogenesis mechanism that can in itself aggravate or cause pulmonary edema. And of course with the pulmonary edema as David has pointed out, we have a widening of the arterial, too, the villa to arterial oxygen difference. We have hypoglycemia and of course this will create the vicious cycle feeding back there to the further hypoxia aggravating the pulmonary and the cerebral edema. Now, what about exercise? It's been said that exercise at altitude? Certainly in the first few days will tend to aggravate the problem. How does this come about? Well, exercise may in fact produce or aggravate the problems by increasing both the pulmonary artery pressure and the systemic artery pressure, thus making the vessels that are already dilated and to some extent extent hypoxia more likely to leak fluid. And so it's possible that exercise and even cold by the changes they exert on pressures in the primary and in the cerebral circulation do tend to cause and aggravate pulmonary and cerebral edema, causing leakage of fluid to the lung and the brain. Now, at this point in time, perhaps we should try and work out precisely what one can do about these problems. The most logical thing of all, of course is to prevent this. No, it's unlikely, nor is it desirable that we'll be able to get people going to high altitudes. We have to accept that as a simple fact people are going to visit these places, but we would like to minimize the chances of these people who are in their prime of life, are stricken and sometimes die from altitude illness. The first of course, the first thing that we should be concerned about is trying to prevent high altitude illness and we know that high altitude illness affects the young, the healthy and the physically active. It usually develops over a period of hours or days and it's very unlikely to occur. It's a shorter time interval than 4-6 hours. We think that it's aggravated by alcohol and it's certainly aggravated by the cold by exercise and by any form of upper respiratory tract illness. We also should be aware of how we can prevent it. Obviously we can prevent it by not going, but we also can prevent it by slow acclimatization. We also should reduce our physical activity for the 1st 24 hours at altitude. And we should also minimize the amount of alcohol we drink in this period of time. In fact, one beer That altitude is like two or 3 back here in Hamilton's. I think that's also rather important to remember. What about if you actually get these symptoms, if you are out on your ski holiday, if you develop a persistent headache, nausea and vomiting, shortness of breath or cough, you should actually descend and rest. You may even need to seek medical advice. Is there anything else that we should bring up at this point, David? Well, there was a concern that I think perhaps many of our viewers might have, and that is the effect of cigarette smoking. We know that cigarette smoking does something which inhibits oxygen transport. How does this affect people's performance at high altitude? Well, in fact, of course, people who smoke are at a disadvantage when going to altitude. But strangely enough, some of the best mountaineers in the world do still smoke. So I can't argue all that strongly about its problems as far as someone going on a ski holiday. However, for the 1st 24 or 48 hours at altitude, I think people would be very well advised to cut down on their smoking. So that means really to cut down on alcohol and smoking perhaps. And a lot of violent activity which cuts down on perhaps people's enjoyment for the first hour. But first day, I should say, but makes it worthwhile for the rest of their holiday. Oh, that's right. I mean, one would hate to take grog smoking and sex out of a ski holiday, but one probably should be rather cautious over the 1st 24 or 48 hours. So to some of our feelings about high altitude illness and to bring it into some sort of perspective, I think with some full warning, some common sense, one can go and really enjoy a ski holiday at high altitude and it's important not to let high altitude illness ruin your ski holiday. And so David, let me thank you for being with me tonight to share our views on high altitude illness. The mechanisms related to causing high altitude pulmonary and cerebral edema and in a practical sense, what we can do to prevent and treat this very important, potentially fatal and largely unrecognized high altitude illness. If you're interested in participating in the evaluation of the Health Care today television programs or if you would like further information on the programs planned for this year, please contact the program. Coordinator Healthcare Today. Room One R. One Faculty of Health Sciences McMaster University Hamilton in Ontario Health care Today was produced in cooperation with Ch ch T. V. The Faculty of Health Sciences McMaster University, the Ontario Medical Association, Mohawk College, the Ontario chapter of the Canadian College of Family Physicians and the Hamiltons Academy of Medicine.