英国纽卡斯尔大学生理学课件0027学习课件.pptVIP

Within hours subjects can develop acute mountain sickness (AMS) which can become extremely serious. Oxygen lack is not a drive to respiration at sea level in healthy subjects. The low PO2 in the lungs (hypoxia) immediately causes redistribution of blood flow around the alveolar capillaries. Those alveoli which are very poorly ventilated and therefore have the lowest PO2 are constricted. This diverts the blood to well ventilated alveoli. Consequences of hyperventilation: little increase in Hb saturation The shape of the O2 dissociation curve is shifted by increased production of 2,3 DPG (2,3 diphosphoglycerate) over a few hours. Hypoxia stimulates red blood cell production by releasing erythropoeitin from the kidney which stimulates bone marrow. This is initiated after about 2-3 days and the production of extra red cells continues for 2 to 3 weeks. The blood haemoglobin increases from about 15g/100ml to a peak of about 22g/100ml. Approximately a 50% increase in Hb and thus a 50% increase in O2 carrying capacity. The increased number of RBC’s increases the blood viscosity and so the heart has to work harder. Within hours subjects can develop acute mountain sickness (AMS) which can become extremely serious. * Adaptation to high altitude hypoxic response compensatory mechanisms hematological changes High 2,500 - 3,600 meters Very High 3,600 - 5,500 Extremely High 5,500+ High altitude P in the alveoli ~ 60 mm Hg The only sure treatment is to descend. · Headache · Malaise · Loss of appetite · Nausea, vomiting · Peripheral edema · Disturbed sleep · Cyanosis Factors that affect the severity of altitude illness ? Rate of ascent- the faster you climb the greater your risk.? Altitude attained (especially sleeping altitude)- the higher you sleep the greater the risk.? Length of exposure- the longer you stay the greater the risk.? Level of exertion- hard exertion, without rest or hydration, increases the risk.? Hydration and di