Introduction to High Altitude Stress
High altitude stress is a pathophysiological effect that occurs to 25-85% of humans7 who increase their altitude without acclimatization. Going from sea level to the top of Mount Everest yields a drastic drop in the partial pressure of oxygen as the pressure goes from 149mmHg at base camp to 43mmHg15 at the summit as seen in Figure 1. Focusing primarily on the renal and respiratory physiology, increasing elevation rapidly (thus experiencing hypoxia) can result in a variety of physiological effects to the body, such as high blood cell concentrations, production of proteins, and two main forms of edema. These physiological conditions can greatly affect the ...view middle of the document...
1, 15 The blood has a higher resultant viscosity, which produces a decrease in the RPF, therefore causing the filtration factor (FF) to increase to compensate. 1 This process takes weeks to reach a steady state, resulting in the increase of the total red blood cell count and concentration.1 Those who surpass the suggested speed for acclimatization to occur can expect a low plasma volume from dehydration, but equally high red blood cell concentration. The higher concentration of blood cells is beneficial because it allows for increased binding sites for the available oxygen to bind and become oxyhemoglobin; thus increasing oxygen transport in the body. Another process that the human body may experience during acclimatization is an increase in the production of vascular endothelial growth factor (VEGF).7, 8 VEGF is what increases the number of new blood vessels from existing ones, which again stimulates increased oxygen transport in the body. Another renal process of acclimatization is increasing the number of mitochondria, which in turn increases myoglobin as seen in Figure 2. This increases the cytochrome oxidase content in tissues allowing for a larger ATP production via oxidative phosophoylation.19
High altitudes do not appear to have any severe pathophysiological effects; however there is a prevalence of proteinuria and microalbuminuria in subjects who reside in these higher elevations for extended periods of time.1, 13 These conditions occur as a result of polycythemia; the increased hematocrit from the stimulated increase of erythropoietin. With proteinuria, the pathogenesis may result in kidney parenchyma, hyperviscosity, elevated right heart pressure, and glomerular capillary hypertension.1, 13 Another pathophysiological effect would be hypovolemia resulting from low humidity and tachypnea.8 This could lead to dehydration during the primary stages of climbing the mountain, however after the hypoxic diuretic response has completed, a subject may now experience fluid accumulation.8
To treat the pathophysiological effects of proteinuria, angiotensin converting enzyme (ACE) inhibitor treatment was effective, because it lowers the hemoglobin count, inhibiting angiotensin II mediated erythropoiesis and improving renal medullary blood flow.1, 13 As seen in Table 1, Acetazolamide has also been found to be effective because it improves the renal plasma flow and arterial oxygenation, since it excretes bicarbonate ultimately increasing acidity in the blood.8, 4 This increase in acidity tricks the body into believing it has high carbon dioxide levels, therefore reacting with increased hyperventilation and increased oxygen levels. To take care of the hypovolemia, drinking water with minimal salt concentration would be beneficial to induce water reabsorption through osmosis. To deal with the fluid accumulation that may occur at a later time, use of diuretics may be beneficial to overcome this issue.8