Renal And Respiratory Pathophysiological Challenges Of High Altitudes, Acclimatization And Possible Methods Of Treatment With A Minor Focus On Ethanol

2029 words - 9 pages

Respiratory System Acclimatization, Prophylaxis, and Treatment
The respiratory system acclimatizes for the majority of elevation gain through the incorporation of hyperventilation.8, 16 The hypoxic conditions of Mount Everest stimulate the peripheral chemoreceptors of the carotid body16, resulting in a hypoxic ventilation response (HVR) from messages sent to the brain as seen in Figure 3. This leads to increased ventilation to compensate for the lower oxygen content available for your body to consume during its normal functions. The physiological advantage to this process is lessening the alveolar partial pressure of oxygen that would normally occur as elevation increased.15 The diffusion capacity of the lungs would also increase, since there is a diffusion limitation under these extraordinary conditions.15, 16 By decreasing the alveolar carbon dioxide levels, subjects experience hypocapnia and respiratory alkalosis from the resultant increase in pH.8 The respiratory alkalosis is what promotes bicarbonate excretion by the kidneys to compensate for the high pH level.
Too rapid of elevation gain can have severe pathophysiological effects on the lungs, and brain resulting from the hypobaric hypoxic environment. Some of the major pathophysiological conditions include acute mountain sickness, high altitude cerebral edema and high altitude pulmonary edema as summarized on Table 2. The symptoms of acute mountain sickness can easily be confused for a viral illness7, 16 from the emergence of similar symptoms (vomiting, fatigue, dizziness, etc.). This sort of “illness” can progress rapidly to cerebral interstitial edema, which results from the blood brain barrier experiencing an imbalance of starling forces, increasing cerebrospinal fluid hydrostatic pressure.18 The presence can be determined by ataxia during a heel to toe walking test and the presence of swelling, and hypertension.7 This feature can progress even quicker into sudden coma and/or death. High altitude pulmonary edema (HAPE) is the result of hypoxic pulmonary vasoconstriction, which increases the capillary pressures.7, 16 This leads to fluid excretion into the alveolar and interstitial spaces, causing difficulty in breathing and disruption of the gas exchange ability of the lungs, since there is now a thicker barrier for gas exchange to occur. Symptoms for this condition can be headaches, insomnia, cyanosis, fluid retention, cough and shortness of breath.7, 16 Another pathophysiological effect of high altitude is the rightward shift of the oxygen dissociation curve, leading to increased offloading of oxygen into the periphery. This occurs because of an increase of 2,3-diphosphoglycerate from the emergence of respiratory alkalosis.17 The shift to the right may lead to increased offloading, however also indicates that the hemoglobin has a lower affinity for oxygen, making it harder to obtain oxyhemoglobin saturation.
Respiratory complications from high...

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