DefinePK

Abstract

Introduction


Hyperventilation is the first physiological adjustment observed in response to sudden exposure to hypoxia. It is initiated by hypoxic stimulation of peripheral arterial chemoreceptors (carotid and aortic bodies) and central integration of chemosensory inputs in brain stem via medullary respiratory center.1 Besides hyperventilation, the lungs undergo several changes which may impair its functions. Several studies2-4 have recorded the reduction in forced vital capacity (FVC) during first week at Mount Everest base camp (5300m elevation) and an increase in forced expiratory flow (FEF 25-75%). The native study on 16 Pakistani lowlander volunteers have revealed a significant reduction in FVC, %FEV1, MVV and PEFR on the first day of arrival at 4570 m altitude.5 Despite reduction in airway resistance due to decreased air density at high altitude the ventilatory muscle endurance may be decreased by hypobaric hypoxia6 which may be a limiting factor in ventilatory function. Therefore, exacerbating hypoxemia at high altitude can impair lung functions which may be associated to the arterial blood gases. Gradual ascent in stages has been the thumb rule to achieve adaptation to high altitude and to prevent untoward effects of hypoxia. However, acetazolamide and/or dexamethasone has been tried to speed up the process of adaptation especially when acute ascent to high altitude is compelled during rescue climbing or military operations. The present study is an effort to evaluate the changes in spirometric lung volumes and flow rates alongwith changes in arterial blood gases in healthy volunteers during acute exposure to hypobaric hypoxia following ascent to 4578 m altitude. Furthermore, it has been tried to assess the role of acetazolamide and/or dexamethasone prophylaxis in ventilatory response during acute ascent to high altitude.