One mmHg is essentially equivalent to one torr. At sea-level, the barometric pressure is 760 mmHg. The percentage of oxygen (O2) in dry air is 20.94%; consequently, the partial

pressure of O2 at sea-level is 159 mmHg (0.2094 × 760). When air is inhaled, it is warmed and saturated with water vapor. At 37°C, the saturated vapor pressure in the lungs is 47 mmHg regardless of altitude; because water vapor displaces oxygen and nitrogen, the partial pressure of inspired oxygen is 149 mmHg (0.2094 × (760 – 47)). The partial pressure of water vapor in the lungs at sea-level accounts for only 6% of the total barometric pressure, but Inhibitors,research,lifescience,medical water vapor becomes increasingly Inhibitors,research,lifescience,medical important at high altitudes. On the summit of Mount Everest, where the barometric pressure is only 250 mmHg, water vapor accounts for nearly 19% of the total barometric pressure, further diminishing the oxygen availability.13 At rest, the partial pressure of carbon dioxide (PCO2) in the lungs is

40 mmHg, which further displaces oxygen. Although the partial pressure of inspired oxygen at sea-level is 159 mmHg, the combined effects of CO2, water vapor, and dead space reduce the partial pressure of oxygen (PO2) in the lungs Inhibitors,research,lifescience,medical to approximately 100 mmHg. Hyperventilation Inhibitors,research,lifescience,medical can reduce the partial pressure of CO2 in the lungs below 40 mmHg, thereby allowing the partial pressure of O2 to rise. This DAPT cell line effect is exaggerated at altitude. On the summit of Mount Everest where the inspired PO2 is only 29% of its value at sea-level, alveolar ventilation is increased

by a factor of 5. This extreme hyperventilation reduces the alveolar PCO2 to 7–8 mmHg, about one-fifth Inhibitors,research,lifescience,medical of its normal value. Because of the reduction of PCO2, the alveolar PO2 can rise and be maintained near 35 mmHg, enough to keep the climber alive.14,15 THE HYPOXIC VENTILATORY RESPONSE Histone demethylase AND CONTROL OF RESPIRATION At higher altitudes, the rate and depth of ventilation increase to compensate for the reduced partial pressure of oxygen (PO2). This increase in ventilation is termed the hypoxic ventilatory response (HVR) and is partially mediated by the carotid body which is located at the bifurcation of the common carotid artery and is sensitive to dissolved oxygen in the blood. The primary stimulus to breath, however, is not hypoxia; it is hypercapnia, an increase in the level of carbon dioxide in the blood. This stimulus is mediated by potent chemoreceptors located in the medulla. Although the blood–brain barrier separates these medullary chemoreceptors from the arterial blood, the blood–brain barrier is permeable to CO2.