Describe the respiratory effects of high altitude during acute exposure and acclimatization.

Outline:

·        Effects of decreased barometric pressure

·        Acute response

·        Acclimatization

Essay:

            As altitude increases, barometric pressure decreases. Therefore the oxygen partial pressure decreases proportionately leading to hypoxia problems in high altitude physiology. At 3000m above sea level, the alveolar PO₂ is about 60 mmHg. Even at high altitudes, carbon dioxide is continually excreted from the pulmonary blood into the alveoli. Also, water vaporizes into the inspired air from the respiratory surfaces. Therefore, these two gases dilute the oxygen in the alveoli, thus reducing the oxygen concentration.

            The body’s immediate response to the hypoxia of high altitude is hyperventilation which is triggered off by the low arterial oxygen partial pressure. Hyperventilation enhances alveolar ventilation, raising the alveolar and arterial PO_2. However, it also removes large quantities of carbon dioxide, reducing the PCO₂ and increasing the pH of body fluids, causing a state of (respiratory) alkalosis. Both these changes inhibit the respiratory center and oppose the effect of low PO₂ to stimulate the peripheral chemoreceptors. During the ensuing 2 to 5 days, this inhibition fades away, allowing the respiratory center to now respond to the chemoreceptor stimuli resulting from hypoxia. There is a steady increase in ventilation over the next 4 days because the active transport of H⁺ into CSF, or possibly a developing lactic acidosis in the brain, causes a fall in CSF pH that increases the response to hypoxia. After 4 days, the ventilatory response begins to decline slowly.

            The initial increase in pH increases the affinity of hemoglobin oxygen, shifting the oxygen dissociation curve to the left. This allows the hemoglobin to pick up more oxygen at lower PO₂ of the lungs. After an acclimatization period of hours to days, the production of 2,3-DPG by red blood cells increases, shifting the curve to the right and offsetting the effects of respiratory alkalosis. 

            The hypoxia of high altitude also triggers the release of the hormone erythropoietin from the kidney and liver. This hormone stimulates red blood cell production. Even though the PO₂ of the blood remains low, the total oxygen-carrying capacity is increased. The increase in hemoglobin and blood volume is a slow process, having no effect until after 2 weeks.

            Changes also take place gradually in the circulatory system and tissues to adapt to the lower arterial PO_{2 .}  There is an increase in diffusing capacity partly caused by increase in pulmonary capillary volume which expands the capillaries and increases the surface through which oxygen can diffuse into the blood. Another part results from an increase in lung volume, which expands the surface area of the alveolar membrane. An increase in pulmonary arterial pressure forces blood into greater numbers of alveolar capillaries. The cardiac output increases after a person ascends to high altitudes, but decreases back toward normal as the blood hematocrit increases. In the tissues, the mitochondria, which are the site of oxidative reactions, increase in number, and there is an increase in myoglobin that facilitates the movement of oxygen into the tissues. There is also an increase in the tissue content of cytochrome oxidase.