Hyperventilation Research Paper

Although the fraction of oxygen, 21%, and other gases in the atmosphere remain constant on increasing altitude the barometric pressure decreases exponentially as we ascend above sea level. At sea level the atmospheric pressure is 760mmHg resulting in an oxygen partial pressure(pO2) of 150mmHg (taking water vapour into consideration.) On ascent to an altitude of 4000m the atmospheric pressure is reduced to 475mmHg resulting in a pO2 of 103mmHg. Because of the fall in pO2 the driving of force of oxygen into the blood is reduced resulting in a decrease alveolar and arterial pO2. It’s because of this decrease in oxygen content in the blood that the human body experiences hypoxia on ascent to altitude where the tissues, and mitochondria in particular,

It seems logical to think that as the atmospheric pO2 decreases, in order to improve the oxygen supply to the blood the alveolar ventilation should be increased. This can be done by increasing the respiratory minute volume meaning pulmonary hyperventilation. This occurs when the alveolar pressure declines below 60mmHg and the respiratory minute volume increases progressively as the alveolar pO2 declines. Hyperventilation at the increased altitude occurs as a result of a stimulation of the peripheral chemoreceptors on the aorta and carotid sinus by hypoxia. The carotid body is a vascularised cluster of type 1 glomus cells which are sensitive to changes in arterial partial pressure of oxygen(PaO2) and carbon dioxide which then signal the respiratory centres in the central nervous system to increase the rate and depth of ventilation. This is known as hypoxic ventilator response. The respiratory centre is triggered in the cerebral pons and medulla in response to the peripheral chemoreceptors and the signals are then passed onto the diaphragm, intercostal muscles and stretch receptors of the lungs. As the ventilation increases the arterial partial pressure of CO2(PaCO2) drops in proportion with the increase in ventilation as more CO2 is removed from the blood while at the same time the alveolar and thus PaO2 will increase as more oxygen enters the lungs. The drop in PaCO2 results in the diminished

As a result of respiratory alkalosis there is an increase in the concentration of 2,3 diphosphoglycerate(DPG). 2,3-DPG is an allosteric regulator of haemoglobin affinity for oxygen. Its binding at an allosteric site leads to increased affinity of haemoglobin for oxygen. which increases the oxygen carrying capacity of the blood resulting in a leftward shift in the oxygen dissociation curve. This would have a positive effect in delivering more oxygen to the tissues and would be especially important if exercise was to be carried out as more oxygen is being use by the tissues. Although the left ward shift would increase the oxygen carrying capacity it could be argued that if there was a rightward shift in the oxygen dissociation curve it could be more beneficial. This shift would cause an increase in the unloading of oxygen into the tissues making more oxygen readily available to the mitochondria of those tissues. In order to determine if a left or right shift does occur the concentration of 2,3 DPG could be measured at altitude and at sea level in a native sea dweller. If in fact there is a left shift as expected there would be an increase in the carrying capacity of the