The first sensor, which has the strongest effect by far on ventilation (at sea level) is the central chemoreceptor. The neurons responsible are located in the medulla. These are close to, but separate, from the neurons that generate the rhythm of breathing. Small changes in the partial pressure of carbon dioxide (PaCO2) in the systemic arterial blood flowing to the medulla produce pronouced changes in ventilation.
The second sensor is the peripheral chemoreceptor, which consists of afferent neurons monitoring the blood in the carotid and aortic bodies. These are close to the baroreceptors, but entirely separate. By contrast with the central chemoreceptor, the peripheral chemoreceptor has little effect on the breathing of a normal person at rest at sea level. But in two important circumstances the peripheral chemoreceptor begins to drive breathing.
Oxygen therapy is usually given when PaO2 is below 55 mm Hg, and, although expensive and cumbersome, the oxygen is helpful in COPD when the oxygen falls below this level. Indeed, the PaO2 can fall much lower than 55 mm Hg in COPD. But several recent studies have found that patients with less severe COPD are not helped by supplemental oxygen.
However, if a respiratory problem primarily involves a shunt, the PaO2 responds poorly to supplemental oxygen. Why is this? (Think about the effect of the supplemental oxygen on the oxygen content of blood flowing through the ventilated alveoli.)
High altitude is a circumstance in which a healthy person must deal with a lowered PaO2. At 14,000 feet, for example, the PO2 in moist tracheal air is only 82 mm Hg, compared to 149 mm Hg at sea level.
For most people acclimated to sea level, a fast ascent to roughly 10,000 feet begins producing symptoms of acute mountain sickness, although some people will experience symptoms at the 7,000 to 9,000 feet. Headache is the most common symptom with lassitude and nausea common as well. The level of physical fitness does not seem to to be important.
The cause of acute mountain sickness is not known. There is evidence that the brain swells somewhat with elevation, and some investigators feel this might be the important factor. One reason for the swelling might be that hypoxia leads to vasodilation of blood vessels, cerebral and otherwise. Various factors mediate this. Another suggestion is that the vasodilation leads to a mild form of edema. But whatever the sequence, the swelling could explain the headache and perhaps other problems.
Another interesting factor at higher elevations is respiratory alkalosis. Why does this occur? (Remember that the peripheral chemoreceptor kicks in if the PaO2 falls below 60 mm Hg.)
In some cases acute mountain sickness progresses to serious cerebral edema or pulmonary edema These are both dangerous conditions which require immediate return to lower elevations.
It's instructive to observe what happens when a normal, healthy person begins breathing oxygen at a higher partial pressure than normal. This occurs, for example, in scuba diving, because the diver must breathe air at the same pressure as that of the surrounding water. Since the water pressure increases by one atmosphere for each 33 feet, a scuba diver often is breathing quite high partial presssures of oxygen.
First think about oxygen transport. About how much would the amount of oxygen in systemic arterial blood increase if the partial pressure of oxgygen in the alveoli were, for example, twice normal?
Next think about the peripheral chemoreceptor. As described above, the peripheral chemoreceptor does not have much effect on ventilation when the PaO2 is above about 60 mm Hg.
Now, what about CO2? Suppose the metabolism of the diver is about the same as at the surface. If so, then CO2 would be produced at about the same rate, and thus the diver would need to breathe at the same rate in order to blow off the CO2. In other words, normal ventilation would keep the PaCO2 at the normal level. And, of course, it is the PaCO2 that is primarily controlling breathing.
Something that is quite obvious in lab is the sudden increase in the ventilation during the exercise tolerance test. In a plot of Ve vs. watts, there is a sudden increase in ventilation at the lactate threshold. What sensor is important for this sudden increase in ventilation?
The RQ also changes at the lactate threshold. At rest, the RQ is usually between approximately 0.8 to 0.9. However, two factors can cause it to rise well above 1.0. The first is hyperventilation, since this increases the rate of exhalation of CO2 without changing the oxygen consumption. The second factor is the addition of lactic acid to the blood. The acid reacts with bicarbonate in the blood, releasing CO2.