RESPONSE TO ALTERED OXYGEN

The response of ventilation to altered alveolar P_O2 is displayed in the curves shown in Figure 7.

FIGURE 7

Ventilatory response to changes in alveolar P_O2. Hypoxic response curves. Note that when the P_CO2, is 36 mm Hg, almost no increase in ventilation occurs until the P_O2 is reduced to about 50 mm Hg. (Modified from HH Loeschke and KH Gertz: Arch Ges Physiol (more...)

The following features of these curves are noteworthy. As alveolar P_O2 decreases below a threshold of about 50 mm Hg at normal P_CO2, ventilation increases. At a given alveolar P_O2, ventilation depends on alveolar P_CO2. Ventilation increases with increasing P_CO2. Thus, increased CO₂ potentiates the response to decreased P_O2. For normal alveolar P_CO2, no increase in ventilation is observed until alveolar P_O2 falls below about 50 mm Hg. Because arterial blood is still highly saturated with oxygen (recall the oxygen dissociation curve, S_O2 ≈ 80% when P_O2 is about 50 mm Hg), there is no great need for sensitivity to P_O2 above about 50 mm Hg. In normal situations, the hypoxic stimulus is not very important. On ascent to high altitude, however, it takes on considerable significance. For example, at an elevation of 10,000 ft, barometric pressure is about 550 mm Hg, yielding an inspired P_O2 of about 100 mm Hg and a P_AO2 of about 50 mm Hg.

CENTRAL AND PERIPHERAL RESPIRATORY CHEMORECEPTORS

The central chemoreceptor response to hypoxia actually depresses ventilation, presumably by depressing oxidative metabolism in neural tissue. The peripheral chemoreceptors are located in the carotid (carotid sinus) and aortic bodies (aortic arch). The carotid bodies respond to arterial hypoxia by increasing the firing rate from the carotid sinus nerve. The carotid bodies are connected to the respiratory centers in the brainstem, and all of the respiratory response from peripheral chemoreception originates in them. The carotid bodies have high blood flow and are not sensitive to CO or anemia. The aortic bodies are connected to the cardiovascular centers in the brainstem, and they are responsible for the cardiovascular response to respiratory-linked chemical factors in the arterial blood. The aortic bodies have lower blood flow than do the carotid bodies, and they are sensitive to CO and anemia. The carotid bodies are small (1–2 mg) organs with an enormous blood flow (1–2 l per min per 100 g tissue). Their O₂ consumption relative to blood flow is negligible, resulting in a small arteriovenous O₂ difference. They continuously sample arterial blood. The mechanism of peripheral chemoreceptor oxygen sensitivity appears to involve P_O2 directly rather than [O₂] or S_O2. The responses by the central and peripheral respiratory chemoreceptors can be summarized by stating that the sensed variable is arterial P_O2 (P_aO2); when it falls below 50 mm Hg, the central chemoreceptors give a non-specific metabolic response that depresses ventilation, whereas the peripheral chemoreceptors stimulate ventilation. Thus, all of the stimulatory response to hypoxia resides in the peripheral chemoreceptors. Elevation of P_aO2 above normal (∼100 mm Hg) generally has no effect on ventilation since the respiratory chemoreceptors appear to be insensitive to changes in P_aO2 above about 50–60 mm Hg.