Ventilatory Response to Arterial Po2, Pco2, and pH
Paco2 when only frequency increases. This helps explain the increase in slope of the ventilatory response to C02 at high of levels C02 (see Fig. 5).
It is difficult to decrease Paco2 below normal in an individual without changing other ventilatory stimuli, but ventilation can decrease if this does occur. This indicates that chemoreceptors are tonically active at normal Paco2 levels (see Fig. 5), so hypocapnia decreases chemoreceptor stimulation and ventilatory drive. However, ventilatory sensitivity to low levels of Paco2 is relatively low, as shown by the low slope of the hypercapnic ventilatory response between 0% and 2% inspired C02, compared with higher levels (see Fig. 6). Ventilation may actually cease if Paco2 is lowered enough to go below the so-called apneic CO2 threshold. It is estimated that about two-thirds of the drive to breathe in normal resting humans is from chemoreceptor stimulation and the balance is from mental state (i.e., wakefulness).
The ventilatory response to C02 is mainly a function of central chemoreceptor stimulation, which explains 75% of the total response. The rest of the response is explained by arterial chemoreceptors, which depend on stimulation by arterial Pco2, as well as H+ from respiratory changes in arterial pH. The direct effect of Pco2 on arterial chemoreceptors probably explains less than 10% of the total ventilatory response. The independent effect of arterial pH on ventilation and important interactions between Pao2 and Paco2 as ventilatory stimuli are described later in separate sections on pH and Po2.
The time course of the ventilatory response to Paco2 begins rapidly (within a few breaths of inhaling C02) from stimulation of arterial chemoreceptors. It requires a few minutes for ventilation to reach a steady value after Paco2 stabilizes at a new level. This probably reflects the time it takes central chemoreceptors to respond to Paco2 by an indirect H+-sensing mechanism (Fig. 4). When Paco2 is experimentally increased in normal subjects over hours to weeks, ventilation remains near the level measured during the first few minutes of exposure to C02. This occurs despite a reduction in arterial chemoreceptor stimulation, as H+ decreases with renal compensation for the respiratory acidosis. Also, it is different than the case in patients with lung disease and chronically high Paco2 (see Integrated Ventilatory Responses section later).
The ventilatory response to changes in arterial pH is the result of arterial chemoreceptor stimulation, and only the carotid bodies contribute to this response in humans. Patients without normal carotid body innervation do not have a response to metabolic changes in pHa. H+ cannot cross the blood-brain barrier, so a metabolic acidosis or alkalosis cannot stimulate central chemoreceptors. The ventilatory response to physiologic changes in pHa of ±0.1 pH units is very small (less than 10% of resting ventilation). Larger increases in pHa (to 7.6) also only cause small decreases in ventilation. However, larger decreases in pH have a stronger effect, so resting ventilation may double at pHa = 7.2. In severe acidosis, ventilation increases even without the involvement of arterial chemoreceptors. Very large increases in arterial [H+] might allow some H+ to cross the blood-brain barrier, or this could represent a generalized response to stress.
Increases in ventilation with chronic metabolic changes in pH are essentially the same as the increase with acute changes. For example, in a diabetic patient with long-term ketoacidosis, ventilation remains elevated despite (1) pH being compensated toward normal, which reduces H+ stimulation of arterial chemorecep-tors; (2) decreased PCO2 stimulation of arterial chemo-receptors, after respiratory compensation of the metabolic acidosis; and (3) decreased central chemo-receptor stimulation from the low PaCO2. Recall that metabolic H+ changes in the blood are not sensed by the central chemoreceptors so the small arterial acidosis (from incomplete compensation) stimulates arterial chemoreceptors and provides the only known stimulus for ventilation. However, chronic decreases in PaCO2 may increase the sensitivity of central chemoreceptors and restore some of that ventilatory drive, at least in the case of normal subjects acclimatizing to chronic hypoxia (see Integrated Ventilatory Responses section later).
The ventilatory response to PaO2 is called the hypoxic ventilatory response, and it is notable for its nonlinearity. Increases in PaO2 have relatively little effect on ventilation, whereas decreases in PaO2 below about 60 mm Hg cause large increases in ventilation (Fig. 7). This nonlinearity is the reason why PaCO2 is more important than PaO2 at controlling ventilation in normal individuals. Increases or decreases in PaCO2 from a normal value of 40 mm Hg are effective at changing ventilation (see Fig. 6). Normally, the hypoxic ventilatory response is not large until PaO2 falls to a level at which O2-hemoglobin saturation starts decreasing significantly (Chapter 20) and ventilation is a linear function of arterial O2 saturation. However, this linear relationship is a coincidence and not a mechanistic explanation because arterial chemoreceptors respond only to O2 partial pressure, and not O2 content or saturation (see Arterial Chemoreceptors section). The hypoxic
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