CONTROLLED SYSTEM EFFECTS ON REGULATION OF BREATHING

The translation of the output of the inspiratory neurons to ventilation involves, as shown in Fig. 8, the successive transformation of nerve impulses to muscle electrical activity, muscle shortening, force, and then ventilation. Usually, moderate changes in the mechanical properties of the muscles or chest bellows have little or no effect on the resting blood gas tensions. Compensating effects by the chemoreceptor and mechanoreceptor reflexes, conscious adjustments, and the intrinsic force-velocity relationships of the muscles themselves allow the force of contraction to increase whenever the rate of contraction is slowed. In the presence of sufficiently severe chest disease, however, gas exchange is inadequate despite all efforts to compensate.

FIG. 8. Steps by which respiratory neural activity is translated into ventilation.

Even when the compensatory responses prove ultimately to be adequate, changes in mechanical conditions (or metabolic rate) cause a transient period in which gas exchange is disturbed and gas tensions are abnormal. The degree to which blood gas tensions deviate from normal in such situations depends on the volume and arrangement of the body stores of O2 and CO2.

CO2 is contained in the body in large amounts as gas in the lungs, but mainly in the form of bicarbonate and carbonate solutions in blood and tissues. O2, on the other hand, is stored in much smaller amounts in alveolar gas, in solution, and in combination with hemoglobin and myoglobin. Disturbances in gas exchange cause small changes in PCO2 because of the large size of the CO2 stores, but large changes in PO2.

Rates of change of PO2 and PCO2 depend not only on the volume of gas stores, but also on organization—that is, the way O2 and CO2 contained in different body tissue compartments are linked by the circulation, rates of perfusion, and metabolic rates in the various body compartments—and the ability of the tissues in each compartment to bind CO2 and O2.

The rate at which peripheral and central chemoreceptors respond to changes in inspired CO2 and O2 depends on the arrangement of the body gas stores. The small size of the arterial compartment and the high rate of carotid body blood flow allow peripheral chemoreceptors to respond quickly to changes in both O2 and CO2. The larger CO2 stores of the brain cause the central chemoreceptors to respond more slowly to changes in inspired CO2. This difference in response time of central and peripheral chemoreceptors has been used to distinguish the contribution of each receptor to the CO2 response.