Under normal conditions, blood Po2 affects breathing only indirectly, by influencing the chemoreceptor sensitivity to changes in PcO2- Chemoreceptor sensitivity to PCO>2 is augmented by a low PO2 (so ventilation is increased at a high altitude, for example) and is decreased by a high PO2. If the blood PO2 is raised by breathing 100% oxygen, therefore, the breath can be held longer because the response to increased PCO2 is blunted.
When the blood PCO2 is held constant by experimental techniques, the PO2 of arterial blood must fall from 100 mmHg to below 50 mmHg before ventilation is significantly stimulated (fig. 16.31). This stimulation is apparently due to a direct effect of PO2 on the carotid bodies. Since this degree of hypoxemia, or low blood oxygen, does not normally occur at sea level, PO2 does not normally exert this direct effect on breathing.
In emphysema, when there is a chronic retention of carbon dioxide, the chemoreceptor response to carbon dioxide becomes blunted. This is because the choroid plexus in the brain (chapter 8)
■ Figure 16.31 Comparing the effects of blood CO2 and O2 on breathing. The graph depicts the effects of increasing blood concentrations of CO2 (see the scale at the top of the graph) on breathing, as measured by the total minute volume. The effects of decreasing concentrations of blood O2 (see the scale at the bottom of the graph) on breathing are also shown for comparison. Notice that breathing increases linearly with increasing CO2 concentration, whereas O2 concentrations must decrease to half the normal value before breathing is stimulated.
secretes more bicarbonate into the cerebrospinal fluid, buffering the fall in cerebrospinal fluid pH. The abnormally high PCO2, however, enhances the sensitivity of the carotid bodies to a fall in PO2. For people with emphysema, therefore, breathing may be stimulated by a hypoxic drive rather than by increases in blood PCO2. Over a long period, however, the chronic hypoxia reduces the sensitivity of the carotid bodies in people with emphysema or other forms of chronic obstructive pulmonary disease, exacerbating their breathing problems.
The effects of changes in the blood PCO2, pH, and PO2 on chemoreceptors and the regulation of ventilation are summarized in table 16.6.
A variety of disease processes can produce cessation of breathing during sleep, or sleep apnea. Sudden infant death syndrome (SIDS) is an especially tragic condition that claims about I in 1,000 babies under 12 months in the United States annually. Victims are apparently healthy 2-to-5-month-old babies who die in their sleep for no obvious reason—hence, the layperson's term "crib death." These deaths seem to be caused by failure of the respiratory control mechanisms in the brain stem and/or by failure of the carotid bodies to be stimulated by reduced arterial oxygen. Since 1992, when the American Academy of Pediatrics began a campaign recommending that parents put infants to sleep on their backs rather than on their stomachs, the number of infants dying from SIDS has dropped by 38%.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...