VO2 and VCO2, mL/min, Multiples of resting level
FIGURE 11 Hypoxic ventilatory response measured in normal adults living at low altitude (controls), adults who were born at low altitude but who have lived at 3100-m altitude for 3-39 years (high-altitude residents), and adults who were born at 3100-m altitude and lived there all of their lives (high-altitude natives). The hypoxic ventilatory response is ''blunted'' between 100 and 60 mm Hg Pao2 in both high-altitude groups. This must be a physiologic mechanism in high-altitude residents, but a genetic component may be involved in high-altitude natives. (After Weil et al, J Clin Invest 1971;50:186.)
oxygen, called long-term oxygen therapy (LTOT). To put this in some perspective, a healthy person has Pao2 < 60 mm Hg when breathing room air at rest at 12,500 ft (3800 m) above sea level.
Ventilatory control in COPD patients is dominated by hypoxic stimulation of arterial chemoreceptors, in contrast to Paco2 being the most important determinant of resting ventilation in healthy subjects. For example, if a patient with COPD has an acute health problem that further impairs gas exchange (e.g., pneumonia), then it is often counterproductive to administer supplemental oxygen. In some patients, supplemental oxygen causes ventilation to decrease, presumably by relieving hypoxic stimulation of arterial chemoreceptors. This will increase Paco2 but it does not appear to stimulate central chemoreceptors as it would in normal subjects. The central chemoreceptors seem to be desensitized to increases in Paco2. Extremely high Pco2 levels
(80 mm Hg) may lead to respiratory failure and further depression through a narcotic effect of C02.
Patients with COPD can be classified into two groups: normal and elevated Paco2. CO2 retention (chronic increases in Paco2) is often associated with a decreased ventilatory response to C02. It is difficult to determine if this represents a time-dependent decrease in the responsiveness of central chemoreceptors, a deficiency in the motor output from the respiratory centers, or reduced function of ventilatory muscles. Increasing airway resistance decreases the ventilatory response to Paco2 in normal individuals, suggesting that patients with obstructive lung disease might retain C02 to minimize the work of breathing. Ventilation in patients with COPD and C02 retention behaves ''as if" the increased Paco2 is no longer increasing H+ ion in the central chemoreceptors. However, pH in the CSF, at least, remains acidotic in people with chronic increases in Paco2, so the mechanism of decreased central chemoreceptor responsiveness in some COPD patients remains unknown.
Ventilatory acclimatization would be expected to reduce the physiologic consequences of chronic hypox-emia, but it is not known if the changes described for ventilatory control in the previous section occur in patients with chronic hypoxemia or not. It is possible that abnormal ventilatory acclimatization in only some patients contributes to differences in the degree of hypoxemia and C02 retention between patients. Certainly genetic differences exist in the acute ventila-tory responses to arterial blood gases in healthy individuals.
Cherniack NS, Widdicombe JG, eds. Control of breathing, Vol II. In Handbook of physiology: Section 3, The respiratory system. Bethesda, MD: American Physiological Society, 1986. Dempsey JA, Forster HV. Mediation of ventilatory adaptations.
Physiol Rev 1982;62:262-346. Dempsey JA, Pack AI, eds. Regulation of breathing, Vol 79, 2nd ed. In Lung biology in health and disease. New York: Marcel Dekker, 1995.
Phillipson EA. Disorders of ventilation. In Isselbacher KJ, Braunwald E, Wilson JD, et al., eds., Harrison's principles of internal medicine, 13th ed. New York: McGraw Hill, 1994, pp 1234-1240.
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