Effects of Anesthetics on Ventilatory Response to
Chemical Stimuli
The effects of inhaled anesthetics on respiratory drive are typically
characterized by the ventilatory response to alterations in arterial carbon dioxide
tension or hypoxia. A complete discussion of chemical control of ventilation may
be found in several excellent reviews.[214]
[299]
[300]
Briefly, central and peripheral chemoreceptors
are critical to
Figure 6-20
Comparison of PaCO2
in anesthetized, spontaneously breathing patients relative to preoperative forced
expiratory volume in 1 second (FEV1.0
). Patients with chronic obstructive
pulmonary disease (COPD) did not exhibit carbon dioxide retention before anesthesia,
but the degree of alveolar hypoventilation is much greater in the more severely obstructed
patients. (Adapted from Pietak S, Weenig CS, Hickey RG, et al: Anesthetic
effects on ventilation in patients with chronic obstructive pulmonary disease. Anesthesiology
42:160, 1975.)
chemical control of respiration. Central chemoreceptors are located near the ventrolateral
medulla and other brainstem locations and respond to changes in hydrogen ion (H+
)
concentration in the cerebrospinal fluid but not to arterial carbon dioxide tension
or pH. Unlike H+
, carbon dioxide rapidly diffuses through the blood-brain
barrier. Central chemoreceptors are more profoundly affected by respiratory alterations
than by metabolic alterations in arterial carbon dioxide tensions. In contrast,
peripheral chemoreceptors located in the carotid bodies are sensitive to changes
in arterial carbon dioxide tension, pH and, most importantly, arterial oxygen tension.
The mechanisms by which peripheral chemoreceptive cells respond to hypoxia and hypercapnia
appear to be separate and synergistic, because hypoxemia potentiates the chemical
drive to a carbon dioxide challenge. Peripheral chemoreceptors appear to contribute
about one third to the total resting minute ventilation at normocapnia and normoxia
as determined by respiratory functional testing. This contribution falls to 15%
during hyperoxic normocapnia, suggesting that central chemoreceptors control 85%
of the carbon dioxide drive during hyperoxia. Both stimuli cause membrane depolarization
and activation of afferent nerve transmission.[301]
Hypercapnia may induce alveolar epithelial cell injury mediated by a NO-dependent
pathway.[302]
The consequences of these observations
on chemoreceptor function are unknown.
