Clinical Implications
The profound depression of hypoxic responsiveness produced by
inhaled anesthetics suggests that patients may
Figure 6-22
The ventilatory responses to acute isocapnic hypoxia
(to approximately 44 mm Hg) in one subject during control (i.e., awake) and at 0.1
and 0.2 minimum alveolar concentrations (MACs) of isoflurane. Solid
bars indicate period A (2-minute period before induction of hypoxia) and
period B (minutes 3 and 4 of hypoxia). V̇E
, minute ventilation.
(Adapted from van den Elsen MJLJ, Dahan A, DeGoede J, et al: Influences
of subanesthetic isoflurane on ventilatory control in humans. Anesthesiology 83:478,
1995.)
have a diminished ventilatory response to hypoxemia in the recovery room for some
time after the agent has been discontinued. The presence of residual anesthetic
(particularly halothane) places the patient at greater risk of hypoventilation in
the absence of other stimuli (e.g., pain) or recovery room personnel activity. Stimulation
of the postoperative patient may attenuate the effects of low residual concentration
of anesthetics
Figure 6-23
Influence of 0.1 minimum alveolar concentration (MAC)
of five volatile anesthetic agents on the ventilatory response to a step decrease
in end-tidal oxygen concentration. Values are given as the mean ± SD. Subanesthetic
concentrations of the volatile anesthetics, except desflurane, profoundly depress
the response to hypoxia. (Adapted from Sarton E, Dahan A, Teppema L, et
al: Acute pain and central nervous system arousal do not restore impaired hypoxic
ventilatory response during sevoflurane sedation. Anesthesiology 85:295, 1996.)
on hypoxic drive. Intraoperative surgical stimulation reduces anesthetic-induced
respiratory depression to some degree, but a similar extent of stimulation does not
prevent impairment of hypoxia and hypercarbia chemoreflexes during administration
of a volatile anesthetic.[344]
[345]
These phenomena may be especially important in patients who depend to some degree
on a hypoxic drive to establish their level of ventilation (e.g., those with chronic
respiratory failure). Under these circumstances, the ability of patients to maintain
adequate spontaneous ventilation during administration of an inhaled anesthetic may
be severely impaired. There appear to be few clinically relevant differences between
volatile anesthetics in depression hypoxia-induced ventilatory response in these
patients.
It has been suggested that volatile anesthetics may augment the
inflammatory response during mechanical ventilation.[346]
[347]
However, in normal lungs of isoflurane-anesthetized
patients, short-term mechanical ventilation with high tidal volumes caused no clinically
relevant increase in systemic proinflammatory or anti-inflammatory cytokines in the
lungs of healthy, isoflurane-anesthetized patients.[348]
However, whether inhaled agents produce a proinflammatory response in pulmonary
parenchyma in the presence of lung disease remains unknown.
