ABSTRACT
Deranged control o f breathing and depression of ventilatory drive is common to most general anesthetic agents. Inhalational agents such as isoflurane and enflurane are quite potent in this regard, and their effects linger in proportion to the duration of the operation. These agents go largely unmetabolized and are distributed throughout tissues such as fat and muscle, ultimately to be eliminated by the lungs. Nitrous oxide (N20 ) has the least ventilatory depressant effects of the inhaled agents and is often used to lower the required concentrations of the other agents. Those volatile agents with the shortest biologic half-lives such as desflurane and sevoflurane allow this effect to be transient, with ventilatory drive normalized within 30 min postoperatively. Patients recovering from the use of any of the inhalation agents often have a rapid respiratory rate but a depressed tidal volume, predisposing them to atelectasis. Virtually all the inhaled agents markedly impair the ventilatory response to hypoxia, even at low concentrations. Intravenous narcot ics, barbiturates, propofol, and other agents are also potent inhibitors of ventilation, both to hypercarbia and hypoxia. However, the use of ultra-short-acting opiates such as remifentanil, a mu-receptor agonist, may minimize this effect to a few minutes postinfusion.
