Search

We have determined that the mixed agonist-antagonist narcotic, butorphanol, improves CO2 response and ventilation after fentanyl anesthesia. A tentative dosage range has been established. Twenty-two patients were anesthetized with isoflurane, nitrous oxide, and fentanyl, which was continuously infused throughout the study. Postoperatively three 1-mg doses of butorphanol were administered IV. Blood pressure, heart rate, plasma epinephrine and norepinephrine concentrations, and pain intensity were essentially unchanged after butorphanol. Most of the improvement in breathing occurred after the first 1-mg dose. Mean respiratory rate increased from 7.8 +/- 5.0 to 11.0 +/- 4.8 min-1 (P less than or equal to 0.005), tidal volume increased from 469 +/- 302 to 844 +/- 390 ml (P less than or equal to 0.005), minute ventilation increased from 4.32 +/- 2.97 to 8.51 +/- 3.14 L/min (P less than or equal to 0.005), and the slope of the ventilatory response to CO2 increased from 0.36 +/- 0.37 to 0.90 +/- 0.80 L X min-1 X mm Hg-1 (P less than or equal to 0.05). Resting PaCO2 decreased from a baseline of 57.8 +/- 11.1 to 51.7 +/- 5.12 mm Hg (P less than or equal to 0.05) after the third dose.

Lower intercostal and abdominal muscles interact with other respiratory muscles to produce inspiration as well as expiration. Intercostal nerve blockade from T6-T12 was produced in seven healthy males to study its effect on: 1) supine pulmonary function, 2) inspiratory effort, 3) hypercapnic ventilatory response, including mouth occlusion pressures with and without an expiratory load, and 4) ventilation during progressive exercise on a cycle ergometer. Studies during control and blocked states were performed on different days. Lower chest and abdominal wall paralysis was documented with electromyography. Findings include a minimal decrease in peak expiratory flows with intercostal blockade (P = 0.02), but no other changes in supine resting pulmonary function tests, inspiratory effort, or hypercapnic ventilatory response slopes. Minute ventilation, respiratory rate, and VT/TI during exercise were also minimally increased, indicating an increase in the drive to breathe, which was unrelated to a change in metabolic rate. During exercise, total time to exhaustion was decreased following intercostal nerve blockade. Bilateral intercostal nerve blockade produced minimal decreases in peak expiratory flow at rest in supine subjects. During seated exercise, there was a slight increase in respiratory drive, probably due to minor alterations in the mechanics of breathing induced by intercostal blockade. The authors conclude that, in healthy young subjects, intercostal nerve blockade does not exert a clinically significant adverse affect on pulmonary mechanics and that ventilatory function is well-maintained even at extremes of ventilatory demand.