Pupillary diameter and ventilatory CO2 sensitivity after epidural morphine and buprenorphine in volunteers.

The aim of this study was to correlate pupillary diameter with respiratory depression for 20 hr after epidural administration of morphine or buprenorphine. Pupillary diameter and the ventilatory sensitivity to CO2 were measured in six healthy volunteers at various times (0, 0.5, 1, 2, 3, 4, 6, 8, 10, 12, and 20 hr) in two sessions, separated by at least 1 week, at which either epidural morphine, 4 mg, or epidural buprenorphine, 0.15 mg, was administered randomly in a double-blind manner. Three of the six volunteers received 0.3 mg buprenorphine epidurally in a third session. Pupillary diameter was measured with a modified Essilor pupillometer. The ventilatory CO2 sensitivity was measured by a modified Read rebreathing technique. The ventilatory parameters measured were mouth occlusion pressure during the first 0.1 sec of inspiration (P0.1), end-tidal CO2 (PETCO2), tidal volume (VT) and respiratory rate (RR). Slopes of the linear regression lines (P0.1/CO2, VT/CO2, VE/CO2, and RR/CO2) and the intercept values of the regression lines and PETCO2 = 7.2 kPa (P0.1:7.2, VT:7.2, VE:7.2, and RR:7.2) were calculated. Pupillary diameter after epidural morphine was smallest at the second hour and had returned to normal after eight hours. After epidural buprenorphine there were two periods of miosis, one at 1-3 hr, the other at 10 hr. With epidural morphine, a statistically significant correlation (P less than 0.05) was found between pupillary diameter and VE/CO2, VE:7.2, P0.1:7.2, and VT:7.2. With epidural buprenorphine 0.15 mg a significant correlation was found between pupillary diameter and VE:7.2 and P0.1:7.2. With epidural buprenorphine 0.3 mg the correlations between pupillary diameter and VE:CO2, VE:7.2, and P0.1:7.2 were significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolonged and biphasic respiratory depression following epidural buprenorphine.

Ventilatory sensitivity to carbon dioxide was measured in six healthy volunteers before, and at various times up to 20 hours after, administration of epidural buprenorphine 0.15 mg with a modified Read rebreathing technique. The carbon dioxide response curves were depressed in a time-dependent, prolonged and biphasic manner. Significant depression was seen in the intercept values at an end tidal carbon dioxide of 7.2 kPa, for mouth occlusion pressure (p less than 0.01), tidal volume (p less than 0.05) and minute ventilation (p less than 0.05). A significant reduction of slope was obtained only for minute ventilation. Linear regression of respiratory rate changes during carbon dioxide stimulation, did not reach statistical significance. In conclusion, these data indicate that epidural buprenorphine, despite a high lipid solubility, causes respiratory depression to the same extent as epidural morphine. Surveillance of patients who receive epidural buprenorphine for postoperative pain relief is necessary.