Uterine activity may be defined in terms of the frequency of contractions of the uterus and the pressure generated by these contractions. Most studies that report an effect of analgesia on labor are retrospective, and, if prospective, are nonrandomized. Drug effects on uterine activity and labor progress are probably dose related, but are also influenced by a myriad of other factors including, but not limited to, the mother's emotional state, degree of cervical change, uterine contractility pattern, phase of labor, and individual differences in pharmacokinetics and drug sensitivity. The latest phase of labor may be prolonged by excessive narcotic or inappropriate timing of regional analgesia. The normal active phase tends to be resistant to the inhibitory effects of the usual amount of any analgesia. A brief period of decreased uterine activity often follows institution of analgesia. This may effectually accelerate labor in some patients by decreasing maternal anxiety and serum concentrations of catecholamines. A combination of sedation epidural blockade, and subsequent oxytocin use may prove effective in correcting a dysfunctional or hyperstimulatory pattern during the active phase. The second stage of labor may be slightly prolonged by effective epidural analgesia, but this delay is not necessarily harmful as long as the fetal heart rate tracing is normal, maternal hydration is adequate, and maternal pain relief is sufficient.