Dysfunctional labor and myometrial lactic acidosis.

OBJECTIVE

Inefficient uterine contractions are the most common cause of poor progress in labor. The global increase in cesarean delivery rate is a cause of considerable concern, and the greatest reason for increase is the result of failure to progress in labor. Following in vitro studies that showed acidification could depress uterine contraction, we hypothesized that it could contribute to dysfunctional labors.

METHODS

A blood sample was taken from the lower segment of the uterus from women having a cesarean delivery, either electively or as a result of dysfunctional labor, and from those having a normal labor. This blood sample was analyzed for pH, O(2) saturation, and lactate levels. Contraction was recorded in myometrial strips, taken from women having elective cesarean delivery, at the pH of normally and dysfunctionally contracting uteri.

RESULTS

The pH of myometrial capillary blood from women having a dysfunctional labor was significantly lower (7.35) than that from women having elective cesarean delivery (7.49) or cesarean delivery with normal contractions, with (7.47) or without (7.48) oxytocin (P <.001). The women in dysfunctional labor had higher capillary lactate and lower capillary O(2) saturation. Furthermore, in vitro, reducing the pH value from 7.5 to 7.3 changes regular uterine contractions to irregular ones of reduced amplitude.

CONCLUSIONS

Myometrial lactic acidosis and a small decrease in O(2) saturation may be contributing factors to dysfunctional labor. Our data may also account for the ineffectiveness in management of dysfunctional labor with oxytocin. Oxytocin with a background of lactate acidosis may not be successful.

LEVEL OF EVIDENCE

II-2