Amide-linked local anesthetic agents, such as lidocaine and bupivacaine, can become "trapped" in their ionized forms on the fetal side of the placenta, and therefore their net transfer across the placenta is increased. An ester-linked local anesthetic agent, 2-chloroprocaine, is rapidly metabolized, and placental transfer is limited. Since the metabolism of 2-chloroprocaine by fetal plasma is slower than in maternal plasma, the potential for ion trapping exists. Fetal pH is slightly lower than maternal (7.32 to 7.38), thus most unionized drugs are "ion trapped" to a degree, even in a healthy fetus. Chloroprocaine (pKa 8.7) is the drug of choice for epidural analgesia and a decompensating fetus, because it does not participate in ion trapping. Placental transfer of 2-chloroprocaine is not influenced by fetal acidosis.^[2]

In vitro half-life of Chloroprocaine is 21 seconds for maternal and 43 seconds for fetal blood. In patients who are homozygous atypical for plasma cholinesterase, Chloroprocaine typically exists for two minutes in circulation.^[3][4]

Chloroprocaine should rarely be used in the subarachnoid space because of the risk of adhesive arachnoiditis. This is likely related to the preservative sodium bisulfate. It is also not used in IV regional anesthesia due to the risk of thrombophlebitis.