Local anesthetics provoke reversible blockade of nerves by interaction with sodium channels in membranes of nerves. The uncharged molecular configuration of the local anesthetic penetrates the membrane from the outside and the charged configuration then interacts with the sodium channel from the inside. The potency of a local anesthetic is determined mainly by lipid solubility, the time of onset by the pK(a) of the substance and the duration of action by protein binding. Local anesthetic molecules consist of a hydrophilic tertiary amine and a lipophilic aromatic system combined by an ester or amide linkage. Local anesthetics may therefore be classified as aminoester or aminoamide compounds. Aminoesters are hydrolysed by plasmacholinesterase whereas aminoamides undergo metabolisation in the liver. Aminoamides cause fewer allergic reactions. Local anesthetics show dose-dependent CNS and cardiac toxicity. Reports of toxicity, mainly involving bupivacaine and etidocaine initiated the development of ropivacaine which is the first aminoamide marketed as a pure S-enantiomer. Recently introduced was levo-bupivacaine, the S-enantiomer of bupivacaine.