Cocaine/Local Anesthetics

The local anesthetics group includes medications that block sodium channels, which in turn block the conduction of nociceptive impulses along nerve tissue. This action is of particular benefit in preventing and/or reducing pain from surgical procedures as well as assisting with minimizing and eliminating central sensitization or “wind-up.” 

Cocaine’s clinical effects were first described in 1884 when used topically to desensitize an eye for surgery at the Congress of the German Society for Ophthalmology23. Soon, other local anesthetics were developed, procaine in 1904, tetracaine in 1932.  Lidocaine, likely one of the most recognizable local anesthetics in veterinary and human medicine, was developed in 1943. 

Lidocaine is unique among local anesthetics in that it can also be administered intravenously as an adjunctive analgesic primarily beneficial for visceral pain and as an antiarrhythmic to treat ventricular premature contractions (VPC) or ventricular tachycardia (VT). 

Lidocaine given by continuous rate infusion (CRI) can provide minimal alveolar concentration (MAC) sparing effects, antiarrhythmic effects and visceral analgesia. It has the potential to modulate an inflammatory response, minimize the negative impact of endotoxemia and possibly act as a pro-kinetic24. It is also used clinically to spray the arytenoids of species prone to laryngeal spasm (i.e. cats, pigs, rabbits etc.) to assist with intubation.

Soon after lidocaine, other local anesthetics with applications in both human and veterinary medicine followed; mepivicaine (1956) and bupivacaine (1957), to name a recognizable few. This group of adjunctive analgesics is likely the most underused and cheapest, effective analgesic option veterinary practitioners have readily available. Minimal side effects occur when used as a local anesthetic by means of an infiltrative, regional nerve block or epidural if proper dosing and administration techniques are followed. 

Each local anesthetic has both a toxic dose and a specific duration. Cats are more sensitive to the toxic effects of lidocaine as they are not as effective at glucuronidation as dogs25. Observed toxic effects are vomiting in the conscious patient, ataxia, seizures or convulsions, followed by CNS depression and eventual respiratory and cardiac arrest26.Hypotension, vasodilation and respiratory depression are also early signals of toxicity in patients under anesthesia. 

In addition to its analgesic effects, there is evidence that lidocaine has antimicrobial effects27 and potentially improves wound healing28. Further investigation is required to see if these touted effects are real and are available at clinically recommended dose rates. 

Selecting the ideal local anesthetic depends on requirements for speed of onset and desired duration. Onset time can be influenced by the lipid solubility and pH of the agent (see table for onset times and durations of three commonly used veterinary local anesthetics). Systemic absorption of a local anesthetic may be influenced by a variety of factors, including the drug dose/volume used, the vascularity of the injection site and if a vasoconstrictor adjunct was utilized. 

Some local anesthetics have been developed into topical products like transdermal patches which can be applied over an incision or as eutectic mixtures (creams) that can be placed on intact skin. 

Local Anesthetic

Maximum Suggested Clinical Dose Rate

Onset time

Duration of action


Dogs 5 mg/kg

Cats 2-3 mg/kg

3-5 minutes

60-120 minutes


Dogs 5 mg/kg

Cats 2 mg/kg

5-10 minutes

90-180 minutes


Dogs 3 mg/kg

Cats 2 mg/kg

20-30 minutes

180-480 minutes