Local Anaesthetics - Specific Drugs MCQs

As previously discussed, this S (–) enantiomer of bupivacaine is somewhat less cardiotoxic than the racemic mixture. It is also less potent, and tends to have a longer duration of action, though the magnitude of these effects is too small to have any substantial clinical significance. Interestingly, recent work with lipid resuscitation suggests a potential advantage of levobupivacaine over ropivacaine, as the former is more effectively sequestered into a so-called lipid sink, implying greater ability to reverse toxic effects should they occur. Reference LANG’ Basic & clinical pharmacology by Bertram G. Katzung, Susen B. Masters and Anthony J. Trevor 12 th edition. Chapter 26- Local Anaesthetics by Dr. Kenneth Drasner,MD. Page no. 460

Aside from the issue of a high incidence of TNS with spinal administration, lidocaine has had an excellent record as an intermediate duration anaesthetic, and remains the reference standard against which most anaesthetics are compared. Reference LANG’ Basic & clinical pharmacology by Bertram G. Katzung, Susen B. Masters and Anthony J. Trevor 12 th edition. Chapter 26- Local Anaesthetics by Dr. Kenneth Drasner,MD. Page no. 460

Bupivacaine is the most cardiotoxic local anaesthetic At toxic doses, local anaesthetics can result in CNS (convulsions) or CVS (hypotension, bradycardia, arrhythmias) symptoms. Diazepam is used to treat convulsions. If not responding, thiopentone may be used. Arrhythmias should be promptly treated using bretylium, amiodarone, disopyramide, magnesium sulphate, esmolol or sotalol. Lignocaine should be avoided as antiarrhythmic because it canexacerbate the CNS toxicity. In refractory arrhythmias, intravenous lipid emulsion (like intralipid)has been found to be extremely useful. Bupivacaine induced cardiotoxicity is enhanced by acidosis, hypercarbia and hypoxemia.

Ropivacaine is an S (–) enantiomer in a homologous series that includes bupivacaine and mepivacaine, distinguished by its chirality, and the propyl group off the piperidine ring ( Table 26–1). Its perceived reduced cardiotoxicity has led to widespread use for high-volume peripheral blocks. It is also a popular choice for epidural infusions for control of labor and postoperative pain. Although there is some evidence to suggest that ropivacaine might produce a more favourable differential block than bupivacaine, the lack of equivalent clinical potency adds complexity to such comparisons. Reference LANG’ Basic & clinical pharmacology by Bertram G. Katzung, Susen B. Masters and Anthony J. Trevor 12 th edition. Chapter 26- Local Anaesthetics by Dr. Kenneth Drasner,MD. Page no. 461

Plasma cholinesterase (PChE), also known as pseudocholinesterase, butyrylcholinesterase, or serum cholinesterase, is a serine hydrolase from the family of human cholinesterase’s. Anesthetic drugs metabolized by PChE include succinylcholine, mivacurium, and all ester local anesthetics (e.g., cocaine, procaine, and chloroprocaine). PChE is produced in the liver, and its plasma half-life is approximately 8 to 12 days. Advanced age, pregnancy, chronic kidney failure, or specific gene variations may result in reduced PChE activity. Reference: FRCA A TO Z , page no 136

Inclusion of an anti-sialagogue in the preoperative medication is often recommended to decrease the likelihood of coughing and laryngospasm due to ketamine-induced salivary secretions Glycopyrrolate may be preferable , as atropine or scopolamine can easily cross the blood-brain barrier and could theoretically increase the incidence of emergence delirium Reference : Stoelting's pharmacology and physiology in anesthetic practice 5th edition

CNS or CVS systemic toxicity may result when standard lidocaine dose is administered to patient with circulatory failure because its concentration is initially higher in relatively well perfused tissue such as brain & heart And reduced cardiac output (in CHF) slows delivery of lidocaine (amide LA) to liver reducing their metabolism (to MEGX=mono ethyl glycine xylidide) à prolonging Lidocaine's plasma half life Toxicity of Lidocaine is due to its own concentration in blood NOT due to its toxic metabolite MEGX can cause seizures in neonates Reference : Stoelting's pharmacology and physiology in anaesthetic practice 5th edition

Ropivacaine has a higher therapeutic index and lesser cardiotoxicity as compared to bupivacaine This is because ropivacaine is the S (-) enantiomer of bupivacaine The cardiotoxicity of bupivacaine is due to the R (+) isomer which blocks the cardiac Na channel s more avidly and dissociates more slowly Ropivacaine is less potent Epidural ropivacaine is 40 % less potent than bupivacaine Ropivacaine has a shorter duration of action and produces less motor block than bupivacaine Reference: Morgan and mikhail's clinical anaesthesiology 6th edition