Local Anesthetics Flashcards
What is the aim of LAs?
Induce local analgesia, meaning local insensitivity to pain
Reduces pain and distress, an effective but safer alternative to GA
Relieves non-surgical pain and diagnoses chronic pain conditions
What do LAs do?
Cause loss of nociception by blocking afferent activity in PNS and CNS
What are the techniques of LA administration?
Topical
Plexus block
Spinal block
IV via Bier block
Trigger points
What are the adverse effects of LAs?
Localized prolonged anesthesia or paresthesia due to infection, hematoma, excessive fluid pressure in a confined cavity and severing of nerves and support tissue
Systemic reactions like depressed CNS syndrome, allergic reactions, vasovagal episodes, cyanosis etc due to injection into a highly vascularized area or accidentally into a BV
Name the amide group LAs
Lidocaine
Mepivacaine
Bupivacaine
Etidocaine
Prilocaine
Name the ester group LAs
Cocaine
Procaine
Chloroprocaine
Tetracaine
Difference between ester and amide LAs?
Ester link more prone to hydrolysis, therefore shorter duration of action
Charged vs uncharged LAs?
LAs are weak bases, dissociating more in acidic environments
Charged form is most active
Uncharged form penetrates lipid membranes
Therefore less effective when injected into acidic tissue
Inject together with sodium bicarbonate to hasten onset
Effects of PK on LA onset?
LAs are injected directly around target nerves, so absorption and distribution do not affect onset much
Effects of PK on LA offset?
Determined by systemic absorption, entering BV and distributing to cause concentration around nerves to drop and dropping to below MEC
Determined by dosage, site of injection, tissue binding strength, use of vasoconstrictors and drug properties
Metabolism and excretion differ between ester and amide LAs, where ester types are rapidly hydrolysed in blood, whereas amide types are metabolised in the liver by CYP450
Therefore, amide type metabolism and excretion is lowered in patients with liver disease, reduced hepatic blood flow, and CYP450 inhibition/competition
Effects of PK on LA offset?
Determined by systemic absorption, entering BV and distributing to cause concentration around nerves to drop and dropping to below MEC
Determined by dosage, site of injection, tissue binding strength, use of vasoconstrictors and drug properties
Metabolism and excretion differ between ester and amide LAs, where ester types are rapidly hydrolysed in blood, whereas amide types are metabolised in the liver by CYP450
Therefore, amide type metabolism and excretion is lowered in patients with liver disease, reduced hepatic blood flow, and CYP450 inhibition/competition
How do LAs work?
They stop the action potential depolarization process by inhibiting sodium ion influx through sodium channels, prolonging repolarization and reducing depolarization
LAs are voltage and time dependent, preferably blocking nerve cells firing rapidly, and therefore LAs are more selective for pain fibers than motor fibers
Has side effects in CNS and heart
What kind of nerves are LAs preferential towards?
Rapidly depolarizing nerves
Smaller, typically unmyelinated nerve fibers
Nerve fibers on the periphery of nerve bundles
How do the durations of LAs differ from drug to drug?
Short acting: Procaine
Medium acting: Lidocaine
Long acting: Bupivacaine
How can the LA effect be prolonged?
Increasing dose
Adding vasoconstrictor
