LA Flashcards
What is LA
any technique to induce absence of sensation in a specific part of the body
What are some non pharmacological methods of inducing LA
electrical nerve stimulation, nerve ablation, pulsed radiofrequency
What do LA drugs do
loss of nociception, blocks afferent activity in peripheral and CNS
What are some adverse effects of LA
prolonged anesthesia/paresthesia due to ( inflection, hematoma, excessive fluid pressure in a confined cavity)
- systemic reaction ( could inadvertently enter the systemic circulation when injected into blood vessel or region of highly vascularised area), leading to depressed CNS syndrome, allergic reaaction, vasovagal episode, cyanosis due to LA toxicity
what is the chemistry of LA
consists of lipophilic group connected via an ester or amide to an ionisable group
whats the difference in the duration of action between ester links and amide links
ester links have shorter duration of action as they are more prone to hydrolysis
what kind of LA are ester group
cocaine, procaine, chloroprocaine, tetracaine
what kind of LA are amide group
lidocaine, mepivacaine, bupivacaine, etidocaine, prilocaine
What form of LA is the most active
charged form as it cannot readily exit closed Na channel
What form of LA is important for rapid penetration of lipid membrane
Uncharged form, less effective when injected into acidic tissue as smaller proportion will be non ionised and available for diffusion into the nerve
What is LA onset of action determined by
offset of action and systemic toxicity, and not by absorption or distribution as LA are usually injected around nerves
What is systemic absorption of LA dependent on
dosage, site of injection, tissue binding, local blood flow, use of vasoconstrictors like epinephrine, drug properties
What is ester type LA hydrolysed by
circulating butyrylcholinesterases into inactive metabolites in the blood
What is amide type LA metabolised by
microsomal CYP450 isoenzymes in the liver.
What type of patients will experience reduced metabolism for amid type LA
reduced metabolism in patients with liver disease, reduced hepatic blood low, or if they are taking concomitant medications competing for or inhibiting cyp450 enzymes
How does the mechanism of LA work
it binds to receptor near intracellular end of sodium channel, inhibit influx of sodium ions through sodium channels. Usually when neurone stimulated, channel assume open state, sodium diffuse into cell, initiating depolarisation. But now further influx is denied while active transport mechanism return sodium to exterior
What is LA’s action on nerve dependent on
smaller fiber diameter( can only passively propagate electrical impulses over a short distance), faster firing frequency, fibre position on nerve fiber
What are the LA route of transmission
topical, plexus, spinal, IV
Compare the duration of LA for procaine, bupivacaine, lidocaine
short: procaine
medium: lidocaine
long: bupivacaine
How can anesthetic effect of LA be prolonged
- increase dose
- add vasoconstrictor
How to increase onset of action of LA
add sodium bicarbonate into solution
choose LA with rapid penetration of skin
What toxic effects do LA have
- Direct neurotoxicity,
- systemic toxicity from rapid absorption or accidental intravascular administration
- CNS( sleepiness, light headedness, visual and auditory disturbance, restlessness), nystagmus, muscle twitching
-CVS ( depress myocardial contractility, arteriolar dilation, systemic hypotension. Arrythmia
- Haematology
( accumulation of prilocaine metabolite may cause methemoglobinaemia
What does an accumulation of prilocaine metabolite cause
methemoglobinemia–> Fe2+ change to Fe3+ in haemoglobin, affecting its binding to oxygen
