Local anesthetic blocks Flashcards
mechanism of action of local anesthetics
- Bind to Na+ channels
– Prevent Na+ from entering the cell - Impede propagation of action potentials
– Cause a conduction blockade
chemical structure of local anestheitcs
aromatic ring: lipophilic
intermediate chain: (amide are the ones in current use)
amine: hydrophilic
Lidocaine onset time (min), duration (min), and clinical dose (mg/kg)
onset: 5-10
duration: 60-90
clinical dose: 2-5
Mepivicaine onset time (min), duration (min), and clinical dose (mg/kg)
onset: 5-10
duration: 90-120
clinical dose: 2-5
Bupivicaine/Ropivicaine onset time (min), duration (min), and clinical dose (mg/kg)
onset: 20-30
duration: 240-360
clinical dose: 1-2
what type of fibres do local anesthetics block?
-every fibre
-notable for pain:
>A-delta (fast pain, temp)
>C (slow pain)
active form vs diffusible chemical form of local anesthetic
DIffusable: RN
Active: RNH+
common uses for local anesthetics, and how they are performed
A. Analgesia/Anesthesia blocks for surgical procedures
* Peripheral administration
* Combined with Sedation or General Anesthesia
B. Equine lameness diagnosis
C. Lidocaine, intravenously
* Analgesic and MAC (minimum alveolar concentration) sparing effects of inhalant anesthetics
advantages of local anesthetics
- Used in standing animal (Large Animals)
- Used with sedation only
- Easy to perform
- decreased resistance/movement
- Inhibition of nociception
– Transduction
– Transmission
– Modulation (epidural, IV administration) - Reduced level of GA / sedation allows for:
– decreased adverse cardiopulmonary effects
– decreased doses of analgesics intra- and postoperatively and their side effects
complications with local anesthetic use
- Toxicity
-unintentional IV injection
-excessive doses
>toxicity dependent on several factors not just dose - Damage to surrounding structures
-traumatic technique, sepsis - Failure of technique
-lack of experience, anatomical abnormalities
how do ester vs amide local anesthitics differ in their toxicities?
- Esters = allergic reactions
- Amides = CNS, CV toxicity
2 examples of ester local anesthetics
Procaine, Tetracaine
describe the toxic process of an ester local anesthetic
– Hydrolysed by plasma cholinesterase
* Metabolite:Para-aminobenzoic acid (PABA) which is allergenic
* Chloroprocaine and tetracaine do not result in PABA
* Cocaine- also to norcocaine via N-demethylation
– USED LESS frequently nowadays
describe the toxic process of an amide local anesthetic
– Enzymatic degradation in liver
* N-dealkylation and Hydroxylation
– Then glucoronidation (cats are defficient)
* Metabolite: Aminocarboxilic acid and a cyclic aniline derivative
examples of amide local anesthetics
Lidocaine, Mepivacaine, Bupivacaine, Ropivacaine
toxicity of a local anesthetic mainly depends on what?
Toxicity = Due to plasma concentrations
-Depends on dose, site of administration, co- administration of other drugs, individual variation
-Depends on rate of absorption in area & vasculature
-Toxicity is additive if using more than one local anesthetic