Local Anesthetics Flashcards
Two classes of local anesthetics?
Ester, Amide
Ester anesthetics?
Procaine, Cocaine, Benzocaine, Tetracaine (Pros do Coke in Benzs while playing Tetris)
Amide anesthetics?
Mepivicaine, Lidocaine, Dibucaine, Prilocaine, Ropivicaine, Bupivicaine (Mark Leets Dubious Past Reeks Bad)
Cocaine?
Ester
Lidocaine?
Amide
Mepivicaine?
Amide
Bupivicaine?
Amide
Procaine?
Ester
Benzocaine?
Ester
Prilocaine?
Amide
Tetracaine?
Ester
Ropivicaine?
Amide
Dibucaine?
Amide
The aromatic ring of LAs determines? What portion of the LA is this?
Potency, Duration of Action. This portion is lipophilic.
The intermediate linkage of LAs determines?
The class: Ester or Amide
The terminal amine of LAs determines? What portion of the LA is this? What form of the LA is active? What form can cross membranes? How does this relate to pKa & pH? What happens as pKa increases? What happens in an acidic (abscess, inflammation) environment? Why would we mix an LA with sodium bicarbonate?
Onset of action. This portion is hydrophilic. The ionized form is active but the unionized form is the form that can cross membranes. So, the onset of action is ultimately related to the pKa of the LA & the pH of the local environment. All LAs have pKas greater than physiological pH (7.4). As pKa increases, more ionized form exists, meaning less unionized form, meaning less diffusion into cells, meaning longer time of onset. In an acidic environment, the ionized form is favored even greater, so onset is prolonged even more. Adding sodium bicarbonate will reduce acidity of the local environment, favor the unionized form, and speed onset.
What are ester LAs limited by? These are metabolize by?
Metabolized by plasma esterases. Limited by short duration (hydrolysis is rapid) & allergies (derivatives of PABA – a known allergen).
Amides are metabolized by?
Hepatic amidases
What is the MOA of LAs?
Bind and block the intracellular portion of the inactivated voltage gated sodium channel.
What is the time of onset in terms of nerve fibers? What other factors determine onset of block?
B (temperature) > C (pain) > Ad (pain) > Ag (proprioception) > Ab (touch & pressure) > Aa (motor). Size (smaller diameter, quicker), Meyelination (myelinated, quicker), Firing frequency (more often, quicker).
Absorption of LAs is determined by? Distribution? Metabolism/Excretion?
Absorption: Site (highly vascular? – ^), Vasoconstrictor (epinephrine? – v), LA used (highly protein bound? – v). Distribution: Perfusion, Tissue/Blood coefficient. Metabolism: Esterase, Amidase, Both classes excreted in kidney.
Systemic toxicity can affect which systems? List affects & treatments.
CNS. Cardiovascular . CNS: decreased inhibition, sensory disturbances, muscle twitching, seizures, coma, respiratory depression. Treat with ABCs, reverse seizures with benzodiazepines. Cardio: vasodilation, depresion, bradycardia, v.fib., arrest. Reverse with intralipid emulsion. Methemoglobinemia can also occur (tx with methylene blue).
Local toxicity can manifest as?
Transient neurological symptoms (TNS), Neuronal injury.
