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12 Cards in this Set

  • Front
  • Back
4 features of all Local Anesthetics
-reversible conduction block
-Act on every nerve fiber type
-Also act of skeletal, cardiac muscle, and brain
-Don't cause any structural damage
The Ideal local anesthetic
-short onset
-long, but not too long duration
Chemical structure of local anesthetics
-3 structural components
-All are weakly basic (HCl added to prolong shelf life)

1. Lipophilic aromatic ring
2. Intermediate aminoESTER (one "i") or aminoAMIDE (two "i"s)
3. Amino group, often with a chiral carbon atom that can affect toxicity. (ex: ropivacaine more cardiotoxic than levobupivacaine)
Neural blockade by local anesthetics:
-Site of binding
-Mechanism of action
-Affect on the membrane potential
-Binds to internal alpha subunit of sodium channels, but only in the open or inactive state
-Blocks the membrane permeability to sodium
-Ionic gradient and resting membrane potential are unchanged
What do local anesthetics do to nerve firing?
-Rate of depolarization
-Impulse conduction
-Refractory period
-decrease AP amplitude
-slow rate of depolarization
-increase firing threshold
-slow impulse conduction
-prolong refractory period
Distribution of local anesthetics
-Alpha phase
-Beta phase
-Gamma phase
-Alpha phase: rapid distribution to well perfused tissues

-Beta phase: less perfused tissues

-Gamma phase: clearance by metabolism and excretion
Metabolism of local anesthetics
-Esters are rapidly hydrolyzed in the plasma by pseudocholinesterase to PABA

-Amides are metabolized in the ER of hepatocytes; they thus have a greater risk of toxcitity.
Physiochemical properites of local anesthetics
-rapidty of onset
- Potency and duration: positive correlation with lipid solubility.

- pKa's closer to physiological pH have a faster onset
CNS toxicity
-Relation to lipid solubility
-Early signs
-Correlated to potency/L.S.
-Convulsions, numbness of tongue, visual problems, etc.
-Halt the injection. In case of seizures, hyperventitlate with 100% 0xygen to cause respiratory acidosis to decrease the effective dose; administer benzodiazepine or thiopental.
CVS toxicity
-Where on dosage scale?
-Direct cause?
-What happens to the heart?
-Occurs after CNS toxicity (except for bupivicaine)

-LA acts directly on the cardiac muscle itself

-Causes negative inotropic and chronotropic effects with ventricular arrhythmias.

-Treat with lipid emulsions (found in TPN)to "absorb" the LA.
Bupivicaine exception to toxicity
-D vs. S isomer
-Dysrhythmias (CVS) seen before and convulsions (CNS)

-Dissociates from the receptor slowly

- D-isomer is 40x more cardiotoxic than the s-isomer.
Clinical pearls and uses of
- Ropivacaine
- Levobupivacaine
- Prilocaine
- Lidocaine
- Cocaine
- s-isomer only; less cardiotoxic than bupivacaine

- s-isomer only; less cardiotoxic than bupivacaine, but with the same sensory nerve blocking capability

-metabolized to alpha-orthotoludine which in doses>600 mg causes methemeglobinemia

-rapid onset, medium duration

-Numb and vasoconstrict nasopharynx

-topical mixture of lidocaine and prilocaine.