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12 Cards in this Set
- Front
- Back
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4 features of all Local Anesthetics
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-reversible conduction block
-Act on every nerve fiber type -Also act of skeletal, cardiac muscle, and brain -Don't cause any structural damage |
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The Ideal local anesthetic
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-nonirritating
-short onset -long, but not too long duration |
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Chemical structure of local anesthetics
-Acidity -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) |
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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 |
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What do local anesthetics do to nerve firing?
-Amplitude -Rate of depolarization -Threshold -Impulse conduction -Refractory period |
-decrease AP amplitude
-slow rate of depolarization -increase firing threshold -slow impulse conduction -prolong refractory period |
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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 |
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Metabolism of local anesthetics
-Esters -Amides |
-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. |
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Physiochemical properites of local anesthetics
-potency -duration -rapidty of onset |
- Potency and duration: positive correlation with lipid solubility.
- pKa's closer to physiological pH have a faster onset |
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CNS toxicity
-Relation to lipid solubility -Early signs -Treatment |
-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. |
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CVS toxicity
-Where on dosage scale? -Direct cause? -What happens to the heart? -Treatment |
-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. |
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Bupivicaine exception to toxicity
-What? -Why? -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. |
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Clinical pearls and uses of
- Ropivacaine - Levobupivacaine - Prilocaine - Lidocaine - Cocaine - EMLA |
Ropivacaine
- s-isomer only; less cardiotoxic than bupivacaine Levobupivacaine - s-isomer only; less cardiotoxic than bupivacaine, but with the same sensory nerve blocking capability Prilocaine -metabolized to alpha-orthotoludine which in doses>600 mg causes methemeglobinemia Lidocaine -rapid onset, medium duration Cocaine -Numb and vasoconstrict nasopharynx EMLA -topical mixture of lidocaine and prilocaine. |
