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Flashcards in Local Anesthetics Deck (24)

What role do local anesthetics play during intubation?

- attenuate sympathetic response to tracheal intubation
- decrease coughing during intubation and extubation
- are antiarrhythmic.


How are local anesthetics classified?

- Aminoesters
- Aminoamides


Name commonly used ester local anesthetics.

procaine, chloroprocaine, cocaine, and tetracaine


Name commonly used amide local anesthetics.

lidocaine, prilocaine, mepivacaine, bupivacaine, levobupivacaine, ropivacaine, and etidocaine


How are ester local anesthetics metabolized?

- Undergo hydrolysis by pseudocholinesterases found principally in plasma.


How are amide local anesthetics metabolized?

- Undergo enzymatic biotransformation primarily in the liver.


Which types of patients are at risk for ester LA toxicity?

- Patients with atypical pseudocholinesterase and severe liver disease in neonates


Which types of patients are at risk for amide LA toxicity?

- Patients with liver disease.


Which (amides or esters) are more likely to cause allergic reactions?

Esters produce metabolites related to p-aminobenzoic acid and are more likely to produce allergic reactions than are amide local anesthetics.


What determines local anesthetic potency?

The higher the lipid solubility, the greater the potency.


What determines local anesthetic duration of action?

The greater the protein binding, the longer the duration of action.


What determines local anesthetic onset time?

pKa and degree of ionization: the closer the pKa of the local anesthetic is to tissue pH, the more rapid the onset time.


Which regional anesthetic blocks are associated with the greatest degree of systemic vascular absorption of local anesthetic?

The rate of LA systemic absorption is greatest with intercostal nerve blocks > caudal > epidural injections > brachial plexus block > intravenous regional > femoral and sciatic nerve blocks > subcutaneous tissue


Why are epinephrine and phenylephrine often added to local anesthetics? What cautions are advisable regarding the use of these drugs?

- cause local tissue vasoconstriction --> limit uptake of LA into vasculature --> prolong effect and reduce toxic potential.

- Epinephrine, usually in 1:200,000 concentration, is also a useful marker of inadvertent intravascular injection.

- Contraindicated for digital blocks or other areas with poor collateral circulation.

- Systemic absorption of epinephrine may also cause HTN and cardiac dysrhythmias, and caution is advised in patients with ischemic heart disease, hypertension, preeclampsia, and other conditions in which such responses may be


How does a patient become toxic from local anesthetics?

Systemic toxicity is caused by elevated plasma LA levels, most often a result of inadvertent IV injection and less frequently a result of systemic absorption of LA from the injection site.


What are the clinical manifestations of local anesthetic toxicity?

CNS and cardiac toxicities are the most common.


What dose of intralipid do you administer in LA toxicity treatment?

Suggested dose is initial bolus of 1.5 ml/kg of 20% intralipid solution, which can be repeated every 3 to 5 minutes up to a total maximum dose of 8 ml/kg.


Describe transient neurologic symptoms.

TNS manifests in the form of moderate-to-severe pain in the lower back, buttocks, and posterior thighs.

- symptoms appear within 24 hours of spinal anesthesia and generally resolve within 7 days.

- Most commonly seen with lidocaine spinal anesthesia and are rare with bupivacaine.

- Patients having surgery in the lithotomy position appear to be at increased risk of neurologic symptoms following either spinal or epidural anesthesia.


Describe cauda equina syndrome in patients receiving LA.

Cauda equina syndrome is a serious neurologic condition where damage to the cauda equina causes acute loss of function of the lumbar plexus. A few cases of diffuse injury to the lumbosacral plexus were initially reported in patients receiving continuous spinal anesthesia with 5% lidocaine dosed via microcatheters. The mechanism of neural injury is thought to be that nonhomogeneous distribution of spinally injected local anesthetic may expose sacral nerve roots to a high concentration of local anesthetic with consequent toxicity. Rare cases in the absence of microcatheters have also been described.


Which local anesthetics are associated with the risk of methemoglobinemia?

Prilocaine and benzocaine


What agent do you give to treat methemoglobinemia?

Methylene blue IV 1-2 mg/kg.


Describe the role of lipid infusion in the treatment of local anesthetic toxicity.

Initially administer intralipid 20% at a dose of 1.5 ml/kg over 1 minute. Follow immediately with an infusion at a rate of 0.25 ml/kg/minute. Continue chest compressions (lipid must circulate). Repeat bolus every 3 to 5 minutes up to 3 ml/kg total dosage until circulation is restored. Continue infusion until hemodynamic stability is restored. Increase the rate to 0.5 ml/kg/min if blood pressure declines. A maximum total dose of 8 ml/kg is recommended.


What is the target of local anesthetics? Where is the binding?

Voltage-gated sodium channels. The binding is intracellular and mediated by hydrophobic interactions.


What is the order of progression of sensory and motor deficits with local anesthetic administration?

Loss of temperature sensation --> loss of proprioception --> loss of motor function --> loss of sharp pain --> loss of light touch

This concept refers to differential blockade, which historically has been thought to be related to diameter of the nerve fibers with the smaller fibers more susceptible to drug blockade than larger fibers.