local anesthetic: pharmaodynamics and pharmacokinetics

2% pain lidocaine

What is no longer allowed in the US

1.8mL

How much L.A. solution is in each car pulse

0.5, 2, 3, 4%

What percentages are L.A. produced in

Sodium hydroxide and sodium chloride

What buffering agents are in L.A. solution

Epinephrine and Levonordefrin

What vasoconstrictors can be used in L.A.

Sodium bisulfite

What vasoconstrictor preservative can be used in L.A.

Sodium bisulfite

What potential component of L.A. solution can increase allergic reactions

Sodium bisulfite

What potential component of L.A. solution can decrease solution pH and delay onset

Methylparaben

What is no longer included in L.A. solution due to many reports of allergic reaction

Higher likelihood of allergic reactions and metabolized by pseudocholinesterase

What are characteristics of ester L.A.s

All injectables are amides, low cross hypersensitivity, metabolized by liver

What are characteristics of Amide L.A.s

Lipophilic Aromatic ring (base form), intermediate linkage, hydrophilic terminal amine (active form)

What is the chemical structure of L.A.s

Determines potency and allows L.A. molecule to cross the membrane (due to lack of H+ ion)

What is the function of the lipophilic aromatic ring (base form)

Determine if L.A. is an ester or amide

What is the function of the intermediate linkage

Dissociates and becomes tertiary amine that can gain an H+ ion inside the nerve and become functional

What is the function of the hydrophilic terminal amine (active form)

Acidic (more hydrophilic terminal amines)

What pH type is L.A. solution before injected

Vasodilators

Are all L.A. vasodilators or vasoconstrictors

Pka low= high amount lipophilic aromatic ring (base form)= rapid onset

How is L.A. function effected with pka is low

Causes L.A. to stay in the acidic hydrophilic terminal amine state that is unable to cross the membrane causing inadequate anesthesia

How does infected tissue effect L.A.s

8-10mm

How much myelinated nerve must be penetrated to cause adequate nerve block

Low pka*, High concentration of L.A., and smaller nerve

What causes rapid onset

As it travels across bodily fluids and anatomic barriers

How can L.A. loss concentration

High lipid solubility and vasoconstriction

What increases potency of L.A.

Small volume of additional L.A. is effective with rapid onset

What happens if you try to re-inject a nerve fiber that is partially recovered from its initial injection

Tachyphylaxis- increased tolerance to L.A. (L.A. ineffective)

What happens if you try to reinfect-inject a fully recovered nerve fiber from initial injection

High protein binding*, low vascularity of site, and high vasoconstriction

What increases duration of L.A.

Low protein binding

What decreases recovery time

Highly vascularized organs

When L.A.s are distributed after absorption, what tissue have the highest concentrations

High total dose, high concentration, and topical L.A., intravascular injection, lack on vasoconstrictor

What increase absorption

Risk for systemic toxicity increases

What happens if half life increases

Lidocaine, mepivaciane, and bupivacaine

What amides are metabolized by the liver only

Prilocaine

What amides are metabolized by the liver and lungs

Articaine

What amides are metabolized by plasma and liver

Articaine

What amide has the shortest half life

Plasma pseudocholinesterase

What metabolizes esters

2% 1:50,000 epi or 1:100,000 epi

What forms does lidocaine come in

3% plain or 2% 1:20,000 levonordefrin

What form does mepivacaine come in

4% plain or 1:200,000 epi

What form does prilocaine come in

4% 1:100,000 epi or 1:200,000 epi

What form does Articaine come in

0.5% 1;200,000 epi

What form does bupivacaine come in

Asthmatic patient or patient allergic to wine, dried fruit/potatoes

What may increase likelihood of bisulfide allergy

3% mepivacaine plain and 4% prilocaine plain

What are the short acting L.A. (30 mins)

0.5% bupivacaine 1:200,000 epi

What are the long acting L.A.s (90 min or more)

Moderate level of L.A. in blood= stimulation

High level of L.A. in blood= depression

What is the CNS effect of L.A.s

Mild overdose= slight stimulation

Moderate overdose= stimulation

High overdose= depression

What is the cardiovascular effect of L.A.s

0.2mg

What is the MRD for epinephrine For a healthy patient

1mg

What is the MRD for levonordefrin for a healthy patient

50% each

How does epinephrine effect alpha and beta receptors

Alpha-75% and beta-25%

How does levonordefrin effect alpha and beta receptors

Appears in 60 seconds and clears after 5-10 min

What happens during overdose of epinephrine

Allergy

What is the absolute contraindication of L.A.s

H2 receptor blocker, beta blocker, CNS depressant, pregnancy, liver disease, renal dysfunction

Whata re the relative contraindications for L.A.s

Prilocaine or lidocaine

What L.A.s should be used while pregnant

Articaine

What L.A.s should be used with liver disease

MI or coronary bypass with in 3-6 months, uncontrolled hypertension, angina, arrhythmia, hyperthyroidism, sulfite allergy, glaucoma, Cocaine/meth use

Whata re the absolute contraindications for vasoconstrictors

CV disease, non selective beta blocker, antidepressants, and digitalis

What are relative contraindications for L.A.

0.04mg or 0.2mg levonordefrin

What is the MRD of vasoconstrictors for CV disease or non selective beta blocker patients

0.04mg epi and no levonordefrin

What is the MRD for vasoconstrictors of patients on antidepressant