Overview. Normally, the process is completely reversible.
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2 Overview Local anesthetics produce a transient and reversible loss of sensation (analgesia) in a circumscribed region of the body without loss of consciousness. Normally, the process is completely reversible.
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4 Local anesthetics are generally classified as either esters or amides and are usually linked to: a lipophilic aromatic group to a hydrophilic, ionizable tertiary (sometimes secondary) amine. Most are weak bases with pka ( 8 9), and at physiologic ph they are primarily in the charged, cationic form.
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6 The potency of local anesthetics is positively correlated with their lipid solubility, which may vary 16-fold, and negatively correlated with their molecular size.
7 These anesthetics are selected for use on the basis of: 1. the duration of drug action Short: 20 min Intermediate: hrs Long: 2 4 hrs 2. effectiveness at the administration site 3. potential for toxicity
8 Mechanism of action Local anesthetics act by blocking sodium channels and the conduction of action potentials along sensory nerves. Blockade is voltage dependent and time dependent.
9 a. At rest, the voltage-dependent sodium (Na+) channels of sensory nerves are in the resting (closed) state. Following the action potential the Na+ channel becomes active (open) and then converts to an inactive (closed) state that is insensitive to depolarization. Following repolarization of the plasma membrane there is a slow reversion of channels from the inactive to the resting state, which can again be activated by depolarization.
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11 During excitation the cationic charged form of local anesthetics interacts preferentially with the inactivated state of the Na+ channels on the inner aspect of the sodium channel to block sodium current and increase the threshold for excitation.
12 b. This results in a dose-dependent decrease in impulse conduction and in the rate of rise and amplitude of the action potential. This is more pronounced in rapidly firing axons Local anesthetics gain access to the inner axonal membrane by: 1. traversing sodium channels while they are more often in an open configuration. 2. passage directly through the plasma membrane.
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14 Pharmacologic properties 1. Administration and absorption a. Local anesthetics, except cocaine, are poorly absorbed from the GI tract. They are administered: topically, by infiltration into tissues to bathe local nerves, by injection directly around nerves and their branches by injection into epidural (on or outside the dura mater) or subarachnoid spaces.
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16 a. The rate and extent of absorption to and from nerves determines: the rate of onset of action termination of action the potential for systemic adverse effects. Absorption rate depends on: relative lipid solubility of the uncharged form the dose the drug's physicochemical properties tissue blood flow drug binding.
17 i. Reduced ph, as in inflamed tissues, increases the prevalence of the cationic form, which reduces diffusion into nerves and thereby reduces local anesthetic effectiveness. ii. Carbonation of local anesthetic solutions (saturation with carbon dioxide) can decrease intracellular ph, which increases the prevalence and activity of the cationic active form inside the nerve.
18 c. All local anesthetics, except cocaine, are vasodilators at therapeutic doses. Coadministration of a vasoconstrictor (e.g., epinephrine) with a local anesthetic (generally of short or intermediate duration of action) reduces local blood flow. This reduces systemic absorption of the local anesthetic from the site of application, prolongs its action, and reduces its potential for toxicity.
19 Epinephrine: should not be coadministered for nerve block in areas such as fingers and toes that are supplied with end-arteries because it may cause ischemia or necrosis it should be used cautiously in patients in labor and in patients with thyrotoxicosis or cardiovascular disease.
20 2. Metabolism a. Ester-type local anesthetics are metabolized by plasma butyrylcholinesterase and thus have very short plasma half-lives. The metabolic rate of these anesthetics is decreased in patients with decreased or genetically atypical cholinesterase.
21 b. Amide-type local anesthetics are metabolized at varying rates and to varying extents by hepatic microsomal enzymes (dealkylation and conjugation). They are excreted in metabolized and uncharged form by the kidney. The rate of metabolism of these anesthetics is decreased: in patients with liver disease or decreased hepatic blood flow, or by drugs that interfere with cytochrome P-450 enzymes (e.g., cimetidine, alfentanil, midazolam).
22 Specific drugs and their therapeutic uses 1. Amides a) Lidocaine, articaine Lidocaine is the prototype amide it has an intermediate duration of action. Lidocaine is generally preferred for: infiltration blocks epidural anesthesia. the duration of drug action 1. Short: 20 min 2. Intermediate: hr 3. Long: 2 4 hr Articaine has a rapid onset of action with the same pka and toxicity as lidocaine.
23 b) Mepivacaine intermediate duration of action that is longer than that of lidocaine. Actions: similar to those of lidocaine it causes less drowsiness and sedation. Mepivacaine is not used topically.
24 c) Prilocaine intermediate duration of action that is longer than that of lidocaine. Actions: similar to those of lidocaine less toxic than lidocaine. Prilocaine should not be used in patients with cardiac or respiratory disease or in those with idiopathic or congenital methemoglobinemia Hgb methylene blue Prilocaine O-toluidine Hgb methemoglobin
25 d) Bupivacaine, Ropivacaine, Etidocaine These drugs have a long duration of action. Bupivacaine has greater cardiotoxicity than other amide local anesthetics. Ropivacaine may have less cardiotoxicity than bupivacaine. Etidocaine has a rapid onset of action.
26 2. Esters a) Procaine (prototype) Procaine is short-acting. Procaine is not effective topically. b) Chloroprocaine Chloroprocaine is very rapidly metabolized by plasma cholinesterase. Chloroprocaine has less toxic than procaine.
27 c) Cocaine Cocaine is a short-acting used only for the topical anesthesia of mucous membranes. Cocaine is a schedule II controlled substance that is subject to abuse.
28 d)tetracaine Tetracaine is long acting but has a slow onset of action (>10 min). Tetracaine is often preferred for: spinal anesthesia ophthalmologic use.
29 e) Dibucaine Dibucaine is long acting but has a slow onset of action (15 min). Dibucaine is used only for: topical spinal anesthesia.
30 f) Benzocaine and butamben picrate. These anesthetics are used topically only to treat sunburn, minor burns, and pruritus. g) Proparacaine used topically for ophthalmology due to: rapid onset short duration.
31 3. Other local anesthetics a) Dyclonine has a rapid onset of action used topically. b) Pramoxine used topically too irritating for the eye or nose.
32 Adverse effects and toxicity of local anesthetics Adverse effects are generally an extension of therapeutic action to block the membrane sodium channel. They are usually the result of overdose or inadvertent injection into the vascular system. Systemic effects are most likely to occur with administration of the amide class.
33 Adverse CNS effects include light-headedness, dizziness, restlessness, tinnitus, tremor, and visual disturbances. Lidocaine and procaine may cause sedation and sleep. At high blood concentrations, local anesthetics produce nystagmus, shivering, tonic-clonic seizures, respiratory depression, coma, and death.
34 Adverse cardiovascular system effects: Develop at relatively higher plasma levels than do adverse CNS effects. Bradycardia develops as a result of the block of cardiac sodium channels and the depression of pacemaker activity. Hypotension develops from arteriolar dilation and decreased cardiac contractility.
35 Allergic reactions include rare rash, edema, and anaphylaxis. These reactions are usually associated with estertype drugs that are metabolized to derivatives of paraaminobenzoic acid.
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