Local Anesthetics Overview

The responsiveness of nerve fibers to local anesthetics, influenced by factors like fiber diameter, myelination, and the type of fiber.

Larger-diameter nerve fibers are less sensitive to local anesthetics than smaller ones.

Myelinated fibers are less sensitive to local anesthetics than unmyelinated fibers of the same diameter.

Local anesthetic inhibition generally follows: autonomic, then sensory, then motor, initially.

Local anesthetics have a lipophilic (fat-loving) and a hydrophilic (water-loving) portion, connected by an ester or amide linkage.

Local anesthetics are categorized as esters or amides based on the linkage type.

Clinical potency is linked to lipid membrane permeability and octanol solubility.

Adding larger alkyl groups to the local anesthetic molecule enhances anesthetic potency.

Potent local anesthetics can cause seizures at lower blood concentrations compared to less potent ones. Benzodiazepines, propofol, and hyperventilation can raise the seizure threshold. Acidosis lowers the seizure threshold.

Drugs that block nerve impulses by preventing sodium ion influx.

Propofol (0.5–2 mg/kg), benzodiazepines, or barbiturates can quickly and reliably stop seizure activity.

Membrane proteins that allow sodium ions to pass through, crucial for nerve impulse transmission.

Inhibition of sodium channels prevents nerve depolarization, thus blocking pain signals.

Lidocaine infusions can prevent ventricular arrhythmias, and decrease cerebral blood flow, affecting intracranial pressure.

Lidocaine and procaine infusions can reduce the minimum alveolar concentration (MAC) of volatile anesthetics, improving the effects of other anesthetics.

The pH at which a drug molecule is 50% ionized and 50% non-ionized.

Measure of how easily a drug dissolves in fats.

Lidocaine infusions can inhibit inflammation and reduce postoperative pain; in some cases, it can reduce opioid requirements and surgery recovery.

Measures the effectiveness of a local anesthetic, often correlated with octanol solubility and lipid membrane permeation.

Cocaine overdose presents with restlessness, vomiting, tremors, convulsions, arrhythmias, respiratory failure, and cardiac arrest.

Large volumes of chloroprocaine injected into the subarachnoid space during epidural attempts can cause total spinal anesthesia, hypotension, and neurological deficits.

Time it takes for a local anesthetic to start working, influenced by lipid solubility and the balance between ionized and non-ionized drug forms.

Chloroprocaine toxicity may result from its low pH and preservative sodium bisulfite.

Length of time a local anesthetic effect lasts, often tied to lipid solubility and how quickly it diffuses out of lipid-rich environments.

Injection of local anesthetics near nerve pathways to block a larger area of the body.

Administering 5% lidocaine in continuous spinal anesthesia has been linked to neurotoxicity (cauda equina syndrome).

The movement of a local anesthetic into the bloodstream.

Maintaining a clear airway with adequate ventilation and oxygenation is critical during local anesthetic use.

Amount of blood vessels in a region.

Membrane proteins allowing sodium ions to pass through nerves, crucial for impulse transmission

Blocking nerve impulses by preventing sodium influx.

How effective a local anesthetic is, often linked to lipid solubility and octanol.

The time it takes for a local anesthetic to start working.

Length of time a local anesthetic's effect lasts.

Movement of local anesthetic into the bloodstream

Amount of blood vessels in an area affecting anesthetic absorption.

The pH at which a drug is 50% ionized and 50% non-ionized.

How easily a drug dissolves in fats

Injecting local anesthetics near nerve pathways to block pain sensations.

Different nerve fibers react differently to local anesthetics based on diameter, myelination, and other factors. Smaller fibers are more sensitive.

The width of the nerve fiber; larger diameter fibers are less sensitive to local anesthetics.

Myelinated fibers (with a protective layer) are less sensitive to local anesthetics compared to unmyelinated fibers of the same diameter.

Local anesthetic effects generally appear in autonomic, then sensory, then motor nerves first, but all at steady state.

Local anesthetics have a lipophilic (fat-loving) and hydrophilic (water-loving) portion and an ester or amide linkage.

Classified as esters or amides based on the linkage between the lipophilic and hydrophilic portions.

Clinical potency is linked with the drug's lipid membrane permeability and octanol solubility, or how rapidly it dissolves in fat and alcohol.

Adding larger alkyl groups to a local anesthetic molecule increases its potency.

The pH at which half of the drug molecules are ionized (water-soluble) and half are non-ionized (lipid-soluble).

How easily a local anesthetic dissolves in fats.

The time it takes for a local anesthetic to start working.

The two forms of a local anesthetic: one water-soluble (ionized) and the other fat-soluble (non-ionized).

Factors affecting the minimum anesthetic concentration needed to block nerve impulse conduction.

Myelinated nerves are less sensitive to local anesthetics than unmyelinated nerves.

An acidic environment hinders nerve block formation.

The process by which local anesthetics enter the bloodstream after topical or injection application influenced by factors like skin integrity, and presence of vasoconstrictors.

Absorption through intact skin requires high concentration of lipid-soluble local anesthetic base.

Vasoconstrictors (e.g., epinephrine) decrease blood flow, reducing systemic absorption and prolonging the duration of local anesthetic action.

Vasoconstrictors more prominently affect duration of shorter-acting local anesthetics compared to longer-acting ones.

Lipid-soluble local anesthetics are absorbed more slowly than less lipid-soluble ones.

Highly perfused tissues (e.g., brain, heart) quickly remove local anesthetics from blood. A slower redistribution follows, to other tissues .

Distribution of local anesthetics depends on organ uptake dictated by tissue perfusion.

A cream containing lidocaine and prilocaine bases in an emulsion, formulated to enhance topical anesthetic absorption through intact skin.

Labor or delivery patients are at higher risk of aspiration, requiring immediate airway protection.

Succinylcholine stops muscle spasms but does not treat the cause of the problem(s).

Drugs like midazolam or propofol are used before succinylcholine to control seizures.

Bupivacaine causes more heart problems than lidocaine (at similar doses) due to slower sodium channel separation.

Acidosis, often after seizures, increases the risk of local anesthetic harming the heart.

Lipid emulsion is preferred over amiodarone to treat bupivacaine-related heart problems.

Epinephrine is used to treat low blood pressure (hypotension) from heart toxicity from local anesthetics.

Test doses and small amounts of local anesthetics reduce accidental intravascular injections during regional anesthesia.

Only the smallest dose needed for the procedure should ever be used during a regional anesthesia procedure

Ropivacaine, a pure S(-) isomer, appears to have a better safety margin (higher therapeutic index) compared to racemic bupivacaine.

Levobupivacaine, the S(−) isomer of bupivacaine, is no longer available in the United States.

Cocaine blocks norepinephrine reuptake, which intensifies adrenergic effects, leading to hypertension and ventricular ectopy.

Initial treatment for systemic cocaine toxicity involves benzodiazepines to manage central nervous system stimulation.

Cocaine-induced arrhythmias can be treated with α-adrenergic antagonists and amiodarone.

Topical application of cocaine causes vasoconstriction, aiding in reducing pain and epistaxis (nosebleed) during nasal intubation.

True allergic reactions to local anesthetics, involving antibodies, are rare compared to systemic toxicity from high doses.

Ester-type local anesthetics, especially those derived from PABA, are more likely to cause allergic reactions.

Direct injection of local anesthetics into muscle tissue can cause mild myotoxicity (muscle damage).

Prolonged local anesthetic infusion into joints can lead to severe chondromalacia (cartilage damage).

Lidocaine slightly inhibits blood clotting and enhances fibrinolysis (blood clot breakdown).