CLASSIFICATION: ESTERS: Procaine, Chlorprocaine Amethocaine(Tetracaine).
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1 Local Anesthetics History The first local anesthetic was Cocaine which was isolated from coca leaves by Albert Niemann in Germany in the 1860s. The very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction. It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect. Kollar first introduced it to clinical ophthalmology as a topical ocular anesthetic. Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia. LOCAL ANESTHETICS o Reversible loss of sensation in a localized area without the loss of consciousness is called Local Anesthesia and the drugs producing this state are called Local Anesthetics. o Local anesthetics are the drugs that when applied directly to the peripheral nerves, block nerve conduction and abolish all sensations in area supplied by the nerve. CLASSIFICATION: Local anesthetics are divided into following groups. NATURAL: Cocaine. SYNTHETIC: Nitrogenous compounds: Non nitrogenous compounds: Non nitrogenous compounds: Benzyl alcohol Propanediol. Nitrogenous compounds: ESTERS: Procaine, Chlorprocaine Amethocaine(Tetracaine). AMIDES: Lignocaine or Lidocaine (Xylocaine), Cinchocaine, Bupivacaine, Mepivacaine and prilocaine.
2 MISCELLANEOUS AGENTS: Clove oil, Phenol, Chlorpromazine Certain antihistamine drugs. Local anesthesia may also be produced by application of ice. GENERAL PROPERTIES: All useful local anesthetics consists of three parts, these are: 1. Hydrophilic amino group. 2. Intermediate chain. 3. Lipophilic aromatic group. PHARMACOKINETICS: Local anesthetics are not absorbed from unbroken skin. When applied on mucous membrane their absorption varies with mucous surface and the agent used. Procaine can not penetrate mucosal cells and is not absorbed when applied on mucous membrane. The absorption of local anesthetics is rapid from trachea due to high vascularity. Local anesthetics are generally injected into the area of nerve fibers. Systemic absorption of local anesthetics from site of injection is modified by several factors such as dosage, site of drug administration, presence vasoconstrictor substance and physicochemical properties of the drug. vasoconstrictor agents: Epinephrine, a vasoconstrictor agent, reduces the systemic absorption of local anesthetics from site of injection by decreasing the blood flow in the area, this causes higher concentration of drug in the local area around the nerve fiber and increased uptake of the drug by nerve fiber. The coadministration of local anesthetics with epinephrine is beneficial in majority of the cases as increased neuronal uptake is associated with prolonged duration of the action and systemic toxicity of local anesthetics is reduced due to decreased absorption. vasoconstrictor agents: Phenylephrine, methoxamie, norepinephrine and other agonists can also be used for this purpose but epinephrine is commonly used. Cocaine itself produces vasoconstrictor effect and should not be combined with epinephrine. Epinephrine should not be used in ring block anesthesia and during surgery on penis. Ester type of local anesthetics are hydrolyzed in plasma by pseudocholinesterase, they have short plasma half lives and short duration of action. Amide type of local anesthetics are hydrolyzed by hepatic microsomal enzymes and toxicity from these drugs is more likely to occur in patients with liver disease.
3 MECHANISM OF ACTION: Local anesthetics prevent the generation and conduction of nerve impulse. Their main site of action is cell membrane. Local anesthetics block the conduction by decreasing the permeability of excitable membrane to sodium ions. This action of local anesthetics is due to their direct effect on voltage sensitive sodium channels. Local anesthetics bind with intracellular end of sodium channels. When increasing concentrations of local anesthetics are applied to a nerve fiber, the threshold for excitation is increased, impulse conduction slows, and the amplitude of action potential decreases and action potential generation is abolished. The incremental effects are due to the binding of local anesthetics to more and more sodium channels. The rapidly firing nerve fibers are more sensitive to local anesthetics than resting fibers. Elevated extra-cellular Ca+2 antagonize and elevated extra-cellular K+ levels potentiate the effects of local anesthetic. Order of sensory function block 1. pain 2. cold 3. warmth 4. touch 5. deep pressure 6. motor PHARMACOLOGICAL ACTIONS: ACTION ON NERVES: Small pain fibers are blocked first, other sensations disappear next and motor functions are blocked in the last, recovery of function appears to occur in reverse direction. Small fibers are blocked earlier than large fibers. Myelinated fibers are blocked earlier than unmyelinated fibers. Rapidly firing fibers are blocked earlier than resting fibers. CARDIOVASCULAR SYSTEM: Local anesthetics produce myocardial depression, decrease heart rate and force of contraction. Excitability threshold and refractory period are increased and conduction is slowed. In higher concentration local anesthetics produce ventricular fibrillation. Procainamide (related to procaine) and lignocaine are used in the treatment of cardiac arrhythmias. Cocaine produces vasoconstriction, all other agents produce vasodilatation and hypotension. CENTRAL NERVOUS SYSTEM: Local anesthetics initially have stimulant effect on CNS that is followed by CNS depression. They produce restlessness, tremors and in toxic doses convulsions, these effects are due to inhibition of inhibitory neuronal circuits. Cocaine in small doses causes euphoria, mental alertness and hallucinations. It is one of the commonly abused drugs.
4 Neuromuscular Junction and Ganglionic Synapse (1) Neuromuscular blocking action - +ACh release (2) Ganglionic blocking action Local Anesthetics and the Placenta (1) Cross placenta (2) Protein binding important Hyper-sensitivity Reactions 1) Occurs most prominently in response to local anesthetics of the ester type 2) Cross-sensitization exists-paraben, other ester types 3) Urticaria, angioedema, bronchospasm, laryngeal edema, hypotension 4) Amide-linked produce very infrequent episodes SIDE EFFECTS: INTOLERANCE: Allergic skin reactions Asthmatic attacks Severe anaphylactic reactions can occur, these are more common with ester type than amide type local anesthetics. o CARDIOVASCULAR SYSTEM: Hypotension, ventricular fibrillation and cardiac arrest. CENTRAL NERVOUS SYSTEM: Local anesthetics produce restlessness, excitation, tremors, visual and auditory disturbances, tonic clonic convulsions. The excitatory effects are followed by CNS depression. Local anesthetics apparently depress the cortical inhibitory pathways, thereby allowing unopposed activity of the excitatory pathways. In general, three categories of agents: Short action (20-45 min) o PROCAINE Intermediate action ( min) LIDOCAINE, o MEPIVACAINE, o PRILOCAINE Long action ( min) o TETRACAINE, o BUPIVACAINE, o ETIDOCAINE TYPES OF LOCAL ANESTHESIA: SURFACE ANESTHESIA: INFILTRATIVE ANESTHESIA.
5 NERVE BLOCK ANESTHESIA: SPINAL ANESTHESIA: TOPICAL BLOCK: PERIDURAL ANESTHESIA: OBJECTIVE Patient requiring anesthesia, administer anesthesia utilizing your knowledge of anesthesia pharmacology and applying the five rights, Right patient, Right drug, Right amount, Right route, Right time, in accordance with manual of anesthesia. Thank you!
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