CHLOROPROCAINE HYDROCHLORIDE- chloroprocaine hydrochloride injection, solution
Hospira, Inc.
Rx only
DESCRIPTION
Chloroprocaine Hydrochloride Injection, USP is a sterile, nonpyrogenic, isotonic, isobaric solution. Each milliliter of 2% solution contains 20 mg of chloroprocaine hydrochloride; 4 mg sodium chloride; with 1.8 mg sodium metabisulfite added in water for injection. Each milliliter of 3% solution contains 30 mg of chloroprocaine hydrochloride; 2.1 mg sodium chloride; with 1.8 mg sodium metabisulfite added in water for injection. May contain hydrochloric acid and/or sodium hydroxide for pH adjustment. It contains no bacteriostat, antimicrobial agent or added buffer. Discard unused portion.
It is intended for production of local anesthesia by nerve block, infiltration, caudal or other epidural blocks.
Chloroprocaine Hydrochloride Injection has a pH of 3.1 (2.7 to 4.0).
Sodium Chloride, USP is chemically designated NaCl, a white crystalline compound freely soluble in water.
Chloroprocaine Hydrochloride Injection is identified chemically as 2-(diethylamino) ethyl 4-amino-2 chlorobenzoate monohydrochloride. Its molecular Formula is: C13 H19 ClN2 O2 �HCl and the molecular weight is 307.22. It has the following structural formula:
structural formula chloroprocaine
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CLINICAL PHARMACOLOGY
Chloroprocaine, like other local anesthetics, blocks the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone.
Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block and ultimately to cardiac arrest. In addition, with toxic blood concentrations myocardial contractility may be depressed and peripheral vasodilation may occur, leading to decreased cardiac output and arterial blood pressure.
Following systemic absorption, toxic blood concentrations of local anesthetics can produce central nervous system stimulation, depression, or both. Apparent central stimulation may be manifested as restlessness, tremors and shivering, which may progress to convulsions. Depression and coma may occur, possibly progressing ultimately to respiratory arrest.
However, the local anesthetics have a primary depressant effect on the medulla and on higher centers. The depressed stage may occur without a prior stage of central nervous system stimulation.
