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LOCAL ANESTHETIC AGENTS
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History of local anesthesia
1500’s Accounts referring to Peruvian Indians chewing on leaves of the coco plant are found 1884 Cark Koller demonstrated the usefulness of the extract from these leaves[cocaine]as a topical anesthetic for the eyes, and earned distinction as the “father of local anesthesia 1884 Willium Halsted used cocaine in the first nerve block [ Inferior alveolar nerve block]. The use of cocaine for anesthesia produced several unwanted side effects including cardiac problem and addiction 1885 James Corning demonstrated the use of a tourniquet to slow absorption of cocaine
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History of local anesthesia
1901 Heinrich Braun demonstrated the use of epinephrine to retard local anesthetic absorption from the site of injection 1904 Alfred Einhorn introduced procaine . Epinephrine was needed to constrict the vessels in the area of administration to lengthen the duration of anesthesia. It was common to see a 1:50,000 concentration for many years 1943 Nils Lofgren introduced lidocaine 1947 Novocol company made the dental aspirating syringe available 1959 Disposable sterile needles made available by Cook- Waite, Roehr Company
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Physiology of nerve conduction
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Sodium-potassium Pump
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Channel Entry
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Local anesthetics: amides vs. esters
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Classification of local anesthetics
Amides Ester Bupivacaine Benzocaine Lidocaine Cocaine Mepivacaine Procaine Prilocaine
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Absorption Site of injection The dose of local anesthetic
Physicochemical properties of local anesthetic The addition of epinephrine
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Distribution Site of injection Systemic absorption heart brain
Skeletal muscle
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Biotransformation and Elimination
Aminoester Aminoamide Plasma esterase Hepatic enzyme Renal excretion
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สภาพของผู้ป่วยกับการขับถ่ายยา
อายุ – ผู้ป่วยสูงอายุขับถ่ายยาได้ช้าลง โรคตับ – ทำให้ half life ของยานานขึ้น cardiac output –ถ้ามี cardiac output ต่ำ จะขับถ่ายยาได้ช้าลง
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Potency: lipid solubility
Onset : pKa, concentration of local anesthetic
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(modified Henderson- Hasselbalch equation)
What is pKa? pKa = pH + log[ RNH+ ] [RN] (modified Henderson- Hasselbalch equation) pKa is the dissociation constant, represents the pH at which the concentration of the ionized base(RNH+) and the non-ionized base (RN) are equal.
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RNH RN H+ Outside membrane Inside membrane RNH RN H+
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Anesthetic pKa %RN at pH 7.4 Onset [min] Mepivacaine 7.6 40 2-4 Etidocaine 7.7 33 Articaine 7.8 29 Lidocaine 7.9 25 Prilocaine Bupivacaine 8.1 18 5-8 Procaine 9.1 2 14-18
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Example at physiologic pH (7.4)
Lidocaine Procaine pKa 7.9 3:1 ionized to non-ionized 8.9 32:1, ionized to non-ionized onset 2 to 3 minutes 6 to 12 minutes if lidocaine (pKa 7.9) is administered into an area of infection (pH 4.9) resulting 1,000:1 ionized to non-ionized indicates a poorer penetration into the nerve tissue and therefore a less effective nerve block
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Quinn and Malamed (1990) and Haegerstam (1990) suggested of administer L.A.
AWAY from the area of inflammation (nerve block) especially in the area of EXTENSIVE CELLULITIS Malamed. Handbook of LOCAL ANESTHESIA 1990. Haegerstam, Introduction to Dental Local anesthesia 1990.
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Duration of action Differential sensory/ motor blockade Adverse reaction
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Clinical use of local anesthesia
Topical anesthesia Infiltration Peripheral nerve block Epidural block Spinal block Intravenous regional anesthesia
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Toxicity
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Clinical sign and symptom LA toxicity
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CNS toxicity Potency The rate of intravenus administration
Acid base status and PaCO2
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Cardiovascular toxicity
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CC/CNS Ratio i.e. the ratio of the LA dosage required for irreversible cardiovascular collapse and the dosage that produces CNS toxicity (convulsions) the higher the CC/CNS ratio the better the safety margin
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Prevention Aspiration before injection Inject slowly
Use smallest quantity of solution and lowest concentration of vasoconstrictor Observe the patient after injection Choose another anesthetic if the patient has tendency for allergic reaction
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The signs and symptoms of allergic reaction include:
generalized body rash or skin redness itching, urticaria (hives) bronchospasm (difficulty breathing) swelling of the throat asthma abdominal cramping irregular heartbeat hypotension (low blood pressure) swelling of the face and lips (angioneurotic edema)
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Adverse reactions of commonly used local anesthetics
Methemoglobinemia associated with prilocaine, articaine, benzocaine Local tissue toxicity
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epinephrine
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Receptor Response Alpha stimulation Vasoconstriction
Peripheral resistance Beta 1 stimulation Heart rate Force of cardiac contraction Cardiac output Beta 2 stimulation Vasodilatation Bronchodilation Coronary blood flow
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Adverse reactions of vasopressor drugs
Signs Elevated BP, HR Symptoms Fear Anxiety Restlessness Throbbing headache Tremor Dizziness Pallor Respiratory difficulty Palpitations
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Contraindication for Epinephrine
Blood pressure over 200 torr systolic or 115 torr diastolic Uncontrolled hypertension Severe cardiovascular disease including less than 6 months after a myocardial infarction or cerebrovascular accident Daily episodes of angina pectoris or unstable angina Cardiac dysrhythmias despite appropriate therapy Medicated with beta blocker,monoamine oxidase inhibitor , or tricyclic antidepressant; or general anesthesia with a halogenated anesthetic like halothane
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New York Heart Association :
แนะนำว่าควรใช้ epinephrine ในขนาด 3 ug. / kg. Body weight แต่ไม่ควรเกิน 0.2 mg. (200 µg) หากผู้ป่วยมีปัญหาเกี่ยวกับ โรคความดันโลหิตสูง โรคหัวใจ ให้ใช้ Epinephrine ในขนาด 40 ug และสูงสุด ไม่ควรเกิน 54 µg ต่อการฉีดยาครั้งหนึ่ง
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วิธีคำนวณปริมาณของ Epinephrine
1 gm / 200,000 ml 1,000 mg / 200,000 ml 1 mg / 200 ml 0.005 mg / 1 ml
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ผู้ป่วยเด็กอายุ 2 ปี หนัก 12 กิโลกรัม
หกล้มมีแผลฉีกขาดที่นิ้ว ต้องเย็บแผล ควรใช้ยาชาชนิดใด ปริมาณและความเข้มข้นเท่าไร
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ผู้ป่วยชายอายุ 25 ปี น้ำหนัก 60 กิโลกรัม
ไม่มีโรคประจำตัว บอกวิธีการให้ยาชาและปริมาณยาที่ใช้กับผู้ป่วย
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