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LOCAL ANESTHETIC AGENTS

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LOCAL ANESTHETIC AGENTS History of local anesthesia 1500 s Accounts referring to Peruvian Indians chewing on leaves of the coco plant are found 1884 Cark Koller ... – PowerPoint PPT presentation

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Title: LOCAL ANESTHETIC AGENTS


1
LOCAL ANESTHETIC AGENTS
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History of local anesthesia
  • 1500s 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 leavescocaineas 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

4
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
    150,000 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
9
Channel Entry
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Local anestheticsamides vs. esters
14
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

17
Distribution
  • Site of injection

Systemic absorption
heart
brain
Skeletal muscle
18
Biotransformation and Elimination
  • Aminoester Aminoamide
  • Plasma esterase Hepatic enzyme
  • Renal excretion

19
?????????????????????????????
  • ???? ???????????????????????????????
  • ?????? ????? half life ????????????
  • cardiac output ????? cardiac output ???
    ???????????????????

20
  • Potency lipid solubility
  • Onset pKa, concentration of local anesthetic

21
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.

22
  • RNH RN H

Outside membrane
Inside membrane
  • RNH RN H

23
Anesthetic pKa RN at pH 7.4 Onset min
Mepivacaine 7.6 40 2-4
Etidocaine 7.7 33 2-4
Articaine 7.8 29 2-4
Lidocaine 7.9 25 2-4
Prilocaine 7.9 25 2-4
Bupivacaine 8.1 18 5-8
Procaine 9.1 2 14-18
24
Example at physiologic pH (7.4)
Lidocaine Procaine
pKa 7.9 31 ionized to non-ionized 8.9 321, 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 1,0001
    ionized to non-ionized indicates a poorer
    penetration into the nerve tissue and therefore a
    less effective nerve block

25
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.

26
  • Duration of action
  • Differential sensory/ motor blockade
  • Adverse reaction

27
Clinical use of local anesthesia
  • Topical anesthesia
  • Infiltration
  • Peripheral nerve block
  • Epidural block
  • Spinal block
  • Intravenous regional anesthesia

28
Toxicity
29
Clinical sign and symptom LA toxicity
30
CNS toxicity
  • Potency
  • The rate of intravenus administration
  • Acid base status and PaCO2

31
Cardiovascular toxicity
32
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

36
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)

37
Adverse reactions of commonly usedlocal
anesthetics
  • Methemoglobinemia
  • associated with prilocaine, articaine,
    benzocaine
  • Local tissue toxicity

38
epinephrine
39
  • 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

40
Adverse reactions of vasopressor drugs
  • Signs
  • Elevated BP, HR
  • Symptoms
  • Fear
  • Anxiety
  • Restlessness
  • Throbbing headache
  • Tremor
  • Dizziness
  • Pallor
  • Respiratory difficulty
  • Palpitations

41
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

42
New York Heart Association
  • ?????????????? epinephrine ?????? 3 ug. / kg.
    Body weight ????????????? 0.2 mg. (200 µg)
  • ?????????????????????????? ??????????????????
    ???????? ?????? Epinephrine ?????? 40 ug
    ????????? ?????????? 54 µg ?????????????????????

43
?????????????????? Epinephrine
  • Epinephrine ???? 1 200,000
  • 1 gm / 200,000 ml
  • 1,000 mg / 200,000 ml
  • 1 mg / 200 ml
  • 0.005 mg / 1 ml

44
??????????????? 2 ?? ???? 12 ???????? ????????????
??????????? ??????????? ???????????????? ?????????
?????????????????
45
?????????????? 25 ?? ??????? 60
???????? ???????????????? ????????????????????????
????????????????????
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