anesthetic drugs pharmacology

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    ANESTHETICS DRUGS

    Depart. of Pharmacology and Therapy

    Medical School -Padjadjaran University

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    TERMINOLOGY

    ANESTHETICS :

    Drugs that caused anesthesia

    ANESTHESIA :

    No pain sensation

    TWO GROUPS OF ANESTHESIA :

    1. General Anesthetics

    2. Local Anesthetic

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    THEORYOF ANESTHESIA

    1. No stimuli from perifer

    2. Stimuli + Block at Gg. cervicalis sup

    3. Stimuli +

    No block at Gg. Cervicalis sup

    No interpretation

    4. Stimuli +No block

    interpretation +

    No response

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    GENERAL ANESTHESIA

    Analgesic, amnesic, unconscious state

    Muscle relaxation

    Suppresion of undesirable reflexes

    BALANCED ANESTHESIA

    PRE ANESTHETIC MEDICATION

    SKELETAL MUSCLE RELAXANTS

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    PRE ANESTHETIC MEDICATION

    SERVES TO :

    Calm the patient

    Relieve pain Protect against undesirable effects of the subsequently

    administered anesthetic or the surgical procedures

    INCLUDING :

    Hipnotic sedatives, anti histamines, anti emetics, opioids,

    anti cholinergics

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    STAGES OF ANESTHESIA

    STAGE I Analgesia

    STAGE II Excitement

    violent combative behavior

    BP

    Respiratory rate

    Reflexes

    Hyper secretion

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    STAGES OF ANESTHESIA

    STAGE III Surgical anesthesia

    Regular respirationSkeletal muscles relaxation

    Eye reflexes

    Eye movementsFixed pupil

    STAGE IV Medullary paralysis

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    STAGES OF ANESTHESIA

    PLANE I PLANE II PLANE III PLANE

    IV

    EYE

    Rovingmovment of

    eye ball.

    Myotic pupil

    midconstriction middilatation dilatation

    REFLEXES

    MUSCLE

    RELAXATION

    Small

    muscles

    Large muscles All muscles All

    muscles

    RESPIRATION Thoracal >

    Abdominal

    Thoracal =

    Abdominal

    Abdominal

    >

    Thoracal

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    EVALUATION

    Rhythm and automatization of respiration

    Conjunctival reflexes

    Gradually loss of Mm. Intercostales activity

    Fixated eye

    DEEP ANESTHESIA

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    GENERAL ANESTHESIA

    INHALATIONAL ANESTHETICS

    INTRAVENOUS ANESTHETICS

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    INHALATIONAL ANESTHETICSMECHANISM OF ACTION

    Non selective action

    Their clinically important effect on the CNS

    also alter the function of various peripheral

    cell types

    Site of action :Reticular activating system

    and cortex cerebri (controlling the overallstate consciousness and response to sensory

    stimuli)

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    INHALATIONAL ANESTHETICSTHE POTENCY

    Defined quantitatively as the MINIMUM ALVEOLAR

    CONCENTRATION (MAC)

    MAC :

    The concentration of gas anesthetic needed to eliminate

    movement among 50% of patient challenged by a

    standardized skin incision

    MAC is small for potent anesthetics and large for theless one

    The more lipid soluble an anesthesia, the lower the

    concentration of anesthetics needed to produce

    anesthesia

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    THE PHARMACOKINETICS OF

    INHALATIONAL ANESTHETICS

    Partial pressure of anesthetic gas driving

    force moves the anesthetics into the

    alveolar space blood brain and body

    compartment

    Steady state :

    The partial pressure in each of these compartments

    is equivalent to that in inspired mixtures

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    THE PHARMACOKINETICS OF

    INHALATIONAL ANESTHETICS

    The steady state depends on :

    Alveolar wash-in

    Solubility in blood

    Blood-gas partition coefficient

    halothane > enflurane > isoflurane > N20

    solubility faster achievement of steadystate

    Tissue uptake

    Wash-out

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    COMMON FEATURES OF

    INHALATIONAL ANESTHETICS

    Decrease cerebrovascular resistance

    resulting in increased perfusion of the brain

    Bronchodilation and decrease minuteventilation

    Potency does correlate with their solubility

    in lipid

    Recovery is due to redistribution from the

    brain

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    HALOTHANE

    Weak analgesic effect

    Vagomimetic, atropine-sensitive bradycardi

    Cardiac output , hipotension

    Cardiac arrhytmia, esp. to whom with hipercapnia

    and high concentration of blood catecholamine

    Toxic metabolites (trifluoroethanol + bromide ion) No hepatotoxic effect for children

    DOC for pediatric patient

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    ENFLURANE

    Less potent than halothane

    Rapid induction and recovery

    The metabolite (fluoride ion) excreted by kidney,

    so its contra indicated in patient with renal failure

    Some differences from halothane:

    Fewer arrhytmia

    less heart sensitization to catecholamines

    greater potentiation of muscle relaxants

    Intra ocular pressure

    Disadvantage : CNS excitation

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    ISOFLURANE

    Low biotransformation and low organ

    toxicity

    Doesnt induce cardiac arrhytmia

    No heart sensitization to catecholamine

    Less fluoride ion is produced

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    METHOXYFLURANE

    High solubility in lipid

    Not for prolonged adminiostration (toxic

    effect to the kidney)

    Indication : obstetrical practice (does not

    relax the uterus)

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    NITROUS OXIDE

    Potent analgesic, weak general anesthetic

    No respiration depression Less effect on CVS

    Increasing cerebral blood flow

    Less hepatotoxic effect

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    INTRAVENOUS ANESTHETICBARBITURATES

    Quickly enter the CNS depress function

    diffusion out of the brain redistributionto other body tissue

    Not significant analgesic

    ADR : apnea, coughing, chest wall spasm,laryngospasm, bronchospasm

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    BENZODIAZEPINES

    Lorazepam and Midazolam are more potent

    than diazepam Facilitate amnesia while causing sedation

    Etomidate : No analgesic effect

    uncontrolled skeletal muscle activity

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    OPIOIDS

    Analgesic effect

    Amnesic effect