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    08 .麻醉用藥 - 邱全秀

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    The document summarizes different types of intravenous anesthetic drugs used in anesthesia including opioids, muscle relaxants, and sedatives. It discusses the mechanisms of action, pharmacokinetics, pharmacodynamics, and key considerations for propofol, barbiturates, benzodiazepines, ketamine, etomidate, dexmedetomidine, succinylcholine, nondepolarizing muscle relaxants like rocuronium and cisatracurium, morphine, fentanyl, sufentanil, alfentanil, remifentanil, and the opioid antagonist naloxone. The document emphasizes proper drug selection and dosing to minimize adverse effects

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    08 .麻醉用藥 - 邱全秀

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    kenny631653
    4 views62 pages
    The document summarizes different types of intravenous anesthetic drugs used in anesthesia including opioids, muscle relaxants, and sedatives. It discusses the mechanisms of action, pharmacokinetics, pharmacodynamics, and key considerations for propofol, barbiturates, benzodiazepines, ketamine, etomidate, dexmedetomidine, succinylcholine, nondepolarizing muscle relaxants like rocuronium and cisatracurium, morphine, fentanyl, sufentanil, alfentanil, remifentanil, and the opioid antagonist naloxone. The document emphasizes proper drug selection and dosing to minimize adverse effects

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    麻醉用藥醫智庫講義

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    The document summarizes different types of intravenous anesthetic drugs used in anesthesia including opioids, muscle relaxants, and sedatives. It discusses the mechanisms of action, pharmacokinetics, pharmacodynamics, and key considerations for propofol, barbiturates, benzodiazepines, ketamine, etomidate, dexmedetomidine, succinylcholine, nondepolarizing muscle relaxants like rocuronium and cisatracurium, morphine, fentanyl, sufentanil, alfentanil, remifentanil, and the opioid antagonist naloxone. The document emphasizes proper drug selection and dosing to minimize adverse effects

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
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    4 views62 pages

    08 .麻醉用藥 - 邱全秀

    Uploaded by

    kenny631653
    The document summarizes different types of intravenous anesthetic drugs used in anesthesia including opioids, muscle relaxants, and sedatives. It discusses the mechanisms of action, pharmacokinetics, pharmacodynamics, and key considerations for propofol, barbiturates, benzodiazepines, ketamine, etomidate, dexmedetomidine, succinylcholine, nondepolarizing muscle relaxants like rocuronium and cisatracurium, morphine, fentanyl, sufentanil, alfentanil, remifentanil, and the opioid antagonist naloxone. The document emphasizes proper drug selection and dosing to minimize adverse effects

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    of 62

    麻醉部 醫智庫

    08-1. 靜脈麻醉用藥
    邱全秀 醫師
    學習大綱

    1. Intravenous injection
    2. 藥物個論
    3. BZD拮抗劑
    4. Key point
    Intravenous injection
    Intravenous injection
     管路
     管徑
     流速
     三讀五對
    三讀：
    藥時、拿藥時、放回時
    五對：
    病人、藥物、劑量、時間、途徑
    藥物個論
    Propofol of Dyspnea
    Mechanism of action
    Activation of GABA receptor

    Increase transmembrane Cl- conductance

    Hyperpolarization of post synaptic membrane

    Functional inhibition of the post synaptic membrane


    Pharmacodynamics
     Effect on the central nervous system decrease cerebral
    blood flow, cerebral blood volume and ICP
     Effect on the respiratory system profound respiratory
    depressant
     Effect on the cardiovascular system drop in systemic
    vascular resistance, preload and cardiac contractility
     Other effects
    Pharmacodynamics
     CNS
    mild degree of sedation to general anesthesia
    anticonvulsant effect
     Respiratory
    dose-related central respiratory depression
     CVS
    hypotension
    decrease heart rate
    circulatory collapse
     Induction and maintenance of anesthesia
     Sedation
     Side effect and contraindication
    pharmacokinetics
     Protein binding：95-99%
     Metabolism：Liver
     Onset of action：15-30 seconds
     Clearance：20-30min
     Duration of action：4-7min
    termination due to redistribution
     Excretion：Liver
    Barbiturates
     GABAA receptors：BZDs, barbiturate, zolpidem,
    zaleplon…

     Less selective in their actions than BZDs


     Also depress the actions of the excitatory
    neurotransmitter glutamic acid via binding to AMPA
    receptor
    Pharmacokinetics
     Metabolism：Liver
     Onset of action：30-45 seconds
     Clearance：huge diversity (4h – 12h)
     Duration of action：4-7min termination due to
    redistribution
     Excretion：Renal (60-90%)
     May precipitate an attack by stimulating γ-aminolevulinic
    acid synthetase, the enzyme responsible for the
    production of porphyrins.
    Benzodiazepines
     Agonists facilitate GABA actions
     Used for induction, maintenance and supplementing
    anesthesia as well as for conscious sedation
     In no anesthetic or opioid is given, the patient becomes
    responsive in 1hr. But, amnesia for 2-3hrs
     Poor analgesics
     Opioid or N2O is added, if the procedure in painful
     In larger doses injected produce sedation, amnesia and
    unconsciousness in 5-10mins
    Phencyclidines (Ketamine)
     Related to phencyclidine-dissociative anesthesia
     Act by inhibiting NMDA receptors
     Site of action：cortical and sub-cortical areas.
     Profound analgesia, immobility, amnesia, feeling of
    dissociation from ones own body
     Dose of 1-3mg/kg i.v. produces the above effects with a
    minute and recovery after 10-15mins, but reamnesic for
    1-2hr.
     Metabolized in the liver and has an elimination T1/2 3-4hrs.
    Etomidate
     Imidazole derivate, whose structure is unlike that of any
    other anesthetic
     For maintenance of anesthesia, and for prolonged
    sedation in critically ill patients
    Dexmedetomidine
     The α2 agonist with sedative and analgesic effect
     Half life：2-3hrs
     Metabolized in liver and excreted mainly as inactive urine
    metabolites
     Adverse effect：hypotension and bradycardiac
    BZD拮抗劑
    Flumazenil
     BZD antagonist, not antagonize the
    action of barbiturates or ethanol
     Competitive antagonist at the BZD
    receptor with minimal agonist activity
     Metabolism：Liver
     In patients using large doses of BZE over
    several weeks or longer, Flumazenil may
    elicit symptoms or withdrawal, including
    seizures.
    Key point
    Summary
     Combination of drugs
     Based on the individual patient’s need for hypnosis,
    amnesia and analgesia
     Drug selection must match the physiology and/or
    pathophysiology of the individual patient with the
    pharmacology of the particular drug(s).
     No single perfect drug for any particular patient.
    閱讀建議

     Miller 9th edition, chapter 23


    麻醉部 醫智庫

    08-2. 肌肉鬆弛劑
    邱全秀 醫師
    學習大綱

    1. 作用機制
    2. 藥物分類
    3. 逆轉方式
    作用機制
    Structure of neuromuscular junction

     Motor neuron
     Axon
     Nerve terminals
     Synaptic cleft
     Postsynaptic membrane
    PRESYNAPSE

    POSTSYNAPSE
    藥物分類
    Succinylcholine
     Succinylcholine = Ach-Ach
     The only one: rapid onset
    & ultrashort duration
     Rapid hydrolysis by
    butyrylcholinesterase
     Side effect
     Duration: 9 ~ 13 min
     0.6 ~1.0 mg/kg for intubation
    Nondepolarizing NMBDs

     Category: aminosteroids & benzylisoquinolinium


    compounds
    ex: rocuronium vs. cisatracurium
    Adverse effects of NMBDs
     Autonomic effects: only succinylcholine
     Histamine release (related to speed of injection)
     Allergic reactions: 1:10,000~20,000
    rocuronium
     0.6 ~ 1.0 mg/kg intubation dose
     Duration 30-40min
     No hemodynamic effects
     Rapid sequence induction
     Sugammadex
    cisatracurium
     Dose 0.15~0.2 mg/kg intubation dose
     Duration 30-45min
     Devoid of histamine releasing properties
    逆轉方式
    Neostigmine
     Reversible anticholinesterase inhibitor
     50 ~ 70 mcg/kg
     Increased Ach in the receptor
     Profound vagal stimulation
     administered with glycopyrrolate or atropine
    sugammadex
     Gamma cyclodextrin
     Aminosteroids group：rocuronium & vecuronium
     No cardiovascular adverse effects
     2~16 mg/kg dose required
    Special considerations
     Myasthenia gravis
     Myotonia
     Burns
     Muscular dystrophy
     UMN lesions
     Malignant hyperthermia
    (dantrolene)
    Key point
     Neuromuscular junction physiology and pathologic
    condition
     Type of muscle relaxant: nondepolarizing & depolarizing
     Interaction between inhaled anesthetics & antibiotics
     Drug selection (induction / maintenance)
    閱讀建議

     Miller 9th edition, chapter 12 & 27


    麻醉部 醫智庫

    08-3. 嗎啡類用藥
    邱全秀 醫師
    學習大綱

    1. 作用機制

    2. 藥物代謝

    3. 藥物個論

    4. 逆轉方式（解毒劑）
    作用機制
    Mechanism of opioid analgesia
     Brain
    inhibit directly the ascending transmission of nociceptive
    information activate pain control circuits that descend from the
    midbrain.
     Spinal cord
    morphine increased 5-HT release in the spinal dorsal horn in the
    spinal cord, opioids act at synapses either pre- or post - synaptically.
     Peripheral mechanism
    immune cells may release endogenous opioid-like substances
    Neurophysiologic effects of opioids
     Decrease cerebral metabolic rate, cause cerebral vasoconstriction
     neuroprotection
     Muscle rigidity
     Neuroexcitatory phenomena
     Pupil size
     Thermoregulation and shivering
     Pruritus
     Opioid-induced hyperalgesia (OIH)
    Respiratory effects of opioids
     Opioids’ most serious adverse
    effect：respiratory depression
     Opioids can affect pharyngeal
    function, airway protection, and
    coordination of breathing and
    swallowing.
     Incidence range from 0.1 ~ 37%
    depending on the route of
    administration
    藥物代謝
    Factors affecting PK & PD of opioids
     Age
     Body weight
     Renal failure
     Hepatic failure
     Cardiopulmonary bypass
     Acid-base changes
     Hemorrhagic shock
     Genetic variation in opioid metabolism
    藥物個論
    Morphine
     SNPs：cancer patients with SNPs (A118G) require more and
    longer opioids for pain management
     Low lipid solubility
     Metabolized by conjugation In the liver M3G & M6G
    Fentanyl
     Metabolites in the liver by N-dealkylation and hydroxylation.
     Norfentanyl , the primary metabolite, is detectable in the
    uring for up to 48h after IV injection.

     Mean plasma-brain equilibration half-times：


    fentanyl： 6.4min
    sufentanil： 6.2min
    alfentanil： 1.1min
    Sufentanil
     Potency ratio 2,000 ~ 4,000 times that of morphine.
     Potency ratio 10 ~ 15 times that of fentanyl.
     Highly selective μ-opioid receptor agonist
     Decrease MAC in a dose-dependent manner
     Metabolism in the liver by N-dealkylation & O-demethylation
     Clearance and elimination half-life in patients with cirrhosis
    are similar to controls.
    Alfentanil
     Potency ratio 10 times that of morphine.
     Potency ratio ¼ ~ 1/10 times that of fentanyl.
     Comparing to fentanyl, the duration of alfentanil is short.
     Mild ventilator depression, increased end-tidal CO2.
     Alfentanil can also cause bradycardia
     Clearance is just half that of fentanyl
     Lower lipid solubility
     Liver dx. Can significantly prolong the elimination half-life
    of alfentanil
    Remifentanil
     An ultrashort-acting opioid which is due to metabolism rather
    than to redistribution
     Metabolized by blood and tissue esterase
     It does not accumulate with repeated dosing or prolonged
    infusion
     Potency ratio 40 times that of
    fentanyl.
    Other opioid agonists
     Codeine
     Oxycodone
     Meperidine (pethidine / Demerol)
    metabolite, normeperidine, causes excitation of CNS, like
    seizure
     Hydromorphone
     Metadone
     Oxymorphone
     tramadol
    逆轉方式 (解毒劑)
    Naloxone
     Pure opioid antagonists at μ-, κ-, and δ- opioid receptors
     Restore spontaneous ventilation
     Reverse opioid-induced nausea and vomiting, pruritus,
    urinary retention, rigidity, and biliary spasm.
     Side effects：
    1. severe hypertension
    2. tachycardia and ventricular dysrhythmias
    3. produing sudden, severe pain in postoperative patients.
    Key point
     Opioids are a vital part of providing the analgesic
    component of anesthesia and often form the foundation
    for postoperative pain management.
     Opioids also affect multiple organ systems, including the
    respiratory and cardiovascular systems, and can cause a
    variety of adverse effects. Proper dosing and monitoring
    may minimize the adverse effects.
     Long-term treatment of chronic noncancer pain might
    increased risks of overdose and addiction.
    閱讀建議

     Miller 9th edition, chapter 24

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