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General Anesthetics (Preanesthetic Medication: 6 As (Anxiolytics: BDZ,..,…

- - - - Volatile (enflurane, isoflurane, desflurane, sevoflurane)
        
        halothane: Narrow margin of safety; high solubility--> slow induction and recovery;
      - gaseous ([xenon])
        
        nitrous oxide: Extremely fast absorption & elimination; low solubility--> Rapid induction & recovery; excellent analgesic; Dentists, or personnel abusers at risk
    - - Uptake & Distribution
        
        A. Factors Controlling Uptake
        
        Inspired concentration and ventilation
        
        Higher inspired [ ]= more rapid induction
        
        Higher ventilation rate = more rapid induction
        
        Solubility
        
        :arrow_up: Lipid solubility = :arrow_up: Potency = :arrow_down: MAC
        
        Lower solubility in blood = more rapid induction
        
        blood:gas partition coefficient: tendency for a given inhaled anesthetic to pass from gas phase of alveolus into pulmonary capillary blood; (an index of solubility);
        
        :arrow_up: Blood solubility =:arrow_up: b:g PC=:arrow_down: Speed of action
        
        Cardiac output
        
        Higher pulmonary blood flow = less rapid induction
        
        Alveolar-venous partial pressure difference
        
        MAC (Minimum Alveolar Concentration): anesthetic [ ] that produces immobility in 50% of pxs exposed to a noxious stimulus; the measure of potency of general anesthetics
        
        halothane: Potent (0.75)
        
        Nitrous Oxide: Low potency (>100); used for short procedures and in combination w/ other anesthetics
        
        Desflurane 6
        Sevoflurane 2
        Enflurane 1.7
        Methoxyflurane 0.16
        
        opiods--> decr MAC; MAC lower in infants and elderly
        
        B. Elimination
        
        1. Ventilation
        
        Clearance by lungs: major route of elimination (Redistribution from brain to blood to air)
        
        Anesthetics relatively insoluble in blood and brain eliminated faster
        
        N2O not metabolized at all in body
        
        2. Metabolism by Liver
        
        halothane: 40% Oxidative metabolism--> chloro-tri-fluoro-ethyl free radical--> immune-mediated responses--> hepatitis
        
        methoxyflurane
        
        10% of isoflurane
    - - Organ System Effects of Inhaled Anesthetics
        
        A. CNS Effects
        
        Enflurane: Alter EEG pattern; Induces seizure in deep anesthesia
        
        Halothane: incr ICP
        
        B. Cardiovascular Effects
        
        Halothane: Sensitize myocardium to arrhythmogenic effects of catecholamines
        
        Isoflurane: Good coronary vasodilatation
        
        all volatile agents tend to decr mean arterial pressure in direct proportion to their alveolar [ ]
        
        halothane & enflurane: caused primarily by myocardial depression (reduced cardiac output) + little change in systemic vascular resistance (enflurane causes more severe resp cardiac depression)
        
        isoflurane, desflurane, and sevoflurane produce greater vasodilation w/ minimal effect on cardiac output; Isoflurane maintains CO and coronary function better than other agents
        
        C. Respiratory Effects
        
        nitrous oxide: The smallest effect on respiration
        
        All volatile anesthetics possess varying degrees of bronchodilating properties
        
        pungency of isoflurane & desflurane: less suitable for induction of anesthesia in pxs w/ active bronchospasm
        
        pungency reactions rarely occur w/ halothane & sevoflurane (nonpungent)--> agents of choice in pxs w/ underlying airway problems
        
        degree of ventilatory depression varies, w/ isoflurane & enflurane being the most depressant
        
        D. Renal Effects
        
        Depression of renal blood flow and urine output
        
        E. Hepatic Effects
        
        F. Effects on Uterine Smooth Muscle
        
        nitrous oxide: Low muscle relaxant effect, a disadvantage
        
        Isoflurane: Good muscle relaxation
        
        High enough concentrations will relax skeletal muscle
        
        Halothane: no muscle relaxant effect
      - Toxicity of Anesthetic Agents
        
        A. Acute Toxicity
        
        Nephrotoxicity
        
        Sevoflurane: Is degraded by contact with the CO2 absorbent in anesthesia machines, yielding a vinyl ether
        
        Enflurane: Metabolism releases fluoride
        ion--renal toxicity
        
        Methoxyflurane
        
        Hematotoxicity
        
        nitrous oxide: inhibits methionine synthetase (precursor to DNA synth) activity in long term use; Megaloblastic Anemia
        
        3. Malignant hyperthermia
        
        halothane
        
        Rare, genetically susceptible: Mutations in gene loci corresponding to ryanodine R (RyR1) & mutant alleles of gene-encoding skeletal muscle L-type calcium channels
        
        Uncontrolled release of Ca++ by SR of skeletal muscle--> muscle spasm, hyperthermia, Tachycardia, HTN, hyperkalemia tachypnea, metabolic acidosis, muscle rigidity, sweating, arrhythmia and May be fatal
        
        Treat w/ Dantrolene (blocks ryanodine R on SR) and supportive management
        
        4. Hepatotoxicity
        
        halothane: postoperative hepatitis (1 in 20-35k)
        
        B. Chronic Toxicity
        
        Mutagenicity, teratogenicity, and reproductive effects
        
        Carcinogenicity
      - Mechanisms of Action:
        
        Activate GABA-A, GlyR and K+ channels
        
        Block Na+ channels and NMDAR
        
        In general, all general anesthetics incr cellular threshold for firing--> decr neuronal activity
        
        Disrupt membrane lipids
  - - - Organ System Effects
        
        A. CNS Effects: Sedative-Anxiolytic effects; Anticonvulsant; anterograde Amnesia; onset of its CNS effects is slower than that of thiopental
        
        D. Other Effects: muscle relaxant;
      - slower onset and recovery
    - - Adrenocortical Suppression
        
        Dose dependent inhibits adrenal biosynthetic enzymes (11β-hydroxylase) required for the production of cortisol and some other steroids
        
        Can be used to treat hypercortisolemia
      - High incidence of nausea & vomiting; minimum effect on resp and cardiac; hypnotic
      - rapid effect; activates GABA R; not analgesic
    - - Rapid onset and recovery
      - pharmacodynamics
        
        :arrow_up: GABA R activity
        
        Organ System Effects
        
        A. CNS Effects: Poor analgesic; decr cerebral blood flow and ICP
        
        B. Cardiovascular Effects: circulatory depressants;
        
        C. Respiratory Effects: Respiratory depressants;
        
        D. Other Effects: poor muscle relaxant;
      - Clinical Uses: for induction of anesthesia and short surgical procedures
    - - Pharmacokinetics
        
        high lipid solubility of ketamine--> rapid onset of its effect
        
        Metabolism primarily in liver--> inactive metabolites excreted in urine
        
        [the only IV anesthetic] that has low pr binding
      - pharmacodynamics
        
        Organ System Effects
        
        B. Cardiovascular Effects: transient but significant incr in systemic BP, HR, and CO, [presumably by centrally mediated sympathetic stimulation]
        
        A. CNS Effects:
        
        [In contrast to other IV anesthetics]: a cerebral vasodilator that incr cerebral blood flow--> not recommended for use in pxs w/ incr ICP
        
        Psychotomimeticagent; a congener of phencyclidine; Unpleasant emergence reactions after administration: vivid colorful dreams, hallucinations, out-of-body experiences, and incr and distorted visual, tactile, and auditory sensitivity; less frequently in children; BDZs reduce it
        
        significant analgesia
        
        charac state after an induction dose: “dissociative anesthesia,”: px's eyes remain open w/ a slow nystagmic gaze (cataleptic state)
        
        inhibition of NMDA R
    - - Pharmacodynamics: Less pain at injection sites; Many pxs experience paresthesias
      - Pharmacokinetics: ALP-->propofol; Onset and recovery both slower than w/ propofol
    - - Centrally acting α2-adrenergic agonist
        Has analgesic and hypnotic actions
      - Is used mainly for short-term sedation in an ICU setting; short elimination half-life
    - - Fentanyl: Slow onset
        
        Recovery from actions of remifentanil faster than recovery from other opioids used in anesthesia bc of its rapid metabolism by blood and tissue esterases
        
        Incr tone of chest muscle
        
        Naloxone reversal available
      - Used in
        
        In combination w/ diazepam used in diagnostic, endscopic and angiographic procedures
        
        balanced anesthesia & conscious sedation;marked analgesia
        
        heart surgeries
    - - Rapid onset (60 sec) and recovery
      - Pharmacodynamics
        
        Organ System Effects
        
        B. Cardiovascular Effects: Vasodilation; :arrow_down: peripheral R
        
        C. Respiratory Effects: Dose dependent respiratory depression
        
        D. Other Effects: antiemetic; Pain during injection: reduced by local anesthetic combination
        
        A. CNS Effects: Sedative-Hypnotic agent BUT NO analgesic effects; :arrow_down: cerebral blood flow and ICP; neuroprotectant; anticonvulsant;
        
        Mechanisms of action: Potentiation of GABA-A R and inhibiting Na channel
      - Clinical Uses: Used in induction and for maintenance
  - - -  procedures of short duration
      -  supplementation of weak inhalation agents such as N2O
      -  induction for inhalation anesthesia (wide use)
    - -  Supplemented with analgesic and muscle relaxants
      -  Decrease vagal reflexes
      -  Prevention of postoperative nausea &vomiting