What is Anesthesia

							What is Anesthesia?

 Franklin Scamman, MD
     Topics to Cover This Lecture
1.   What is “anesthesia”
2.   History and mechanism of anesthesia
3.   Uptake and distribution of inhaled anesthetics
4.   CNS effects of anesthesia
5.   Minimal alveolar concentration (MAC)
6.   Properties of inhaled anesthetics
7.   System effects of inhaled anesthetics
8.   Delivery systems for inhaled anesthetics
             “Anesthesia”
• Insensitivity to pain
• May be from local or general agents
• Term introduced by Oliver Wendell
  Holmes in 1847 in response to work by
  WTG Morton using ether
       History of Anesthesia
• Greeks and Romans: aware of opium and
  derivatives; oral ethanol
• Japan: 1820s, mandrake causing
  cholinergic crisis and unconsciousness
• TWG Morton, MGH, October 16, 1846
  using diethyl ether
• However, Crawford Long in 1849
  described his use of it in 1842
MGH “Ether Dome” 1846
      Mechanisms of Anesthesia

• No single macroscopic site of action
• Specific brain areas affected by inhalational
  Anesthetics causing amnesia
  –   Reticular activating system,
  –   Cerebral cortex
  –   Cuneate nucleus
  –   Olfactory cortex
  –   Hippocampus
• Anesthetics depress excitatory transmission in
  the spinal cord supressing movement
    Mechanisms of Anesthesia
• General anesthetic action could be due to
  alterations in any one of several cellular systems
  including ligand-gated ion channels, second
  messenger functions, or neurotransmitter
  receptors.
• Many anesthetics (the potent agents) enhance
  (GABA) inhibition of the central nervous system.
• Other agents (nitrous oxide and xenon) are
  NMDA agonists with good pain relief, just like
  ketamine
• Potency of inhalation agents correlates directly
  with their lipid solubility (Meyer–Overton rule)
Rate of Rise of Alveolar
    Concentration
    Factors Determining the Speed
             of Induction
•   Vaporizer setting (concentration)
•   Fresh gas flow
•   Alveolar minute ventilation
•   Blood-gas partition coefficient (solubility)
•   Cardiac output
•   Alveolar-to-venous partial-pressure difference
•   Brain-blood partition coefficient
•   Cerebral blood flow
 How fast do you go asleep?
The higher the blood/gas coefficient

The greater the anesthetic's solubility

The greater its uptake by the pulmonary
circulation.

 Alveolar partial pressure rises more slowly


Slow induction
     Many of the factors that speed
     induction also speed recovery
•   Elimination of rebreathing
•   High fresh gas flows,
•   low anesthetic-circuit volume,
•   low absorption by the anesthetic circuit,
•   Decreased solubility,
•   High cerebral blood flow,
•   Increased ventilation.
Minimal Alveolar Concentration
• Percent alveolar concentration to prevent
  purposeful movement in 50% of individuals
• Corresponds to the ED-50 of oral or IV drugs
• Lower at extremes of age
• Lower with other depressant drugs
• Lower in pregnancy
• Maximum at 37-39 degrees
• Maximum age 2-24 (roughly)
       Properties of the Vapors
              Desflurane   Nitrous   Isoflurane   Sevoflurane
                           Oxide

Blood/Gas       0.42        0.47       1.43          0.69


Brain/Blood     1.29        1.1        1.57          1.70


Fat/Blood       27.2        2.3        44.9          47.5


 MAC %           6.0        104         1.2           2.0
        Depth of Anesthesia
• Anesthesia depth can be assessed by
  – Lack of movement in non-paralyzed state
  – Respiration rate and pattern
  – Respiratory depression (ET CO2 and VE )
  – Eye signs
  – BP and P less valuable
  – BIS and Entropy analysis
         Respiratory Effects
• Abolish the hypoxic response at less than
  half MAC concentrations
• Fantastic bronchodilators by direct action
  on smooth muscle
    Cardiovascular Effects (1)
• All cause cardiac depression
• Cardiac depression causes an increased
  rate of concentration rise
• An increased concentration causes more
  cardiac depression
• Positive feedback -> cardiac arrest if not
  careful
    Cardiovascular Effects (2)
• Isoflurane and desflurane cause increased
  heart rate which may mask depression
• Systemic vascular resistance
  – Isoflurane and desflurane decrease (great for
    starting IVs)
  – Halothane and nitrous oxide do not change
             Renal Effects
• All decrease arterial pressure
• RBF and GFR will be maintained until
  threshold of autoregulation, absent other
  influences (sympathetic tone, renin)
• Urine output is variable, depending on
  ADH and aldosterone and other humeral
  agents
• Creatinine clearance not effected by UO