Sevoflurane


  • Sevoflurane is a polyfluorinated isopropyl methyl ester
  • It is an achiral molecule
  • SEVoflurane has SEVen fluoride ions
Time constant graph

MAC Blood:gas coefficient Oil:gas coefficient Molecular weight Boiling point SVP at 20ºC Safe ppm
1.8% 0.7 80 200.1 58.5ºC 22.7kPa No set limit


One pot method

  • All the ingredients to make sevoflurane are mixed, then water added to 300ppm

Chloro-fluoro method

  • The basic molecular architecture is created but with chlorine molecules
  • Fluorine is then substituted for chlorine to produce sevoflurane

  • A Lewis acid is any substance that can accept an electron pair
  • It includes many metal oxides, H+ and glass

  • Sevoflurane is formulated with 300ppm water as this is an inhibitor of Lewis acids
    • If the concentration of water is <100ppm, the Lewis acids attack at sevoflurane's ether and halogen bonds
    • This releases the highly toxic substance hydrofluoric acid
  • Hydrofluoric acid can also corrode glass, exposing the sevoflurane to further Lewis acids
  • Sevoflurane is therefore kept in a polyethylene naphthalate bottle

  • A dry formulation containing <130ppm water is available, and kept in an aluminium bottle with an epoxyphenolic resin lacquer

Metabolism

  • 3.5 - 5% metabolised by CYP2E1 subfamily to:
    • Organic fluoride - hexafluroisopropanol (HFIP)
    • Inorganic fluoride ions (renal toxicity)
  • It is not metabolised to trifluoroacetic acid therefore not linked with hepatitis

Respiratory

  • Non-irritant with a pleasant odour
  • Dose dependent respiratory depression
  • Reduces VT to a greater extent than it stimulates respiratory rate, and therefore there is a rise PaCO2
  • Relaxes bronchial smooth muscle via histamine/acetylcholine

Cardiovascular

  • Reduces vascular resistance: SVR, coronary and cerebral circulations
  • Blood pressure is therefore reduced
  • There is, however, no change to splanchnic blood flow

  • No catecholamine sensitisation
  • Can lengthen QTc

Neurological

  • Increases CBF and reduces CMRO2
  • Potentiates muscle relaxation, including some relaxation of the uterus
  • Can cause burst suppression on EEG
  • Purportedly some analgesic properties
  • Incidence of excitatory phenomenon on gas induction/waking most common with sevoflurane

  • In the presence of CO2 absorbers, sevoflurane forms compounds A-E
    • Only compound A and B are present in sufficient amount to analyse
    • Formation is favoured in KOH-based absorbents (vs. NaOH), especially when dry
    • Reaction releases heat and consumes sevoflurane

  • Compound A
    • A tri-fluoro-methyl vinyl ester
    • LC50 of compound A in rats is 300-400ppm after 3hrs
    • This suggests human nephrotoxic threshold of 150-200ppm

    • However, with flow rates of 0.25L/min for 5hrs, peak compound A concentration <20ppm and no change to renal function
    • Humans also have 20x reduced levels of β-lyase vs. rats and therefore there is reduced conversion of compound A to toxic metabolites
    • Evidence demonstrates sevoflurane use does not increase risk of renal injury (BJA, 2022)
    • However some concern it may cause nephrogenic diabetes insipidus if used for prolonged sedation on ICU (BJA, 2022)