Desflurane

8 min read Last updated April 8, 2026

Where it fits clinically

  • Very rapid changes in depth due to low blood–gas solubility; useful when fast wake-up is desired.
    • Common use: maintenance of anaesthesia (often with TIVA/opioid adjuncts) where rapid emergence is advantageous (e.g. short cases, neuro, bariatrics).
  • Airway irritant: avoid for inhalational induction; can provoke coughing, breath-holding, laryngospasm.
    • Particularly problematic with high inspired concentrations or rapid increases.
  • Sympathoadrenal stimulation with rapid increases in concentration (tachycardia, hypertension).
    • Blunted by opioids, beta-blockers, and slower up-titration.
  • Requires a heated, pressurised vaporiser (Tec 6 / D-Vapor type) because of physical properties.
    • Not used in standard variable bypass vaporizers designed for other agents.

Immediate practical points

  • MAC in adults ≈ 6% (high MAC) → often needs adjuncts for balanced anaesthesia.
    • MAC decreases with age; lower requirements in elderly.
  • Low metabolism (~0.02%) → minimal risk of fluoride-related nephrotoxicity; very small hepatic biotransformation.
    • Main elimination is via exhalation.
  • Potent greenhouse gas; minimise fresh gas flows where appropriate and use scavenging.
    • Environmental impact is disproportionately high compared with sevo/isoflurane per MAC-hour.

Chemical & physical properties

  • Halogenated methyl ethyl ether; structurally similar to isoflurane but with fluorine substitution that reduces intermolecular forces.
  • Boiling point ~23°C (close to room temperature) → high vapour pressure (~669 mmHg at 20°C).
    • At room temperature it is near boiling; output from a standard variable bypass vaporiser would be unstable/inaccurate.
  • Blood:gas partition coefficient ~0.42 (very low) → rapid onset/offset; alveolar concentration tracks inspired concentration closely.
  • Oil:gas partition coefficient ~18–19 (low) → relatively low potency (high MAC).
  • Non-pungent? No: it is pungent/irritant compared with sevoflurane.

Pharmacodynamics (system effects)

  • CNS: dose-dependent depression; reduces CMRO2; cerebral vasodilation increases CBF and can increase ICP at higher concentrations (attenuate with controlled ventilation).
    • EEG: similar to other volatiles; burst suppression at high dose.
  • Cardiovascular: reduces SVR (vasodilation) → dose-dependent fall in arterial pressure; HR may increase especially with rapid concentration increases.
    • Myocardial depression is modest; CO often maintained by tachycardia.
    • Coronary steal: theoretical with potent coronary vasodilators; not clearly clinically significant in routine practice.
  • Respiratory: dose-dependent respiratory depression; bronchodilation but airway irritation can provoke reflex bronchoconstriction/coughing.
    • Rapid increases can cause breath-holding and laryngospasm, especially in light planes.
  • Neuromuscular: potentiates non-depolarising neuromuscular blockers.
  • Uterus: relaxant effect like other volatiles (dose-dependent).

Pharmacokinetics (uptake, distribution, elimination)

  • Low blood solubility → fast FA/FI rise and fall; emergence relatively independent of duration compared with more soluble agents.
    • Still influenced by context: high fat solubility is low-ish but prolonged cases can still accumulate in fat to some extent.
  • Metabolism ~0.02% (CYP2E1) → trifluoroacetic acid (TFA) and inorganic fluoride produced in very small amounts.
    • Much lower fluoride exposure than sevoflurane; clinically significant nephrotoxicity not expected.
  • Malignant hyperthermia trigger: yes (as with all potent volatile agents).

Vaporiser and delivery

  • Special vaporiser (heated to ~39°C and pressurised) delivers desflurane as a controlled vapour; output is not a simple function of fresh gas flow as in variable bypass designs.
    • Agent-specific filling system reduces misfilling risk; still requires vigilance.
  • Because MAC is high, inspired concentrations commonly 3–10% depending on stage, adjuncts, and age.

Adverse effects, cautions, and interactions

  • Airway reactivity: avoid in severe reactive airways or when smooth inhalational induction required; consider sevoflurane instead.
  • Sympathetic stimulation: rapid increases can cause tachycardia/hypertension and increased myocardial oxygen demand; caution in IHD, severe aortic stenosis, uncontrolled hypertension.
  • CO formation with desiccated CO2 absorbent: possible with all volatiles; risk increased with dry absorbent and prolonged high flows; modern absorbents reduce risk.
    • Sevoflurane has additional concern of Compound A; not a key issue for desflurane.
  • PONV: similar to other volatiles; risk reduction via multimodal prophylaxis and minimising volatile exposure where appropriate.
  • Environmental: high global warming potential; consider alternatives (TIVA, lower-impact volatiles) when clinically appropriate.

Comparisons (high-yield)

  • vs Sevoflurane: desflurane is more pungent/irritant; faster wash-in/wash-out (both fast, des often fastest); sevo better for inhalational induction.
  • vs Isoflurane: desflurane much less soluble (faster), higher MAC, requires special vaporiser; isoflurane is pungent but less airway-irritant than des at equivalent MAC changes.
Describe the key physical properties of desflurane and explain how they influence its clinical use.

Aim to link numbers to consequences (speed, potency, vaporiser requirements).

  • Blood:gas partition coefficient ~0.42 → very rapid changes in alveolar and brain partial pressure → fast onset and fast emergence.
  • Oil:gas ~18–19 → low potency → MAC ~6% in adults (age-dependent).
  • Boiling point ~23°C and vapour pressure ~669 mmHg → cannot be delivered accurately with a standard variable bypass vaporiser; needs heated, pressurised vaporiser.
  • Pungent/airway irritant → unsuitable for inhalational induction; can cause coughing, laryngospasm, breath-holding.
Why does desflurane require a special vaporiser? Outline the principle of its vaporiser.

This is a common viva theme: relate vapour pressure/boiling point to vaporiser design.

  • At room temperature, desflurane has very high vapour pressure and a boiling point near ambient → output from a variable bypass vaporiser would be excessive and unstable.
  • Desflurane vaporisers heat the agent (≈39°C) and pressurise it to produce a stable saturated vapour, then meter vapour into the fresh gas stream to achieve the set concentration.
  • Agent-specific filling and temperature/pressure compensation are used to maintain consistent output.
Explain why desflurane gives rapid wake-up. What factors still slow emergence?

Examiners want the solubility story plus context sensitivity and confounders.

  • Low blood solubility → little uptake into blood → alveolar partial pressure falls quickly when turned off → rapid decrease in brain partial pressure.
  • Emergence can still be slowed by: high alveolar concentration at end, long duration (some tissue accumulation), obesity (fat reservoir), low alveolar ventilation, high cardiac output (during wash-in), and co-administered sedatives/opioids.
  • Circuit factors: low fresh gas flows and large circuit volume can slow washout unless flows increased at end.
A patient becomes tachycardic and hypertensive shortly after you increase desflurane. Explain the mechanism and how you would manage it.

Classic desflurane-specific issue: sympathetic stimulation with rapid increases.

  • Rapid increases in inspired desflurane can stimulate airway receptors and sympathetic outflow → catecholamine release → tachycardia and hypertension.
  • Management: reduce/slow the increase in desflurane; deepen with opioid/propofol; treat haemodynamics (e.g. beta-blocker) if appropriate; ensure adequate analgesia and exclude other causes (light anaesthesia, hypovolaemia, hypercarbia).
Compare desflurane and sevoflurane for inhalational induction and for maintenance.
  • Induction: sevoflurane is non-pungent and better tolerated; desflurane is pungent/irritant → coughing, breath-holding, laryngospasm.
  • Maintenance: both allow rapid titration; desflurane often gives the fastest emergence, especially after longer cases, but may cause sympathetic responses with rapid increases.
  • Metabolism: desflurane ~0.02% (very low); sevoflurane higher metabolism with fluoride/Compound A considerations (mainly theoretical/low clinical risk with modern practice).
What are the cardiovascular effects of desflurane? How does it compare with other volatiles?
  • Dose-dependent reduction in arterial pressure mainly via decreased SVR (vasodilation).
  • Heart rate may rise, especially with rapid increases in concentration (more prominent than with sevoflurane).
  • Myocardial depression occurs but is usually modest; CO may be maintained by tachycardia.
Outline the effects of desflurane on the brain and intracranial dynamics.
  • Reduces CMRO2; causes cerebral vasodilation → increased CBF; at higher doses can increase ICP (especially if ventilation allows hypercapnia).
  • Control PaCO2 with ventilation to mitigate ICP rise; consider adjuncts (opioids/propofol) to reduce volatile requirement.
Describe the metabolism of desflurane and its clinical relevance (renal/hepatic).
  • Very low hepatic metabolism (~0.02%, CYP2E1) producing small amounts of TFA and fluoride ions; most is exhaled unchanged.
  • Clinically significant fluoride nephrotoxicity is not expected; risk of immune-mediated halothane-like hepatitis is extremely low but cross-sensitisation to TFA-protein adducts is a theoretical consideration.
What are the key contraindications/cautions for desflurane?
  • Avoid inhalational induction; caution in asthma/reactive airways due to airway irritation.
  • Caution where tachycardia/hypertension is undesirable (IHD, severe aortic stenosis, uncontrolled hypertension).
  • Contraindicated/avoid in MH-susceptible patients (trigger).
Explain how low blood–gas solubility affects the FA/FI curve and what this means for control of anaesthetic depth.
  • Low solubility means less uptake into blood → alveolar partial pressure rises quickly (FA approaches FI rapidly).
  • Clinical consequence: rapid titratability—small changes in vaporiser setting produce relatively quick changes in end-tidal concentration and depth.
  • Also means rapid washout at the end, especially with increased alveolar ventilation and adequate fresh gas flow.
List the blood:gas partition coefficients of common volatile agents and identify where desflurane sits. How does this influence recovery?

Numbers vary slightly by source; exam answers should show relative ranking and implications.

  • Approximate blood:gas: desflurane ~0.42 (lowest), sevoflurane ~0.65, isoflurane ~1.4, halothane ~2.4.
  • Lower blood:gas → faster wash-in and wash-out → faster emergence and less dependence on duration compared with more soluble agents.
Explain why desflurane has a high MAC and relate this to the Meyer–Overton rule.
  • Meyer–Overton: potency correlates with lipid solubility (oil:gas). Desflurane has low oil:gas (~18–19) → low potency → high MAC (~6%).
  • Clinical implication: higher inspired concentrations needed; often combined with opioids/adjuncts to reduce MAC requirement.
A vaporiser question: compare variable bypass vaporisers with desflurane vaporisers.
  • Variable bypass: splits fresh gas flow through bypass and vaporising chamber; relies on predictable saturated vapour pressure at ambient temperature and agent-specific calibration.
  • Desflurane vaporiser: heats and pressurises agent to create stable vapour, then injects/meters vapour to achieve set concentration; less dependent on ambient temperature.
  • Reason: desflurane’s high vapour pressure and low boiling point make variable bypass delivery inaccurate and potentially dangerous.

0 comments