Understand the history of Sevoflurane
2. Recognize the pharmacological properties
3. Recognize its specific advantages in
4. Must appreciate unfavourable conditions
produced by Sevoflurane
History started with inhalational
Past 50 years- 3 gases,13 inhalational
anaesthetics were introduced.
Inhalational anaesthetics are routinely
They are potent.
Development of Sevoflurane is an unusual
and truly remarkable story.
1960’S-Three investigators evaluated
Thomas Cook, Richard Mazze & Michael
Bio transformation- increase in inorganic
flouride in urine.
Dunken Holaday& Burnell Brown observed
sweet smell,low solubility & no
1981- phase 1 trials.
After 10years Yasuda etal compared Sevo
Baxter sold sevo to BOC which later
OHMEDA sold Sevo to Mariushi japan.
Mariushi used Sevo in japan .
Approached ABBOTT for FDA approval in
Later phase 2 &3 trials were done.
Approved by FDA in 1994.
Freely available by 1995.
It is 1, 1,1,3,3,3,hexafluro-2- fluro methoxy propane.
Boiling point(at sea level)-58.6c
Specific gravity at 20c-1.520-1.525
Partition coefficient at 37c
Refractive index n20-1.2740 - 1.2760
Purity by gas chromatography-99.975% or
SEVOFLURANE IN N2O 65%
3 - <5
5 - 12
Non corrosive to stainless
steel, brass, aluminium,nickle plated
brass,chrome plated brass.
Stored at 25c not refrigerated.
Tightly closed amber colouredbottles.
Should not be used after expiry date.
Impact on intracranial dynamics
Indirect vasoconstriction vs direct
Effect on ICP& surgical condition.
Effect on auto regulation.
Studies that have compared the use of
different agents in patients with intra cranial
lesions with a certain degree of increased
The possibility of a quick awakening
allowing for rapid post operative
Low solubility of agents such as
Animal studies only,at this time.
Relationship between metabolism and CBF.
Volatile anaesthetics act indirectly on CBF
by reducing metabolism.
Directly they are vasodilators.
Net effect depends on agent & dosage
Sevo is the least vasodilating agent
followed by Iso and Des.
Sevo has net vasoconsticting effect.
Preserves autoregulation upto 2 MAC.
Iso&Des disruots auto regulation at
Threshold under which CBF is not
sufficient to meet the cerebral metabolic
needs is called critical CBF.
Below critical CBF brain becomes ischemic.
On awake patients it is 25ml/100gms/min.
The critical CBF with Iso
10ml/100gms/min, with Sevo 11.5ml& with
Strong evidence showing cytoprotection in
animal experiments by volatile anaesthetics.
Same applies to Propofol but more benificial
if given in reperfusion period.
Volatile anaesthetics shown to have
preconditioning in rodents.
They allow ischemic tolerance of brain
Preconditioning is not seen with Propofol.
The choice of specific agent in anaesthesia in
a patient with cerebral ischemia solely
depends on CPP,ICP& autoregulation.
Solubility : low blood gas solubility
Potency : highly potent MAC averaging at 2%
can be given with high 02
does not suppress SSEP.
Air way properties:
pleasant smell,no irritation, fast induction
Dose dependent fall in BP
No sensitization to catecholamines
Protective property on myocardium
Dose dependent in tidal volume
Slight in end tidal & arterial co2
Less effect on HPVC
Dose dependent in total &
regional blood flow
Slight in ICP
Protection against ischemia
3-5% metobolised .
in inorganic flourides.
Reacts with sodalime and baralime.
More in low FGF,when soda lime is dryer&
hotter and also with high Sevo.
CompoundA 19 ppm at clinical conditions.
very little effect on hepatic blood flow
Low blood gas solubility co-efficient
Rapid induction and recovery
Potent, can be used with oxygen only
Pleasant,non-irritating to respiratory system
Minimal or no stimulation of air way reflexes
Suitable for all ages
Compatable with epinephrine
Cerebral autoregulation maintained
10. Coupling of metabolism and o2 demand
11. Rapid recovery and early neurological
12. Pre-conditioning of the brain for ischemic
13. Protects brain cells
15. No long term effects on vital organs
16. Maintains co2 reactivity
1. Triggering agent for malignant
2. Emergence dysphoria in children
3. Nausea and vomiting
5. Co production
induces less cerebral
vasodilation than isoflurane at the same
A-line1autoregressive index level
A. HOLMSTRO¨ M and J. A°KESON
Department of Anesthesia and Intensive Care, Malmo¨ University Hospital, Lund
University, Malmo¨, Sweden
Dynamic Cerebral Autoregulation During
SevofluraneAnesthesia: A Comparison with
IsofluraneAndrew C. Summors, BSc, MBBS, FRCA, Arun K.
Gupta, MBBS, FRCA, and Basil F. Matta, MB, ChB, BA, FRCA
Intracranial Pressure, Middle Cerebral Artery
FlowVelocity, and Plasma Inorganic Fluoride
Concentrations inNeurosurgical Patients
Receiving Sevoflurane or lsoflurane Alan A.
Artru, MD*, Arthur M. Lam, MD*, Joel 0.
Johnson, MD, PhDt, andRichard J. Sperry, MD, PhDtDepartment of
Anesthesiology, University of Washington School of
Medicine, Seattle, Washington; and tDepartment
ofAnesthesiology, University of Utah School of Medicine, Salt Lake
Direct Cerebral Vasodilatory Effects of
Sevofluraneand IsofluraneBasil F.
Matta, M.B.B.Ch., B.A., F.R.C.A.,* Karen J. Heath, M.B.B.S., F.R.C.A.,†
Kate Tipping, M.B.B.S.,‡
Andrew C. Summors, B.Sc., M.B.B.S., F.R.C.A.‡
Sevoflurane-induced preconditioning of rat
brainin vitro and the role of KATP channels
Franz Kehla,*, Ralphiel S. Payneb, Norbert Roewera, Avital SchurrbaDepartment
of Anesthesiology, Klinik und Poliklinik fu¨r Ana¨sthesiologie, Zentrum
Operative Medizin, Julius-Maximilans-Universita¨ t, Oberdu¨rrbacher Str.
6, Wu¨rzburg 97080, Germany
Sevoflurane Provides Faster Recovery and
PostoperativeNeurological Assessment Than
Isoflurane in Long-DurationNeurosurgical Cases
Alain Gauthier, MD*, Francois Girard, MD, FRCPC*, Daniel
Boudreault, MD, FRCPC*, Monique Ruel, RN*, and Alexandre
Todorov, PhD†Department of Anesthesiology, Centre Hospitalier de
l’Universite´ de Montre´al, Hopital Notre-Dame, Montre´al, Canada; and
†Department of Psychiatry, Washington University Medical Center, St.
results in higher cerebral
blood flow than sevoflurane or isoflurane
at hypocapnia in pigs A. HOLMSTRO¨ M 1, I. ROSE ´ N 2
and J. A°KESON Departments of 1Anaesthesia and Intensive
Care, Experimental Research and 2Clinical Neurophysiology, Malmo¨
University Hospital, Lund University, Malmo¨, Sweden
Effects of Prolonged Low-Flow
Sevoflurane Anesthesia on Renal and
Hepatic Function Ryoji Obata, MD, Hiromichi
Bito, MD, Morihiro Ohmura, Goroku Moriwaki, MD, Yukako
Ikeuchi, MD, Takasumi Katoh, MD, and Shigehito Sato,
MD Department of Anesthesiology and Intensive Care, Hamamatsu
University School of Medicine, Hamamatsu, Japan
Comparison of propofol/remifentanil and
sevoflurane/remifentanil for maintenance of
anaesthesia for elective intracranial surgery J. R.
Sneyd1*, C. J. H. Andrews2 and T. Tsubokawa21Peninsula Medical School, C310
Portland Square, University of Plymouth, Drake Circus, Plymouth PL4 8AA, UK.
2Department of Anaesthesia, Pain Management and Critical Care Medicine,
Derriford Hospital, Plymouth PL6 8DH, UK
The Long-Term Effect of Sevoflurane on
Neuronal Cell Damage and Expression of
Apoptotic Factors After Cerebral Ischemia and
Reperfusion in Rats Monika Pape, MD*Kristin Engelhard,
MD*Eva Eberspa¨cher, Regina Hollweck‡Kristine Kellermann,
DVM‡Susanne Zintner, DVM‡Peter Hutzler, PhD§Christian Werner, MD
A review of recovery from sevoflurane
anaesthesia:Comparisons with isoflurane and
propofol includingComparisons with isoflurane
and propofol including meta-analysis B. J.
ROBINSON, T. D. UHRICH and T. J. EBERT Medical College of Wisconsin
and VA Medical Center, Milwaukee, Wisconsin, USA
Low-flow Sevoflurane Compared with Lowflow Isoflurane Anesthesia in Patients with
Stable Renal Insufficiency
Peter F. Conzen, M.D.,* Evan D. Kharasch, M.D., Ph.D.,† Stephan F. A.
Czerner, M.D.,‡ Alan A. Artru, M.D.,† Florian M. Reichle, M.D.,‡ Piotr
Michalowski, M.D., Ph.D.,§ G. Alec Rooke, M.D., Ph.D.,_ Branko M.
Weiss, M.D.,# Thomas J. Ebert, M.D., Ph.D.**