2. 1.
Understand the history of Sevoflurane
2.
Recognize the pharmacological properties
of Sevoflurane
3.
Recognize its specific advantages in
neuroanaesthesia
4.
Must appreciate unfavourable conditions
produced by Sevoflurane

3. 
History started with inhalational
anaesthesia.

Past 50 years- 3 gases,13 inhalational
anaesthetics were introduced.

Inhalational anaesthetics are routinely
used.

They are potent.

Balanced anaesthesia.

4. 
Development of Sevoflurane is an unusual
and truly remarkable story.

1960’S-Three investigators evaluated
halogenated ethers.

Thomas Cook, Richard Mazze & Michael
Halsey-on animals.

Bio transformation- increase in inorganic
flouride in urine.

5. 
Dunken Holaday& Burnell Brown observed
sweet smell,low solubility & no arrhythmias.

1981- phase 1 trials.

After 10years Yasuda etal compared Sevo
with Iso.

Baxter sold sevo to BOC which later
became OHMEDA.

OHMEDA sold Sevo to Mariushi japan.

6. 
Mariushi used Sevo in japan .

Approached ABBOTT for FDA approval in
USA.

Later phase 2 &3 trials were done.

Approved by FDA in 1994.

Freely available by 1995.

7. It is 1, 1,1,3,3,3,hexafluro-2- fluro methoxy propane.

8. Non flammable
 Pleasant smell
 Volatile
 Molecular weight-200.05
 Boiling point(at sea level)-58.6c
 Specific gravity at 20c-1.520-1.525
 Partition coefficient at 37c
water/gas- 0.36
blood/gas-0.63-0.69


9. 
Refractive index n20-1.2740 - 1.2760

Purity by gas chromatography-99.975% or
better
Vapour
pressure
Temp°C
mmHg
20
157
25
197
36
317

10. MAC values
AGE OF
PATIENT
(YEARS)
SEVOFLURANE IN
O2
SEVOFLURANE IN N2O 65%
O2 35%
<3
3.3-2.6%
2.0%
3 - <5
2.5%
Not available
5 - 12
2.4%
Not available
25
2.5%
1.4%
35
2.2%
1.2%
40
2.05%
1.1%
50
1.8%
0.98%
60
1.6%
0.87%
80
1.4%
0.70%

11. 
Non corrosive to stainless steel, brass,
aluminium,nickle plated brass,chrome
plated brass.

Stored at 25c not refrigerated.

Tightly closed amber coloured bottles.

Should not be used after expiry date.

12. Impact on intracranial dynamics

Indirect vasoconstriction vs direct
vasodilatation.

Effect on ICP& surgical condition.

Effect on auto regulation.
CO2 reactivity.


Studies that have compared the use of
different agents in patients with intra cranial
lesions with a certain degree of increased

13. 
The possibility of a quick awakening
allowing for rapid post operative
neurological assessment.
Low solubility of agents such as
Sevoflurane.

Cytoprotective effect.
Animal studies only,at this time.

14. 
Relationship between metabolism and CBF.

Volatile anaesthetics act indirectly on CBF
by reducing metabolism.

Directly they are vasodilators.

Net effect depends on agent & dosage used.

16. 
Sevo is the least vasodilating agent followed
by Iso and Des.

Sevo has net vasoconsticting effect.

Preserves autoregulation upto 2 MAC.
Iso&Des disrupts auto regulation at 1.5&0.5
MAC.

17. 
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
Halothane 20ml/100gms/min.

18. 
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 tissue.

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.

19. 
Solubility : low blood gas solubility
coefficient.

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
no laryngospasm.

20. Circulatory
effects:
Dose dependent fall in BP
No sensitization to catecholamines
Protective property on myocardium
Coronary vasodilation

21. Respiratory
effects:
Dose dependent in tidal volume
Slight in end tidal & arterial co2
Bronchodilatation
No irritation
Less effect on HPVC

22. CNS
effects
Dose dependent in total &
regional blood flow
CMRO2
Slight in ICP
Protection against ischemia
Preconditioning possible.

23. Renal
effects:
3-5% metobolised .
in inorganic flourides.
Reacts with sodalime and baralime.
CompoundA produced.
More in low FGF,when soda lime is dryer&
hotter and also with high Sevo.
CompoundA 19 ppm at clinical conditions.

24.  Hepatic
:
very little effect on hepatic blood flow
and function

25. Favourable
points
Low blood gas solubility co-efficient
2. Rapid induction and recovery -(Sevoflurane Provides
1.
Faster Recovery and Postoperative Neurological Assessment Than Isoflurane in LongDuration Neuro surgical Cases)
Potent, can be used with oxygen only
4. Pleasant,non-irritating to respiratory
system
5. Minimal or no stimulation of air way
reflexes
6. Laryngospasm uncommon
7. Suitable for all ages
8. Compatable with epinephrine
3.

26. 9.
Cerebral autoregulation maintained
(Dynamic Cerebral Autoregulation During SevofluraneAnesthesia: A Comparison with
Isoflurane)
10.
Coupling of metabolism and o2 demand
maintained
(Intracranial Pressure, Middle Cerebral Artery FlowVelocity, and Plasma Inorganic
Fluoride Concentrations inNeurosurgical Patients Receiving Sevoflurane or lsoflurane)
11.
Rapid recovery and early neurological
assessment possible (A comparative study between Sevo and
Propofol for intracranial surgery for assessment of rapid recovery)
12.
Pre-conditioning of the brain for ischemic
attacks (The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and
Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats)—
(sevoflurane induced preconditioning of rat brain invitro and the role of KATP
channels.)

27. 13.
Protects brain cells
(the effect of Sevoflurane on recovery of
brain energy metabolism after cerebral ischmia in the rat)
15.
Non-inflammable
No long term effects on vital
16.
Maintains co2 reactivity
14.
organs(Low-flow
Sevoflurane Compared with Low-flow Isoflurane Anesthesia in Patients with Stable
Renal Insufficiency) (The Effects of Prolonged Low-Flow Sevoflurane Anesthesia
on Renal and Hepatic Function)

28. 
1.
2.
3.
4.
5.
Unfavourable points
Triggering agent for malignant
hyperthermia
Emergence dysphoria in children
Nausea and vomiting
Seizures
CO production

30.  Sevoflurane
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

31. 
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 City,
Utah

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.‡
*

32. 
Sevoflurane-induced preconditioning of rat
brain invitro 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. Louis, Missouri

33.  Desflurane
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
 The
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

34. 
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

35. 
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.**