1. Several gases were discovered to have anesthetic properties throughout the 19th century, including nitrous oxide, diethyl ether, and chloroform. 2. Between 1920-1940, newer inhaled anesthetics like ethylene, cyclopropane, and divinyl ether were introduced with faster induction and recovery times but also serious drawbacks like flammability and toxicity. 3. Modern inhaled anesthetics developed through fluorination have greater stability and lesser toxicity compared to earlier agents. Their uptake and distribution involves transfer between the anesthesia machine, breathing circuit, alveoli, and pulmonary blood based on partial pressures and solubility properties.

1. Inhalational agents
Dr Tess Jose
Resident anaesthesia

2. History
• Humphry Davy first observed the analgesic
effects of nitrous oxide as long ago as 1800,and
called it "laughing gas:' He used in the treatment
of pulmonary tuberculosis.
• However, it was not until 1844 that Horace Wells
described the use of nitrous oxide to facilitate the
extraction of a tooth.
• Unfortunately, the first public demonstration of
his technique ended in failure. Despite this, he
continued to use the gas, and eventually the
qualities of nitrous oxide were recognized; it is
still in use today.

3. • • Diethyl Ether
• • William Morton, a dentist, noticed that diethyl ether,
during “ether frolics” in which ether had similar effects as
nitrous oxide. Like Wells, Morton applied ether in his dental
practice and then demonstrated its anesthetic properties at
the Massachusetts General Hospital on October 16, 1846
(“ether day”). In contrast to Wells’s debacle, Morton’s
demonstration was received with great enthusiasm. The
results of successful ether anesthetics were soon published
in the Boston Medical and Surgical Journal.Following this
event, the use of ether and other volatile anesthetics
became widespread in Western medicine.

5. • • Chloroform
• • James Simpson, an obstetrician from Scotland,
developed chloroform, which did not share the
protracted induction, flammability, and postoperative
nausea seen with diethyl ether. Chloroform soon
became popular as an inhaled anesthetic in England,
although diethyl ether dominated medical practice in
North America. Unfortunately, chloroform was
associated with several unexplained intraoperative
deaths of otherwise healthy patients and numerous
cases of hepatotoxicity.

6. INHALED ANESTHETICS BETWEEN 1920 AND 1940
• Between 1920 and 1940, ethylene, cyclopropane, and divinyl ether
were introduced into use as anesthetics, gaining acceptance over
the older inhaled anesthetics by producing a faster, more pleasant
induction of anesthesia and by allowing faster awakening at the
conclusion of surgery.
• However, each had serious drawbacks. Many were flammable (i.e.,
diethyl ether, divinyl ether, ethylene, and cyclopropane), whereas
others, halogenated entirely with chlorine, were toxic (i.e.,
chloroform, ethyl chloride, and trichloroethylene)
• Techniques of fluorine chemistry, was beneficial in providing a
method of synthesizing modern inhaled anesthetics . Modern
inhaled anesthetics are halogenated partly or entirely with fluorine
. Fluorination provides greater stability and lesser toxicity.

8. BIOPHYSICAL PROPERTIES OF INHALED ANESTHETICS
• 1.Partial pressure is the portion of total pressure
contributed by one component of a gas mixture,
where each component contributes pressure in
direct proportion to its molar fraction.
• For example, 1.5% isoflurane in air (21% O2 and
79% N2) at 1 standard atmosphere (atm) (760 mm
Hg)
mixture of O2 at 157.2 mm Hg, N2 at 591.4 mm Hg,
and isoflurane at 11.4 mm Hg.

9. • 2.Hydrophobicity
• The molecular property of general anesthetics that
do not readily form hydrogen bonds and therefore
display low water solubility.
• Hydrophobic compounds are also usually lipophilic,
demonstrating high solubility in low polarity
solvents such as oils

10. • 3.Partition coefficients
• Usually represented by the Greek letter lambda (λ),
• a partition coefficient is the ratio of two solute
concentrations at equilibrium (i.e., at equal partial
pressure) in two separate but adjacent solvents or
compartments such that the solute moves freely
between the compartments

12. Flow diagram for
uptake and
distribution of inhaled
anesthetics

14. 1.FROM ANESTHESIA MACHINE TO BREATHING CIRCUIT .
• Wash-in of the ventilator
breathing circuit represents an
example of bulk transfer
exchange, wherein the gas in
circuit components is replaced
by fresh gases emerging from
the gas outlet of the
anesthesia machine.

15. • The delivered concentration depends on the fresh
gas flow and the vaporizer output. For example,
when 6 L/min of FGF are delivered with a vaporizer
setting of sevoflurane of 2%, amount of sevoflurane
vapor delivered to the breathing circuit is
calculated as:
• 2% = 2 ml of sevoflurane vapor for every 100 ml of
FGF
• So, for 6000 ml of FGF, 6000 x 2/100 = 120 ml of
sevoflurane vapor is delivered per minute to the
breathing circuit

16. • Inspired concentration Fi
• As anaesthetic gas comes intocircuit Fiwill rise
based on first order kinetics
• Time constant = Volume/Flow = Breathing circuit
volume/ FGF.
• Principles of first order kinetics mandates that
• In 1 time constant, 63% equilibration occurs
• In 2 time constants, 86% equilibration
• In 3 time constants, 95% equilibration occurs
• In 5 time constants, 99% equilibration occurs

18. • Consider a typical situation where FGF at the beginning of an anesthetic is 6
L/min, and the gas volume inside the components of a breathing circuit is 6 L.
• If FGF is doubled to 12 L/min, then wash-in will proceed at twice the rate
(halving the time).
• Conversely, if the Vcirc doubles to 12 L, then wash-in will proceed at half the
rate (doubling the time).
• Therefore,we can increase inspired concentration
by increasing FGF or increasingfractional
concentration that we set

19. • The magnitude and direction of net
anesthetic gas flow depends on the
difference in partial
pressure/concentration between
delivered and inspired mixture.
• At induction, where FI(or Pcirc ) is less
than FD (Pdel ), it moves from anesthetic
machine to circuit.
• At recovery, Pcirc is more than Pdel and
movement of anesthetic molecules is
reversed, and anesthetic is removed from
circuit gas.

20. 2.FROM BREATHING CIRCUIT TO THE ALVEOLI
• Alveolar concentration of the anesthetic
• The alveolar concentration of an anesthetic is
determined by a balance between that introduced
into the lungs by ventilation and that removed
through uptake by blood.
• The increase in alveolar concentration or
equilibration of alveoli with circuit is described in
terms of FA/FI curves
• (FA – fraction of anesthetic in alveoli and FI –
Fraction of anesthetic in inspired gas

21. The shape of the FA/FI curve
shows an initial upslope, a knee,
and an alveolar plateau which is
upsloping with a second knee.
The rapid upslope is because of
the wash in. There is no
anesthetic in the lungs in the first
minute of administration of
inhalational anesthetic.
This results in a large gradient
between inspired gas and alveolar
gas, leading to a rapid rise in the
concentration of anesthetic in the
alveoli.

22. • The first knee in the curve is because of the effect of
cardiac output, which results in uptake or removal of
the anesthetic from the alveoli, tapering the rapid
rate of rise of alveolar concentration
• The second knee in the curve leads to an upsloping
alveolar plateau. This is because of the anesthetic
concentration in the mixed venous blood. Mixed
venous blood returning to the lungs has increasing
concentrations of anesthetic with time

23. • The alveolar concentration is the balance of what is
delivered to the lungs and what is removed by pulmonary
blood flow. For a less soluble agent like desflurane, less
anesthetic is removed by the blood (small arrow)
compared to sevoflurane (large arrow) which is more
compared to isoflurane (very large arrow)

24. 3.FROM ALVEOLI TO PULMONARY CAPILLARY BLOOD – UPTAKE

25. • factors affecting alveolar uptake.
Anesthetic uptake into blood also depends on the
pulmonary blood flow (which is typically close to
cardiac output (Q)
The more soluble an anesthetic is in blood (i.e., the
higher its λb/g), the greater is the capacity for each
volume of blood to take up anesthetic from alveolar
gases
partial pressure gradient between alveolar gas
(Palv) and mixed venous blood (Pmv) entering the
pulmonary arteries. The net flow of anesthetic
reverses during anesthetic wash-out when Palv
drops below PMV.

26. Blood gas coefficient

27. • A higher blood-gas partition coefficient (higher
solubility) leads to greater uptake by the pulmonary
circulation,
• Blood-gas partition coefficients depend on the
concentrations of serum constituents such as
albumin, globulin, triglycerides and cholesterol.
These serum molecules effectively act as molecular
sinks to bind anesthetic agents.
•

28. • Lower blood gas coefficients are seen with •
Hemodilution
Obesity
Hypoalbuminemia and starvation
• Higher blood gas coefficients are seen with
 Adults versus children
Hypothermia
Postprandially

30. Effect of cardiac output and presence of shunt
• In the absence of shunt, pulmonary blood flow equals
cardiac output. Higher cardiac output results in a greater
uptake of anesthetic from the lungs and more rapid
delivery to the issues including the CNS.
• However, this does not hasten induction, as the alveolar
concentration is lowered by the high uptake of
anesthetic.
• Presence of shunt results in blood not reaching the lungs .
This shunted blood has no inhaled anesthetic, and mixes
with blood from the lungs containing inhaled anesthetic.
The shunt thus effectively dilutes the concentration of
inhaled anesthetic in the arterial blood, that is Pa
decreases.

31. Concentration effect
• When an inhaled anesthetic, such as nitrous oxide is
administered in high concentrations, the gas is
rapidly taken up into blood, at a very high rate
initially (1 L/min).
• Since Nitrous oxide is about 30 times more soluble
than nitrogen, the volume of N2O entering the
pulmonary capillaries is greater than the N2 leaving
the blood and entering the alveolus.
• This leads to a reduction in lung volume,

32. • This reduction in lung volume augments ventilation
as more inspired gas is now drawn into the alveolus
to compensate for the diminished alveolar volume.
• So, there are two reasons for the increase in
alveolar concentration, a concentrating effect in a
smaller lung volume and an augmentation of
ventilation, bringing further anesthetic into the
alveoli

33. second gas effect
• The second gas effect refers to the effect of nitrous oxide
administration in increasing the alveolar concentration of a
concurrently administered volatile inhalational agent.
• If a second gas (like halothane, is administered at the same time
as nitrous oxide, the concentration of the second gas rises faster
in the alveoli, than it would in the absence of nitrous oxide.
• This is termed the second gas effect and is due to the uptake of
large volumes of nitrous oxide in the alveoli that leads to both
concentrating the residual second gas in a smaller lung volume
and an augmentation of alveolar ventilation.
• This process can speed induction of inhalational anesthesia

36. Over pressure effect
• At induction, we compensate for the high uptake of
anesthetic by delivering a far higher concentration
of inhalational agent than we hope to achieve in
the alveoli.
• For example, using 8% sevoflurane at induction to
achieve an alveolar concentration of 2%.
• This is called the overpressure effect and is used to
speed up the process of inhalational induction

37. 4.FROM ARTERIAL BLOOD TO TISSUES

39. Based on perfusion

40. Mapleson’s water analogue

41. With a more soluble anesthetic like halothane, all the tissue containers are
much larger than with a less soluble agent like nitrous oxide, because of the
greater solubility of halothane, especially in fat.

42. 5.FROM TISSUES BACK TO VENOUS BLOOD AND
6. FROM MIXED VENOUS BLOOD BACK TO ALVEOLI
• Recovery occurs when concentration in brain
• After a short period of inhalation and uptake, anesthetic
clearance from blood is rapid through both exhalation and
distribution to muscle and other tissues
• Aside from pulmonary exchange, some portion of inhaled
anesthetics is lost by diffusion through other large area
interfaces between the body and surrounding air.
• Metabolism of inhaled anesthetics in tissues, particularly
liver, contributes a variable degree to drug clearance

43. • Diffusion Hypoxia (Fink Effect)
• Towards the end of surgery when nitrous oxide
delivery is stopped, the gradient reverses and the
nitrous oxide from blood gushes in alveoli replacing
the oxygen from there causing hypoxia. This is
called as diffusion hypoxia. To avoid this diffusion
hypoxia 100% oxygen should be given for 5-10
minutes after discontinuing nitrous oxide

44. Why Pediatric inductions are
faster ?
Larger ratio of alveolar ventilation to
functional residual capacity
 Greater delivery of cardiac output to
vessel rich tissues
Lower albumin and cholesterol levels
leading to a reduction in blood-gas
solubility coefficients.

45. minimum alveolar concentration (MAC)
• minimum alveolar concentration (MAC) which is
defined as minimum concentration of agent required to
produce immobility in 50% of the subjects given
noxious stimuli, which is skin incision in human beings
and tail clamping in rats.
• More important from clinical point of view is MAC95
(MAC producing effect in 95% individuals). MAC95 is
1.3 times of MAC50
• MACawake. It is MAC at which patient is not
unconscious but remains amnestic. It is 0.3 times
ofMAC50.

46. • Factors Decreasing the MAC Age:
• 1. Maximum MAC in human beings is at the age of 6 months, thereafter
decreasing steadily throughout the life (except a slight increase at puberty).
• 2. Temperature: Decreasing the temperature decreases the MAC. Increasing
temperature (up to 42°C) also decreases the MAC.
• 3. Anemia (Hb < 5 gm%), Hypoxia (pO2 < 40 mm Hg) and Hypercarbia (pCO2
> 95 mm Hg) decreases the MAC, only if they are severe.
• 4. Alcohol: Acute alcohol or acute administration of amphetamines
decreases the MAC.
• 5. Pregnancy: lnhalarional anesthetics should be used in lower
concentrations in pregnancy.
• 6. Concurrent administration of lntravenous anesthetics and alpha2
agonists.
• 7. Local anesthetics: All local anesthetics except cocaine decreases the
MAC.
• 8. Electrolytes imbalances decreasing MAC are: Hyponatremia,
Hypercalcemia and Hypermagnesemia.

47. • Factors Increasing the MAC
• 1. Hyperthermia > 42°C
• 2. Chronic intoxication of alcohol and
amphetamines Cocaine, ephedrine
• 3. Barometric pressure: Increasing pressure
increases the MAC (pressure reversal theory of
anesthesia)
• 4. Hypernatremia

48. NITROUS OXIDE
• Nitrous oxide is also called as 'laughing gas' (name given by
Humpry Davy). It was firs t prepared by Joseph Pristley in
1774.
• Preparation Prepared by heating ammonium nitrate between
245 and 270°C.
• Physical Properties
• It is colorless, non-irritating and sweet smelling. Critical
temperature is 36.5°C which is above room temperature,
therefore can be stored in liquefied state at room
temperature.
• It is stored in blue color cylinders at a pre sure of760 psi.
• 1.5 times heavier than air.
• 35 times more soluble than nitrogen

49. • Anesthetic Properties
• It is not a complete anesthetic (to act as complete
anesthetic, the agent must be given in concentration
above MAC.
• MAC of nitrous oxide is 104% and maximum
concentration of nitrous oxide which can be given is
66%).
• Along with the oxygen it acts as a carrier to carry other
volatile agents.
• Blood gas coefficient of 0.47 makes it an agent with
faster induction and recovery

50. • Although it is non-inflammable and non explosive,
but it can support fire.
• Good analgesic.
• Not a muscle relaxant.

51. • Systemic Actions
• Cardiovascular system :
• In vitro it depresses myocardium but in vivo this
effect is countered by stimulation of sympathetic
system, therefore can be used safely for cardiac
patients and shock.
• Cerebral:
• Increases cerebral metabolic rate and raises the
intracranial tension.
• Res piratory system:
• Respiration is minimally depressed
• Immunologic system: Effects chemotaxis and motility
of leukocytes.

52. Contraindicated
• Pneumothorax: Nitrous oxide doubles the
pneumorhorax volume in 1O minutes and triples in
30 minutes producing severe cardiorespiratory
compromise.
• Pneumoperitoneum.
• Pneumoencephalus: Entry of nitrous oxide can
significantly increase the intracranialtension. Once
the patient develops pneumoencephalus nitrous
oxide cannot be used for l week

53. • Middle ear surgery and tympanoplasties: Pressure in middle
ear cavity may rise ro 20- 50 mm Hg which can displace the
graft.
• Posterior fossa surgeries: There is increased risk of venous air
embolism
• Laparoscopic surgeries: Chances of air embolism are high in
laparoscopies.
• Acute intestinal obstruction and volvulus of gut: increase the
gut distension.
• Diaphragmatic hernia: Increased gut distension causes further
atelectasis worsening the hypoxia
• Eye surgeries: It can expand sulfur hexafluoride bubble
increasing intraocular pressure.
• - Microlaryngeal surgeries (MLS): By diffusing through the
tracheal tube cuff (which is filled with air), it may double or
triple the cuff volume aggravating the post-surgical edema,
which can cause upper airway obstruction.

54. Side Effects
• Hematological system:
• It inactivates vitamin B12, impairs methionine and
deoxythymidine synthesis which leads to defect in folate
metabolism a nd therefore bone marrow depression
causing aplastic and megaloblastic anemia. Vitamin B12
inactivation is seen, if nitrous oxide is used for more
than 12 hours.
• Neurological system: Vitamin B12 deficiency by
impairing DNA syn thesis can cause Subacute
degeneration of spinal cord and encephalopathy
(sometimes presenting as psychosis).
• Teratogenic effects: Teratogenicity and increased risk of
abortion has been observed in animals, h owever, h
uman s tudies are inconclusive.

55. HALOTHANE
• Physical Properties
• Colorless
• Pleasant to smell, nonirritant makes induction to become smooth,
therefore, can be used as an alternative to sevofiurane for
induction in children.
• Stored in amber-colored bottles and contains thymol 0.01 % as
preservative (to prevent decomposition by light).
• Non-inflammable, non-explosive.
• Boiling point 50°C.
• Halothane has highest fat/ blood coefficient [can get deposited in
adipose tissue after prolonged exposure).
• In the presence of moisture halothane can corrode metals of
vaporizers (aluminum, brass and tin) and plastic.
• Halothane is significantly absorbed by rubber tubing of circuits.

56. • Anesthetic Properties
• It is potent anesthetic (MAC= 0.74)
• Blood gas coefficient: 2.4 makes it agent with slow
induction and recovery time {slowest among the
agents used nowadays}
• Not a good analgesic

57. • Metabolism
• Halothane undergoes extensive metabolism (20%)
by oxidation as well as reduction.
• Metabolic products are:
Trifluoroacetic acid: It is the major metabolic
product
Chloride (Cl-).
 Bromide (Br-).
 Fluoride (F-) only under anaerobic conditions

58. Systemic Effects
• Cardiovascular system:
• Halothane causes significant decrease in cardiac output which is
because of direct depression of myocardium and bradycardia (beta
blocking action).
• Blunts the baroreceptor reflex.
• Blood pressure is decreased by direct action on smooth muscle of blood
vessels as well as decreased central sympathetic tone.
• It sensitizes heart to adrenaline (exogenous to heart) producing
ventricular arrhythmias therefore maximum permissible dose of
adrenaline with halothane for local ischemia is 1.5 µg/kg (otherwise 5
µm / kg is the maximum permissible dose) or not more than 30 mL/hr
of I in 1,00,000 solution. For the same reason, it is contraindicated in
pheochromocytoma.
• So, it can be concluded that halothane should not be used in cardiac
patients

59. • Respiratory system:
• Depresses respiration and blunts hypercarbic and
hypoxic reflexes
• In spite of being a potent bronchodilator, it should
be avoided in asthma patients as by sensitizing
myocardium to catecholamines, it increases the
possibility of arrhythmias in patients on B-agonist
and aminophylline.
• (lnhalational agent of choice for asthmatics in
present day practice is Sevoflurane

60. • Central nervous system: There is marked increase in
intracranial tension with halotbane.
• Renal: Both GFR and urinary flow is decreased because
of decrease in cardiac output.
• Uterus: Like other inhalational agents in current day
practice, it produces similar degree of uterine
relaxation.
• Thermoregulation: Postoperative shivering (halothane
shakes) and hypothermia is maximum with halothane
as compared to other inhalational agents.

61. • Liver:
• Halothane hepatitis, although rare (1 in 35,000), but is
clinically significant as it carries very high mortality
(>70%).
• The most important risk /actor for halothane is multiple
and frequent exposures. Other risk factors are hypoxia,
middle age, obesity, female gender and patients suffering
from autoimmune diseases.
• Pathologic lesion is centrilobular necrosis.
• Guidelines for use ofhalothane are:
Avoid repeated use, at least an interval of 3 months is
mandatory between two exposures.
Avoid in patients with coexisting autoimmune diseases

62. ISOFLURANE
• It is fluorinated methyled1yl ether. It is an isomer of
enflurane.
• Physical Properties
• Pungent ethereal odor therefore induction is unpleasant.
• Vapor pressure is similar to halothane (240 mm Hg).
• Anesthetic Properties
• It is the agent with moderate potency (MAC 1.15) and
moderate induction and recovery time (B/G coeffi cient
1.38),

63. • Systemic Effects
• Cardiovascular system:
• Hypotension is maximum with isoflurane ( It is the
inhalational agent of choice for controlled hypotension),
• however, at the same time, minimally depress
myocardium, does not cause bradycardia and
baroreceptor reflex is preserved, therefore, cardiac
output is best maintained among all inhalational agents
making isoflurane as inhalalional agent of choice for
cardiac patients except for myocardial ischemia patients.
• In MI patients, it can cause coronary steal however,
coronary steal is just a theoretical phenomenon and
Isoflurane can be used in MI patients, if necessary. It does
not sensitize myocardium to adrenaline.

64. • Cerebral: Decrease in cerebral metabolic rate,
brain's oxygen consumption and not very
significant rise in ICT makes Isoflurane as 2nd best
choice for neurosurgical procedures.
• Liver: lsonurane on metabolism produces
trifluroacetic acid, therefore theoretically can
produce hepa ti tis, however, the amount of
trifiuoroacetic produced is too minimal to initiate
the production of antibodies.

65. DESFLURANE
• It is the isomer of lsoflurane (ch lorine atom
replaced by fluorine atom),

66. • Physical Properties
• As it is an ethereal product therefore has pungent
odor and unpleasant induction.
• Vapor pressure is very high (681 mm Hg) and
boiling poin t is less than 23°C, therefore can boils
at room temperature and that is why a special
vaporizer (TEC 6) which is temperature and
pressure compensated is required for its delivery.

67. • Anesthetic Properties
• Because of the lowest blood gas coefficient (0.42) its
induction and recovery is most rapid among the agents
used nowadays.
• Potency is low (MAC-6%).
• Unpleasant induction may manifes ts as coughing,
breath-holding or laryngospasm.
• Produces maximum muscle relaxation among the agents
used nowadays.
• Very low fat/gas coefficient therefore excellent for obese
patients.

68. Fat / gas coefficient
Halothane
197
Isoflurane 90.8
Enflurane
98.5
Sevoflurane 47
Desflurane 19
Nitrous oxide 1.3

69. • Systemic Effects
• Cardiovascular system:
• As it is an isomer of lsoflurane, its actions are similar to
isoflurane with an added advantage that it does not
causes coronary steal however, at concentrations more
than 1 MAC ( >6%) (particularly, if this concentration is
achieved rapidly) it stimulate sympathetic system .
• Metabolism
• Undergoes minimal metabolism ( <0.02%), therefore
does not produce any fluoride.

70. • Uses
• Because of minimal metabolism Desflurane is the agent of choice
for:
Prolonged duration surgeries (no risk of accumulation of any
metabolites in spite of prolonged exposure)
Old age patients who may have impaired hepatic or renal
functions
 Renal diseases ( does not produce fluoride)
Obese patients: Least fat/ gas coefficient and least metabolism
(In obese patients, the metabolism of inhalational agents may be
increased by 30-40%)
• An excellent alternative to Sevoflurane for hepatic patients
• Because of fast recovery, it is inhalational agent of choice for day
care surgery.
• • Because of stimulation or sympathetic system at cone. >6%, it is
inhalational agent of choice for shock patients.

71. SEVOFLURANE
• Physical Properties
• Sweet odor.
• Anesthetic Properties
• Faster (B/G coefficient 0.69), pleasant and smooth
induction makes sevoflurane as an agent of choice
for induction in children.

72. • Systemic Effects
• Cardiovascular system: Cardiac output is
moderately decreased.
• Respiration: Effects similar to other agents, i.e.
depresses respiration and blunts ventilatory
responses. Excellent bronchodilatation makes
Sevoflurane as the inhalational agent of choice for
asthmatics in present day practice.
• Cerebral:

73. • Cerebral: Minimum increase in ICT, significant
reduction in cerebral metabolic rate and smoother
recovery makes sevoflurane as an inhalational
agent of choice for neurosurgery in current day
anesthetic practice.
• • Although incidence is very low but sevoflurane
can produce convulsions (usually at higher
concentrarions ).

74. • Hepatic: It decreases portal blood flow but at the same
time, increases hepatic artery blood flow therefore
hepatic blood flow is best rnaintained. Does not produce
trifluoroacetic acid, therefore, cannot cause immunologic
hepatitis. These properties make sevoflurane as an
inhalational agent of choice for hepatic patients.
• Renal: The clearance of Sevoflurane is so rapid that in
spite of producing high fluoride nephrotoxicity has not
been reported, however, if the renal functions are
compromised, it can cause nephrotoxicity making
sevoflurane unsuitable for renal patients.

75. • Disadvantages •
• With sodalime and Barylime (Barylime > Sodalime), it can
produce an olefin called as compound A, which can cause
nephrotoxicity. The methods to decrease the production of
compound A are:
Use fresh gas flow> 2 liters/ min.
Use Amsorb or lithium containing CO2 absorbents.
• With desiccated sodalime, it produceshydrogen fluoride which
can cause burns of respiratory tract.
• Sevoflurane with Barylime can produce fire and explosions in
breathing circuits
• Although very rare but can cause Convulsions. Produces high
fluoride

76. AGENTS NO MORE IN CLINICAL
USE
• ENFLURANE
• Has been recently obsoleted due to the following
reasons:
• Highly epileptogenic
• Systemic side effects, i.e. decrease in cardiac
output, respiratory depression and increase in
intracranial pressure was significant
• Due to slow excretion fluoride may accumulate in
renal tubules to cause nephrotoxicity.

77. • ETHER
• First public demonstration of ether was given by WTG Morton
on 16th October 1846 for the removal of jaw tumor.
• only anesthetic till date which can be considered complete, i.e.
has all three basic properties of anesthesia, viz. narcos is,
analgesia and muscle relaxation.
• Safest inhalalional anesthetic: Does not produce any cardiac or
respiratory depression, the only agent which preserves ciliary
activity.
• Can be given by open drop method. High safety profile, all
anesthetic properties, use without equipment (open drop
method)
• low cost make ether not only the agent of choice for remote
locations (like wars and disasters) and with less experienced
hands

78. • Disadvantages
• High inflammable and explosive: There have been
death reports following burns by ether.
• Pungent smelling therefore induction and recovery
is very unpleasant.
• Can be easily decomposed by light and heat,
therefore, stored in dark color bottles wrapped in
black paper.
• By increasing tracheobronchial secretions it can
induce laryngospasm.
• Very high incidence of nausea and vomiting, in
postoperative period

79. • METHOXYFLURANE
• Overall most potent (MAC 0.16%) and slowest induction
and recovery (blood gas coefficient 15)
• Highly soluble in rubber lubing of closed circuit.
Undergoes maximum metabolism yielding highest con
centration of fluoride (F-) producing vasopressin-resistant
high output (polyuric) renal failure.
• CYCLOPROPANE
• Highly inflammable and explosive.
• • Used to be stored in orange color cylinders at a pressure
of75 psi.

80. • TRICHLOROETHYLENE (TRILENE)
• Most potent analgesic among inhalational agents,
therefore was popular in past for labor analgesia.
• It can react with sodalime producing
dichloroacetylene which is neurotoxic effecting
cranial nerves (most commonly involved are V and
VII)and phosgene gas which can cause ARDS.
• CHLOROFORM
• Number of cardiac arrest and death has been
reported due to ventricular fibrillation