Handout for Inhalational Anaesthesia CME held in 2013 by the Department of Anaesthesiology, JNMC, Belagavi. Authors have been credited in each chapter.

1. 1

2. 2
TABLE OF CONTENTS
Dr. M. Ravishankar, Professor & Head of Anesthesia, MGMC & RI,
Pondicherry – Low flow anesthesia- -------------------------Page No.2
Dr. Ashok Deshpande, Intensivist, Bharti Medical College, Sangli -
Uptake and redistribution of inhalational anesthetics-----Page No. 37
Dr. Vithal Dhulkhed, Professor and Head of Anesthesiology, Krishna
Institute of Medical Sciences, Deemed University, Karad - Paediatric
inhalational induction--------------------------------------------Page No.59
Dr. Vidya Patil, Professor of Anesthesiology, Shri B.M. Patil Medical
College, Bijapur – Intravenous induction of anesthesia in paediatric
patients-----------------------------------------------------------Page No.72

3. 3
LOW FLOW ANAESTHESIA
Dr. M. Ravishankar, Professor & Head of Anesthesia, MGMC & RI,
Pondicherry.
INTRODUCTION:
The technique of reusing the expired gas for alveolar
ventilation after absorption of carbon dioxide can be traced to the
very beginning of Anaesthesia when Dr. John Snow used caustic
potash to absorb CO2 from the expired gas. This concept was
considerably simplified by the introduction of “To and Fro”
system by Waters and the circle system by Brian Sword, which
utilised soda lime for absorption of CO2. It reigned supreme in
the early half of this century when expensive and explosive agents
like cyclopropane were utilised. The introduction of non-explosive
agents like halothane and plenum vaporisers that performed
optimally only in the presence of higher flows, resulted low flow
anaesthesia becoming less popular. With the added knowledge of
the disadvantages of using high percentages of O2 for prolonged
periods and the necessity to use a second gas to control the
percentage of oxygen, coupled with the complexities involved in
the calculation of uptake of anaesthetic agents during the closed
circuit anaesthesia, made this technique even less popular.
However, the awareness of the dangers of theatre pollution with
trace amounts of the anaesthetic agents and the prohibitively high

4. 4
cost of the new inhalational agents, have helped in the rediscovery
of low flow anaesthesia.
DEFINITION
Low flow anesthesia has various definitions. Any technique that
utilizes a fresh gas flow (FGF) that is less than the alveolar
ventilation can be classified as ‘Low flow anesthesia’. Baum et al 1
had defined it as a technique wherein at least 50% of the expired
gases had been returned to the lungs after carbon dioxide
absorption. This would be satisfied when the FGF was less than
about two liters per minute.
Baker2, in his editorial had classified the FGF used in anesthetic
practice into the following categories:
Metabolic
flow
: about 250 ml /min
Minimal
flow
: 250-500 ml/min.
Low flow : 500- 1000 ml/min.
Medium
flow
: 1 - 2 l/min.
For most practical considerations, utilization of a fresh gas flow
less than 2 liters/min may be considered as low flow anesthesia.

5. 5
The need for low flow anaesthesia.
Completely closed circuit anesthesia is based upon the reasoning
that anesthesia can be safely be maintained if the gases which are
taken up by the body alone are replaced into the circuit taking
care to remove the expired carbon dioxide with soda lime. No gas
escapes out of the circuit and would provide for maximal
efficiency for the utilization of the fresh gas flow. The very nature
of this system requires that the exact amount of anesthetic agent
taken up by the body be known, since that exact amount has to be
added into the circuit. Any error in this could lead to potentially
dangerous level of anesthetic agent be present in the inspired
mixture with its attended complications. Hence, there exists a
need for a system that provided the advantages of the completely
closed circuit and at the same time, reduced the dangers
associated with it. Low flow anesthesia fulfilled these
requirements.
Low flow anaesthesia involves utilising a fresh gas flow
which is higher than the metabolic flows but which is considerably
lesser than the conventional flows. The larger than metabolic
flows provides for considerably greater margin of safety and
allows variations in the fresh gas flow composition and strict
compliance to the uptake is not necessary. Hence, the conduct of

6. 6
anaesthesia is greatly simplified and at the same time provides for
the economy of the fresh gas flows.
Equipment
The minimum requirement for conduct of low flow anesthesia is
absorption of CO2 from the expired gas, so that it can be
reutilized for alveolar ventilation. Two systems were commonly
used in the past, i.e., “To and Fro” system introduced by Waters
and the circle system introduced by Brian Sword. The ‘To and Fro’
system because of its bulkiness near the patient and other
disadvantages has gone out of vogue. The circle system using large
soda lime canisters is in common use. The circle system should
have the basic configuration with two unidirectional valves on
either side of the soda lime canister, fresh gas entry, reservoir bag,
pop off valve, and corrugated tubes and ‘Y’ piece to connect to the
patient. The relative position of fresh gas entry, pop off valve, and
reservoir bag are immaterial as long as they are positioned
between the expiratory and the inspiratory unidirectional valves
that functions properly and CO2 absorption is efficient at all
times.
Monitoring
Inspired O2 concentration should be monitored at all times if
N2O is used in more than 65% concentration, as one of the

7. 7
adjuvant gas. EtCO2 monitoring seems to be necessary to ensure
proper functioning of the absorber. If monitoring of end tidal
anesthetic concentration is available, the administration of low
flow anesthesia becomes very easy. In the absence of that a few
calculations have to be carried out for deciding on the amount of
anesthetic agent to be added to the system.
THE PRACTICE OF LOW FLOW ANAESTHESIA:
The practice of low flow anesthesia can be dealt with under the
following three categories:
1. Initiation of Low flow anesthesia
2. Maintenance of Low flow anesthesia
3. Termination of Low flow anesthesia.
INITIATION OF LOW FLOW ANAESTHESIA.
Primary aim at the start of low flow anesthesia is to achieve an
alveolar concentration of the anesthetic agent that is adequate for
producing surgical anesthesia (approximately 1.3 MAC). The
factors that can influence the buildup of alveolar concentration
should all be considered while trying to reach the desired alveolar
concentration. These factors can broadly be classified into three
groups (fig. 1); 1) Factors governing the inhaled tension of the
anesthetic, 2) Factors responsible for rise in alveolar tension, 3)

8. 8
Factors responsible for uptake from the lungs thus reducing the
alveolar tension.
Factors governing the inhaled tension of the anaesthetic:
1. The circle system is often bulky and has a volume roughly equal
to 6-7 litres. Besides this, the FRC of the patient, which is roughly
3 litres, together constitutes a reserve volume of 10 litres to which
the anaesthetic gases and vapours have to be added. With the
addition of FGF, the rate of change of composition of the reserve
volume is exponential. The time required for the changes to occur
is governed by the time constant, which is equal to this reserve
volume divided by the fresh gas flow. This represents the time
required for 67% change to occur in the gas concentration. Three
time constants are needed for a 95% change in the gas
FACTORS AFFECTING THE
INHALED TENSION
FACTORS AFFECTING THE
RISE IN ALVEOLAR TENSION
UPTAKE BY THE
BLOOD
1. BREATHING CIRCUIT VOLUME
2. RUBBER GAS SOLUBILITY
3. SET INSPIRED CONCENTRATION
1. CONCENTRATION EFFECT
2. ALVEOLAR VENTILATION
1. CARDIAC OUTPUT
2. BLOOD GAS
SOLUBILITY
3. ALV – VENOUS
GRADIENT
Fig 1. Factors affecting the build up of alveolar tension

9. 9
concentration to occur. Hence, if a FGF of 1L/min is used, then
30 minutes will be required for the circuit concentration to reflect
the gas concentration of the FGF. If the FGF is still lower, then
correspondingly longer time will be required.
2.The functional residual capacity of the lung and the body as a
whole contain nitrogen which will try to equilibrate with the
circuit volume and alter the gas concentration if satisfactory
denitrogenation is not achieved at the start of anaesthesia.
Hence, as a prelude to the initiation of closed or low flow
anaesthesia, thorough denitrogenation must be achieved with
either a non-rebreathing circuit or the closed circuit with a large
flow of oxygen and a tight fitting facemask.
3.The anaesthetic agent could be lost from the breathing system
due to solubility of the agent in rubber, and permeability through
the corrugated tubes. Though the amount of loss will be minimal,
it should be considered at the start if the aimed anaesthetic
concentration is low.
Factors responsible for rise in alveolar tension of the
anaesthetic agent:
1. Concentration effect: The concentration effect helps in raising
the alveolar tension towards the inspired tension, but hinders
with it if an insoluble gas is present in the mixture. The rate of
rise of alveolar partial pressure of the anaesthetic agent must

10. 10
bear a direct relationship to the inspired concentration. Higher
the inspired concentration, the more rapid is the rise in alveolar
concentration. At low inspired concentration, the alveolar
concentration results from a balance between the ventilatory
input and circulatory uptake. If the later removes half the
anaesthetic introduced by ventilation, then the alveolar
concentration is half that inspired. The concentration effect
modifies this influence of uptake. When appreciable volumes are
taken up rapidly, the lungs do not collapse; instead the sub
atmospheric pressure created in the lung by the anaesthetic
uptake causes passive inspiration of an additional volume of gas
to replace that lost by uptake, thus increasing the alveolar
concentration and offsetting the mathematical calculations.
Similarly, if an insoluble gas (e.g., nitrogen) is present in the
inspired mixture, as the blood takes up the anaesthetic gas, the
concentration of the insoluble gas will go up in the alveoli,
reducing the concentration of the anaesthetic agent.
2.Alveolar ventilation: The second factor governing the delivery of
anaesthetic agent to the lung is the level of alveolar ventilation.
The greater the alveolar ventilation, the more rapid is the rise of
alveolar concentration towards the inspired concentration. This
effect is limited only by the lung volume, the larger the functional
residual capacity, the slower the wash in of the new anaesthetic
gas.

11. 11
Factors responsible for uptake from the lungs thus
reducing the alveolar tension:
Uptake from the lung is the product of three factors: solubility
of the agent in the blood, the cardiac output and the alveolar to
venous partial pressure gradient.
1. Blood gas solubility: “Solubility” is the term used to describe how
a gas or vapour is distributed between two media. At equilibrium,
that is when the partial pressure of the anaesthetic in the two
phases is equal, the concentration of the anaesthetic in the two
phases might differ. This is calculated as a coefficient. When it is
between blood and gas it is called blood gas solubility coefficient.
If other things are equal, the greater the blood/ gas solubility
coefficient, the greater the uptake of anaesthetic, and slower the
rate of rise of alveolar concentration.
2.Cardiac output: Because blood carries anaesthetic away from the
lungs, the greater the cardiac output, the greater the uptake, and
consequently the slower the rate of rise of alveolar tension. The
magnitude of this effect is related to the solubility: the most
soluble agents are affected more than the least soluble agents.
3.Alveolar to venous partial pressure gradient: During induction
the tissues remove all the anaesthetic brought to them by the
blood. This lowers the venous anaesthetic partial pressure far
below that of the arterial blood. The result is a large alveolar to

12. 12
venous anaesthetic partial pressure difference, which causes
maximum anaesthetic uptake and hence lowers the alveolar
partial pressure.
Considering the above mentioned factors at the start of
anaesthesia, two facts become apparent:
1. Induction if performed using low flows would take an
unacceptably long time.
2.If induction is done with an intravenous agent, unless special
precautions are taken, it may take very long time to achieve the
desired alveolar concentrations. Once the desired concentration
is achieved, it will be difficult to change it. Hence, termination of
action would take a long time after the discontinuation of the
agents.
Methods to achieve desired gas and agent concentration
Use of high flows for a short time:
This is by and far the commonest and the most effective technique
of initiating closed circuit. By using high flows for a short time,
the time constant is reduced thereby bringing the circuit
concentration to the desired concentration rapidly. Often, a fresh
gas flow of 10L of the desired gas concentration and 2 MAC agent
concentration is used so that by the end of three minutes (three
time constants) the circuit would be brought to the desired

13. 13
concentration. The large flows and high agent concentration also
compensate for the large uptake seen at the start of the
anesthesia. Mapleson3 using a spreadsheet model of a circle
breathing system has calculated that, by using a FGF equal to
minute ventilation and setting the anesthetic agent partial
pressure to 3 MAC, the end expired partial pressure of halothane
will reach 1 MAC in 4 minutes and that of isoflurane in 1.5
minutes. The major advantages of this method are the rapidity
with which the desired concentration is achieved, the ability to
prevent unexpected raise in the agent concentration and the
ability to use the commonly available plenum vaporizers to
achieve the desired concentration. This also has the added
advantage of achieving better denitrogenation, so vital to the
conduct of the low flow anesthesia. The chief disadvantage would
be the high flows required which would compromise on the
economy of the gas utilization and the need for scavenging
systems to prevent theatre pollution. This period of using high
flows for a short period at initiation goes by the name of “loading”.
Prefilled circuit.
The second method is utilizing a different circuit like Magills for
preoxygenation. Simultaneously, the circle is fitted with a test
lung and the entire circuit is filled with the gas mixture of the
desired concentration. Following intubation, the patient is

14. 14
connected to the circuit thereby ensuring rapid achievement of
the desired concentration in the circuit. But all the factors
discussed above will be effective in preventing fast buildup of the
alveolar concentration to attain surgical anesthesia.
Use of large doses of anaesthetic agents.
The third method consists of adding large amounts of anesthetic
agent into the circuit so that the circuit volume + FRC rapidly
achieves the desired concentration as well as compensates for the
initial large anesthetic gas uptake. To execute this, the patient is
connected to the circuit, which is filled with oxygen (used for
preoxygenation), after intubation. Fresh gas flow is started with
metabolic flows of oxygen and a large amount of nitrous oxide
often in the range of 3-5 liters per minute. Oxygen concentration
in the circuit, which gradually falls, is continuously monitored and
the nitrous oxide flow is reduced once the desired oxygen
concentration is achieved (33 - 40%). The obvious disadvantage of
this method is the potential for errors and hypoxia if the oxygen
monitor were to malfunction. Hence this method is seldom used
for N2O.
The method discussed above is often used to build up the agent
concentration in the circuit. The commonly used agents are
halothane and isoflurane. This involves setting the VOC to deliver
a large amount of the agent while using low to moderate flows so

15. 15
that the required amount of vapor is added into the circuit. The
usual requirement of anesthetic agent is approximately 400 - 500
ml of vapor in the first 10 minutes which implies an average need
of 40 - 50 ml of vapor per minute during the first 10 minutes.
Most of the vaporizers allow a maximal concentration of 5% to be
delivered. At a setting 5% in the vaporizer, with a FGF of one
liter/minute, the required mass of 500 ml of vapor could be added
to the circuit so that the alveolar concentration could be built up.
The setting in the vaporizer can be brought down to 0.5 – 0.8 %
after 10 minutes and titrated according to the surgical needs.
Injection techniques.
An alternative method for administering the large amounts of the
agents is by directly injecting the agent into the circuit, a form of
VIC4,5,6,7,8. This is an old, time-tested method and is extremely
reliable. Each ml of the liquid halothane, on vaporization yields
226 ml of vapor and each ml of liquid isoflurane yields 196 ml of
vapor at 20oC . Hence, the requirement of about 2ml of the agent
is injected in small increments into the circuit. The high volatility
coupled with the high temperature in the circle results in
instantaneous vaporization of the agent. The injection is made
through a self-sealing rubber diaphragm covering one limb of a
metal t piece or a sampling port, inserted into either the
inspiratory or the expiratory limb (fig. 2).

16. 16
Fig 2. Closed circuit configuration for injection technique
The injection is made using a small bore needle and a glass
syringe. Placing a gauze piece or a wire mesh inside the T piece
often helps in the vaporization of the liquid. The intermittent
injections are often made in 0.2-0.5 ml aliquots manually. Doses
should never exceed 1ml at a time. Doses exceeding 2 ml bolus
invite disaster. Intermittent injections can often be easily
substituted with a continuous infusion with the added advantage
of doing away with the peaks and troughs associated with
intermittent injections.
The exact dose to be used is calculated thus:
Priming dose (ml
vapor) =
Desired concentration x {( FRC +
Circuit volume) +( Cardiac output
x BG Coeff.)}

17. 17
The Cardiac output and the FRC can be estimated for the patient
based on standard normograms. This priming dose is the dose
required to bring the circuit volume + FRC to the desired
concentration and is injected over the first few minutes of the
closed circuit anesthesia. Besides this, an amount of agent
necessary to compensate for the uptake of the body must also be
added and this is calculated depending on the uptake model being
used (vide infra).
THE MAINTENANCE OF LOW FLOW ANAESTHESIA.
This is the most important phase as this is stretched over a period
of time and financial savings result directly from this. This phase
is characterized by
1. Need for a steady state anaesthesia often meaning a steady
alveolar concentration of respiratory gases.
2.Minimal uptake of the anaesthetic agents by the body.
3.Need to prevent hypoxic gas mixtures.
Since the uptake of the anesthetic agent is small in this phase, the
low flow anesthesia is eminently practical. Adding small amounts
of the anesthetic gases to match the uptake and providing oxygen
for the basal metabolism should suffice. If CCA is used, this would
be directly equal to the uptake and hence provides for the
monitoring of the oxygen consumption and the agent uptake. If
low flow anesthesia is used, then besides the uptake, the amount

18. 18
of gas, which is vented, is also added to the circuit to maintain
steady state anesthesia.
Management of the oxygen and nitrous oxide flow during
the maintenance phase:
The need to discuss the flow rates of N2O and O2 arises
specifically because of the possible danger of administration of a
hypoxic mixture. Let us analyze the following example. 33%
oxygen is set using a flow of 500 ml of O2 and 1000 ml of N2O.
Oxygen is taken up from the lungs at a constant rate of about 4
ml/kg/min. N2O is a relatively insoluble gas and after the initial
equilibration with the FRC and vessel rich group of tissues, the up
take is considerably reduced. In this situation, there is a constant
removal of O2 at a rate of 200 - 250 ml/min, whereas the
insoluble gas N2O uptake is minimal. Hence the gas returning to
the circuit will have more N2O and less of O2. Over a period of
time, due to concentration effect, the percentage of N2O will go up
and that of O2 will fall, sometimes dangerously to produce
hypoxic mixtures.
Various short cuts are available to make low flow anesthesia easy
of which the most popular technique is the 'Gothenburg
technique' 9. Most of the other technique approximate to this and
hence, deserves a special mention.

19. 19
The Gothenburg Technique:
Initially high flows, oxygen at 1.5 l/min and nitrous oxide at 3.5
l/min had to be used for a period of six minutes after the
induction of anesthesia and this constitutes the loading phase.
This is followed by the maintenance phase in which the oxygen
flow is reduced to about 4ml/kg and nitrous oxide flow adjusted
to maintain a constant oxygen concentration in the circuit. The
usual desired oxygen concentration is about 40%. The use of an
oxygen analyzer is very important since the nitrous oxide added is
directly based on its readings and hence any errors would be
dangerous.
Other authors have made similar recommendations 10,11,12,13,14.
Most of the authors opine that the oxygen consumption under
anesthesia is about 200 - 250 ml. However, there is wide disparity
in the amount of nitrous oxide to be added into the circuit. This
controversy is consistent with the basic controversy surrounding
the uptake of the anesthetic agents and is dealt with in detail in a
later stage. For most practical purposes, in the absence of oxygen
analyzer the following technique is safe to use. A high flow of 10
lit/min at the start, for a period of 3 minutes, is followed by a flow
of 400 ml of O2 and 600 ml of N2O for the initial 20 minutes and
a flow of 500 ml of O2 and 500 ml of N2O thereafter. This has

20. 20
been shown to maintain the oxygen concentration between 33 and
40 % at all times.
Management of the potent anaesthetic agents during
maintenance phase.
This is easily accomplished by dialing in the calculated
concentration on the plenum vaporizer for the flow being used.
For example, suppose the anesthetic uptake for a desired
concentration of 0.5% halothane is 7.5ml/min (vide infra). If a
FGF of 500ml/min is being used, then the dial setting should be
1.5% for at this setting and for the used flow, the total vapor
output would be 7.5ml/min. If a flow of 1000ml/min is being
used, then the dial setting should be 0.8%. In practice the actual
dial setting often over estimates the actual output since the
plenum vaporizer under delivers the agent at low flows. Hence,
the dial setting is fine-tuned depending on the endpoints being
achieved.
During completely closed circuit anesthesia, the most popular
method of adding agents into the circuit is by the injection
technique. This is often used to initiate the closed circuit
anesthesia as described earlier. Later, the same setup is used to
continue the anesthesia by adding either small boluses or by
constant infusion into the circuit. The dose to be added depends
on the uptake model being used for the conduct of the closed

21. 21
circuit. The endpoint for adding the agent can be the achievement
of the desired end tidal agent concentration, measured using an
agent analyzer. This would be the most accurate method. The end
point may also be based on the hemodynamic stability 15.
Simple rule of the thumb techniques16,17 for adding the
anesthetic agents into the circuit both during the loading phase
and the maintenance phase has been suggested.
Weir and Kennedy4 recommend infusion of halothane (in liquid
ml/hr) at the following rates for a 50 kg adult at different time
intervals.
0-5 min 27 ml/hr
5-30
min
5.71
ml/hr
30-60
min
3.33ml/
hr
60-120
min
2.36
ml/hr
These infusion rates had been derived from the Lowe's theory of
the uptake of anesthetic agent (vide infra). They had
approximated isoflurane infusion (in liquid ml/hr) based on the
Lowe's formula as follows:

22. 22
0 - 5
min.
14 + 0.4X wt.
ml/hr.
5 - 30
min.
0.2 X initial
rate.
30-60
min.
0.12Xinitial
rate.
60-
120min.
0.08X initial
rate.
For halothane infusion, they had suggested that the above said
rates be multiplied by 0.8 and for enflurane, multiplied by 1.6.
These rates had been suggested to produce 1.3 MAC without the
use of nitrous oxide. The infusion rates had to be halved if nitrous
oxide is used.
The other salient points to be considered during the maintenance
phase are the following: a) Leaks must be meticulously sought for
and prevented since they would decrease the efficacy of the
system. Flows must be adjusted to compensate for the gas lost in
the leaks. b) Most of the gas monitors sample gases at the rate of
200 ml/min, which may be sometimes as high as half the FGF.
Hence, care must be taken to return the sample back to the circuit
to maximize the economy of FGF utilization. Some gas analyzers
like Ohmeda Rascal add air to the sample exhaust. This if
returned to the circuit would result in dilution of the anesthetic

23. 23
mixture and accumulation of nitrogen within the circuit and
hence should be vented. This mandates utilization of a flow
adequate to compensate for this loss. Recent studies18 have
shown that venting of the gas from the analyzer does not alter the
dynamics to any large extent and can safely be done.
CONTROVERSIES IN THE UPTAKE MODELS OF
ANAESTHETIC AGENTS
EXPONENTIAL OR LINEAR?
Knowledge of uptake of anaesthetic agent is very important in
the practice of closed and low flow anaesthesia since, the very
technique calls for the addition of an amount of anaesthetic agent
which is taken up by the body. In fact, mutually contradicting
models exist on the uptake of anaesthetic agents. The Lowe's theory
13,14 which has wider acceptance ascribes the anaesthetic uptake
to an exponential model. It states that the uptake of agent is
inversely proportional to the square root of the time, implying that
the uptake decreases exponentially with time. It necessitates
calculation of unit dose (Appendix 1). This unit dose is the amount
of anaesthetic agent to be added to the closed circuit during the
time intervals of 0-1 min, 1-4 min, 4-9 min, 9-16 min, and so on.
Besides that the circuit and the FRC and the circulating blood of

24. 24
the patient had to be brought to the desired concentration with a
prime dose.
Prime dose = {(circuit volume + FRC) + (Q x )} x desired
concentration.
This prime dose had to be added into the circuit during the first 9
minutes of closed circuit anesthesia.
The practical implication of this is that to maintain closed circuit,
one must calculate the agent and gases to be added into the circuit
using hair-splitting exponential equations, often frightening the
anesthetist. It has been one of the main causes for the reluctance
in the widespread usage of the closed circuit anesthesia.
In total contrast to this exponential theory is the linear model
proposed by CY Lin 12,19. He states that the uptake of anesthetic
agents is a near constant over the clinically important
concentrations. Hence, he advocated adding the anesthetic agent
as a constant rate infusion into the circuit throughout the
anesthetic procedure. Lin had contended that the FRC constituted
an extension of the breathing circuit and the washing into it could
not be considered as uptake by the body. He had suggested a
simple method of conducting the closed circuit anesthesia: It had
consisted of using a high flow of nitrous oxide and oxygen (6
L/min and 4 L/min respectively) for 3 minutes (three time

25. 25
constants). At the end of 3 minutes, the flows had been reduced to
metabolic flows and closed circuit started. Potent agents had been
added either through a VOC (like a copper kettle) or by direct
injection into the circuit. The anesthetic agent required to
washing the circuit volume and the FRC of the patient had
constituted the prime dose and it should be added to the circuit
during the first ten minutes, besides the dose required to
compensate the uptake of the agent. The formula to calculate the
amount of agent to be added into the circuit to equal the uptake
had been:
uptake of anaesthetic
agent =
desired concentration X
alveolar ventilation X fractional
uptake ( ml of vapour)
The fractional uptake (= 1 - FA / FI) for halothane had been
calculated as 0.5 and that for enflurane, as 0.4. He had concluded
that anesthesia thus conducted produced a nearly constant
inspired and expired concentration implying that the uptake of
the anesthetic agents had been a near constant.
Unfortunately very little literature exists on the efficacy of either
of these models. The study conducted to compare these two
models in our Institute, revealed that predictive performance of
both the models were statistically similar, and linear uptake
model had scope for improvement whereas the exponential model

26. 26
had no such scope. Lin's linear model however has a distinct
superiority in the form of simplicity.
Our subsequent experience in simplifying low flow
anaesthesia
100 patients of ASA physical status 1 or 2 undergoing general
surgical procedures under general anesthesia were induced with
thiopentone and intubation facilitated with succinylcholine after
preoxygenation with 100% oxygen for 3 minutes. Total FGF of
100 ml / kg was used for initial 10 min, N2O to O2 ratio of 60:40
along with 1.5% isoflurane, after connecting patients to the circle
breathing system. FGF was reduced to 300ml/min of N2O and
300ml/min of O2 at the end of 10 min but the dial setting of 1.5 %
isoflurane was not changed for the rest of the period. In the
control group, after the initial 10 minutes, patients were given a
flow of 4L/min in the ratio of 65:35 of N2O:O2.
During the course of low flows, inspired O2 concentration never
fell below 0.3(30 v/v %). Initially as N2O was being used up
rapidly, initial inspired O2 concentration increased and the End
tidal O2 concentration was higher than the inspired O2
concentration. After a period of 20 minutes, N2O usage decreased
and a period of constant uptake is present. Least value of inspired
O2 concentration recorded was 0.31. After one hour the mean

27. 27
value of FiO2 was 0.41(41 v/v %) and 0.39(39 v/v %) at the end of
2 hours (fig 3).
For the first five minutes in high flows, the inspired isoflurane
concentration was around 1.1 v/v%. This value settled to around
0.7v/v%. This value was more or less constant throughout the
period. Initially, the concentration of end tidal isoflurane was
0.59±0.027. This value rose during high flow period to
0.78±0.015 v/v%. During low flows the mean concentration was
0.55± 0.007 v/v%.
Changes in O2 & N2O conc over time
25
30
35
40
45
50
55
60
65
3 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120
Time in Minutes
Concentration%
Fio2
FiN2O
EtO2
EtN2O

28. 28
The combined MAC value computed from the end tidal
concentration of N2O and Isoflurane was maintained at 1.1 to 1.2
MAC and this along with IV narcotics provided adequate depth of
anesthesia for all patients (fig 4). N2 accumulation was found to
decrease during the initial high flow period and subsequently in
the low flow period, there was a gradual increase in its
concentration up to a mean of around 3. But this did not
necessitate change in flow rates to wash it off as FiO2 did not fall
below 0.31. Conduct of anesthesia proved to be safe with no
adverse outcome.
Total gases consumed for 120 min were calculated and the
usage was 66 L of N2O, 55 L of O2 and 9.3 ml of liquid Isoflurane
Changes in Isoflurane over time
0
0.2
0.4
0.6
0.8
1
1.2
1.4
1.6
3 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120
Time in Minutes
Isofluraneconcentration
Mean Et
Mean Fi
Dial setting
combined MAC

29. 29
in the low flow group. In the high flow group, 176.5L of O2 and
320 L of N2O and 25.83 ml of liquid isoflurane were used. The
total cost in high flows was Rs. 532.69 and Rs. 192 in the low flow
group leading to a cost reduction of 64%.
Sevoflurane controversy
Sevoflurane, like all currently used volatile anaesthetics, is
degraded by carbon dioxide absorbents. The most significant
degradant is a haloalkene known as "compound A" being
nephrotoxic in rats at an exposure of 150 – 340 ppm-h. Applying
low-flow sevoflurane in volunteers one study group found an intact
renal function using validated markers of renal function (creatinine
clearance, serum BUN and creatinine), but a transient increase of
experimental markers of renal function (urine excretion of protein,
glucose, and certain tubular enzymes). This “transient renal injury”
was attributed to compound A. Additionally, the study group
claimed a threshold value of compound A of about 150 ppm-h to
induce transient renal injury and postulated a similar renal
sensitivity to compound A in humans as in rats.
However, over the years these results and conclusions could not
be confirmed by other study groups. Several studies found that
the renal uptake and metabolism of the glutathione and cysteine
conjugates of compound A are different in rats and humans. Thus,
the threshold for nephrotoxicity of compound A in rats does not

30. 30
apply to humans. Furthermore, summarizing all data about
protein excretion on postoperative day 3 (as “sensitive marker” of
renal dysfunction) after low-flow sevoflurane from surgical
patients and volunteers did not show a threshold even though
exposures up to almost 500 ppm-h had been documented.
Considering all of the studies published to date in patients or
volunteers (other than that reported by Eger et al.), and even
using proteinuria as a so-called “sensitive” (albeit not validated
and experimental) marker of renal dysfunction, there is no
difference between the renal effects of low-flow sevoflurane and
other anesthetics (isoflurane, desflurane, enflurane and propofol).
This also applies to patients with preexisting renal impairment.
Furthermore, there have been no case reports of compound A-
associated renal injury reported in humans so far. Thus, low-flow,
minimal-flow and closed-loop anesthesia with sevoflurane is as
safe as anesthesia with other anesthetics. In conclusion,
compound A is no longer a matter of concern.
Compound A is produced by degradation of sevoflurane in the
presence of soda lime or Bary lime. As such, it is not a metabolite
produced by biotransformation of sevoflurane in the body, but is
rather a degradation product generated in the anesthesia circuit.
Changing the composition of the absorbent by eliminating the
potassium hydroxide has reduced the formation of compound A to

31. 31
a large extent. Eliminating the NaOH also has made it safer.
Amsorb® plus is now available in India.
Absorbent
Hydroxide
content
Compound A Menthol
Bary lime
KOH 4.7%
Ba(OH)2 7.4%
64.6 373
Soda lime
KOH 2.9%
NaOH 1.4%
56.4 606
Sofnolime NaOH 2.6% 2.2 91
Amsorb®
plus
Ca(OH)2
Cacl2
Negligible -
TERMINATION OF LOW FLOW ANAESTHESIA.
Unlike the initiation or the maintenance of the closed circuit,
termination is less controversial. There are only two recognized
methods of termination of the closed circuit. They are as follows:
Towards the end of the anesthesia, the circuit is opened and a
high flow of gas is used to flush out the anesthetic agents which
accelerates the washout of the anesthetic agents. This has the

32. 32
obvious advantage of simplicity but would result in wastage of
gases.
The second method is the use of activated charcoal8. Activated
charcoal when heated to 220oC adsorbs the potent vapors almost
completely. Hence, a charcoal-containing canister with a bypass is
placed in the circuit. Towards the end of the anesthesia, the gas is
directed through the activated charcoal canister. This results in
the activated charcoal adsorbing the anesthetic agent resulting in
rapid recovery and at the same time, reducing theatre pollution.
Nitrous oxide, due to its low solubility is washed off towards the
end by using 100% oxygen.
To conclude the low flow closed circuit anesthesia has many
advantages to offer. To list a few,
1. Enormous financial savings due to use of low fresh gas flows as
well as the agent.
2.High humidity in the system leads to fewer post anaesthetic
complications.
3.Maintenance of body temperature during prolonged procedures
due to conservation of heat.
4.Reduction in the theatre pollution.
The perceived disadvantages are not real:

33. 33
1. The need to accurately adjust the flows of gases. The system is
inherently stable once a steady state is reached and small errors
in the dosage of the agents or the gases would be of no concern.
2.Accumulation of trace gases20. It has, however, been often
overestimated21.
3.Need for monitoring equipment. Oxygen monitor is necessary
but not mandatory if the recommended flow rates are used.
EtCO2 monitor is indicated to ensure satisfactory CO2
absorption and maintenance of normocarbia.
With a proper understanding of the concepts of practice, the low
flow anaesthesia technique can safely be used in all surgical
procedures lasting more than an hour.

34. 34
APPENDIX

35. 35
REFERENCES
1. Baum JA, Aithkenhead: Low flow Anaesthesia. Anaesthesia. 50 (suppl).: 37-44,
1995
2. Baker AB: Editorial. Low flow and Closed Circuits. Anaesthesia and Intensive
Care. 22: 341-342, 1994
3. Mapleson W: The theoretical ideal fresh gas flow sequence at the start of low flow
anaesthesia. Anaesthesia 53(3): 264-72, 1998
4. Weir HM, Kennedy RR: Infusing liquid anaesthetic agents into the closed circle
anaesthesia. Anaesthesia and Intensive Care. 22: 376-379, 1994
5. Wolfson B: Closed Circuit Anaesthesia by Intermittent Injections of Halothane.
British Journal of Anaesthesia. 34: 733 - 737., 1962
6. Thorpe CM, Kennedy RR: Vaporisation of Isoflurane by Liquid Infusion.
Anaesthesia and Intensive Care. 22: 380-82, 1994
7. Hampton JL, Flickinger H: Closed Circuit Anesthesia utilising known increments
of Halothane. Anesthesiology 22: 413-418, 1961
8. Philip JH: 'Closed Circuit Anesthesia' in 'Anesthesia Equipment: Principles and
Applications'. Edited by Ehrenwerth J, Eisenkraft JB, Mosby Year Book Inc., 1993,
Chap 30.
9. Dale O, Stenqvist O: Low flow Anesthesia: Available today - A routine tomorrow.
Survey of Anesthesiology. 36: 334-336, 1992
10. Cullen SC: Who is watching the patient? Anesthesiology 37: 361-362, 1972

36. 36
11. Baker AB: Back to Basics - A Simplified Non - Mathematical Approach to Low
Flow Techniques in Anaesthesia. Anaesthesia and Intensive Care. 22: 394-395., 1994
12. Lin CY, Benson JW, Mostert DW: Closed Circle Systems - A new direction in the
practice of Anaesthesia. Acta Anaesthesiologica Scandinavica. 24: 354-361., 1980
13. Lowe HJ: 'The Anesthetic Continuum' in the book, 'Low flow and closed circuit
anesthesia'. Edited by Aldrete JA, Lowe HJ, Virtue RW, Grune & Stratton, 1979, pp
11-38
14. Lowe H: 'Closed- circuit anesthesia', in the book 'Clinical Anesthesiology' Edited
by Morgan GE, Mikhail MS, Appleton and Lange, 1992, pp 112 - 115.
15. Da Silva CJM, Mapleson WW, Vickers MD: Quantitative study of Lowe's square
root of time method of closed system anaesthesia. British Journal of Anaesthesia. 79:
103-112., 1997
16. El - Attar AM: Guided Isoflurane injection in a totally closed circuit. Anaesthesia.
46.: 1059-1063., 1991.
17. Eger II E: “Uptake and Distribution”, in the book “Anesthesia”, Edited by Miller
RD, Ed 4, Churchill Livingstone,1994, p118.
18. Bengtson J, Bengtsson J, Bengtsson A, Stenqvist O: Sampled gas need not be
returned during low-flow anaesthesia. Journal of Clinical Monitoring 9(5): 330-4,
1993
19. Lin CY: Uptake of Anaesthetic Gases and Vapours. Anaesthesia and Intensive
Care. 22: 363-373, 1994

37. 37
20. Morita S, Latta W, Hambro K, Snider MT: Accumilation of methane, acetone and
nitrogen in the inspired gas during closed circuit anesthesia. Anesthesia and
analgesia. 64: 343-347, 1985
21. Baumgarten R: Much ado about nothing: Trace gaseous metabolites in closed
circuit. Anesthesia and Analgesia. 64: 1029-1030, 1985

38. 38
UPTAKE AND DISTRIBUTION OF THE
INHALATIONAL ANAESTHETICS
Dr. Ashok Deshpande, Intensivist, Bharti Medical College, Sangli
The goal in inhalational anesthesia is the development of the
critical level of the anesthetic agent in the brain .
Factors for this are -----
1. Production and delivery of suitable concentration of the
anesthetic drug for inhalation
2. Distribution of the agent to the lung
3. Uptake of the agent from the lungs
4. Distribution of the agent to the brain and other tissues.
5. Metabolism of the anesthetic agent
UPTAKE AND DISTRIBUTION OF THE
INHALATIONAL AGENT
Anesthetic agent has to achieve a level in the lungs
called as alveolar level . This is the result of the two factors ---
1. Factors responsible for delivery to the lung
2. Factor responsible for uptake from the lung
Factors for delivery ---

39. 39
1. Inspired conc of the agent
2. Level of the alveolar ventilation
Inspired conc of the agent Inspired conc is the
amount of the agent present in the inspired gases . Rate of
rise of the agent is directly proportional to the inspired
concentration This has lead us to Concentration effect. This rules
as , higher the inspired conc ,rapid is the rise of alveolar conc .
This is the result of –
1. Concentrating Effect
Imagine the lung filled with 100% anesthetic agent ,
some gas is removed by circulation of the blood but
concentration should remain 100%
Fig 1
If this is filled with 80% anesthetic agent
and 20 % insoluble gas , as the anesthetic agent is absorbed ,

40. 40
the proportion of the agent in the lung must alter as the
diluent gas is same . So, a diluent gas represents large
proportion and concentration of the anesthetic falls . This rate
and degree of fall depends on the solubility of the agent in
the blood ( Fig. 2)
Fig. 2
2. Inspired Ventilation
When appreciable amount of the anesthetic agent is taken
up by the blood the lung do not collapse, on the other
hand as pressure drops it leads to sub atmospheric
pressure resulting in the inspiration of the additional vol.
of gas to replace the one which is absorbed.
This concentration effect modifies the influence of the
uptake from the lungs , on the rate of rise of the alveolar
conc to conc Inspired .

41. 41
Alveolar Concentration = Ventilatory input -- Circulatory
uptake
If the circulation removes half of the anesthetic
introduced by ventilation the Alveolar concentration will
be half of the Inspired concentration. The influence of
the uptake on alveolar concentration diminishes as
inspired conc increases to 100 % .Thus uptake ceases to
influence alveolar conc and then ,
alveolar conc depends on the ventilation to FRC .As the
FRC will be saturated with anesthetic agent the alveolar
conc will rise .
Second gas effect---- As the inspired ventilation
increases there is rapid uptake of the anesthetic agent .If
a second gas such as halothane is added , then as alveolar
ventilation is high ,halothane is also inspired more .
Because of this the level of the halothane in the blood
rises fast in spite of its inspired concentration This is
second gas effect .
LEVEL OF THE ALVEOLAR VENTILATION
With the increased level of the ventilation , the conc. of
the agent in the alveolus also increases rapidly i.e. F A
.This tries to equalize with the inspired conc F I. Thus FI =
FA. The limiting factor for this is FRC ( Functional
Residual Capacity ). The level of the new gas in the

42. 42
inspired mixture decreases because the air in FRC has
to be replaced by the new gas .
Suppose FRC 2 lit. 100 % N2O as induction agent , each
breath (TV ) 500 ml , alveolar ventilation 4 lit. /min
At the end of the first breath alveolar concentration of
nitrous oxide will be
(500ml N20 TV + 2000 ml FRC) = 2500 ml (TV+FRC)
20% will be alveolar conc of N2O
At the end of the second breath ----
500ml (fresh Breath) N2O + 400ml (20 % 0f 2000) N2O +
2000 ml FRC. Thus N2O will be 900 ml in 2500 ml, so it will
be 36%. Like this at the end of the 1 set min it will be
86% .
Time Constant --- is the time required for the flow (
Ventilation ) through a container to equal the capacity of
container OR Time required for the 63% wash in of the
new gas into the lung . (Lung = FRC)
Capacity 10 lit.

43. 43
5 Lit N2O / min
Fig. 3
Time constant = Capacity / flow = 10 / 5 = 2 min. (Fig 3)
So in the above example when flow is 4 lit/min , capacity
is 2 lit ( FRC ) , then time constant will be 2/4 = 0.5 min.
So conc of N2O after ½ min will be 63% and after 1 min
86 % by doubling the time from ½ to 1 min.
Alveolar level of the anesthetic is the result of the rate
of delivery and rate of uptake .
Uptake depends on the three factors and it is a product of
three factors ----
1. Solubility of the agent in the blood
2. Cardiac output
3. Alveolar – Venous level of the agent
Increase in any component will increase uptake and vice
versa and will decrease the rate of rise of the alveolar
tension .

44. 44
1. Solubility ---- Term used to describe the distribution
of the Gas / Vapor in two media , Blood / Gas and
Tissue / blood. It is also called as Partition Coefficient.
If Blood / Gas partition coefficient is greater the uptake
of the anesthetic is also greater and so the rate of rise of
the alveolar conc is slow
Higher B/G coefficient -------- slow induction (Ether)
Lower the B/G Coefficient ------ Fast induction
(Sevoflurane)
Induction is also made faster in spite of high solubility
by increasing the inspired concentration to a much higher
level .
Agent B/G
COEFFICIENT
T/G brain
COEFFICIENT
Nitrous Oxide 0.47 1.06
Sevoflurane 0.65 1.7
Isoflurane 1.4 1.6
Enflurane 1.8 1.4
Halothane 2.36 2.6
Ether 12.1 1.14
Methoxyflurane 15 1.4

45. 45
Above figure 4 shows derivation of the Blood /Gas coefficient
Behavior of the drug and Solubility
1. Totally insoluble in blood B/G= 0 No Uptake
Alveolar Conc will increase fast and will be equal to
inspired conc
FA = FI (fig 5)
Fig 5 Fig 6
2. Low blood gas solubility -- Small amount of the agent
is taken by the blood. This increases alveolar
concentration rapidly as well as the concentration in the
blood as it is less soluble . This blood reaches the tissue ,
tissue takes up some molecules of the agent , so venous
blood will have less concentration of the agent . (Fig 6)
This blood reaches the lung where alveolus has full
concentration of the agent . So the tension of the agent
in the alveolus is more and tension of agent in venous
blood is less. So blood will pick up more molecules of
the agents and the cycle goes on ( Fig 7 )

46. 46
Fig 7
3. Highly Soluble --- Blood will absorb more agent like
a bloating paper and so the alveolar concentration will
rise slowly .
As alveolar concentration is less , concentration in blood
is less and the induction is slow ( Fig 8 )
Fig 8
Approach of the alveolar conc to inspired conc is related
inversely to solubility .So it is slow with highly soluble and fast
with insoluble agents.

47. 47
2 Cardiac Output ----
It is the pulmonary blood flow which carries the
anesthetic agent with it from the lungs . So when there is,
This relationship affects more soluble agents than least soluble
agent as follows ---

48. 48
If the Cardiac output is doubled , then uptake is not doubled
. So induction in thyrotoxicosis , nervous patients will take
longer time with highly soluble agents . But if the Cardiac
Output is reduced as in hemorrhage , heart disease rate of
induction of anesthetic will be greatly increased .
3. Influence of Alveolar to Venous difference -----
Tissues remove all the anesthetic brought to them by the
arteries .This leads to fall of the venous anesthetic level far
below the arterial . Alveolar to venous anesthetic
difference is more , so diffusion of the anesthetic vapors
from alveolus to blood in the capillaries is rapid, so uptake
is more . With time the tissue level increases leading to
lesser uptake by tissue ,so the venous level of the
anesthetic also increases , causing a reduction in the

49. 49
difference in the Alveolar--- Venous concentration . This
reduces the uptake of the anesthetic
DISTRIBUTION OF ANAESTHETIC
Up take from the Lung = Up take by the tissue. If there
is no uptake by tissue then the alveolar to venous difference
will be zero . So FA=FI
Uptake by the tissue is governed by --
1. Solubility of the drug in tissue
2. Tissue blood flow
3. Partial pressure difference in arterial blood and tissue
If any of the factors is zero , then uptake is zero . If any
of the factors is increased , then uptake is more and if
any of them is decreased , then uptake is decreased . As
tissue is saturated with the anesthetic, the uptake is
decreased and may become zero .

50. 50
Capacity of the tissue to hold the anesthetic depends on
the size of the tissue , affinity of the anesthetic in the
tissue , solubility of the anesthetic in the tissues .
Therefore
Capacity of the tissue to
Absorb anesthetic drug = Tissue solubility X Tissue
volume
so if tissue solubility and/ or volume is more , then
capacity is also more .
If the tissue has large capacity and the perfusion of
blood is less than the rate of rise of the anesthetic
level is also slow ,so the uptake will be for long time .
Opposite of this - If the tissue is highly perfused
with blood , then the uptake is also fast and uptake time is
also less. Ultimately uptake ceases also fast .This uptake of
the agent is governed by the Tissue / Blood coefficient .
Variation in the tissue / blood coefficient is very less as
against the Blood / Gas coefficient . Tissue / Blood coefficient
varies between 1 for N2O and 4 for halothane . Ultimately

51. 51
when the tissue is fully saturated tissue anesthetic partial
pressure = arterial anesthetic partial pressure but the time
required for this is different for different type of tissues . The
limiting factor for this is the blood supply to the tissue . On
this basis the tissues are divided in to four groups . Each
group makes contribution for the uptake in total.
The four groups of tissue are ---
1. Vessel rich group
2. Muscle Group
3. Vessel poor group
4. Fat group
Vessel rich
group
A. Heart , Brain ,
Kidney , Liver ,
Endocrine
Gland
Splanchnic Bed
,
B. 10 % of body
mass
C. 70 % Cardiac
Output
D. High flow per
unit vol. of the
tissue
E. Rapid
equilibration
with arterial
partial
pressure
Muscle Group
A. Muscle and
Skin
B. 50 % of body
mass
C. 24 % Cardiac
Output
D. average flow
per unit mass
E. Equilibration
takes fast but
slower than VRG
F. Uptake of
anesthetic is fast
Very Poor
Group
A. Skeleton ,
Ligaments ,
Cartilages,
B. 18 % of body
mass
C. 1 % Cardiac
Output
D. very low flow
per unit mass
E. Equilibration
takes long time
F. Uptake of
anesthetic is
slowest
Fat Group
A. Fatty tissue
B. 22 % of body mass
C. 6 % Cardiac Output
D. low flow per unit
mass
E. Equilibration takes
very long time may be
hours
F. Uptake of anesthetic
is very slow

52. 52
Effect of tissue uptake on the rate of rise of alveolar
concentration .
Greater the solubility of anesthetic in tissue , lesser is the
rate of rise of alveolar concentration
Alveolar concentration rises first regardless of the solubility
because at the beginning of anesthesia alveolar
concentration is zero .Later on, it rises fast initially but
alveolar to mixed venous anesthetic partial pressure
difference is small , so uptake is less .After few minutes the
partial pressure difference develops due to uptake .
So slowly ,uptake of anesthetic from alveoli = input by the
ventilation .Thus rapid rise slows down producing the first
bend A . If uptake continues at the same rate the curve
would have been plateau . But due to the saturation of the
VRG initial uptake is not maintained . Also due to
saturation of VRG , the venous blood conc of the anesthetic
is same as arterial . This reduces the alveolar venous
difference leading to decrease in uptake and on top of it
F. Uptake of the
anesthetic is
very fast
G. 5—15 min for
induction
G. Most anesthetics are
HIGHLY Soluble in fat

53. 53
continued ventilation increases alveolar ventilation . Due to
saturation of VRG , second bend is seen .
Next is uptake by MG and FG which is very slow , so the
curve is flat and continues for a long time
Effect of abnormalities of the Cardio pulmonary
function on uptake of anesthetic agent
Diseases and drugs affect the cardiac and/ or pulmonary
function. So it changes the uptake. Hyperventilation ,
Ventilation Perfusion inequalities , decrease cardiac output
changes the Cerebral Blood Flow .
Hyperventilation -------
Increases rate of delivery of the anesthetic to alveoli
Decreases level of CO2
Decreases cerebral blood flow
Decreases rate of rise of the anesthetic in brain

54. 54
Increase in the Alveolar concentration of agent
If solubility is high, there is faster induction with
hyperventilation
If solubility is intermediate ,such as halothane , it balances
the increased alveolar concentration and decreased
perfusion of brain .
Reduction in the Cardiac Output and Cerebral
blood flow
Decrease in cardiac output Decreases uptake
Increases the alveolar conc.
Decrease in cardiac output with decrease in cerebral blood
flow ----- decreases the uptake by brain . If the anesthetic
agent is soluble ,It increases rate of rise of anesthetic in
the lungs . So it balances decrease in cerebral flow and
uptake remains the same . Due to this there is increase in
the level in the brain , but due to increase in alveolar
partial pressure and due to decrease in cardiac output ,it
causes higher brain levels in spite of the difference in
solubility .
Effect of the venous admixture -----
Venous admixture due to physiological shunt is normal. It is
due to pleural veins, bronchial veins, Thebesian veins. It is 5 %
of cardiac output. Many cardiopulmonary diseases increase
venous admixture

55. 55
All agent is delivered to B as A is blocked , so B increases
the uptake of the agent to compensate for A . But this is
not exactly as would have been by both .
Venous Admixture ----
Blood to left side of the heart –
1. Blood from alveoli
2. Mixed venous blood
Less oxygenated blood is responsible for venous
admixture.
1. True shunt - Blood from right to left of the heart
without oxygenation .

56. 56
2. Blood with some oxygen from alveoli but not fully
oxygenated , due to under perfused / over ventilated
zones of lung
Normal Abnormal
Extra
pulmonary
Thebesian
vessels
Congenital heart disease
with
right –left shunt
Intrapulmonary Bronchial
veins
Slight
Atelectasis
Atelectasis ,Pulmonary
infection
Pul. A V shunts ,Neoplasms
Contused, edematous ,
damaged alveolar perfusion
Anatomical shunts are true shunts
Pathological shunts are not present in normal people
,ex- CHD with R – L shunt
Physiological shunts Normal admixture due to true
shunt and due to over ventilated / under perfused zones
of lung
Atelectic shunt Blood passing to collapsed alveoli
Venous admixture causes Increase in PaCO2 and
decrease in PaO2. Small decrease in O2 content is reflected
by large reduction in PaO2

57. 57
So arterial PO2 is the indicator of venous admixture . It is
due to
1. True shunt
2. V—P Shunt
Give 100 % oxygen to breathe , if PO2 increases by
small amount , it is a true shunt . Normal admixture is 5%
Effect of the anesthetic agent on air and gases in
closed cavities
Middle Ear, Intestine, Pleural Cavity, Pneumothorax,
Pneumo encephalogram.
If 70:30 N2O : O2 is used then it enters the cavity and
it increases in volume as N2O is 34 times more soluble
than N2 in blood .As the difference in the partial
pressure between N2O in blood and air in body cavity is
more , so large quantity of N2O will enter the cavity
than the amount of N2 that will come out from cavity .
When the wall is elastic , there is distension but when
the wall is rigid there is pressure .
Recovery from anesthesia after stopping the anesthetic
and the gases leads to Diffusion Hypoxia

58. 58
At the end of the surgery, patient breathes room air.
Alveoli contains N2 + O2 + CO2 + H2O Blood contains
N2O which comes out 34 times more than N2 .So in the
1st minute 1500 ml , 2nd min 1200 ml , 3rd min 1000 ml .
Volume of expiration is more than inspiration. CO2 is
removed from the alveoli , decrease in ventilation drive
leads to apnea . As N2O comes in alveoli dilutes alveolar
oxygen.
Usually Alveolar O2 is 14% but with N2O it is 10 %
leading to hypoxia which is dangerous in elderly and
critically ill.
If hypoxia is for 10 min , there is little significance in
health ; but if ventilation is reduced, it is dangerous . So
to prevent this give OXYGEN to patient during recovery
.
If Cardiac Output is decreased and ventilation is also
decreased , then there is rapid fall in the alveolar
anesthetic concentration . If the cardiac output and
ventilation increases, then recovery is accelerated
Increased perfusion should go to the low perfusing
tissue muscle and fat .
Recovery point is difficult to define called as END POINT

59. 59
End Point ---- 1. Awake sufficiently 2. Recovery of reflexes 3.
Maintain safe airway 4. Tolerates postural changes without
fall in B P
MAC awake - It is the state at which patient will obey
commands and will maintain airway without assistance
MAC awake is 0.6 of MAC value of anesthetic agent.

60. 60
PAEDIATRIC INHALATIONAL INDUCTION
Dr. Vithal Dhulkhed, Professor and Head of Anesthesiology, Krishna
Institute of Medical Sciences, Deemed University, Karad
Introduction
"Infants should preferably be anesthetized in the mother's or
nurse's arms. Care should be taken in anesthetizing children to
make the operation as informal as possible... Mental suggestion
here plays a great part, as well as gentleness in voice and
movement..."
-Gwathmey J: Anesthesia 1914
Inhalational induction is a commonly used technique in
pediatric anesthesia management. Introduction of Sevoflurane
into anesthesia practice has made this technique even more
attractive.
Factors Influencing Choice of Technique
How old is the patient?
What is her/his underlying illness, general medical condition,
ASA physical status?
What is the surgical procedure planned?
How cooperative is the patient?

61. 61
Will a parent be present?
Does s/he have an IV?
Key points supporting inhaled anesthesia 1
Each inhalational anesthetic satisfies the four pillars of
anesthesia.
Induction is easy without IV access. Avoids the psychological
trauma associated with the fear of needles
Can be given by increments, reversible.
Induction of anesthesia is quick, simple and pain free by mask.
Relies less on manual dexterity than intravenous techniques.
Easy to estimate blood tension of inhalational anesthetics
noninvasively
Intravenous agents demonstrate excessive inter individual
variability and cannot be estimated.
Personal Indications for inhalation induction 2
Child’s preference, particularly in those who have had multiple
procedures and anesthetics
A child with a real needle phobia

62. 62
A child with marginal or difficult airways
A child with difficult vein access
After failed attempts at vein cannulation
The goals of preoperative preparation
Presence of the parents
"The presence of the parents during induction has virtually
eliminated the need for sedative premedication." -Fred Berry,
MD, 1990. Parental presence is especially helpful for children
older than 4 years who have calm parents. Pediatric anesthesia
is a family affair. Psychological preparation involves
recognizing and ameliorating stress experienced by the child
and family which is caused by separation, strange surroundings
("fear of the unknown"), painful procedures, fear of the
procedures and survival. Anesthesiologists have to realize the
importance of developing and using checklists. The patient
needs to be educated regarding the procedure to decrease
anxiety and facilitate recovery. The important considerations
are preoperative theatre visit, mock inductions, rewards, and
family counselling, the role of play therapists or clinical
psychologists in preoperative phase.2,3 A child/family friendly

63. 63
ward, holding area, anesthetic room, operating theater and
recovery area, games and reading material for a range of ages
help preparing a child and the family in coping up with the
stress.3,4
Honest communication and positive suggestion are the
key. The appropriate use of premedication options is to be
considered. Opinion regarding their preferred route of
induction of anesthesia and premedication should be sought
from children greater than 2 years of age at the preoperative
visit .5
Midazolam is often more effective than parental presence. - Zee
Kain, 1998 Anxiety can even be associated with oral midazolam
administration and can be significantly reduced in children
who had earlier received a toy to play with. - Golden et al,
2006.
A simple "try on your mask" test may be used to help predict
the likelihood of a smooth, calm inhalational induction. Just
demonstrate how the mask is to be worn on her/himself, then
hold the mask out to the child. If the child promptly and
happily takes the mask and places it correctly on her/his face,
the likelihood of smooth inhalation induction is high. At the
other extreme, if the child cries and refuses to touch the mask,

64. 64
preoperative pharmacologic sedation and/or an alternate
induction technique should be considered.
It is rather the absence of breakfast, which can make the
children very irritable. More liberal fasting guidelines make the
whole experience a good deal more pleasant and decrease the
likelihood of a stormy induction regardless of the chosen
technique.
Pharmacological premedication
Midazolam (Versed) is commonly used.
 PO: 0.5 to 1.0 mg/kg up to 10 mg max.
 Bioavailability = 30%
 Peak serum levels after about 45 minutes
 Peak sedation by about 30 minutes
 85% peaceful separation
 Mix with grape concentrate or acetaminophen syrup or
elixir (10 mg/kg of the 2% suspension) Mother may
administer to child for better acceptance
 Beware: total volume of dose should probably not exceed
0.4-0.5 ml/kg (NPO!)
 0.75 mg/kg may delay PACU discharge 30 minutes 6

65. 65
Ketamine
 PO: 6 to 10 mg/kg, may slightly prolong time to discharge
after a short case
 IM: 3 to 4 mg/kg sedation;
 2 mg/kg does not delay recovery
Midazolam + Ketamine
 PO 0.4 mg/kg + 4 mg/kg respectively
 100% successful separation,
 85% easy mask induction
(Reglan)
PO or IV: 0.2 mg/kg
Ranitidine (Zantac)
PO 2.5 mg/kg
Glycopyrrolate
Consider for selected patients for planned airway
instrumentation; e.g.: fiber optic endoscopy, oral or upper

66. 66
airway surgery, cleft palate)
5-10 mcg/kg IV; 10 mcg/kg IM
My choice of induction technique in younger pediatric age
group who refuse intravenous cannulation has tilted in favor of
inhalational induction particularly with the introduction of
sevoflurane into our practice. Its unique physical properties,
pharmacokinetics and dynamics have a dominating influence in
the choice of induction technique. Whether they are used for
induction or maintenance of anesthesia, inhalational
anesthetics are pervasive because they are effective, reliable,
safe, easy to deliver, stable, and without major end organ
sequelae. Sevoflurane is useful for both sedation and general
anesthesia, and while there is an increased likelihood of
emergence delirium, it is not exclusive to this agent and can be
managed. It is less expensive than
Propofol, does not sting or burn, and ordinarily does not cause
apnea, or unpredictable bradycardia. In children in whom
vascular access is an issue, the vasodilation is very helpful.
It is volatile halogenated ether anesthetic agent, Fluromethyl 2,
2, 2,-trifluoro-1-[trifluoromethyl] ether ether; nonflammable,
non-irritating, minimal odor, no pungency

67. 67
Vapor Pressure 160 mmHg at 20oC, colorless liquid containing
no additives, low solubility in blood
Blood: gas partition coefficient 0.69 Adults (Halothane 2.57,
Isoflurane. 1.38), 0.66 Newborns MAC 2.05 in 100% oxygen;
child MAC 2.5%, infant MAC 3.2% Full-term neonate MAC
3.2% Preterm neonate MAC values generally decrease by 20-
30%
MAC (%) Halothan
e Isofluran
e
sevofluran
e
Enfluran
e Desflurane
Newborns 0.87 1.6 3.3 – 9.2
1 to 6 mth 1.2 1.87 3.1 – 9.4
0.5 to 1 yr. 0.97 1.8 2.7 – 9.9
1 to 12 yrs. 0.89 1.6 2.55 1.7 8.0 to 8.7
Adults 0.77 1.15 1.71 1.6 6
MAC values for anesthetic agent according to age [Gregory 1994; Inomata
1994]
Its degradation products were a concern i.e. gas flow and
temperature dependent degradation in clinical setting with the

68. 68
CO2 absorbents soda lime and Bary lime to Compound A
(PIFE) and trace amounts of Compound B (PMFE). Clinical
experience does not substantiate concerns about Compound A
and plasma F- ions No renal impairment in children, plasma F-
levels remain below theoretical toxic threshold -the affinity of
renal CYP450 2E1 for sevoflurane is fivefold less than for
Methoxyflurane. 7 Potential for hepatotoxicity appears
negligible. Several recent generation absorbents (Amsorb plus,
Superia, and Loflosorb )that produce neither compound A nor
carbon monoxide, even when desiccated, have been developed.
Sevoflurane has advantage over halothane for induction of
anesthesia. Halothane which has been popular as induction
agent is applied with considerably higher MAC values than
sevoflurane aggravating hemodynamic depression and
dysrhythmias. LMA insertion time is faster with sevoflurane
compared to halothane with less coughing and laryngospasm.8,9
PONV is less often than halothane. Potential to cause MH –
very rare case reports
Small FRC in neonates results in a more rapid induction with
inhaled anesthetics. Increased closing volume and decreased

69. 69
FRC make neonate prone to atelectasis and rapid desaturation
rendering them dependent on PEEP during anesthesia.
Changes in depth of sevoflurane anesthesia rapidly follow
changes in the inspired concentration. Premature Babies have
high oxygen consumption in order to meet their high metabolic
rate. They are unable to increase their tidal volume, instead
compensating for increased respiratory demands through a
raised respiratory rate, which can lead to early fatigue.
Perhaps the least understood, but most important, difference is
the neonate’s response to inhalation anesthetic agents. We still
do not know why the minimum alveolar concentration (MAC)
is higher compared with older children. The rate of rise of
inhalation agent depends upon the combination of delivery of
drug to and removal from the lungs. A steady state exists once
the alveolar and the inspired concentrations (FA/FI)
equilibrate; this equilibrium is more rapid in children.10,11
In neonates, the greater CO increases the equilibration of
FA/FI -high distribution to vessel rich groups (~ 18% neonate
vs. ~ 8% adult). The rate varies inversely with the solubility in
blood: nitrous oxide > desflurane > sevoflurane > isoflurane >
enflurane > halothane > methoxyflurane. This alveolar
‘washing’, (FA approaches FI) in children is about 50% higher
for 7% sevoflurane than 4.3% halothane with nitrous oxide.12

70. 70
Tissue/gas solubility- which is half of adult decreases the time
for partial pressure equilibration.
Anesthesia depth monitoring
Monitoring MAC value is all that is required for inhalational
anesthesia which is easier to do since present monitors with
anesthesia gas monitoring facility are commonplace, simple
robust reliable and easier to use.0.7 MAC sevoflurane yields a
similar incidence of awareness as a depth of anesthesia
monitors. During intravenous anesthesia, such comparable
technique is unavailable hence a supplemental depth of
anesthesia monitor is required, since awareness is twice as
frequently as during inhalational anesthesia.
Administration
Inspired concentration up to 8% (max on vaporizer) with
nitrous oxide and oxygen primed in the anesthetic with a single
breath from FRC ensures rapid induction within 20-40 sec
rapid induction, 13
Sevoflurane plus oxygen without nitrous oxide can afford more
margin of safety. The TEC vaporizer simplifies induction

71. 71
whereas the IV induction requires, EMLA cream application, IV
route, syringe pumps etc. For IV access EMLA used, requires 1
hour to act, causes undesired vasoconstriction
At the antecubital fossa injection of thiopentone into the artery
is a possibility.
What are the skills and preferences of the anesthesiologist?
If no IV is present, then inhalational induction is the gentle,
pleasant best technique, allowing the anesthesiologist to
practice her/his art as psychologist, physiologist, and
pharmacologist.
The child receives timely praise and positive reinforcement and
it is pointed out that this wearing of the mask is ALL she/he
will have to do in the operating room or induction area.
It is better and simpler to just trust the child to breath as s/he
has been doing all her/his life and calmly provide distracting
reassurance with a soft touch and a soothing, story-telling tone
of voice
It is preferable to induce them sitting up, or in a lap. Younger
children may also be less likely to be adequately sedated with
midazolam premedication (51). The only goal is to get 3 or 4
breaths of 8%, and then the child can be moved onto the OR

72. 72
table, is laid down, and restrained only if they become excited,
and not everyone does. There are psychological benefits in
gentle inhalational induction. Children over 6, who are
cooperative and are able to hold their breath, can be successful
with single-breath techniques. Often some children tolerate a
cupped hand, if they object to direct placement of the mask on
their face.
In fact, the sight, hearing and touch of the alert, vigilant
anesthesiologist comprise an entirely sufficient monitor for
initiation of inhalational induction in a healthy but anxious
child. As the child loses consciousness, the experienced
pediatric anesthesiologist will often recognize and correct
minor episodes of upper airway obstruction before a pulse
oximeter would have demonstrated any change. Rapid
emergence can be lifesaving if the airway becomes difficult to
manage with a bag and mask
Once the child has lost consciousness, the next most important
monitors, a precordial stethoscope and a pulse oximeter probe
may be gently applied. Subsequently, blood pressure cuff and
ECG leads may be added. A sick infant or child, especially if
unstable, should have these and any other appropriate
monitors applied before induction

73. 73
13-year-old describes her inhalational induction:
"I ended up going to sleep with a mask induction, and it wasn't
so bad after all. They gave me a liquid sedative beforehand to
make me very relaxed and a little sleepy, too. When they put
the mask on me, I noticed the smell of the gas, but didn't really
care because of the sedative. My eyelids got heavy, and I could
feel myself drifting off, and then it was all over."
A less well-known unexpected consequence of a Propofol
induction has been cardiac arrest in several neonates at
induction of anesthesia .14 .both the long-chain triglycerides
and Propofol have been implicated in poisoning the cardiac
mitochondria and causing cardiac arrest, which explains the
difficult and poor outcomes after resuscitation15
There are a few absolute contraindications: malignant
hyperthermia and probably muscular dystrophies 16
Environmental impact
The ozone layer, the environmental impact of polyhalogenated
anesthetics.17
Inhalational anesthetics are large molecules, MW of 180–200,
do not reach stratosphere

74. 74
Nitrous oxide is a small molecule with a MW of only 44 can
reach stratosphere. But only less than 5% of the nitrous oxide
that is released into the atmosphere arises from medical
sources; rest is from industrial sources.
Conclusion
Inhalational induction is widely practiced in pediatric
anesthesia. Preoperative preparation includes psychological
preparation of both parents and child in addition to
appropriate premedication. Sevoflurane is the preferred
inhalational agent. Majority of children prefer mask of
induction.
References
1. Jerrold Lerman, Martin Johr. Pro–Con Debate Inhalational anesthesia vs total
intravenous anesthesia (TIVA) for pediatric anesthesia Pediatric Anesthesia 2009 19:
521–534
2. Marzena Zielinska, Helen Holtby, Andrew Wolf. Pro–con debate: intravenous vs
inhalation induction of anesthesia in children Pediatric Anesthesia; 2011 21 :159–168
3. Margolis O, Ginsberg B, Dear Gl, et al. Paediatric preoperative teaching: effects at
induction and postoperatively. Paediatr Anaesth; 1998, 8:17-23.
4. Tatman A: The screaming child. In: Stoddart PA, Lauder GR, editors. Problems in
anesthesia: paediatric anesthesia. London: Taylor & Francis; 2004, pp. 145-152
5. Van den Berg AA, Muir J.Inhalational or Intravenous Induction of Anesthesia in
Children? An Audit of Patient and Parent Preference. J Anesthe Clinic Res 2011;2:156.
6. Cote Cj, Cohen IT, Suresh S, et al: A comparison of three doses of a commercially
prepared oral midazolam syrup in children. Anesth Analg; 2002, 94:1-3.

75. 75
7. Kharasch ED, Thummel KE. Identification of cytochrome P450 2E1 as the predominant
enzyme catalyzing human liver microsomal defluorination of sevoflurane, isoflurane,
and methoxyflurane. Anesthesiology 1993; 79: 795–807
8. Inagakai et al Anesth Analg 1997 Feb; 84 Suppl.
9. Kwek et al Anaesth Intensive Care 1997 Aug; 25:413-6
10. Salanitre E, Rackow H. The pulmonary exchange of nitrous oxide and halothane in
infants and children. Anesthesiology 1969; 30: 388-94
11. Yasuda N, Lockhart SH, Eger EI2, et al. Comparison of kinetics of sevoflurane and
isoflurane in humans. Anesth.Analg. 1991; 72: 316-24
12. Gallagher TM, Black GW. Uptake of volatile anesthetics in children. Anesthesia 1985;
40: 1073-7
13. Baum et al Anesth Analg 1997;85:313-6
14. Veyckemans F. Propofol for intubation of the newborn? Paediatr Anaesth 2001; 11:
15. Vasile B, Rasulo F, Candiani A et al. The pathophysiology of propofol infusion
syndrome: a simple name for a complex syndrome. Intensive Care Med 2003; 29:
1417–1425.
16. Hayes J, Veykemans F, Bissonnette B. Duchenne muscular dystrophy: an old
anesthesia problem revisited. Pediatr Anesth 2008; 18:100–106.
17. Logan M, Farmer JG. Anesthesia and the ozone layer. Br J Anaesth 1989; 63: 645–647.

76. 76
INTRAVENOUS INDUCTION OF ANAESTHESIA
IN PAEDIATRIC PATIENTS
Dr. Vidya Patil, Professor of Anesthesiology, Shri B.M. Patil Medical
College, Bijapur
A child is certainly not a small adult and hence anesthetic
management has to be tailor-made for each and every patient. A
technique chosen for induction in a particular child varies with
the age of the child, the underlying illness, the surgical procedure,
the location of procedure, the presence of other co-morbid
conditions, the availability of drugs and equipment, the skill & the
preference of the anesthesiologist……The list is endless.
Induction of anesthesia in paediatric patients is generally a
more sensitive process. One needs to be aware of the possibilities
of problems such as preoperative anxiety, emergence delirium,
emergence agitation, behavioral disturbances which can have long
term repercussions like sleep disturbances, behavioral regression,
maladaptive physical and mental manifestations that occur
following stormy inductions. These can persist for up to two
weeks after surgery and are highly disturbing to the parents and
the child.
In defense of IV induction let’s first consider the much hyped
“needle phobia”.
While much attention is given to the issue of ‘needle phobia’,
there exists mask phobia as well. Aversion to the smell and even
sight of masks is evident in a good number of patients, especially
children. Phobia of suffocation with mask is also known. Quite a
few children struggle to accept the presence of any foreign body

77. 77
on their face. The mask becomes all the more unacceptable when
it is applied against their faces despite their protests.
Added to the problem is the unfamiliar, unpleasant and often
pungent smell of the volatile agents, causing even the best
prepared child to lose composure? Moreover the needle is not the
only reason for preoperative anxiety. There are other reasons like,
 Separation from their parents
 Unfamiliar surroundings
 Strangers all around
 Frightening equipment
 Needle: The needle happens to be just one in the list .I would
like to emphasize the fact that all the standard text books and
other reliable literature and all experienced anesthesiologists
are of the view that if an IV line is present, then there cannot
be a better induction technique considering the safety of
induction and minimum incidence of postoperative
emergence & behavioral problems. (Unless it is
contraindicated for some reasons like a difficult airway, a
really difficult venous access and a child with a ‘real needle
phobia’)
Now, to tackle the problem of needle prick, we have reliable
topical anesthetic applications. EMLA cream applied an hour
before venipuncture takes care of the pain. Using a small dose of
Fentanyl just before Propofol or administering Lignocaine a while
before or with Propofol can provide effective pain relief for the IV
administration of Propofol for induction.
Two needle technique –Topical EMLA cream is applied an hour
before induction. A smaller gauge butterfly cannula is shown to
the child and pricked. The child is asked if he/she experienced
pain. The child is surprised at the absence of pain and stops
crying. After induction a wider bore cannula can be inserted.

78. 78
Indications for intravenous induction
IV induction is particularly preferable when
1. Rapid-sequence of induction is required eg—full stomach,
gastro-esophageal reflux, and emergency anesthesia.
2. A child with high-risk of malignant hyperthermia.
3. Child for neurosurgical procedure who require neuroprotection.
4. Child with behavioral disturbances.
5. Child with epilepsy.
6. Child chooses this method.
7. Certain operative procedures such as laryngoscopy,
bronchoscopy, and thoracic surgery where it may be difficult or
impossible to use inhalational agents.
8. Certain procedures where TIVA is the choice of anesthetic
technique preferred.
9. Anesthesia at remote locations-like for MRI, CT
10. In patients where an appropriate mask seal on the face is
difficult/not possible.
Advantages of Intravenous induction
1. Rapid onset of action.
2. Better quality of emergence.
3. Reduced PONV-avoiding inhalational agents is considered as
the prime option in preventing PONV.
There are certain plus points of the intravenous agents when used
as inducing agents.
Intravenous anesthetic agents
Propofol
Although Ketamine, Thiopental are also widely used for induction
of anesthesia in paediatric patients, Propofol is preferred,
because,

79. 79
1. It produces rapid and smooth induction.
2. Early and prompt wake-up.
Its rapid redistribution and metabolism gives it the
advantage of short duration of action and allows for repeat
administration without accumulation.
3. Like thiopental sodium Propofol has neuroprotective
properties—
a. It decreases CMRO2, cerebral blood flow and ICP.
b. Cerebral auto regulation is preserved.
c. Cerebral responsiveness is also preserved.
4. When an adequate dose of propofol is used for induction,
there are no involuntary movements seen. The blame is
baseless .Dose-3.5 t0 4mg/kg
5. Prevents PONV.
Ketamine-
A very good analgesic .It is advantageous in situations of volume
depletion & low cardiac states and where bronchodilation is
beneficial. Airway maintenance without use of an oropharyngeal
airway during short surgical procedures like incision & drainage.
Thiopental sodium
Preferred in patients where neuroprotection is needed.
Dosage-5-6 mg/kg in unpremeditated children.

80. 80
2-4 mg/kg in well premeditated children.
Infants-6-8 mg/kg in unpremeditated
Remifentanyl
It is broken down by nonspecific plasma and tissue plasma
choline esterase and has a brief plasma half-life. This favorable
pharmacokinetics provides a deeper plane of anesthesia while
avoiding cardiovascular depression and the need for postoperative
ventilation. Used with Propofol it produces good anesthesia.
Contrary to what usually one tends to believe, there are certain
problems with inhalational agents
Problems with inhalational agents
‘Induction with inhalational agents’ has become almost
synonymous with ‘Induction with Sevoflurane’
As all other inhalational agents are excluded because of any one or
more of the following reasons-
a. Take a long time for induction.
b. Irritant to the airway.
c. Not pleasant smelling or may be even pungent.
D .Require a dangerously high concentration to be delivered to
induce anesthesia.
c. Need of vaporizer for induction.
Sevoflorane is almost the only suitable inhalational agent
available for induction of anesthesia, despite quite a few notable
adverse actions.

81. 81
The disadvantages of Sevoflurane when used as
induction agents are-
1. The MAC multiple concentrations of Sevoflurane in the
first few minutes of induction are less than those of
halothane during the same period. This exposes a
weakness of Sevoflurane, that for reduced solubility in
blood, the potency is also decreased. And hence with the
maximum concentrations of Sevoflurane from
commercial vaporizers limited to 8% there is loss of
consciousness without analgesia. Sevoflurane is not an
analgesic and probably opposes the analgesic properties
of Nitrous oxide.
2. This is why movement has been reported when IV
cannulation is attempted following Sevoflurane induction
which is due to limited depth of anesthesia.
3. Hence it becomes imperative to maintain a large inspired
concentration of Sevoflurane (and continue 70%N20)
early during the induction and be patient before
establishing IV access.
4. For the same reason, the laryngeal and pharyngeal
reflexes are lost only in deeper planes of anesthesia.
Therefore one has to really, patiently wait for the
suppression of laryngeal and pharyngeal reflexes before
inserting a LMA, an orpharyngeal airway or a
laryngoscope. Administration of either Propofol or
Fentanyl becomes necessary before laryngoscopy or LMA
insertion.

82. 82
5. Coughing, swallowing, breath holding, laryngospasm can
occur while inserting LMA, and can be mistaken for
incorrect placement.
6. PONV occur with up to 20% of children who receive
inhalational induction compared to IV induction.
7. Post-operative emergence agitation /delirium .Some
clinical trials in dentistry have proved that Propofol can
be used to treat Sevoflurane induced emergence
delirium/agitation.
8. Behavioral changes in the postoperative period such as
fear of dark, nightmares, difficulty in getting the child to
sleep & desire to sleep with parent.
9. Epileptiform EEG activity is noted in normal children and
children with seizure disorders, when concentration of
Sevoflurane higher than 5 vol% is used, which is essential
for induction. It is even higher when combined with
hyperventilation.
10. Hypoxic pulmonary vasoconstriction may be more
adversely affected by Sevoflurane compared to Propofol.
11. Sevoflurane like other inhalational agents increases the
CBF and thereby the ICP and therefore cannot be used in
patients requiring neuroprotection.
12. Studies have shown that QT interval is significantly
longer in children who received Sevoflurane for induction

83. 83
compared to those who received Propofol. Hence
propofol could be preferred for induction in children with
predisposition to arrhythmias.
13. Evoked potentials are suppressed or even abolished by
inhalational agents and hence evoked potential
monitoring during neurosurgeries cannot be done.
14. Inhalational agents for induction would be rejected in
up to 24% of patients who have experienced it.
Conclusion:-
Induction of general anesthesia is not simply a technical exercise.
Selection of a single method and extrapolating it in all
circumstances is not only scientifically unfeasible, but can also
prove disastrous to the children.
Delivery of a safe and effective anesthesia with minimal side
effects and ensuring a rapid, clear headed recovery is important.
And, this is exactly why each child requires an intelligently
tailored approach.
Today, it has become possible to use “Total intravenous
anesthesia” with increasing frequency in children because of
obvious advantages of the intravenous agents, like hemodynamic
stability, a very low incidence of PONV, rapid, and smooth
emergence. This is because a combination of current intravenous
anesthetic agents permits a very rapid and accurate titration of
the anesthetic depth akin to inhalational agents. In days to come,
IV anesthetic induction may prove clearly better than inhalational
induction.

84. 84
REFERENCES
o A practical approach to paediatric anesthesia
Robert S.Holzman, David M. Polaner
o SMITH”S Anesthesia for Infants and Children
o Paediatric Anesthesia
George and Gregory.
o A Practice of Anesthesia for Infants and Children.
Cote Todres Goudsouzian Ryan.
o A Practice of Anesthesia 7th Edn
Wylie and Churchhill-Davidson”s
o Clinical Anesthesia Practice
Kirby Gravenstein, Lobato Gravenstein.
o Miller’s Anesthesia 7th Edn
o British Journal of Anesthesia 1997:78;362-365.
o European journal Anaesthesiology,2006 Jun:23(6);470-5
o Paediatric Anesthesia 2009 19; 521-534
o Paediatric Anesthesia 21(2011) 159-168
o Paediatric Anesthesia 2003 JUL;501-7 T
o Journal of Turkish Anesthesiology & Intensive care society; July 2010,vol 38
o Anesthesia Progress ;A journal for pain & anxiety control in dentistry.

85. 85
Thank You