July 29, 2025 • 27 mins
Continue your journey to mastering anaesthesia—one chapter at a time.
In this episode, Dr. J.R. Decker reads and discusses Chapter 8 (Part 2) of Morgan & Mikhail’s Clinical Anesthesiology (7th Edition).
Follow as you read along to strengthen your foundations in anaesthesia, one clear and engaging session at a time.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:02):
Morgan and Michael's Clinical Anesthesiology, 7th Edition,
Chapter 8, Part 2. Concentration.
The slowing of induction due to uptake from alveolar gas can be
(00:26):
counteracted by increasing the inspired concentration.
Interestingly, increasing the inspired concentration not only
increases the alveolar concentration but also
increasing its rate of rise, that is, increases FA over FI
(00:52):
because the two phenomena that produce a so-called
concentrating effect because of two phenomena that produce a
so-called concentrating effect. 1st.
If 50% of an anaesthetic is taken up by the pulmonary
(01:14):
circulation, an inspired concentration of 20%, that is 20
parts of anaesthetic per hundredparts of gas, will result in an
alveolar concentration of 11%, that is 10 parts of anaesthetic
remaining in a total volume of 90 parts of gas.
(01:41):
On the other hand, if the inspired concentration is raised
to 80%, that is 80 parts of anaesthetic per hundred parts of
gas, the alveolar concentration will be 67%, that is, 40 parts
(02:01):
of anaesthetic remaining in a total volume of 60 parts of gas.
Thus, even though 50% of the anaesthetic is taken up, in both
examples a higher inspired concentration results in a
(02:22):
disproportionately higher alveolar concentration.
In this example, increasing the inspired concentration fourfold
results in a six fold increase in alveolar concentration.
(02:44):
The extreme case is an inspired concentration of 100%, that is,
100 parts of 100, which despite a 50% uptake will result in an
alveolar concentration of 100%, that is, 50 parts of anaesthetic
(03:06):
remaining in a total volume of 50 parts of gas.
The second phenomenon responsible for the
concentration effect is the augmented inflow effect.
Using the example above, the 10 parts of absorbed gas must be
(03:30):
replaced by an equal volume of the 20% mixture to prevent
alveolar collapse. Thus, the alveolar concentration
becomes 12%, that is, 10 + 2 parts of anaesthetic in a total
(03:53):
of 100 parts of gas. In contrast, after absorption of
50% of the anaesthetic in the 80% gas mixture, 40 parts of 80%
gas must be inspired. This further increases the
(04:18):
alveolar concentration from 67% to 72%, that is 440 + 32 parts
of anaesthetic in a volume of 100 parts of gas.
(04:38):
The concentration effect is moresignificant with nitrous oxide
than with volatile anaesthetics,as the former can be used in
much higher concentrations. Nonetheless, a high
concentration of nitrous oxide will augment by the same
(05:02):
mechanism not only its own uptake but theoretically also
that of a concurrently administered volatile
anaesthetic. The concentration effect of one
gas upon another is called the second gas effect, which despite
(05:27):
its persistence in examination questions, is probably
insignificant in the clinical practise of anaesthesiology.
Factors affecting arterial concentration, that is, FA
(05:50):
ventilation, perfusion mismatch.Normally alveolar and arterial
anaesthetic partial pressures are assumed to be equal, but in
fact the arterial partial pressure is consistently less
(06:13):
than end expiratory gas would predict.
Reasons for this may include venous admixture, alveolar Dead
Space, and non uniform alveolar gas distribution.
(06:38):
Furthermore, the existence of ventilation perfusion
mismatching will increase the alveolar arterial difference.
Mismatch acts as a restriction to flow.
It raises the pressure in front of the restriction.
(07:02):
Lowers the pressure beyond the restriction and reduces the flow
through the restriction. The overall effect of
ventilation perfusion mismatch is an increase in the alveolar
partial pressure that is particularly for highly soluble
(07:25):
agents, and a decrease in the arterial partial pressure that
is particularly for poorly soluble agents.
Thus, bronchial intubation or a right to left intracardiac shunt
(07:47):
will slow the rate of induction with nitrous oxide more than
with several fluorine factors affecting elimination.
Recovery from anaesthesia depends on lowering the
(08:08):
concentration of anaesthetic in brain tissue.
Anaesthetics can be eliminated by bio transformation,
transcutaneous loss or exhalation.
(08:28):
Biotransformation usually accounts for a minimal increase
in the rate of decline of alveolar partial pressure.
It's greatest impact is on the elimination of soluble
anaesthetics that undergo extensive metabolism, for
(08:51):
example methoxy fluorine. The greater biotransformation of
halothane compared with isofluorine accounts for
halothane's faster elimination even though it is more soluble.
(09:11):
The CYP group of isozymes, specifically CYP 2 EI, seems to
be important in the metabolism of some volatile anaesthetics.
The diffusion of anaesthetic through the skin is
(09:33):
insignificant 4. The most important route for the
elimination of inhalation anaesthetics is the alveolar
membrane. Many of the factors that speed
(09:55):
induction also speed recovery, elimination of rebreathing,
fresh high fresh gas flows, low anaesthetic circuit volume, low
absorption by the anaesthetic circuit, decreased solubility,
(10:21):
high cerebral blood flow and increased ventilation.
Elimination of nitrous oxide is so rapid that oxygen and carbon
dioxide concentrations in alveolar gas are diluted.
(10:46):
The resulting diffusion hypoxia is prevented by administering
100% oxygen for five to 10 minutes after discontinuing
nitrous oxide. The rate of recovery is usually
(11:08):
faster than induction because tissues that have not reached
steady state will continue to take up anaesthetic until the
alveolar partial pressure falls below the tissue partial
pressure. For instance, fat will continue
(11:31):
to take up anaesthetic and hasting recovery until the
partial pressure exceeds the alveolar partial pressure.
This redistribution is not as useful after prolonged
anaesthesia. That is, fat partial pressures
(11:51):
of anaesthetic will have will have come closer to arterial
partial pressures. At the same time, the
anaesthetic was removed from fresh gas.
Thus, the speed of recovery alsodepends on the length of time
the anaesthetic has been administered.
(12:17):
Pharmacodynamics of inhalation anaesthetics.
Theories of anaesthetic action. General anaesthesia is an
altered physiological state characterised by reversible loss
(12:43):
of consciousness, analgesia, amnesia and some degree of
muscle relaxation. The multitude of substances
capable of producing general anaesthesia is remarkable.
(13:07):
Inert elements, that is xenon. Simple inorganic compounds, that
is nitrous oxide, halogenated hydrocarbons, that is halothane
(13:27):
esters, that is isofluorine, cervofluorine, desfluorine and
complex organic structures, thatis propofol, etomidate,
ketamine. A unifying theory explaining
(13:49):
anaesthetic action would have toaccommodate this diversity of
structure. In fact, the various agents
probably produce anaesthesia by differing sets of molecular
mechanisms. Inhalation agents.
Inhalational agents interact with numerous ion channels
(14:14):
present in the CNS and peripheral nervous system.
Nitrous oxide and xenon are believed to inhibit N methyl D
aspartate NMDA receptors. NMDA receptors are exciting 3
(14:35):
receptors in the brain. Other inhalational agents as
well as ectomidate and midazolammay interact with other
receptors, for example, gamma amino aminobutyric acid, GABA,
(14:56):
activated chloride channel conductance leading to
anaesthetic effects. It is possible that inhalational
anaesthetics act on multiple protein receptors that block
excitatory channels and promote the activity of inhibitory
(15:18):
channels affecting neuronal activity.
Specific brain areas affected byinhaled anaesthetics include the
reticular activating system, thecerebral cortex, the cunate
(15:38):
nucleus, the olfactory cortex and the hippocampus.
However, general anaesthetics bind throughout the CNS.
Anaesthetics have also been shown to depress excitatory
(16:02):
transmission in the spinal cord,particularly at the level of the
dorsal horn interneurons that are involved in pain
transmission. Different aspects of anaesthesia
may be related to different sites of anaesthetic action.
(16:27):
For example, unconsciousness andamnesia are probably mediated by
cortical anaesthetic action, whereas the suppression of
purposeful withdrawal from pain likely relates to subcortical
(16:47):
structures such as the spinal cord or brain stem.
One study in rats revealed that removal of the cerebral cortex
did not alter the potency of theanaesthetic.
(17:10):
Indeed, measures of minimum alveolar concentration, that is,
Mac, the anaesthetic concentration that prevents
movement in 50% of subjects or animals, are dependent upon
anaesthetic effects at the spinal cord and not at the
(17:34):
cortex. 5. Past understanding of
anaesthetic action attempted to identify a unitary hypothesis of
anaesthetic effects. This hypothesis proposes that
(17:55):
all inhalation agents share a common mechanism of action at
the molecular level. This was previously supported by
the observation that the anaesthetic potency of
inhalation agents correlates directly with their lipid
solubility, that is the mere overturn rule.
(18:22):
The implication is that anaesthesia results from
molecules dissolving at specificlipophilic sites.
Of course, not all lipid solublemolecules are anaesthetics.
Some are actually convulsants, and the correlation between an
(18:43):
aesthetic potency and lipid solubility is only approximate.
Next we get to Figure 8-4 that states that there is a good but
not perfect correlation between an aesthetic potency and lipid
(19:04):
solubility. Kindly pause this reading to
study Figure 8-4. General anaesthetic action could
be due to alterations in anyone or a combination of several
(19:27):
cellular systems including voltage gated ion channels,
ligand gated ion channels, second messenger functions or
neurotransmitter receptors. There seems to be a strong
(19:52):
correlation between anaesthetic potency and actions on Garber
receptors. Thus anaesthetic action may
relate. To binding in relatively
hydrophobic domains in channel proteins, that is, Garba
(20:14):
receptors. Modulation of Garba function may
prove to be a principal mechanism of action for many
anaesthetic drugs. The glycine receptor A1
subunits, whose function is enhanced by inhalation and
(20:38):
aesthetics, is another potentialand aesthetic site of action.
Other ligand gated ion channels whose modulation may play a role
in an aesthetic action include nicotinic acetylcholine
receptors and MDNMDA receptors. Investigations into mechanisms
(21:08):
of anaesthetic action are likelyto remain ongoing for many years
because many protein channels may be affected by individual
anaesthetic agents with no obligatory site as has yet been
identified. So let's take it again.
(21:33):
Investigations into mechanisms of anaesthetic action are likely
to remain ongoing for many yearsbecause many protein channels
may be affected by individual anaesthetic agents and no
obligatory site has yet been identified.
(21:54):
Selecting among so many molecular targets for the ones
that provide optimum effects with minimal adverse actions
will be the challenge in designing better inhalational
agents. Anaesthetic neurotoxicity.
(22:24):
In recent years there has been ongoing concern that general
anaesthetics damage the developing brain.
Concern has been raised that anaesthetic exposure affects the
development and the elimination of synapses in the infant's
(22:44):
brain and can promote cognitive impairment later in later life.
For example, animal studies havedemonstrated that isofluorine
exposure promotes neuronal apoptosis, altering cellular
(23:06):
calcium hemostatic mechanisms with subsequent learning
disability. Human studies exploring whether
anaesthesia is harmful in children are difficult because
conducting A randomised controlled trial for that
(23:27):
purpose only would be for that purpose only would be unethical.
Studies that compare populationsof children who have had
anaesthetics with those who havenot are also complicated by the
real reality that the former population is likewise having
(23:49):
surgery and receiving the attention of the medical
community. Consequently, children receiving
anaesthetics may be more likely to be diagnosed with learning
difficulties in the first place.Human, animal, and lab
(24:14):
laboratory trials demonstrating or refusing that anaesthetic
neurotoxicity leads to developmental disability in
children are on the way. Smart Thoughts, a partnership
between the International Anaesthesia Research Society and
(24:35):
the US Food and Drug Administration that is FDA
coordinates and funds research related to anaesthesia in
infants and young children. As their consensus statement
notes, it is not yet possible toknow whether anaesthetic drugs
(24:58):
are safe for children in a single, short duration
procedure. Similarly, it is not yet
possible to know whether the useof these drugs poses a risk and,
if so, whether the risk is largeenough to outweigh the benefits
(25:19):
of needed surgery, tests or other procedures.
Concerns regarding the unknown risk of anaesthetic exposure to
the child's brain development must be weighed against
potential harm associated with counselling or delaying a needed
(25:41):
procedure. Of notes, The FDA has issued a
warning that repeated or prolonged use of general
anaesthetics or sedatives in children younger than three
years may affect brain development.
(26:06):
Nevertheless, various chemical studies have failed to
demonstrate adverse outcomes from single brief anaesthetic
exposures in children, and thereis a developing consensus that
single anaesthetic exposures in infants and young children are
(26:27):
very unlikely to result in harm.Some have advocated mitigation
strategies to limit anaesthetic exposure in children and
incorporate dex methadomidene into anaesthetic management.
(26:48):
It has been suggested that Dex methadomidene may have
neuroprotective properties against anaesthetic induced
neurotoxicity. Other investigators are
examining the role of xenon in combination with other
(27:08):
inhalational anaesthetics to promote anti apoptosis.
Anaesthetic agents have also been suggested to contribute to
Tau protein hyperphosphorylation.
Tau hyperphosphorylation is associated with Alzheimer's
(27:32):
disease and it has been hypothesised that anaesthetic
exposures may contribute to AD progression.
Anzerman's disease progression. However, the proposed
association between anaesthetic delivery, surgery and AD
(27:55):
development has not been sufficiently investigated to
draw definitive conclusions.
Morgan and Michael's Clinical Anesthesiology, 7th Edition,
Chapter 8, Part 2. Concentration.
The slowing of induction due to uptake from alveolar gas can be
(00:26):
counteracted by increasing the inspired concentration.
Interestingly, increasing the inspired concentration not only
increases the alveolar concentration but also
increasing its rate of rise, that is, increases FA over FI
(00:52):
because the two phenomena that produce a so-called
concentrating effect because of two phenomena that produce a
so-called concentrating effect. 1st.
If 50% of an anaesthetic is taken up by the pulmonary
(01:14):
circulation, an inspired concentration of 20%, that is 20
parts of anaesthetic per hundredparts of gas, will result in an
alveolar concentration of 11%, that is 10 parts of anaesthetic
remaining in a total volume of 90 parts of gas.
(01:41):
On the other hand, if the inspired concentration is raised
to 80%, that is 80 parts of anaesthetic per hundred parts of
gas, the alveolar concentration will be 67%, that is, 40 parts
(02:01):
of anaesthetic remaining in a total volume of 60 parts of gas.
Thus, even though 50% of the anaesthetic is taken up, in both
examples a higher inspired concentration results in a
(02:22):
disproportionately higher alveolar concentration.
In this example, increasing the inspired concentration fourfold
results in a six fold increase in alveolar concentration.
(02:44):
The extreme case is an inspired concentration of 100%, that is,
100 parts of 100, which despite a 50% uptake will result in an
alveolar concentration of 100%, that is, 50 parts of anaesthetic
(03:06):
remaining in a total volume of 50 parts of gas.
The second phenomenon responsible for the
concentration effect is the augmented inflow effect.
Using the example above, the 10 parts of absorbed gas must be
(03:30):
replaced by an equal volume of the 20% mixture to prevent
alveolar collapse. Thus, the alveolar concentration
becomes 12%, that is, 10 + 2 parts of anaesthetic in a total
(03:53):
of 100 parts of gas. In contrast, after absorption of
50% of the anaesthetic in the 80% gas mixture, 40 parts of 80%
gas must be inspired. This further increases the
(04:18):
alveolar concentration from 67% to 72%, that is 440 + 32 parts
of anaesthetic in a volume of 100 parts of gas.
(04:38):
The concentration effect is moresignificant with nitrous oxide
than with volatile anaesthetics,as the former can be used in
much higher concentrations. Nonetheless, a high
concentration of nitrous oxide will augment by the same
(05:02):
mechanism not only its own uptake but theoretically also
that of a concurrently administered volatile
anaesthetic. The concentration effect of one
gas upon another is called the second gas effect, which despite
(05:27):
its persistence in examination questions, is probably
insignificant in the clinical practise of anaesthesiology.
Factors affecting arterial concentration, that is, FA
(05:50):
ventilation, perfusion mismatch.Normally alveolar and arterial
anaesthetic partial pressures are assumed to be equal, but in
fact the arterial partial pressure is consistently less
(06:13):
than end expiratory gas would predict.
Reasons for this may include venous admixture, alveolar Dead
Space, and non uniform alveolar gas distribution.
(06:38):
Furthermore, the existence of ventilation perfusion
mismatching will increase the alveolar arterial difference.
Mismatch acts as a restriction to flow.
It raises the pressure in front of the restriction.
(07:02):
Lowers the pressure beyond the restriction and reduces the flow
through the restriction. The overall effect of
ventilation perfusion mismatch is an increase in the alveolar
partial pressure that is particularly for highly soluble
(07:25):
agents, and a decrease in the arterial partial pressure that
is particularly for poorly soluble agents.
Thus, bronchial intubation or a right to left intracardiac shunt
(07:47):
will slow the rate of induction with nitrous oxide more than
with several fluorine factors affecting elimination.
Recovery from anaesthesia depends on lowering the
(08:08):
concentration of anaesthetic in brain tissue.
Anaesthetics can be eliminated by bio transformation,
transcutaneous loss or exhalation.
(08:28):
Biotransformation usually accounts for a minimal increase
in the rate of decline of alveolar partial pressure.
It's greatest impact is on the elimination of soluble
anaesthetics that undergo extensive metabolism, for
(08:51):
example methoxy fluorine. The greater biotransformation of
halothane compared with isofluorine accounts for
halothane's faster elimination even though it is more soluble.
(09:11):
The CYP group of isozymes, specifically CYP 2 EI, seems to
be important in the metabolism of some volatile anaesthetics.
The diffusion of anaesthetic through the skin is
(09:33):
insignificant 4. The most important route for the
elimination of inhalation anaesthetics is the alveolar
membrane. Many of the factors that speed
(09:55):
induction also speed recovery, elimination of rebreathing,
fresh high fresh gas flows, low anaesthetic circuit volume, low
absorption by the anaesthetic circuit, decreased solubility,
(10:21):
high cerebral blood flow and increased ventilation.
Elimination of nitrous oxide is so rapid that oxygen and carbon
dioxide concentrations in alveolar gas are diluted.
(10:46):
The resulting diffusion hypoxia is prevented by administering
100% oxygen for five to 10 minutes after discontinuing
nitrous oxide. The rate of recovery is usually
(11:08):
faster than induction because tissues that have not reached
steady state will continue to take up anaesthetic until the
alveolar partial pressure falls below the tissue partial
pressure. For instance, fat will continue
(11:31):
to take up anaesthetic and hasting recovery until the
partial pressure exceeds the alveolar partial pressure.
This redistribution is not as useful after prolonged
anaesthesia. That is, fat partial pressures
(11:51):
of anaesthetic will have will have come closer to arterial
partial pressures. At the same time, the
anaesthetic was removed from fresh gas.
Thus, the speed of recovery alsodepends on the length of time
the anaesthetic has been administered.
(12:17):
Pharmacodynamics of inhalation anaesthetics.
Theories of anaesthetic action. General anaesthesia is an
altered physiological state characterised by reversible loss
(12:43):
of consciousness, analgesia, amnesia and some degree of
muscle relaxation. The multitude of substances
capable of producing general anaesthesia is remarkable.
(13:07):
Inert elements, that is xenon. Simple inorganic compounds, that
is nitrous oxide, halogenated hydrocarbons, that is halothane
(13:27):
esters, that is isofluorine, cervofluorine, desfluorine and
complex organic structures, thatis propofol, etomidate,
ketamine. A unifying theory explaining
(13:49):
anaesthetic action would have toaccommodate this diversity of
structure. In fact, the various agents
probably produce anaesthesia by differing sets of molecular
mechanisms. Inhalation agents.
Inhalational agents interact with numerous ion channels
(14:14):
present in the CNS and peripheral nervous system.
Nitrous oxide and xenon are believed to inhibit N methyl D
aspartate NMDA receptors. NMDA receptors are exciting 3
(14:35):
receptors in the brain. Other inhalational agents as
well as ectomidate and midazolammay interact with other
receptors, for example, gamma amino aminobutyric acid, GABA,
(14:56):
activated chloride channel conductance leading to
anaesthetic effects. It is possible that inhalational
anaesthetics act on multiple protein receptors that block
excitatory channels and promote the activity of inhibitory
(15:18):
channels affecting neuronal activity.
Specific brain areas affected byinhaled anaesthetics include the
reticular activating system, thecerebral cortex, the cunate
(15:38):
nucleus, the olfactory cortex and the hippocampus.
However, general anaesthetics bind throughout the CNS.
Anaesthetics have also been shown to depress excitatory
(16:02):
transmission in the spinal cord,particularly at the level of the
dorsal horn interneurons that are involved in pain
transmission. Different aspects of anaesthesia
may be related to different sites of anaesthetic action.
(16:27):
For example, unconsciousness andamnesia are probably mediated by
cortical anaesthetic action, whereas the suppression of
purposeful withdrawal from pain likely relates to subcortical
(16:47):
structures such as the spinal cord or brain stem.
One study in rats revealed that removal of the cerebral cortex
did not alter the potency of theanaesthetic.
(17:10):
Indeed, measures of minimum alveolar concentration, that is,
Mac, the anaesthetic concentration that prevents
movement in 50% of subjects or animals, are dependent upon
anaesthetic effects at the spinal cord and not at the
(17:34):
cortex. 5. Past understanding of
anaesthetic action attempted to identify a unitary hypothesis of
anaesthetic effects. This hypothesis proposes that
(17:55):
all inhalation agents share a common mechanism of action at
the molecular level. This was previously supported by
the observation that the anaesthetic potency of
inhalation agents correlates directly with their lipid
solubility, that is the mere overturn rule.
(18:22):
The implication is that anaesthesia results from
molecules dissolving at specificlipophilic sites.
Of course, not all lipid solublemolecules are anaesthetics.
Some are actually convulsants, and the correlation between an
(18:43):
aesthetic potency and lipid solubility is only approximate.
Next we get to Figure 8-4 that states that there is a good but
not perfect correlation between an aesthetic potency and lipid
(19:04):
solubility. Kindly pause this reading to
study Figure 8-4. General anaesthetic action could
be due to alterations in anyone or a combination of several
(19:27):
cellular systems including voltage gated ion channels,
ligand gated ion channels, second messenger functions or
neurotransmitter receptors. There seems to be a strong
(19:52):
correlation between anaesthetic potency and actions on Garber
receptors. Thus anaesthetic action may
relate. To binding in relatively
hydrophobic domains in channel proteins, that is, Garba
(20:14):
receptors. Modulation of Garba function may
prove to be a principal mechanism of action for many
anaesthetic drugs. The glycine receptor A1
subunits, whose function is enhanced by inhalation and
(20:38):
aesthetics, is another potentialand aesthetic site of action.
Other ligand gated ion channels whose modulation may play a role
in an aesthetic action include nicotinic acetylcholine
receptors and MDNMDA receptors. Investigations into mechanisms
(21:08):
of anaesthetic action are likelyto remain ongoing for many years
because many protein channels may be affected by individual
anaesthetic agents with no obligatory site as has yet been
identified. So let's take it again.
(21:33):
Investigations into mechanisms of anaesthetic action are likely
to remain ongoing for many yearsbecause many protein channels
may be affected by individual anaesthetic agents and no
obligatory site has yet been identified.
(21:54):
Selecting among so many molecular targets for the ones
that provide optimum effects with minimal adverse actions
will be the challenge in designing better inhalational
agents. Anaesthetic neurotoxicity.
(22:24):
In recent years there has been ongoing concern that general
anaesthetics damage the developing brain.
Concern has been raised that anaesthetic exposure affects the
development and the elimination of synapses in the infant's
(22:44):
brain and can promote cognitive impairment later in later life.
For example, animal studies havedemonstrated that isofluorine
exposure promotes neuronal apoptosis, altering cellular
(23:06):
calcium hemostatic mechanisms with subsequent learning
disability. Human studies exploring whether
anaesthesia is harmful in children are difficult because
conducting A randomised controlled trial for that
(23:27):
purpose only would be for that purpose only would be unethical.
Studies that compare populationsof children who have had
anaesthetics with those who havenot are also complicated by the
real reality that the former population is likewise having
(23:49):
surgery and receiving the attention of the medical
community. Consequently, children receiving
anaesthetics may be more likely to be diagnosed with learning
difficulties in the first place.Human, animal, and lab
(24:14):
laboratory trials demonstrating or refusing that anaesthetic
neurotoxicity leads to developmental disability in
children are on the way. Smart Thoughts, a partnership
between the International Anaesthesia Research Society and
(24:35):
the US Food and Drug Administration that is FDA
coordinates and funds research related to anaesthesia in
infants and young children. As their consensus statement
notes, it is not yet possible toknow whether anaesthetic drugs
(24:58):
are safe for children in a single, short duration
procedure. Similarly, it is not yet
possible to know whether the useof these drugs poses a risk and,
if so, whether the risk is largeenough to outweigh the benefits
(25:19):
of needed surgery, tests or other procedures.
Concerns regarding the unknown risk of anaesthetic exposure to
the child's brain development must be weighed against
potential harm associated with counselling or delaying a needed
(25:41):
procedure. Of notes, The FDA has issued a
warning that repeated or prolonged use of general
anaesthetics or sedatives in children younger than three
years may affect brain development.
(26:06):
Nevertheless, various chemical studies have failed to
demonstrate adverse outcomes from single brief anaesthetic
exposures in children, and thereis a developing consensus that
single anaesthetic exposures in infants and young children are
(26:27):
very unlikely to result in harm.Some have advocated mitigation
strategies to limit anaesthetic exposure in children and
incorporate dex methadomidene into anaesthetic management.
(26:48):
It has been suggested that Dex methadomidene may have
neuroprotective properties against anaesthetic induced
neurotoxicity. Other investigators are
examining the role of xenon in combination with other
(27:08):
inhalational anaesthetics to promote anti apoptosis.
Anaesthetic agents have also been suggested to contribute to
Tau protein hyperphosphorylation.
Tau hyperphosphorylation is associated with Alzheimer's
(27:32):
disease and it has been hypothesised that anaesthetic
exposures may contribute to AD progression.
Anzerman's disease progression. However, the proposed
association between anaesthetic delivery, surgery and AD
(27:55):
development has not been sufficiently investigated to
draw definitive conclusions.
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