July 26, 2025 • 26 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 1) 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.
(00:01):
Morgan and Michael's Clinical anesthesiology, 7th edition,
Chapter 8. Inhalation anaesthetics.
Key concepts. One, the greater the uptake of
(00:27):
anaesthetic agents, the greater the difference between inspired
and alveolar concentrations and the slower the rate of induction
2 Three factors affect anaesthetic uptake.
(00:49):
Solubility in the blood. Alveolar blood flow and the
difference in partial pressure between alveolar gas and venous
blood 3. Low output states predispose
patients to overdosage with soluble agents as the rate of
(01:16):
rise in alveolar concentrations will be markedly increased. 4.
Many of the factors that speed induction also speed recovery,
elimination of rebreathing, highfresh gas flows, low anaesthetic
(01:42):
circuit volume, low absorption by the anaesthetic circuits,
decreased solubility, high cerebral blood flow and
increased ventilation 5. The unitary hypothesis proposes
(02:10):
that all inhalation agents sharea 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
(02:33):
solubility, that is the mere overturn rule.
The implication is that anaesthesia results from
molecules dissolving at specificlipophilic sites.
However, the correlation is onlyapproximate 6.
(02:56):
The minimum alveolar concentration, that is, Mac of
an inhaled anaesthetic is the alveolar concentration that
prevents movement in 50% of patients in response to a
standardised stimulus, for example, surgical incision 7.
(03:24):
Prolonged exposure to anaesthetic concentrations of
Nitro nitrous oxide can result in bone marrow depression, that
is megaloblastic anaemia, and even neurologic deficiencies,
that is peripheral neuropathies 8.
(03:48):
Hallothane hepatitis is extremely rare.
Patients exposed to multiple hallothane anaesthetics at short
intervals, middle age obese women, and persons with a
familial predisposition to hallothane toxicity or a
(04:08):
personal history of toxicity areconsidered to be at increased
risk. 9 Isoflorane dilates coronary arteries, but not
nearly as potently as nitroglycerin or adenosine.
(04:32):
Dilation of normal coronary arteries could theoretically
divert blood away from fixed stenotic lesions 10.
The low solubility of DES fluorine in blood and body
(04:52):
tissues causes very rapid induction of an emergence from
anaesthesia 11. Rapid increases in DES fluorine
concentration lead to transient but sometimes worrisome
(05:14):
elevations in heart rate, blood pressure, and catecholamine
levels that are more pronounced than occur with isofluorine,
particularly in patients with cardiovascular disease 12 Non
(05:37):
pungency and rapid increases in alveolar and aesthetic
concentration make several fluorine an excellent choice for
smooth and rapid inhalation inductions in paediatric and
adult patients. Nitrous oxide, chloroform and
(06:02):
ether We're the first universally accepted general
anaesthetics. Currently used inhalation agents
include nitrous oxide, halothane, isoflorane,
desflorane and sevoflorane. The cause of a general
(06:24):
anaesthetic can be divided into 3 phases. 1 Induction, two
maintenance and three emergence.Inhalation and aesthetics.
(06:44):
Notably, halothane and cerval fluorine are particularly useful
for the inhalation induction of paediatric patients in whom it
may be difficult to start an intravenous line.
Although adults are usually induced with intravenous agents,
(07:07):
the non pungency and rapid onsetof several fluorine makes
inhalation induction practical for them as well.
Regardless of the patient's age,anaesthesia is often maintained
with inhalation agents. Emergence depends primarily upon
(07:32):
redistribution of the agents from the brain, followed by
pulmonary elimination. Because of their unique route of
administration, inhalation and aesthetics have useful
pharmacological properties not shared by other anaesthetic
(07:54):
agents. Pharmacokinetics of inhalation
and aesthetics. Although the mechanism of action
of inhalation and aesthetics is not yet fully understood, their
ultimate effects clearly depend on attaining A therapeutic
(08:19):
tissue concentration in the central nervous system.
There are many steps between theanaesthetic vaporizer and the
anaesthetics deposition in the brain.
(08:41):
Next, we get to Figure 8-1, talking about the fact that
inhalation anaesthetic agents must pass through many barriers
between the anaesthesia machine and the brain.
(09:01):
Kindly take some time to go through Figure 8-1 Factors
affecting inspiratory concentration, that is, FI.
(09:24):
The fresh gas leaving the anaesthesia machine mixes with
gases in the breathing circuits before being inspired by the
patient. Therefore, the patient is not
necessarily receiving the concentration set on the
vaporizer. The actual composition of the
(09:49):
inspired gas mixture depends mainly on the fresh gas flow
rate, the volume of the breathing system, and any
absorption by the machine or breathing circuit.
(10:10):
The greater the fresh gas flow rate, the smaller the breathing
system volume, and the lower thecircuit absorption, the closer
the inspired gas concentration will be to the fresh gas
concentration. Factors affecting alveolar
(10:37):
concentration. FA Optic If there were no optic
of anaesthetic agents by the body, the alveolar gas
concentration FA would rapidly approach the inspired gas
(10:59):
concentration FI. Because anaesthetic agents are
taken up by the pulmonary circulation during induction,
alveolar concentrations lag behind inspired concentrations.
That is, FA over FI is less thanone.
(11:27):
The greater the uptake, the slower the rate of rise of the
alveolar concentration and the lower the FA to FI ratio. 1
Because the concentration of a gas is directly proportional to
(11:50):
its partial pressure, the alveolar partial pressure will
also be slow to rise. The alveolar partial pressure is
important because it determines the partial pressure of an
aesthetic in the blood and ultimately in the brain.
(12:14):
Similarly, the partial pressure of the anaesthetic in the brain
is directly proportional to its brain tissue concentration,
which determines the clinical effect.
The faster the uptake of anaesthetic agent, the greater
(12:37):
the difference between inspired and alveolar concentrations and
the slower the rate of induction. 2.
Three factors affect anaestheticuptake.
(12:59):
Solubility in the blood, alveolar blood flow, and the
difference in partial pressure between alveolar gas and venous
blood. Relatively insoluble agents such
(13:20):
as nitrous oxide are taken up bythe blood less avidly than more
soluble agents such as cerval fluorine.
As a consequence, the alveolar concentration of nitrous oxide
(13:41):
rises and achieves a steady state faster than that of
several fluorine. The relative solubilities of an
anaesthetic in air, blood and tissues are expressed as
partition coefficients. Each coefficient is the ratio of
(14:09):
the concentrations of the anaesthetic gas in each of two
phases at steady state. Steady state is defined as equal
partial pressures in the two phases.
For instance, the blood gas partition coefficient Lambda b /
(14:35):
g of nitrous oxide at 37°C is 0.47.
In other words, at steady state,one meal of blood contains 0.47
(14:56):
as much nitrous oxide as does one meal of alveolar gas, even
though the partial pressures arethe same.
Stated another way, blood has 47% of the capacity for nitrous
(15:18):
oxide as alveolar gas. Nitrous oxide is much less
soluble in blood than is halothene, which has a blood gas
partition coefficient as at 37°Cof 2.4.
(15:43):
Thus, almost five times more halothine than nitrous oxide
must be dissolved to raise the partial pressure of blood by the
same amount. The higher the blood gas
coefficient, the greater the anaesthetics solubility and the
(16:07):
greater its uptake by the pulmonary circulation.
As a consequence of this increased solubility, alveolar
partial pressure rises to a steady state more slowly.
(16:28):
Because fat blood partition coefficients are greater than
one blood gas, solubility is increased by postprandial
lipidemia and is decreased by anaemia.
(16:53):
Next we get to Table 8-1 talkingabout the partition coefficients
of volatile anaesthetics at 37°C.
These values are averages derived from multiple studies
(17:15):
and should be used for comparison purposes and not as
exact numbers. Kindly pause this recording to
go through this very important Table IT-1. 3 The second factor
(17:46):
that affects uptake is alveolar blood flow, which in the absence
of pulmonary shunting is equal to cardiac output.
If the cardiac output drops to 0, so will anaesthetic uptake.
(18:11):
As cardiac output increases, anaesthetic uptake increases,
the rise in avula partial pressure slows and induction is
delayed. The effect of changing cardiac
output is less pronounced for insoluble anaesthetics as so
(18:36):
little is taken up regardless ofalveolar blood flow.
Low output states predispose patients to overdosage with
soluble agents, as the rate overdosage with soluble agents
(18:56):
as the rate of alveolar concentrations will be markedly
increased. The final factor affecting the
uptake of an aesthetic by the pulmonary circulation is the
partial pressure difference between alveolar gas and venous
(19:17):
blood. This gradient depends on tissue
uptake. If anaesthetics did not pass
into organs such as the brain, venous and alveolar partial
pressures would become identicaland there would be no pulmonary
(19:40):
uptake. The transfer of anaesthetic from
blood to tissues is determined by three factors analogous to
system uptake. Tissue solubility of the agent
that is tissue blood partition coefficient, tissue blood flow
(20:07):
and the difference in partial pressure between arterial blood
and the tissue. To better understand inhaled
anaesthetic uptake and distribution, tissues have been
classified into four groups. Based on their solubility and
(20:30):
blood flow, the highly perfused vessel rich group that is brain,
heart, liver, kidney, endocrine organs is the first to encounter
appreciable amounts of anaesthetic.
(20:54):
Moderate solubility and small volume limits the capacity of
this group, so it is also the first to approach steady state,
that is, arterial and tissue partial pressures are equal.
(21:17):
The muscle group that is skin and muscle is not as well
perfused, so uptake is slower. In addition, it has a greater
capacity due to a larger volume and uptake will be sustained for
(21:41):
hours. Perfusion of the fat group
nearly equals that of the musclegroup, but the tremendous
solubility of anaesthetic in fatleads to a total capacity, that
is tissue over blood. Solubility times tissue volume
(22:06):
that would take days to approachsteady state.
The minimal perfusion of the vessel pore group, that is
bones, ligaments, teeth, hair, cartilage results in
(22:26):
insignificant uptake. Next we get to Table 8-2, tissue
groups based on perfusion and solubilities.
Kindly pause this recording to go through Table 8-2.
(22:55):
Anaesthetic optic produces a characteristic curve that
relates the rise in alveolar concentration to time.
The shape of this graph is determined by the optics of
individual tissue groups. The initial steep rise in FA
(23:19):
over FI is due to unopposed feeling of the alveoli by
ventilation. The rate of rise slows as the
vessel reach group and eventually the muscle group
approaches steady state levels of saturation.
(23:46):
Next we get to Figure 8-2. FA rises toward FI faster with
nitrous oxide and insoluble agents than with halothane, A
soluble agent. Kindly pause this recording to
go through Figure 8-2, explaining these differences.
(24:17):
Next we get to Figure 8-3, showing the rise and fall of in
alveolar partial pressure preceding that of other tissues.
Kindly pause this recording to go through Figure 8-3, which
(24:41):
shows the breakdown between the fat group, the muscle group, the
vessel rich group and the alveolar the the partial
pressure differences between them.
Ventilation. The lowering of alveolar partial
(25:07):
pressure by optic can be countered by increasing alveolar
ventilation. In other words, constantly
replacing an aesthetic taking upby the pulmonary bloodstream
results in better maintenance ofalveolar concentration.
(25:33):
The effects of increasing ventilation will be the most
obvious in raising the FA over FI for soluble anaesthetics
because they are more subject touptake.
Because the FA over FI very rapidly approaches one for
(25:58):
insoluble agents, increasing ventilation has minimal effects,
in contrast to the effect of anaesthetics on cardiac output.
Anaesthetics and other drugs, for example opioids that depress
(26:19):
spontaneous ventilation. We'll decrease the rate of rise
in alveolar concentration and create a negative feedback loop.
Morgan and Michael's Clinical anesthesiology, 7th edition,
Chapter 8. Inhalation anaesthetics.
Key concepts. One, the greater the uptake of
(00:27):
anaesthetic agents, the greater the difference between inspired
and alveolar concentrations and the slower the rate of induction
2 Three factors affect anaesthetic uptake.
(00:49):
Solubility in the blood. Alveolar blood flow and the
difference in partial pressure between alveolar gas and venous
blood 3. Low output states predispose
patients to overdosage with soluble agents as the rate of
(01:16):
rise in alveolar concentrations will be markedly increased. 4.
Many of the factors that speed induction also speed recovery,
elimination of rebreathing, highfresh gas flows, low anaesthetic
(01:42):
circuit volume, low absorption by the anaesthetic circuits,
decreased solubility, high cerebral blood flow and
increased ventilation 5. The unitary hypothesis proposes
(02:10):
that all inhalation agents sharea 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
(02:33):
solubility, that is the mere overturn rule.
The implication is that anaesthesia results from
molecules dissolving at specificlipophilic sites.
However, the correlation is onlyapproximate 6.
(02:56):
The minimum alveolar concentration, that is, Mac of
an inhaled anaesthetic is the alveolar concentration that
prevents movement in 50% of patients in response to a
standardised stimulus, for example, surgical incision 7.
(03:24):
Prolonged exposure to anaesthetic concentrations of
Nitro nitrous oxide can result in bone marrow depression, that
is megaloblastic anaemia, and even neurologic deficiencies,
that is peripheral neuropathies 8.
(03:48):
Hallothane hepatitis is extremely rare.
Patients exposed to multiple hallothane anaesthetics at short
intervals, middle age obese women, and persons with a
familial predisposition to hallothane toxicity or a
(04:08):
personal history of toxicity areconsidered to be at increased
risk. 9 Isoflorane dilates coronary arteries, but not
nearly as potently as nitroglycerin or adenosine.
(04:32):
Dilation of normal coronary arteries could theoretically
divert blood away from fixed stenotic lesions 10.
The low solubility of DES fluorine in blood and body
(04:52):
tissues causes very rapid induction of an emergence from
anaesthesia 11. Rapid increases in DES fluorine
concentration lead to transient but sometimes worrisome
(05:14):
elevations in heart rate, blood pressure, and catecholamine
levels that are more pronounced than occur with isofluorine,
particularly in patients with cardiovascular disease 12 Non
(05:37):
pungency and rapid increases in alveolar and aesthetic
concentration make several fluorine an excellent choice for
smooth and rapid inhalation inductions in paediatric and
adult patients. Nitrous oxide, chloroform and
(06:02):
ether We're the first universally accepted general
anaesthetics. Currently used inhalation agents
include nitrous oxide, halothane, isoflorane,
desflorane and sevoflorane. The cause of a general
(06:24):
anaesthetic can be divided into 3 phases. 1 Induction, two
maintenance and three emergence.Inhalation and aesthetics.
(06:44):
Notably, halothane and cerval fluorine are particularly useful
for the inhalation induction of paediatric patients in whom it
may be difficult to start an intravenous line.
Although adults are usually induced with intravenous agents,
(07:07):
the non pungency and rapid onsetof several fluorine makes
inhalation induction practical for them as well.
Regardless of the patient's age,anaesthesia is often maintained
with inhalation agents. Emergence depends primarily upon
(07:32):
redistribution of the agents from the brain, followed by
pulmonary elimination. Because of their unique route of
administration, inhalation and aesthetics have useful
pharmacological properties not shared by other anaesthetic
(07:54):
agents. Pharmacokinetics of inhalation
and aesthetics. Although the mechanism of action
of inhalation and aesthetics is not yet fully understood, their
ultimate effects clearly depend on attaining A therapeutic
(08:19):
tissue concentration in the central nervous system.
There are many steps between theanaesthetic vaporizer and the
anaesthetics deposition in the brain.
(08:41):
Next, we get to Figure 8-1, talking about the fact that
inhalation anaesthetic agents must pass through many barriers
between the anaesthesia machine and the brain.
(09:01):
Kindly take some time to go through Figure 8-1 Factors
affecting inspiratory concentration, that is, FI.
(09:24):
The fresh gas leaving the anaesthesia machine mixes with
gases in the breathing circuits before being inspired by the
patient. Therefore, the patient is not
necessarily receiving the concentration set on the
vaporizer. The actual composition of the
(09:49):
inspired gas mixture depends mainly on the fresh gas flow
rate, the volume of the breathing system, and any
absorption by the machine or breathing circuit.
(10:10):
The greater the fresh gas flow rate, the smaller the breathing
system volume, and the lower thecircuit absorption, the closer
the inspired gas concentration will be to the fresh gas
concentration. Factors affecting alveolar
(10:37):
concentration. FA Optic If there were no optic
of anaesthetic agents by the body, the alveolar gas
concentration FA would rapidly approach the inspired gas
(10:59):
concentration FI. Because anaesthetic agents are
taken up by the pulmonary circulation during induction,
alveolar concentrations lag behind inspired concentrations.
That is, FA over FI is less thanone.
(11:27):
The greater the uptake, the slower the rate of rise of the
alveolar concentration and the lower the FA to FI ratio. 1
Because the concentration of a gas is directly proportional to
(11:50):
its partial pressure, the alveolar partial pressure will
also be slow to rise. The alveolar partial pressure is
important because it determines the partial pressure of an
aesthetic in the blood and ultimately in the brain.
(12:14):
Similarly, the partial pressure of the anaesthetic in the brain
is directly proportional to its brain tissue concentration,
which determines the clinical effect.
The faster the uptake of anaesthetic agent, the greater
(12:37):
the difference between inspired and alveolar concentrations and
the slower the rate of induction. 2.
Three factors affect anaestheticuptake.
(12:59):
Solubility in the blood, alveolar blood flow, and the
difference in partial pressure between alveolar gas and venous
blood. Relatively insoluble agents such
(13:20):
as nitrous oxide are taken up bythe blood less avidly than more
soluble agents such as cerval fluorine.
As a consequence, the alveolar concentration of nitrous oxide
(13:41):
rises and achieves a steady state faster than that of
several fluorine. The relative solubilities of an
anaesthetic in air, blood and tissues are expressed as
partition coefficients. Each coefficient is the ratio of
(14:09):
the concentrations of the anaesthetic gas in each of two
phases at steady state. Steady state is defined as equal
partial pressures in the two phases.
For instance, the blood gas partition coefficient Lambda b /
(14:35):
g of nitrous oxide at 37°C is 0.47.
In other words, at steady state,one meal of blood contains 0.47
(14:56):
as much nitrous oxide as does one meal of alveolar gas, even
though the partial pressures arethe same.
Stated another way, blood has 47% of the capacity for nitrous
(15:18):
oxide as alveolar gas. Nitrous oxide is much less
soluble in blood than is halothene, which has a blood gas
partition coefficient as at 37°Cof 2.4.
(15:43):
Thus, almost five times more halothine than nitrous oxide
must be dissolved to raise the partial pressure of blood by the
same amount. The higher the blood gas
coefficient, the greater the anaesthetics solubility and the
(16:07):
greater its uptake by the pulmonary circulation.
As a consequence of this increased solubility, alveolar
partial pressure rises to a steady state more slowly.
(16:28):
Because fat blood partition coefficients are greater than
one blood gas, solubility is increased by postprandial
lipidemia and is decreased by anaemia.
(16:53):
Next we get to Table 8-1 talkingabout the partition coefficients
of volatile anaesthetics at 37°C.
These values are averages derived from multiple studies
(17:15):
and should be used for comparison purposes and not as
exact numbers. Kindly pause this recording to
go through this very important Table IT-1. 3 The second factor
(17:46):
that affects uptake is alveolar blood flow, which in the absence
of pulmonary shunting is equal to cardiac output.
If the cardiac output drops to 0, so will anaesthetic uptake.
(18:11):
As cardiac output increases, anaesthetic uptake increases,
the rise in avula partial pressure slows and induction is
delayed. The effect of changing cardiac
output is less pronounced for insoluble anaesthetics as so
(18:36):
little is taken up regardless ofalveolar blood flow.
Low output states predispose patients to overdosage with
soluble agents, as the rate overdosage with soluble agents
(18:56):
as the rate of alveolar concentrations will be markedly
increased. The final factor affecting the
uptake of an aesthetic by the pulmonary circulation is the
partial pressure difference between alveolar gas and venous
(19:17):
blood. This gradient depends on tissue
uptake. If anaesthetics did not pass
into organs such as the brain, venous and alveolar partial
pressures would become identicaland there would be no pulmonary
(19:40):
uptake. The transfer of anaesthetic from
blood to tissues is determined by three factors analogous to
system uptake. Tissue solubility of the agent
that is tissue blood partition coefficient, tissue blood flow
(20:07):
and the difference in partial pressure between arterial blood
and the tissue. To better understand inhaled
anaesthetic uptake and distribution, tissues have been
classified into four groups. Based on their solubility and
(20:30):
blood flow, the highly perfused vessel rich group that is brain,
heart, liver, kidney, endocrine organs is the first to encounter
appreciable amounts of anaesthetic.
(20:54):
Moderate solubility and small volume limits the capacity of
this group, so it is also the first to approach steady state,
that is, arterial and tissue partial pressures are equal.
(21:17):
The muscle group that is skin and muscle is not as well
perfused, so uptake is slower. In addition, it has a greater
capacity due to a larger volume and uptake will be sustained for
(21:41):
hours. Perfusion of the fat group
nearly equals that of the musclegroup, but the tremendous
solubility of anaesthetic in fatleads to a total capacity, that
is tissue over blood. Solubility times tissue volume
(22:06):
that would take days to approachsteady state.
The minimal perfusion of the vessel pore group, that is
bones, ligaments, teeth, hair, cartilage results in
(22:26):
insignificant uptake. Next we get to Table 8-2, tissue
groups based on perfusion and solubilities.
Kindly pause this recording to go through Table 8-2.
(22:55):
Anaesthetic optic produces a characteristic curve that
relates the rise in alveolar concentration to time.
The shape of this graph is determined by the optics of
individual tissue groups. The initial steep rise in FA
(23:19):
over FI is due to unopposed feeling of the alveoli by
ventilation. The rate of rise slows as the
vessel reach group and eventually the muscle group
approaches steady state levels of saturation.
(23:46):
Next we get to Figure 8-2. FA rises toward FI faster with
nitrous oxide and insoluble agents than with halothane, A
soluble agent. Kindly pause this recording to
go through Figure 8-2, explaining these differences.
(24:17):
Next we get to Figure 8-3, showing the rise and fall of in
alveolar partial pressure preceding that of other tissues.
Kindly pause this recording to go through Figure 8-3, which
(24:41):
shows the breakdown between the fat group, the muscle group, the
vessel rich group and the alveolar the the partial
pressure differences between them.
Ventilation. The lowering of alveolar partial
(25:07):
pressure by optic can be countered by increasing alveolar
ventilation. In other words, constantly
replacing an aesthetic taking upby the pulmonary bloodstream
results in better maintenance ofalveolar concentration.
(25:33):
The effects of increasing ventilation will be the most
obvious in raising the FA over FI for soluble anaesthetics
because they are more subject touptake.
Because the FA over FI very rapidly approaches one for
(25:58):
insoluble agents, increasing ventilation has minimal effects,
in contrast to the effect of anaesthetics on cardiac output.
Anaesthetics and other drugs, for example opioids that depress
(26:19):
spontaneous ventilation. We'll decrease the rate of rise
in alveolar concentration and create a negative feedback loop.
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