May 15, 2025 • 49 mins
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This episode features a full reading of “The Physiology of Oxygen Delivery” from Update in Anaesthesia, Volume 24, Number 2.
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(00:01):
Updates in Anaesthesia, volume 24 #2 The Physiology of oxygen
delivery by Rob Law and Henry Burkweiwa.
(00:22):
Summary In order to survive, humans have to be able to
extract oxygen from the atmosphere and transport it to
their cells, where it is utilised for essential metabolic
processes. Some cells can produce energy
(00:45):
without oxygen, that is, anaerobic metabolism, for a
short time, although it is inefficient.
Other organs, for example the brain, are made-up of cells that
can only produce the energy necessary for survival in the
presence of a continual supply of oxygen, that is anaerobic
(01:10):
metabolism. Tissues differ in their ability
to withstand anoxia, that is a lack of oxygen.
The brain and the heart are the most sensitive.
Oxygen transport from the air tothe tissues.
(01:38):
Oxygen is transported from the air that we breed to each cell
in the body. In general, gases move from an
area of high concentration or pressure to areas of low
concentration or pressure. If there is a mixture of gases
(02:00):
in a container, the pressure of each gas, that is, the partial
pressure indicated by the symbolP, is equal to the pressure that
each gas would produce if it occupied the container alone.
(02:20):
The total pressure of the gas mixture is the sum of the
partial pressures of all the individual gases.
Oxygen cascade. Oxygen moves down the pressure
or concentration gradients from a relatively high level in the
(02:45):
air to the levels in the respiratory tracts and then
alveolar gas, the arterial bloodcapillaries, and finally the
cell. The partial pressure of oxygen
(03:06):
reaches the lowest level that is1 to 1.5 kilopascals in the
mitochondria, the structures in cells responsible for energy
production. These decrease in partial
pressure of oxygen from air to the mitochondrion is known as
(03:30):
the oxygen cascade. The success successive steps
down in PO2 or call for physiological reasons, but they
can be influenced by pathological states, for
instance, hypoventilation, ventilation, perfusion,
(03:54):
inequality or diffusion abnormality that will result in
tissue hypoxia. Atmosphere to alveolus.
The air that is atmosphere around us has a total pressure
(04:19):
of 101 kilopascals. Note that one atmosphere of
pressure is equal to 760 millimetres of mercury, which is
equal to 101 kilopascals. Air is made-up of 21% oxygen,
(04:39):
78% nitrogen and small quantities of carbon dioxide,
argon and helium. The pressure exerted by oxygen
and nitrogen when added togetherapproximates to atmospheric
(05:02):
pressure. The pressure of oxygen PO2 or
dry air at sea level is therefore 21.2 kilopascals, That
is, 21 / 100 * 1 O1 is equals to21.2 kilopascals.
(05:30):
However, by the time the inspired air reaches the
trachea, it has been warmed and humidified by the upper
respiratory tract. The humidity is formed by water
vapour, which is a gas, so exerts a pressure.
(05:57):
Next we get to Figure 1, explaining the oxygen cascade.
The effects of hyperventilation are shown as the grey line and
the effects of a pathological shunt are shown as a dashed
line. Kindly pause this recording and
(06:19):
take a moment to go through Figure 1.
At 37°C the water vapour pressure in the trachea is 6.3
kilopascals. Taking the water vapour pressure
(06:40):
into account, the PO2 in the trachea when breathing air is
one O 1 - 6.3 * 21 / 100 which is equal to 19.9 kilopascals.
(07:03):
By the time the oxygen has reached the alveoli, the
pressure of oxygen has fallen toabout 13.4 kilopascals.
This is This is because the pressure of oxygen of the gas in
the alveoli, that is PAO 2 is further reduced by dilution with
(07:27):
carbon dioxide entering the alveoli from the pulmonary
capillaries. The pressure of oxygen pressure,
the PO2 of the gas in the alveoli can be calculated using
(07:49):
the alveolar gas equation which is PAO 2 equals Fio 2 -.
P A CO2 over RQ where RQ is a respiratory quotient.
(08:11):
The ratio of carbon diazide production to oxygen
consumption, usually about 0.8 alveolus to blood.
Blood returning to the heart from the tissues has a low
(08:35):
preserve oxygen that is 4.3 kilopascals and travels to the
lungs via the pulmonary arteries.
The pulmonary arteries form pulmonary capillaries which
surround alveoli. Oxygen diffuses, that is, moves
(09:01):
through the membrane separating the air and the blood from the
high partial pressure in the alveoli, that is 13 kilopascals,
to the area of lower partial pressure, that is the blood in
the pulmonary capillaries, whichis 4.3 kilopascals.
(09:23):
After oxygenation, blood moves into the pulmonary veins and
returns to the left side of the heart to be pumped to the
systemic tissues. In a perfect lung, the pressure
of oxygen of pulmonary venous blood will be equal to the
(09:47):
pressure of oxygen in the alveolus, that is the PAO 2. 2
main factors cause the pressure of oxygen of pulmonary venous
blood to be less than the than the PAO 2 that is to increase
(10:10):
the alveolar arterial difference.
These are ventilation perfusion mismatch either which is either
increased Dead Space, that is either increased Dead Space or
shunt and slow diffusion across the alveolar capillary membrane.
(10:40):
Ventilation perfusion that is VQmismatch.
In a perfect long, all alveoli would receive an equal share of
alveolar ventilation, and the pulmonary capillaries that
(11:00):
surround different alveoli wouldreceive an equal share of
cardiac output. That is, alveolar minute
ventilation and perfusion would be perfectly matched.
VQ is equal to 1. Even in health this is not
(11:25):
achieved and at almost all levels in a normal lung there is
a relative imbalance of perfusion and ventilation.
Perfusion is best at the base ofthe lung and gradually reduces
towards the top of the lung, largely due to the effects of
(11:49):
gravity. The alveoli at the base of a
normal lung are at a lower resting volume in exploration,
that is, at functional residual capacity FRC, but they are
better ventilated, that is, theyincrease their volume
(12:13):
proportionately more during inspiration.
This concept is not intuitive and of course, because our major
muscle of inspiration, the diaphragm, lies below the lung,
(12:33):
contributing to better lung compliance towards the base of
the lung. Next we get to Figure 2 talking
about the graph to show perfusion and ventilation in
different segments. Moving up the long take a while
(12:57):
to go through this. Next we get to figure 3.
Explaining is the schematic diagram showing 3 long units
that the ideal situation and thetwo extremes of VQ mismatch that
(13:20):
is shunt and Dead Space. Assume pause this recording to
go through Figure 3 please. Both ventilation and profusion
improve as you move down the lung towards its base, but they
(13:42):
are not perfectly matched areas of the lung.
Areas at the top of the lung arerelatively more ventilated than
perfused. That is, the extreme example of
this is Dead Space, where the long volume is ventilated but
(14:05):
there is insufficient profusion for gas exchange to occur.
In other words, VQ is greater than one.
Areas towards the beasts are perfused more than ventilated.
That is, the extreme example of this is a shunt.
(14:27):
VQ is less than one. Both extreme examples of the
spectrum of possible VQ mismatches are illustrated in
Figure 3, where blood flows pastalveoli with no gas exchange
(14:52):
taking place, that is, shunt. As seen in figure three, well
ventilated alveoli with high oxygen pressure in capillary
blood cannot compensate for the lack of oxygen transfer in the
under perfused alveoli with a low pressure of oxygen in the
(15:16):
capillary blood. This is because there is a
maximum amount of oxygen that can combine with haemoglobin.
That is, this is known by the oxygen haemoglobin dissociation
curve. Later arterial oxygen PAO 2 is
(15:41):
therefore lower than the alveolar oxygen PAO 2.
Lung pathology that exacerbates the physiological shunt includes
atelectasis, consolidation of the lung, pulmonary edoema, or
(16:08):
small airway closure. Pulmonary embolism causes
increased physiological Dead Space diffusion.
Oxygen diffuses from the alveolus to the capillary until
(16:31):
the PCO 2 is equal to that in the alveolus.
This process is rapid, about 0.25 seconds, and normally
complete by the time the blood has passed about 1/3 of the way
(16:53):
along the pulmonary capillary. The total transit time through
the capillary is 0.75 seconds inthe normal lung.
Even if the cardiac output and blood flow past the alveoli is
(17:14):
increased during exercise, thereis enough time for
equilibration. Pulmonary disease may cause an
abnormality of the alveolar capillary membrane, thus
impairing transfer of oxygen from the alveolus to the
(17:36):
capillary, that is diffusion abnormality.
At rest there may still be time for the PAO to to equilibrate
with alveolar oxygen, but on exercise full oxygen transfer is
(17:59):
impossible and hypoxemia develops.
However, the ability of the lungto compensate is great and
problems caused by poor gas diffusion are a rare case Rare
cause for hypoxia except with diseases such as alveolar
(18:24):
fibrosis. Hypoxic pulmonary
vasoconstriction. In order to minimise the
detrimental effects that shunt has on oxygenation, the blood
vessels in the lung are adapted to vasoconstrict in response to
(18:50):
low oxygen levels and therefore reduce blood flow to areas that
are under ventilated. This is termed hypoxic pulmonary
vasoconstriction and reduces theeffects of shunt oxygen carriage
(19:20):
by the blood. Oxygen is carried in the blood
in two forms. Most is carried combined with
haemoglobin and a small amount is dissolved in the plasma.
(19:43):
Each gramme of haemoglobin can carry 1.34 mils of oxygen when
fully saturated. Therefore, every litre of blood
with a haemoglobin concentrationof 15 grammes per deal can carry
about 200 mils of oxygen when fully saturated with oxygen that
(20:09):
is exposed to a pressure of oxygen greater than 13
kilopascals. At this pressure of oxygen, only
three mils of oxygen will dissolve in each litre.
Of plasma. Next we go to Figure 4,
(20:31):
explaining the diffusion from the alveolus to the capillary
and other things. Kindly pause this recording to
go through Figure 4. If the PAO 2 is increased
(20:55):
significantly by breathing 100% of oxygen, then a small amount
of extra oxygen will dissolve inthe plasma at a rate of 0.025
mills of oxygen over 100 mills of blood per kilopascal PO2.
(21:22):
But there will normally be no significant increase in the
amount carried by haemoglobin asit is already greater than 95%
saturated with oxygen. Oxygen delivery When considering
(21:48):
the adequacy of oxygen delivery to the tissues, 3 factors need
to be taken into account, haemoglobin concentration,
cardiac output and oxygenation. Next we get to Figure 5,
(22:08):
explaining the oxygen haemoglobin dissociation curve.
Take a while to go through this.The quantity of oxygen made
available to the body in one minute is known as the oxygen
(22:31):
delivery. Oxygen delivery in miles of
oxygen per minute is equals to cardiac output in litres per
minute multiplied by haemoglobinconcentrations in gramme per
litre multiplied by 1.34 in mills of oxygen per gramme,
(23:03):
mills of oxygen gramme per HB multiplied by percentage
saturation which is finally equal to 1000 mills of oxygen
per minute oxygen consumption. Approximately 250 mills of
(23:34):
oxygen are used every minute by a conscious resting person, that
is resting oxygen consumption and therefore about 25% of the
arterial oxygen content is used every minute.
(23:59):
The haemoglobin is mixed. The haemoglobin in mixed venous
blood is about 73% saturated, that is 98% -, 25% At rest.
Oxygen delivery to the cells of the body exceeds oxygen
(24:24):
consumption. During exercise, oxygen
consumption increases. The increased oxygen requirement
is usually provided by an increased cardiac output as
shown in the formula above. A low cardiac output, low
(24:52):
haemoglobin concentration, that is, anaemia, or low oxygen
saturation will result in reduced tissue oxygen delivery
unless there is a compensatory change in one of the other
factors. If oxygen delivery falls
(25:14):
relatively relative to oxygen consumption, the tissues extract
more oxygen from the haemoglobinand the saturation of mixed
venous blood falls below 70%. Below a setting point, decreased
(25:35):
oxygen delivery cannot be compensated for by an increased
oxygen extraction and this results in anaerobic metabolism
and lactic acidosis. This situation is known as
supply dependent oxygenation. Oxygen stores In spite of our
(26:08):
reliance on oxygen, the sources of oxygen in the body are small
and would be unable to sustain life for more than a few minutes
if breathing ceases. Oxygen stores are limited to the
oxygen in the lung and oxygen inthe blood.
(26:33):
The amount of oxygen in the blood depends on the blood
volume and haemoglobin concentration as described
above. The amount of oxygen in the lung
is dependent on the lung volume at functional residual capacity,
(26:55):
FRC, and the alveolar concentration of oxygen.
The FRC is the volume of air that is about 3 litres in an
adult that is present in the lungs at the end of a normal
expiration. At this volume, the elastic
(27:19):
recoil of the lung, that is its tendency to collapse, is
balanced by the tendency of the chest wall and diaphragm to
resist lung collapse when breathing air.
The total oxygen stalls, that isin the blood and lung are small.
(27:45):
The major component of this stall is the oxygen bound to
haemoglobin. Only a small part of these
stalls can be released without an unacceptable reduction in PA
O2. That is, when haemoglobin is 50%
(28:08):
saturated, the PAO 2 will have fallen to 3.5 kilopascals.
Breathing 100% oxygen causes a large increase in the total
oxygen stalls as the functional reserve capacity fills with
(28:28):
oxygen. The major component of the store
is now in the lung and 80% of this oxygen can be used without
any reduction in haemoglobin saturation.
That is, PO2 is still about 14 kilopascals.
(28:54):
This is the reason why pre oxygenation is so effective.
Next, we get to Figure 6, showing a graph showing the
balance between oxygen delivery and oxygen consumption.
(29:17):
Kindly pause this recording to go through Figure 6.
From there we get to Table 1, the principal stores of oxygen
in the body. The titles are Breathing air or
(29:41):
breathing 100% oxygen. Oxygen stored in the lungs at
FRC. Breathing air is 450 mils.
Breathing 100% oxygen is 3000 mils.
(30:08):
Oxygen stall bound to haemoglobin.
Breathing air is 850 mils. Breathing 100% oxygen is 950
mils oxygen dissolved or bound in tissues.
(30:34):
Breathing air is 250 mils and breathing 100% oxygen IS300
mils. So the total oxygen store in the
body while breathing air is 1550mils and while breeding 100%
(30:59):
oxygen is 4250 mills. Oxygen transport.
The effects of anaesthesia. Hyper ventilation may occur
(31:23):
during anaesthesia due to airwayobstruction.
The effects of volatile anaesthetic agents, opioids and
other sedatives. Ketamine and ether.
Ether at less than one MEC causeless respiratory depression than
(31:51):
other anaesthetic agents. The PAO 2 is a balance between
the oxygen supplied by breathingand that's used by metabolic
processes in the body. Hypoventilation and a decreased
(32:15):
inspired oxygen concentration will therefore cause a reduction
in PAO 2. The increased utilisation of
oxygen when metabolic rate is raised, for example during
postoperative shivering or pyrexia, also causes a reduction
(32:39):
in PAO 2 if the PAO 2 falls to less than 8 kilopascals.
The aortic and carotid body chemoreceptors respond by
causing hyperventilation and increasing cardiac output
(33:03):
through sympathetic nervous system stimulation.
This normal protective response to hypoxia is reduced by
anaesthetic drugs. This effect extends into the
post operative period. Following induction of
(33:30):
anaesthesia. There is a rapid reduction in
functional reserve capacity, largely attributable to loss of
tone in the respiratory muscles and chest wall.
Functional reserve capacity drops below the closing volume
(33:53):
in the lung, the expiratory volume at which airway closure
first occurs. This primarily occurs in small
Airways in dependent parts of the lung.
These areas may remain closed throughout the respiratory cycle
(34:15):
to result in a shunt as described above.
VQ mismatch due to airway closure, that is, shunt will
increase the alveolar arterial difference.
(34:36):
This venous admixture increases from 1% to around 10% following
induction of anaesthesia. Next we go to Figure 7,
(34:57):
explaining the effects on PA O2 of increasing the FIO 2 from 21%
to 30%. That's thin curve to heavy curve
at a constant oxygen concentration of 200 mils per
minute. Kindly pause this recording to
(35:21):
go through Figure 7. With the possible exception of
patients spontaneously breathingwhile anaesthetized with
ketamine, this increase in venous admixture occurs
irrespective of the anaesthetic agent used and whether muscle
(35:45):
relaxants are used or not. It should be viewed as an
unavoidable adverse effect of anaesthesia and explains the
universal requirement for supplementary oxygen during
surgery to achieve normal oxygenation.
(36:08):
Furthermore, volatile anaesthetic agents suppress
hypoxic pulmonary vessel constriction and blood flow to
under ventilated or collapsed alveoli is not reduced
(36:28):
appropriately. In addition, many anaesthetic
agents depress cardiac output and therefore decrease oxygen
delivery. Reduced tissue oxygen delivery
during anaesthesia is partially compensated for by the fact that
(36:54):
anaesthesia causes a 15% reduction in metabolic rates and
therefore a reduction in oxygen requirements.
Artificial ventilation causes a further 6% reduction in oxygen
requirements as the work of breathing is removed.
(37:21):
Anaesthetic agents do not affectthe carriage of oxygen by
haemoglobin. Partial use.
Sorry. Practical use of oxygen inspired
(37:43):
oxygen concentration. The efficiency of oxygenation
during anaesthesia is reduced due to hypoventilation and
venous admixture. Inspired oxygen in the range of
25% to 30% is usually effective in restoring the PAO 2 to normal
(38:11):
when hypoxemia is due to hyperventilation.
When hypoxemia is due to venous admixture, it is possible to
restore the PAO 2 by increasing the inspired oxygen
concentration if the venous admixture does not exceed the
(38:36):
equivalent of a 30% shunt. The inspired oxygen
concentration during maintenanceof anaesthesia should routinely
be increased to 30% whenever possible to compensate for hyper
ventilation and shunt, which normally accompany anaesthesia.
(39:04):
Additional oxygen may need to beadministered to patients at risk
of decreased oxygen delivery, that is, anaemia or decreased
cardiac output, or increased oxygen consumption, that is
fever. Next we get to Figure 8 talking
(39:30):
about the effects on POPA O2 on the which is on the vertical
vertical axis of an increasing FIO 2 which is on the horizontal
axis in the presence of different sized shunts.
Kindly pause this recording to go through Figure 8 pre
(39:57):
oxygenation. The small volume of the oxygen
stores of a patient breathing air means that there will be a
rapid fall in oxygen saturation during apnea, for example
following induction of anaesthesia, during laryngos
(40:19):
spasm or during upper airway obstruction.
Pre oxygenation involves breathing 100% oxygen for three
minutes through an anaesthetic circuit with a face mask firmly
(40:39):
applied to the face. This is the time taken to
replace the nitrogen in the FF in the FRC with oxygen using
normal tidal ventilation, also known as denitrogenation.
(41:02):
Although the functional reserve capacity falls on induction of
anaesthesia, the extra oxygen contained within the FRC
provides an essential store of oxygen for periods of apnea,
particularly during rapid sequence induction or difficult
(41:25):
intubation. Patients with a small functional
reserve capacity, that is infants, pregnancy, the obese or
a low haemoglobin concentration and therefore smaller oxygen
stores desaturate more rapidly and pre oxygenation is
(41:50):
especially indicated in these patients.
Crisis management. When managing emergencies during
anaesthesia, consideration should always be given to the
immediate administration of 100%oxygen while the case is found
(42:15):
and rectified. It is the most appropriate
treatments for acute deterioration in
cardiorespiratory function. Anoxic gas mixtures If during
(42:37):
the course of an anaesthetic, 100% nitrous oxide is given to
the patient in error, the fall in PAO 2 will be much more rapid
than during apnea. The PAO 2 can fall, so can fall
to dangerously low levels in as little as 10 seconds.
(43:05):
This is because the oxygen in the patient's lungs and blood,
that is oxygen stalls, is being actively washed out with each
breath that contains no oxygen. The fall in PO2 is therefore
more rapid than would occur if it was only being used up by the
(43:29):
metabolic needs of the body, that is 250 miles per minute.
Modern anaesthesia machines include a hypoxic link to
prevent 100% nitrous oxide beingadministered in error diffusion
(43:54):
hypoxia. Nitrous oxide is 40 times more
soluble in blood than nitrogen. When nitrous oxide is
discontinued at the end of anaesthesia, nitrous oxide
diffuses out of the blood into the alveoli in large volumes
(44:18):
during the next two to three minutes.
If the patient is allowed to breathe air at this time, the
combination of nitrous oxide andnitrogen in the alveoli reduces
the PA O2. This is called diffusion hypoxia
(44:40):
and it's avoided by increasing the alveolar concentration of
oxygen by the administration of 100% oxygen for two to three
minutes after discontinuing nitrous oxide post operative
(45:02):
oxygen. The causes of increased venous
admixture, that is VQ mismatch, shunt and airway closure, and
the abnormal response to hypoxiacontinue into the post op period
(45:23):
for up to three days following major surgery.
Post operative hyperventilation is common and may be due to the
residual effect of anaesthesia, the use of opioid analgesia,
pain or airway obstruction. Shivering in the immediate post
(45:52):
operative period causes an increase in oxygen consumption.
Additional oxygen should therefore be given to all
unconscious patients in recoveryand to those awake patients who
either shiver, hyperventilate, are desaturated or who are
(46:17):
considered to be at increased risk, for example, ischemic
heart disease on the ward duringthe post operative period.
Episodes of airway obstruction during sleep are common and may
aggravate borderline oxygenationdue to the above factors.
(46:44):
This is usually due to the use of opioid analgesia and a change
in sleep pattern that occurs on the second and third post
operative nights after major surgery.
The risk of hypoxemia extends well into the post operative
(47:07):
period. Small degrees of cyanosis are
not easy to detect clinically, especially in anaemic patients,
and therefore oxygen should be given to those.
These patients wherever possible, especially overnight
(47:32):
post operative pain should be treat to be effectively treated,
particularly following abdominalor thoracic surgery.
If opioid analgesics are indicated, hyperventilation
should be anticipated and oxygensaturation monitored as a
(47:58):
routine problems associated withoxygen administration.
It is it has been suggested thathigh concentrations of oxygen
that is 90 to 100% administered to patients for a prolonged
(48:24):
period of several days may causepulmonary damage.
Whilst this is a concern, it should never prevent the use of
oxygen to treat severe hypoxia. High concentrations of oxygen
(48:45):
encourage collapse of alveoli with low ventilation stroke
perfusion ratios. Oxygen is rapidly and completely
absorbed from this alveoli and when it is the only gas being
(49:06):
given, these under ventilated alveoli collapse, that is
absorption atelectasis. When air and oxygen is used, the
nitrogen present is absorbed more slowly and prevents the
(49:31):
alveolus from collapsing. It is therefore sensible to
administer the lowest FIO tool that achieves adequate
oxygenation as guided by pulse oximetry.
(49:52):
Oxygen therapy may rarely depress ventilation in patients
suffering from severe chronic obstructive Airways disease.
Patients who chronically retain carbon dioxide lose the
hypercarponic stimulus to maintain ventilation and are
(50:17):
therefore reliant on their hypoxic drive to self ventilate.
Administration of oxygen may remove this drive and result in
respiratory arrest. In practise this situation is
rare, but again it is sensitive.It is sensible to gradually try
(50:43):
treat the FIO 2 to achieve a realistic oxygenation goal.
It is often appropriate to tolerate moderate hypoxia in
these patients. That is a maximum SA O2 of 90 to
(51:03):
94%.
Updates in Anaesthesia, volume 24 #2 The Physiology of oxygen
delivery by Rob Law and Henry Burkweiwa.
(00:22):
Summary In order to survive, humans have to be able to
extract oxygen from the atmosphere and transport it to
their cells, where it is utilised for essential metabolic
processes. Some cells can produce energy
(00:45):
without oxygen, that is, anaerobic metabolism, for a
short time, although it is inefficient.
Other organs, for example the brain, are made-up of cells that
can only produce the energy necessary for survival in the
presence of a continual supply of oxygen, that is anaerobic
(01:10):
metabolism. Tissues differ in their ability
to withstand anoxia, that is a lack of oxygen.
The brain and the heart are the most sensitive.
Oxygen transport from the air tothe tissues.
(01:38):
Oxygen is transported from the air that we breed to each cell
in the body. In general, gases move from an
area of high concentration or pressure to areas of low
concentration or pressure. If there is a mixture of gases
(02:00):
in a container, the pressure of each gas, that is, the partial
pressure indicated by the symbolP, is equal to the pressure that
each gas would produce if it occupied the container alone.
(02:20):
The total pressure of the gas mixture is the sum of the
partial pressures of all the individual gases.
Oxygen cascade. Oxygen moves down the pressure
or concentration gradients from a relatively high level in the
(02:45):
air to the levels in the respiratory tracts and then
alveolar gas, the arterial bloodcapillaries, and finally the
cell. The partial pressure of oxygen
(03:06):
reaches the lowest level that is1 to 1.5 kilopascals in the
mitochondria, the structures in cells responsible for energy
production. These decrease in partial
pressure of oxygen from air to the mitochondrion is known as
(03:30):
the oxygen cascade. The success successive steps
down in PO2 or call for physiological reasons, but they
can be influenced by pathological states, for
instance, hypoventilation, ventilation, perfusion,
(03:54):
inequality or diffusion abnormality that will result in
tissue hypoxia. Atmosphere to alveolus.
The air that is atmosphere around us has a total pressure
(04:19):
of 101 kilopascals. Note that one atmosphere of
pressure is equal to 760 millimetres of mercury, which is
equal to 101 kilopascals. Air is made-up of 21% oxygen,
(04:39):
78% nitrogen and small quantities of carbon dioxide,
argon and helium. The pressure exerted by oxygen
and nitrogen when added togetherapproximates to atmospheric
(05:02):
pressure. The pressure of oxygen PO2 or
dry air at sea level is therefore 21.2 kilopascals, That
is, 21 / 100 * 1 O1 is equals to21.2 kilopascals.
(05:30):
However, by the time the inspired air reaches the
trachea, it has been warmed and humidified by the upper
respiratory tract. The humidity is formed by water
vapour, which is a gas, so exerts a pressure.
(05:57):
Next we get to Figure 1, explaining the oxygen cascade.
The effects of hyperventilation are shown as the grey line and
the effects of a pathological shunt are shown as a dashed
line. Kindly pause this recording and
(06:19):
take a moment to go through Figure 1.
At 37°C the water vapour pressure in the trachea is 6.3
kilopascals. Taking the water vapour pressure
(06:40):
into account, the PO2 in the trachea when breathing air is
one O 1 - 6.3 * 21 / 100 which is equal to 19.9 kilopascals.
(07:03):
By the time the oxygen has reached the alveoli, the
pressure of oxygen has fallen toabout 13.4 kilopascals.
This is This is because the pressure of oxygen of the gas in
the alveoli, that is PAO 2 is further reduced by dilution with
(07:27):
carbon dioxide entering the alveoli from the pulmonary
capillaries. The pressure of oxygen pressure,
the PO2 of the gas in the alveoli can be calculated using
(07:49):
the alveolar gas equation which is PAO 2 equals Fio 2 -.
P A CO2 over RQ where RQ is a respiratory quotient.
(08:11):
The ratio of carbon diazide production to oxygen
consumption, usually about 0.8 alveolus to blood.
Blood returning to the heart from the tissues has a low
(08:35):
preserve oxygen that is 4.3 kilopascals and travels to the
lungs via the pulmonary arteries.
The pulmonary arteries form pulmonary capillaries which
surround alveoli. Oxygen diffuses, that is, moves
(09:01):
through the membrane separating the air and the blood from the
high partial pressure in the alveoli, that is 13 kilopascals,
to the area of lower partial pressure, that is the blood in
the pulmonary capillaries, whichis 4.3 kilopascals.
(09:23):
After oxygenation, blood moves into the pulmonary veins and
returns to the left side of the heart to be pumped to the
systemic tissues. In a perfect lung, the pressure
of oxygen of pulmonary venous blood will be equal to the
(09:47):
pressure of oxygen in the alveolus, that is the PAO 2. 2
main factors cause the pressure of oxygen of pulmonary venous
blood to be less than the than the PAO 2 that is to increase
(10:10):
the alveolar arterial difference.
These are ventilation perfusion mismatch either which is either
increased Dead Space, that is either increased Dead Space or
shunt and slow diffusion across the alveolar capillary membrane.
(10:40):
Ventilation perfusion that is VQmismatch.
In a perfect long, all alveoli would receive an equal share of
alveolar ventilation, and the pulmonary capillaries that
(11:00):
surround different alveoli wouldreceive an equal share of
cardiac output. That is, alveolar minute
ventilation and perfusion would be perfectly matched.
VQ is equal to 1. Even in health this is not
(11:25):
achieved and at almost all levels in a normal lung there is
a relative imbalance of perfusion and ventilation.
Perfusion is best at the base ofthe lung and gradually reduces
towards the top of the lung, largely due to the effects of
(11:49):
gravity. The alveoli at the base of a
normal lung are at a lower resting volume in exploration,
that is, at functional residual capacity FRC, but they are
better ventilated, that is, theyincrease their volume
(12:13):
proportionately more during inspiration.
This concept is not intuitive and of course, because our major
muscle of inspiration, the diaphragm, lies below the lung,
(12:33):
contributing to better lung compliance towards the base of
the lung. Next we get to Figure 2 talking
about the graph to show perfusion and ventilation in
different segments. Moving up the long take a while
(12:57):
to go through this. Next we get to figure 3.
Explaining is the schematic diagram showing 3 long units
that the ideal situation and thetwo extremes of VQ mismatch that
(13:20):
is shunt and Dead Space. Assume pause this recording to
go through Figure 3 please. Both ventilation and profusion
improve as you move down the lung towards its base, but they
(13:42):
are not perfectly matched areas of the lung.
Areas at the top of the lung arerelatively more ventilated than
perfused. That is, the extreme example of
this is Dead Space, where the long volume is ventilated but
(14:05):
there is insufficient profusion for gas exchange to occur.
In other words, VQ is greater than one.
Areas towards the beasts are perfused more than ventilated.
That is, the extreme example of this is a shunt.
(14:27):
VQ is less than one. Both extreme examples of the
spectrum of possible VQ mismatches are illustrated in
Figure 3, where blood flows pastalveoli with no gas exchange
(14:52):
taking place, that is, shunt. As seen in figure three, well
ventilated alveoli with high oxygen pressure in capillary
blood cannot compensate for the lack of oxygen transfer in the
under perfused alveoli with a low pressure of oxygen in the
(15:16):
capillary blood. This is because there is a
maximum amount of oxygen that can combine with haemoglobin.
That is, this is known by the oxygen haemoglobin dissociation
curve. Later arterial oxygen PAO 2 is
(15:41):
therefore lower than the alveolar oxygen PAO 2.
Lung pathology that exacerbates the physiological shunt includes
atelectasis, consolidation of the lung, pulmonary edoema, or
(16:08):
small airway closure. Pulmonary embolism causes
increased physiological Dead Space diffusion.
Oxygen diffuses from the alveolus to the capillary until
(16:31):
the PCO 2 is equal to that in the alveolus.
This process is rapid, about 0.25 seconds, and normally
complete by the time the blood has passed about 1/3 of the way
(16:53):
along the pulmonary capillary. The total transit time through
the capillary is 0.75 seconds inthe normal lung.
Even if the cardiac output and blood flow past the alveoli is
(17:14):
increased during exercise, thereis enough time for
equilibration. Pulmonary disease may cause an
abnormality of the alveolar capillary membrane, thus
impairing transfer of oxygen from the alveolus to the
(17:36):
capillary, that is diffusion abnormality.
At rest there may still be time for the PAO to to equilibrate
with alveolar oxygen, but on exercise full oxygen transfer is
(17:59):
impossible and hypoxemia develops.
However, the ability of the lungto compensate is great and
problems caused by poor gas diffusion are a rare case Rare
cause for hypoxia except with diseases such as alveolar
(18:24):
fibrosis. Hypoxic pulmonary
vasoconstriction. In order to minimise the
detrimental effects that shunt has on oxygenation, the blood
vessels in the lung are adapted to vasoconstrict in response to
(18:50):
low oxygen levels and therefore reduce blood flow to areas that
are under ventilated. This is termed hypoxic pulmonary
vasoconstriction and reduces theeffects of shunt oxygen carriage
(19:20):
by the blood. Oxygen is carried in the blood
in two forms. Most is carried combined with
haemoglobin and a small amount is dissolved in the plasma.
(19:43):
Each gramme of haemoglobin can carry 1.34 mils of oxygen when
fully saturated. Therefore, every litre of blood
with a haemoglobin concentrationof 15 grammes per deal can carry
about 200 mils of oxygen when fully saturated with oxygen that
(20:09):
is exposed to a pressure of oxygen greater than 13
kilopascals. At this pressure of oxygen, only
three mils of oxygen will dissolve in each litre.
Of plasma. Next we go to Figure 4,
(20:31):
explaining the diffusion from the alveolus to the capillary
and other things. Kindly pause this recording to
go through Figure 4. If the PAO 2 is increased
(20:55):
significantly by breathing 100% of oxygen, then a small amount
of extra oxygen will dissolve inthe plasma at a rate of 0.025
mills of oxygen over 100 mills of blood per kilopascal PO2.
(21:22):
But there will normally be no significant increase in the
amount carried by haemoglobin asit is already greater than 95%
saturated with oxygen. Oxygen delivery When considering
(21:48):
the adequacy of oxygen delivery to the tissues, 3 factors need
to be taken into account, haemoglobin concentration,
cardiac output and oxygenation. Next we get to Figure 5,
(22:08):
explaining the oxygen haemoglobin dissociation curve.
Take a while to go through this.The quantity of oxygen made
available to the body in one minute is known as the oxygen
(22:31):
delivery. Oxygen delivery in miles of
oxygen per minute is equals to cardiac output in litres per
minute multiplied by haemoglobinconcentrations in gramme per
litre multiplied by 1.34 in mills of oxygen per gramme,
(23:03):
mills of oxygen gramme per HB multiplied by percentage
saturation which is finally equal to 1000 mills of oxygen
per minute oxygen consumption. Approximately 250 mills of
(23:34):
oxygen are used every minute by a conscious resting person, that
is resting oxygen consumption and therefore about 25% of the
arterial oxygen content is used every minute.
(23:59):
The haemoglobin is mixed. The haemoglobin in mixed venous
blood is about 73% saturated, that is 98% -, 25% At rest.
Oxygen delivery to the cells of the body exceeds oxygen
(24:24):
consumption. During exercise, oxygen
consumption increases. The increased oxygen requirement
is usually provided by an increased cardiac output as
shown in the formula above. A low cardiac output, low
(24:52):
haemoglobin concentration, that is, anaemia, or low oxygen
saturation will result in reduced tissue oxygen delivery
unless there is a compensatory change in one of the other
factors. If oxygen delivery falls
(25:14):
relatively relative to oxygen consumption, the tissues extract
more oxygen from the haemoglobinand the saturation of mixed
venous blood falls below 70%. Below a setting point, decreased
(25:35):
oxygen delivery cannot be compensated for by an increased
oxygen extraction and this results in anaerobic metabolism
and lactic acidosis. This situation is known as
supply dependent oxygenation. Oxygen stores In spite of our
(26:08):
reliance on oxygen, the sources of oxygen in the body are small
and would be unable to sustain life for more than a few minutes
if breathing ceases. Oxygen stores are limited to the
oxygen in the lung and oxygen inthe blood.
(26:33):
The amount of oxygen in the blood depends on the blood
volume and haemoglobin concentration as described
above. The amount of oxygen in the lung
is dependent on the lung volume at functional residual capacity,
(26:55):
FRC, and the alveolar concentration of oxygen.
The FRC is the volume of air that is about 3 litres in an
adult that is present in the lungs at the end of a normal
expiration. At this volume, the elastic
(27:19):
recoil of the lung, that is its tendency to collapse, is
balanced by the tendency of the chest wall and diaphragm to
resist lung collapse when breathing air.
The total oxygen stalls, that isin the blood and lung are small.
(27:45):
The major component of this stall is the oxygen bound to
haemoglobin. Only a small part of these
stalls can be released without an unacceptable reduction in PA
O2. That is, when haemoglobin is 50%
(28:08):
saturated, the PAO 2 will have fallen to 3.5 kilopascals.
Breathing 100% oxygen causes a large increase in the total
oxygen stalls as the functional reserve capacity fills with
(28:28):
oxygen. The major component of the store
is now in the lung and 80% of this oxygen can be used without
any reduction in haemoglobin saturation.
That is, PO2 is still about 14 kilopascals.
(28:54):
This is the reason why pre oxygenation is so effective.
Next, we get to Figure 6, showing a graph showing the
balance between oxygen delivery and oxygen consumption.
(29:17):
Kindly pause this recording to go through Figure 6.
From there we get to Table 1, the principal stores of oxygen
in the body. The titles are Breathing air or
(29:41):
breathing 100% oxygen. Oxygen stored in the lungs at
FRC. Breathing air is 450 mils.
Breathing 100% oxygen is 3000 mils.
(30:08):
Oxygen stall bound to haemoglobin.
Breathing air is 850 mils. Breathing 100% oxygen is 950
mils oxygen dissolved or bound in tissues.
(30:34):
Breathing air is 250 mils and breathing 100% oxygen IS300
mils. So the total oxygen store in the
body while breathing air is 1550mils and while breeding 100%
(30:59):
oxygen is 4250 mills. Oxygen transport.
The effects of anaesthesia. Hyper ventilation may occur
(31:23):
during anaesthesia due to airwayobstruction.
The effects of volatile anaesthetic agents, opioids and
other sedatives. Ketamine and ether.
Ether at less than one MEC causeless respiratory depression than
(31:51):
other anaesthetic agents. The PAO 2 is a balance between
the oxygen supplied by breathingand that's used by metabolic
processes in the body. Hypoventilation and a decreased
(32:15):
inspired oxygen concentration will therefore cause a reduction
in PAO 2. The increased utilisation of
oxygen when metabolic rate is raised, for example during
postoperative shivering or pyrexia, also causes a reduction
(32:39):
in PAO 2 if the PAO 2 falls to less than 8 kilopascals.
The aortic and carotid body chemoreceptors respond by
causing hyperventilation and increasing cardiac output
(33:03):
through sympathetic nervous system stimulation.
This normal protective response to hypoxia is reduced by
anaesthetic drugs. This effect extends into the
post operative period. Following induction of
(33:30):
anaesthesia. There is a rapid reduction in
functional reserve capacity, largely attributable to loss of
tone in the respiratory muscles and chest wall.
Functional reserve capacity drops below the closing volume
(33:53):
in the lung, the expiratory volume at which airway closure
first occurs. This primarily occurs in small
Airways in dependent parts of the lung.
These areas may remain closed throughout the respiratory cycle
(34:15):
to result in a shunt as described above.
VQ mismatch due to airway closure, that is, shunt will
increase the alveolar arterial difference.
(34:36):
This venous admixture increases from 1% to around 10% following
induction of anaesthesia. Next we go to Figure 7,
(34:57):
explaining the effects on PA O2 of increasing the FIO 2 from 21%
to 30%. That's thin curve to heavy curve
at a constant oxygen concentration of 200 mils per
minute. Kindly pause this recording to
(35:21):
go through Figure 7. With the possible exception of
patients spontaneously breathingwhile anaesthetized with
ketamine, this increase in venous admixture occurs
irrespective of the anaesthetic agent used and whether muscle
(35:45):
relaxants are used or not. It should be viewed as an
unavoidable adverse effect of anaesthesia and explains the
universal requirement for supplementary oxygen during
surgery to achieve normal oxygenation.
(36:08):
Furthermore, volatile anaesthetic agents suppress
hypoxic pulmonary vessel constriction and blood flow to
under ventilated or collapsed alveoli is not reduced
(36:28):
appropriately. In addition, many anaesthetic
agents depress cardiac output and therefore decrease oxygen
delivery. Reduced tissue oxygen delivery
during anaesthesia is partially compensated for by the fact that
(36:54):
anaesthesia causes a 15% reduction in metabolic rates and
therefore a reduction in oxygen requirements.
Artificial ventilation causes a further 6% reduction in oxygen
requirements as the work of breathing is removed.
(37:21):
Anaesthetic agents do not affectthe carriage of oxygen by
haemoglobin. Partial use.
Sorry. Practical use of oxygen inspired
(37:43):
oxygen concentration. The efficiency of oxygenation
during anaesthesia is reduced due to hypoventilation and
venous admixture. Inspired oxygen in the range of
25% to 30% is usually effective in restoring the PAO 2 to normal
(38:11):
when hypoxemia is due to hyperventilation.
When hypoxemia is due to venous admixture, it is possible to
restore the PAO 2 by increasing the inspired oxygen
concentration if the venous admixture does not exceed the
(38:36):
equivalent of a 30% shunt. The inspired oxygen
concentration during maintenanceof anaesthesia should routinely
be increased to 30% whenever possible to compensate for hyper
ventilation and shunt, which normally accompany anaesthesia.
(39:04):
Additional oxygen may need to beadministered to patients at risk
of decreased oxygen delivery, that is, anaemia or decreased
cardiac output, or increased oxygen consumption, that is
fever. Next we get to Figure 8 talking
(39:30):
about the effects on POPA O2 on the which is on the vertical
vertical axis of an increasing FIO 2 which is on the horizontal
axis in the presence of different sized shunts.
Kindly pause this recording to go through Figure 8 pre
(39:57):
oxygenation. The small volume of the oxygen
stores of a patient breathing air means that there will be a
rapid fall in oxygen saturation during apnea, for example
following induction of anaesthesia, during laryngos
(40:19):
spasm or during upper airway obstruction.
Pre oxygenation involves breathing 100% oxygen for three
minutes through an anaesthetic circuit with a face mask firmly
(40:39):
applied to the face. This is the time taken to
replace the nitrogen in the FF in the FRC with oxygen using
normal tidal ventilation, also known as denitrogenation.
(41:02):
Although the functional reserve capacity falls on induction of
anaesthesia, the extra oxygen contained within the FRC
provides an essential store of oxygen for periods of apnea,
particularly during rapid sequence induction or difficult
(41:25):
intubation. Patients with a small functional
reserve capacity, that is infants, pregnancy, the obese or
a low haemoglobin concentration and therefore smaller oxygen
stores desaturate more rapidly and pre oxygenation is
(41:50):
especially indicated in these patients.
Crisis management. When managing emergencies during
anaesthesia, consideration should always be given to the
immediate administration of 100%oxygen while the case is found
(42:15):
and rectified. It is the most appropriate
treatments for acute deterioration in
cardiorespiratory function. Anoxic gas mixtures If during
(42:37):
the course of an anaesthetic, 100% nitrous oxide is given to
the patient in error, the fall in PAO 2 will be much more rapid
than during apnea. The PAO 2 can fall, so can fall
to dangerously low levels in as little as 10 seconds.
(43:05):
This is because the oxygen in the patient's lungs and blood,
that is oxygen stalls, is being actively washed out with each
breath that contains no oxygen. The fall in PO2 is therefore
more rapid than would occur if it was only being used up by the
(43:29):
metabolic needs of the body, that is 250 miles per minute.
Modern anaesthesia machines include a hypoxic link to
prevent 100% nitrous oxide beingadministered in error diffusion
(43:54):
hypoxia. Nitrous oxide is 40 times more
soluble in blood than nitrogen. When nitrous oxide is
discontinued at the end of anaesthesia, nitrous oxide
diffuses out of the blood into the alveoli in large volumes
(44:18):
during the next two to three minutes.
If the patient is allowed to breathe air at this time, the
combination of nitrous oxide andnitrogen in the alveoli reduces
the PA O2. This is called diffusion hypoxia
(44:40):
and it's avoided by increasing the alveolar concentration of
oxygen by the administration of 100% oxygen for two to three
minutes after discontinuing nitrous oxide post operative
(45:02):
oxygen. The causes of increased venous
admixture, that is VQ mismatch, shunt and airway closure, and
the abnormal response to hypoxiacontinue into the post op period
(45:23):
for up to three days following major surgery.
Post operative hyperventilation is common and may be due to the
residual effect of anaesthesia, the use of opioid analgesia,
pain or airway obstruction. Shivering in the immediate post
(45:52):
operative period causes an increase in oxygen consumption.
Additional oxygen should therefore be given to all
unconscious patients in recoveryand to those awake patients who
either shiver, hyperventilate, are desaturated or who are
(46:17):
considered to be at increased risk, for example, ischemic
heart disease on the ward duringthe post operative period.
Episodes of airway obstruction during sleep are common and may
aggravate borderline oxygenationdue to the above factors.
(46:44):
This is usually due to the use of opioid analgesia and a change
in sleep pattern that occurs on the second and third post
operative nights after major surgery.
The risk of hypoxemia extends well into the post operative
(47:07):
period. Small degrees of cyanosis are
not easy to detect clinically, especially in anaemic patients,
and therefore oxygen should be given to those.
These patients wherever possible, especially overnight
(47:32):
post operative pain should be treat to be effectively treated,
particularly following abdominalor thoracic surgery.
If opioid analgesics are indicated, hyperventilation
should be anticipated and oxygensaturation monitored as a
(47:58):
routine problems associated withoxygen administration.
It is it has been suggested thathigh concentrations of oxygen
that is 90 to 100% administered to patients for a prolonged
(48:24):
period of several days may causepulmonary damage.
Whilst this is a concern, it should never prevent the use of
oxygen to treat severe hypoxia. High concentrations of oxygen
(48:45):
encourage collapse of alveoli with low ventilation stroke
perfusion ratios. Oxygen is rapidly and completely
absorbed from this alveoli and when it is the only gas being
(49:06):
given, these under ventilated alveoli collapse, that is
absorption atelectasis. When air and oxygen is used, the
nitrogen present is absorbed more slowly and prevents the
(49:31):
alveolus from collapsing. It is therefore sensible to
administer the lowest FIO tool that achieves adequate
oxygenation as guided by pulse oximetry.
(49:52):
Oxygen therapy may rarely depress ventilation in patients
suffering from severe chronic obstructive Airways disease.
Patients who chronically retain carbon dioxide lose the
hypercarponic stimulus to maintain ventilation and are
(50:17):
therefore reliant on their hypoxic drive to self ventilate.
Administration of oxygen may remove this drive and result in
respiratory arrest. In practise this situation is
rare, but again it is sensitive.It is sensible to gradually try
(50:43):
treat the FIO 2 to achieve a realistic oxygenation goal.
It is often appropriate to tolerate moderate hypoxia in
these patients. That is a maximum SA O2 of 90 to
(51:03):
94%.
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