May 20, 2025 • 33 mins
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This is an independent educational project not affiliated with the World Federation of Societies of Anaesthesiologists (WFSA). Content is drawn from publicly available issues of Update in Anaesthesia.
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This episode features a full reading of “Carbon Dioxide Transport” from Update in Anaesthesia, Volume 24, Number 2.
Read along with the original article or simply listen in for a clear, guided walkthrough.
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(00:01):
Update in anaesthesia, volume 24#2.
Carbon dioxide transport by GJ authors and M Sudhakar.
(00:22):
Summary Carbon dioxide is transported in the blood in
three ways, 1 dissolved in solution, 2 buffered with water
as carbonic acid and three boundto proteins, particularly
(00:50):
haemoglobin, at a haemoglobin concentration of 15 grammes per
DL and a mixed venous PCO 2 of 6.1 kilopascals.
Venous blood contains 52 meals per DL of carbon dioxide.
(01:17):
Arterial blood with APCO 2 of 5.3 kilopascals contains 48 mils
per DL. The effects of carbon dioxide
production in the tissues include increased plasma
(01:39):
chloride, increased red blood cell mean corpuscular volume and
haemoglobin becoming less acidotic than oxygenated
haemoglobin. Introduction Carbon dioxide is
(02:04):
produced by cell metabolism in the mitochondria.
The amount produced depends on the rate of metabolism and the
relative amounts of carbohydrates, Fat and protein
(02:25):
metabolised. The amount is about 200 meals
per minute when at rest and eating a mixed diet.
This utilises 80% of the oxygen consumed giving a respiratory
(02:46):
quotient of 0.8. That is, respiratory quotient is
equals to the rate of carbon dioxide production divided by
the rate of oxygen consumption. A carbon a carbohydrate diet
(03:08):
gives a quotient of one and a fat diet. 0.7 Carbon dioxide
transport in the blood Carbon dioxide is transported in the
(03:28):
blood from the tissues to the lungs in three ways.
One dissolved in solution, two buffered with water as carbonic
acid, three bound to proteins, particularly haemoglobin.
(04:01):
Approximately 75% of carbon dioxide is transported in the
red blood cell and 25% in the plasma.
The relatively small amount in plasma is attributable to a lack
of carbonic anhydrides in plasma, so associated with water
(04:27):
is slow. Plasma plays little role in
buffering the and combination with plasma proteins is poor.
There is a difference between the percentage of the total
carbon dioxide carried in each form and the percentage exhaled
(04:51):
from them. For example, 5% of the total is
in solution, but 10% of exhaled carbon dioxide comes from this
source. 10% is protein bound, particularly with haemoglobin,
(05:15):
but this supplies 30% of the exhaled amount, dissolved carbon
dioxide. Carbon dioxide is 20 times more
(05:35):
soluble than oxygen. It obeys Harry's law, which
states that the number of molecules in solution is
proportional to the partial pressure of the gas at the
liquid surface. The carbon dioxide solubility
(05:58):
coefficient is 0.0308 millimolesper litre per millimetre per
millimetres of hydro mercury, or0.231 millimoles per litre per
(06:22):
kilopascal. At 37°C.
Solubility increases as the temperature falls.
This corresponds to 0.5 mills per kilopascal carbon dioxide in
(06:48):
100 mills blood at 37°C. The partial pressure of carbon
dioxide is 5.3 kilo. I mean PKA in arterial blood and
6.1 K kilopascals, sorry 6.1 kpain mixed venous blood.
(07:23):
Therefore, arterial blood will remain will contain about 2.5
mils per 100 mils of dissolved carbon dioxide and venous blood
3 mils per 100 mills. A cardiac output of five litres
(07:45):
per minute will carry 150 mills of dissolved carbon dioxide to
the lung, of which 25 mills willbe exhaled.
Because of this high solubility and diffusion capacity, the
(08:08):
partial pressure of carbon dioxide in alveolar and
pulmonary end capillary blood are virtually the same.
Even a large shunt of 50% will only cause a an end pulmonary
capillary stroke. Arterial carbon dioxide gradient
(08:31):
of about 0.4 kilopascals. Carbonic acid.
Carbon dioxide combines with water to form carbonic acid, a
reaction accelerated by carbonicanhydrase.
(08:58):
The carbonic acid then freely dissociates, as seen in equation
1. Carbon dioxide plus water
catalysed by carbonic anhydridesgives birth to carbonic acid.
(09:18):
Then carbonic acid breaks down to hydrogen and bicarbonate.
The enzyme carbonic anhydrase ispresent in a number of organs of
(09:40):
the body, including the eye, kidney and brain.
However, for this purpose, it isthe red blood cell carbonic
anhydrase that is important. Once carbonic acid is formed, it
(10:01):
dissociates easily so that the ratio of carbonic acid to
bicarbonate is 1 to 20. As seen in equation 2, carbon
dioxide and water diffuse freelyinto the red blood cell and are
(10:27):
converted to carbonic acid, which dissociates into hydrogen
and bicarbonate ions. Hydrogen ions do not pass
through cell membranes but carbonic, but carbon dioxide
passes readily. This situation cannot be
(10:49):
sustained as the intracellular hydrogen ion and bicarbonate ion
concentration, osmolarity, and cell size will rise and rupture
the cell. The bicarbonate ion diffuses out
to the plasma to be exchanged for chloride ions.
(11:15):
This is known as the chloride shift, that is the Gibbs donor
equilibrium or Hamburger effect.An ion exchange transporter
protein in the cell membrane called band 3 for chloride and
(11:40):
bicarbonate facilitates chlorideshift.
A buildup of hydrogen ion in thered blood cell would also
prevent further conversion and production of bicarbonate ion.
(12:02):
However, hydrogen ions bind easily to reduced haemoglobin,
which is made available when oxygen is released.
Therefore free hydrogen ions areremoved from solution.
(12:24):
Reduced haemoglobin is less acidic than oxygenated
haemoglobin. This is another way of stating
the Haldane effects, which explains that at any given
partial pressure of carbon dioxide, the carbon dioxide
(12:47):
content of deoxygenated blood isgreater than that of oxygenated
blood. As a result of the shift of
chloride ions into the red cell and the buffering of hydrogen
ions into reduced haemoglobin, the intercellular osmolarity
(13:14):
increases slightly and water enters, causing the cell to
swell. This can be measured as an
increase in mean corpuscular volume, MCV.
The reverse process occurs as the red blood cell passes
(13:37):
through the lung, bound to haemoglobin and other proteins.
Carbon dioxide combines rapidly to the terminal uncharged amino
groups, that is RNH 2 to form carbamino compounds as seen in
(14:03):
equation 3. In most proteins, it is only the
terminal amino acid group that combines with carbon dioxide.
Haemoglobin is different when forming carbaminohemoglobin.
(14:25):
Reduced haemoglobin is the only effective protein buffer of
hydrogen ion at physiological pHbecause of its high content of
amino acid histidine. Hydrogen ions attached to the
imidazole group of the histidine.
(14:48):
About 30% of exhaled carbon dioxide was transported combined
with haemoglobin protein. The amount of carbon dioxide
held in blood in the carbamino form is small, but it accounts
(15:09):
1/3 of the difference between venous and arterial carbon
dioxide content. The Haldane effect reflects the
difference in carbon dioxide content between oxygenated and
reduced haemoglobin at the same partial pressure of carbon
(15:31):
dioxide. This effect is partly
attributable to the ability of haemoglobin to buffer hydrogen
ions, and partly due to the factthat reduced haemoglobin is 3.5
times more effective in combining with carbon dioxide
(15:55):
than oxyhemoglobin. Different hemoglobins vary in
their affinity for carbon dioxide, carbon monoxide and
oxygen. Carbon dioxide combines readily
with haemoglobin to form a carbamino bond at a lower
(16:19):
partial pressure than oxygen, but haemoglobin carries less
than 1/4 of the amount of carbondioxide compared with oxygen.
By contrast, foetal haemoglobin combines with oxygen at a lower
(16:43):
partial pressure due to the replacement of the B chain with
G chains. Carbon monoxide has a greater
affinity for haemoglobin and so displaces oxygen.
(17:05):
Carbon dioxide transports in thetissues Carbon dioxide transport
in the tissue is summarised in Figure 1.
Carbon dioxide combines with water to form carbonic acid.
(17:29):
This reaction is very slow in plasma but fast within the red
blood cell owing to the presenceof the enzyme carbonic anhydrous
carbonic acid, that is, H2CO3 dissociates with hydrogen ion
(17:51):
and bicarbonate ions. Therefore, the concentration of
both hydrogen ions and bicarbonate ions is increased in
the red blood cell. Bicarbonate ions can diffuse out
of the red blood cells into plasma, whereas hydrogen cannot.
(18:22):
In order to maintain electrical neutrality.
Chloride ions diffuse into the red blood cell from the plasma
as bicarbonate ions diffuses out.
Hydrogen ions are taken up by reduced haemoglobin.
(18:46):
The imidazole group of the aminoacid histidine gives haemoglobin
a very significant buffering capacity not present in other
amino acids. These buffering capacity is made
possible by the fact that each tetrama of haemoglobin contains
(19:11):
38 histidine residues, and the dissociation constant of the
imidazole groups of the four histidine residues to which the
HEM groups are attached is affected by the state of
oxygenation of the HEM. In the acidic state, the oxygen
(19:37):
bond is weakened, while reduction of haemoglobin causes
the imidazole group to become more basic in the tissues.
The acidic form of the imidazolegroup weakens the strength of
the oxygen bond at the same timeas hydrogen ions are being
(20:03):
buffered by the more basic. Haemoglobin Next we get to
Figure 1, explaining the movement of gases at tissue
level with the chloride shift highlighted carbon dioxide
(20:27):
transport in the lungs. The combination of oxygen with
haemoglobin is facilitated by the histidine group becoming
more basic, which increases the affinity of the haem group for
(20:50):
oxygen as the carbon dioxide is lost.
This is one reason for the bore effect.
Next is an equation explaining the boy effect.
(21:12):
No, sorry, explaining the what we just discussed.
Release of haemoglobin shifts the equilibrium in favour of
carbon dioxide formation and elimination bicarbonates.
Ion concentration decreases as carbon dioxide is formed and
(21:37):
eliminated, as seen in Figure 2.Next we get to Figure 2,
explaining the movement of gasesat alveolar level.
Kindly pause this recording to go through Figure 2.
(22:01):
Carbon dioxide dissociation curves Carbon dioxide
dissociation curves relate PA CO2 in kilopascal, or
millimetres of mercury to the amount of carbon dioxide in
(22:22):
mills carried in blood, as seen in Figure 3.
The amount of dissolved carbon dioxide and bicarbonate vary
with PCO 2 but a little affectedby the state of haemoglobin.
(22:51):
However, the amount of carbaminohemoglobin is much
affected by the state of oxygenation of haemoglobin, less
so by the partial pressure of carbon dioxide in mixed venous
(23:15):
blood. Venous pressure of carbon
dioxide is 6.1 kilopascals, thatis 46 millimetres of mercury,
and in arterial blood the arterial pressure of oxygen is
5.3 kilopascals, that is 40 millimetres of mercury.
(23:45):
Total carbon dioxide in venous blood is 52 mills per 100 mills
and in arterial blood 48 mills per 100 mills.
Consequently, the curve is more linear than the oxygen
(24:06):
haemoglobin dissociation curve. Next we get to Figure 3, talking
about the total carbon dioxide transports in whole blood, and
Figure 4, talking about the partial pressure of oxygen and
(24:29):
carbon dioxide. Kindly pause this recording to
go through these figures. Figure 4 illustrates the
difference between the content in blood of oxygen and carbon
dioxide with change in partial pressure.
(24:55):
It emphasises that the carbon dioxide content rises throughout
the increase in partial pressure.
Oxygen content rises more steeply until a point at which
the haemoglobin is fully saturated.
(25:15):
After that, the increase is small because of the small
increased amount in solution. Differences between venous and
arterial blood. The differences between arterial
(25:38):
and venous blood are summarised in Figure 5.
The high content of carbon dioxide in venous capillary
blood reduces the affinity of haemoglobin for oxygen, leading
(25:59):
to release of oxygen to the tissues.
The oxygen dissociation curve shifts to the right, that is
bore effect deoxygenated haemoglobin.
(26:22):
It takes up more carbon dioxide than oxygenated haemoglobin.
That is Haldane effect removal of oxygen from haemoglobin in
the tissue. Capillaries cause the
haemoglobin molecule to behave more like a base, that is a
(26:46):
better proton acceptor. Therefore, haemoglobin increases
the amount of carbon dioxide that is carried in venous blood.
Equation 4. Each carbon dioxide molecule
(27:11):
added to the red blood cell increases the intracellular
osmotic pressure by an increase in either bicarbonate or
chloride ions. Therefore, the red blood cell
increases in size and the hematocrit of very of venous
(27:34):
blood is some 3% more than arterial blood.
The plasma concentration of chloride ions is lower, but
bicarbonate ion concentration isgreater. pH of red blood cells.
(28:02):
The total reduction of all haemoglobin would result in a
rise in blood pH by 0.03. At 25% oxygen saturation the pH
increases by 0.007, that is at constant partial pressure of
(28:28):
carbon dioxide. If the partial pressure of
carbon dioxide rises by 0.8 kilopascals, that is 6
millimetres of mercury, IE the difference between mixed venous
(28:49):
an arterial blood, the pH will reduce by 0.04.
The net effect is a fall in pH of 0.033 from 7.4 to 7.36.
(29:18):
Changes in red blood cells during passage through the
lungs. In pulmonary capillary blood,
the red blood cell releases carbon dioxide and the
haemoglobin affinity for oxygen is increased.
(29:40):
The oxygenated haemoglobin bindsfewer hydrogen ions, making it
more acidic, but the fall in partial pressure of carbon
dioxide and the shift in chloride and bicarbonate ions
make the red blood cell less acidic.
(30:05):
The outward shift of water givesa smaller MCV and reduced
hematocrit. The oxygen dissociation curve
will shift to the left, that is bore effect.
(30:28):
The plasma concentration of chloride ion is higher in
arterial compared with venous blood.
Bicarbonate concentration is lower the role of carbon dioxide
(30:49):
in acid elimination. Every minute, 200 miles of
carbon dioxide is exhaled. This is the equivalent of 12 to
13 moles of hydrogen ions in 24 hours.
(31:12):
Urine pH varies from 4.5 to 8.0.Aph of 4.0 represents 10 raised
to the power of 4 millimoles perlitre of hydrogen ions.
(31:34):
Therefore, the passage of three litres of urine accounts for a
relatively small amount of hydrogen ion elimination in 24
hours. However, this includes the the
phosphate and sulphate ions thatcannot be converted to carbon
(31:58):
dioxide. Next, we move to Figure 5,
explaining the distribution of carbon dioxide in arterial and
venous blood. Kindly pause this recording to
go through Figure 5. Effects of apnea The total body
(32:27):
content of carbon dioxide including bicarbonate ion is 120
litres or 100 times that of oxygen.
If there is apnea and all the carbon dioxide is retained in
the body, the partial pressure of carbon dioxide will rise by
(32:50):
0.4 to 0.8 kilopascals per minute, that is 3 to 6
millimetres of mercury per minute.
Alveolar gas will rapidly equatewith venous blood giving an
(33:14):
alveolar partial pressure of carbon dioxide rise from 5.3 to
6.1 kilopascals and the partial pressure of oxygen fall from 14
to 5.3 kilopascals in one minute.
(33:37):
Therefore the patient becomes rapidly hypoxemic.
If the patient is pre oxygenatedwith oxygen 100%, the arterial
oxygen tension would remain above 13 kilopascals and 100%
(33:59):
saturation is maintained for several minutes AS250 meals per
minute of oxygen is used from a high partial pressure in the
lung. However, the arterial carbon
(34:20):
dioxide pressure will steadily rise after 5 minutes will
steadily rise after 5 minutes. It will be approaching 10
kilopascals with an associated fall in pH.
Update in anaesthesia, volume 24#2.
Carbon dioxide transport by GJ authors and M Sudhakar.
(00:22):
Summary Carbon dioxide is transported in the blood in
three ways, 1 dissolved in solution, 2 buffered with water
as carbonic acid and three boundto proteins, particularly
(00:50):
haemoglobin, at a haemoglobin concentration of 15 grammes per
DL and a mixed venous PCO 2 of 6.1 kilopascals.
Venous blood contains 52 meals per DL of carbon dioxide.
(01:17):
Arterial blood with APCO 2 of 5.3 kilopascals contains 48 mils
per DL. The effects of carbon dioxide
production in the tissues include increased plasma
(01:39):
chloride, increased red blood cell mean corpuscular volume and
haemoglobin becoming less acidotic than oxygenated
haemoglobin. Introduction Carbon dioxide is
(02:04):
produced by cell metabolism in the mitochondria.
The amount produced depends on the rate of metabolism and the
relative amounts of carbohydrates, Fat and protein
(02:25):
metabolised. The amount is about 200 meals
per minute when at rest and eating a mixed diet.
This utilises 80% of the oxygen consumed giving a respiratory
(02:46):
quotient of 0.8. That is, respiratory quotient is
equals to the rate of carbon dioxide production divided by
the rate of oxygen consumption. A carbon a carbohydrate diet
(03:08):
gives a quotient of one and a fat diet. 0.7 Carbon dioxide
transport in the blood Carbon dioxide is transported in the
(03:28):
blood from the tissues to the lungs in three ways.
One dissolved in solution, two buffered with water as carbonic
acid, three bound to proteins, particularly haemoglobin.
(04:01):
Approximately 75% of carbon dioxide is transported in the
red blood cell and 25% in the plasma.
The relatively small amount in plasma is attributable to a lack
of carbonic anhydrides in plasma, so associated with water
(04:27):
is slow. Plasma plays little role in
buffering the and combination with plasma proteins is poor.
There is a difference between the percentage of the total
carbon dioxide carried in each form and the percentage exhaled
(04:51):
from them. For example, 5% of the total is
in solution, but 10% of exhaled carbon dioxide comes from this
source. 10% is protein bound, particularly with haemoglobin,
(05:15):
but this supplies 30% of the exhaled amount, dissolved carbon
dioxide. Carbon dioxide is 20 times more
(05:35):
soluble than oxygen. It obeys Harry's law, which
states that the number of molecules in solution is
proportional to the partial pressure of the gas at the
liquid surface. The carbon dioxide solubility
(05:58):
coefficient is 0.0308 millimolesper litre per millimetre per
millimetres of hydro mercury, or0.231 millimoles per litre per
(06:22):
kilopascal. At 37°C.
Solubility increases as the temperature falls.
This corresponds to 0.5 mills per kilopascal carbon dioxide in
(06:48):
100 mills blood at 37°C. The partial pressure of carbon
dioxide is 5.3 kilo. I mean PKA in arterial blood and
6.1 K kilopascals, sorry 6.1 kpain mixed venous blood.
(07:23):
Therefore, arterial blood will remain will contain about 2.5
mils per 100 mils of dissolved carbon dioxide and venous blood
3 mils per 100 mills. A cardiac output of five litres
(07:45):
per minute will carry 150 mills of dissolved carbon dioxide to
the lung, of which 25 mills willbe exhaled.
Because of this high solubility and diffusion capacity, the
(08:08):
partial pressure of carbon dioxide in alveolar and
pulmonary end capillary blood are virtually the same.
Even a large shunt of 50% will only cause a an end pulmonary
capillary stroke. Arterial carbon dioxide gradient
(08:31):
of about 0.4 kilopascals. Carbonic acid.
Carbon dioxide combines with water to form carbonic acid, a
reaction accelerated by carbonicanhydrase.
(08:58):
The carbonic acid then freely dissociates, as seen in equation
1. Carbon dioxide plus water
catalysed by carbonic anhydridesgives birth to carbonic acid.
(09:18):
Then carbonic acid breaks down to hydrogen and bicarbonate.
The enzyme carbonic anhydrase ispresent in a number of organs of
(09:40):
the body, including the eye, kidney and brain.
However, for this purpose, it isthe red blood cell carbonic
anhydrase that is important. Once carbonic acid is formed, it
(10:01):
dissociates easily so that the ratio of carbonic acid to
bicarbonate is 1 to 20. As seen in equation 2, carbon
dioxide and water diffuse freelyinto the red blood cell and are
(10:27):
converted to carbonic acid, which dissociates into hydrogen
and bicarbonate ions. Hydrogen ions do not pass
through cell membranes but carbonic, but carbon dioxide
passes readily. This situation cannot be
(10:49):
sustained as the intracellular hydrogen ion and bicarbonate ion
concentration, osmolarity, and cell size will rise and rupture
the cell. The bicarbonate ion diffuses out
to the plasma to be exchanged for chloride ions.
(11:15):
This is known as the chloride shift, that is the Gibbs donor
equilibrium or Hamburger effect.An ion exchange transporter
protein in the cell membrane called band 3 for chloride and
(11:40):
bicarbonate facilitates chlorideshift.
A buildup of hydrogen ion in thered blood cell would also
prevent further conversion and production of bicarbonate ion.
(12:02):
However, hydrogen ions bind easily to reduced haemoglobin,
which is made available when oxygen is released.
Therefore free hydrogen ions areremoved from solution.
(12:24):
Reduced haemoglobin is less acidic than oxygenated
haemoglobin. This is another way of stating
the Haldane effects, which explains that at any given
partial pressure of carbon dioxide, the carbon dioxide
(12:47):
content of deoxygenated blood isgreater than that of oxygenated
blood. As a result of the shift of
chloride ions into the red cell and the buffering of hydrogen
ions into reduced haemoglobin, the intercellular osmolarity
(13:14):
increases slightly and water enters, causing the cell to
swell. This can be measured as an
increase in mean corpuscular volume, MCV.
The reverse process occurs as the red blood cell passes
(13:37):
through the lung, bound to haemoglobin and other proteins.
Carbon dioxide combines rapidly to the terminal uncharged amino
groups, that is RNH 2 to form carbamino compounds as seen in
(14:03):
equation 3. In most proteins, it is only the
terminal amino acid group that combines with carbon dioxide.
Haemoglobin is different when forming carbaminohemoglobin.
(14:25):
Reduced haemoglobin is the only effective protein buffer of
hydrogen ion at physiological pHbecause of its high content of
amino acid histidine. Hydrogen ions attached to the
imidazole group of the histidine.
(14:48):
About 30% of exhaled carbon dioxide was transported combined
with haemoglobin protein. The amount of carbon dioxide
held in blood in the carbamino form is small, but it accounts
(15:09):
1/3 of the difference between venous and arterial carbon
dioxide content. The Haldane effect reflects the
difference in carbon dioxide content between oxygenated and
reduced haemoglobin at the same partial pressure of carbon
(15:31):
dioxide. This effect is partly
attributable to the ability of haemoglobin to buffer hydrogen
ions, and partly due to the factthat reduced haemoglobin is 3.5
times more effective in combining with carbon dioxide
(15:55):
than oxyhemoglobin. Different hemoglobins vary in
their affinity for carbon dioxide, carbon monoxide and
oxygen. Carbon dioxide combines readily
with haemoglobin to form a carbamino bond at a lower
(16:19):
partial pressure than oxygen, but haemoglobin carries less
than 1/4 of the amount of carbondioxide compared with oxygen.
By contrast, foetal haemoglobin combines with oxygen at a lower
(16:43):
partial pressure due to the replacement of the B chain with
G chains. Carbon monoxide has a greater
affinity for haemoglobin and so displaces oxygen.
(17:05):
Carbon dioxide transports in thetissues Carbon dioxide transport
in the tissue is summarised in Figure 1.
Carbon dioxide combines with water to form carbonic acid.
(17:29):
This reaction is very slow in plasma but fast within the red
blood cell owing to the presenceof the enzyme carbonic anhydrous
carbonic acid, that is, H2CO3 dissociates with hydrogen ion
(17:51):
and bicarbonate ions. Therefore, the concentration of
both hydrogen ions and bicarbonate ions is increased in
the red blood cell. Bicarbonate ions can diffuse out
of the red blood cells into plasma, whereas hydrogen cannot.
(18:22):
In order to maintain electrical neutrality.
Chloride ions diffuse into the red blood cell from the plasma
as bicarbonate ions diffuses out.
Hydrogen ions are taken up by reduced haemoglobin.
(18:46):
The imidazole group of the aminoacid histidine gives haemoglobin
a very significant buffering capacity not present in other
amino acids. These buffering capacity is made
possible by the fact that each tetrama of haemoglobin contains
(19:11):
38 histidine residues, and the dissociation constant of the
imidazole groups of the four histidine residues to which the
HEM groups are attached is affected by the state of
oxygenation of the HEM. In the acidic state, the oxygen
(19:37):
bond is weakened, while reduction of haemoglobin causes
the imidazole group to become more basic in the tissues.
The acidic form of the imidazolegroup weakens the strength of
the oxygen bond at the same timeas hydrogen ions are being
(20:03):
buffered by the more basic. Haemoglobin Next we get to
Figure 1, explaining the movement of gases at tissue
level with the chloride shift highlighted carbon dioxide
(20:27):
transport in the lungs. The combination of oxygen with
haemoglobin is facilitated by the histidine group becoming
more basic, which increases the affinity of the haem group for
(20:50):
oxygen as the carbon dioxide is lost.
This is one reason for the bore effect.
Next is an equation explaining the boy effect.
(21:12):
No, sorry, explaining the what we just discussed.
Release of haemoglobin shifts the equilibrium in favour of
carbon dioxide formation and elimination bicarbonates.
Ion concentration decreases as carbon dioxide is formed and
(21:37):
eliminated, as seen in Figure 2.Next we get to Figure 2,
explaining the movement of gasesat alveolar level.
Kindly pause this recording to go through Figure 2.
(22:01):
Carbon dioxide dissociation curves Carbon dioxide
dissociation curves relate PA CO2 in kilopascal, or
millimetres of mercury to the amount of carbon dioxide in
(22:22):
mills carried in blood, as seen in Figure 3.
The amount of dissolved carbon dioxide and bicarbonate vary
with PCO 2 but a little affectedby the state of haemoglobin.
(22:51):
However, the amount of carbaminohemoglobin is much
affected by the state of oxygenation of haemoglobin, less
so by the partial pressure of carbon dioxide in mixed venous
(23:15):
blood. Venous pressure of carbon
dioxide is 6.1 kilopascals, thatis 46 millimetres of mercury,
and in arterial blood the arterial pressure of oxygen is
5.3 kilopascals, that is 40 millimetres of mercury.
(23:45):
Total carbon dioxide in venous blood is 52 mills per 100 mills
and in arterial blood 48 mills per 100 mills.
Consequently, the curve is more linear than the oxygen
(24:06):
haemoglobin dissociation curve. Next we get to Figure 3, talking
about the total carbon dioxide transports in whole blood, and
Figure 4, talking about the partial pressure of oxygen and
(24:29):
carbon dioxide. Kindly pause this recording to
go through these figures. Figure 4 illustrates the
difference between the content in blood of oxygen and carbon
dioxide with change in partial pressure.
(24:55):
It emphasises that the carbon dioxide content rises throughout
the increase in partial pressure.
Oxygen content rises more steeply until a point at which
the haemoglobin is fully saturated.
(25:15):
After that, the increase is small because of the small
increased amount in solution. Differences between venous and
arterial blood. The differences between arterial
(25:38):
and venous blood are summarised in Figure 5.
The high content of carbon dioxide in venous capillary
blood reduces the affinity of haemoglobin for oxygen, leading
(25:59):
to release of oxygen to the tissues.
The oxygen dissociation curve shifts to the right, that is
bore effect deoxygenated haemoglobin.
(26:22):
It takes up more carbon dioxide than oxygenated haemoglobin.
That is Haldane effect removal of oxygen from haemoglobin in
the tissue. Capillaries cause the
haemoglobin molecule to behave more like a base, that is a
(26:46):
better proton acceptor. Therefore, haemoglobin increases
the amount of carbon dioxide that is carried in venous blood.
Equation 4. Each carbon dioxide molecule
(27:11):
added to the red blood cell increases the intracellular
osmotic pressure by an increase in either bicarbonate or
chloride ions. Therefore, the red blood cell
increases in size and the hematocrit of very of venous
(27:34):
blood is some 3% more than arterial blood.
The plasma concentration of chloride ions is lower, but
bicarbonate ion concentration isgreater. pH of red blood cells.
(28:02):
The total reduction of all haemoglobin would result in a
rise in blood pH by 0.03. At 25% oxygen saturation the pH
increases by 0.007, that is at constant partial pressure of
(28:28):
carbon dioxide. If the partial pressure of
carbon dioxide rises by 0.8 kilopascals, that is 6
millimetres of mercury, IE the difference between mixed venous
(28:49):
an arterial blood, the pH will reduce by 0.04.
The net effect is a fall in pH of 0.033 from 7.4 to 7.36.
(29:18):
Changes in red blood cells during passage through the
lungs. In pulmonary capillary blood,
the red blood cell releases carbon dioxide and the
haemoglobin affinity for oxygen is increased.
(29:40):
The oxygenated haemoglobin bindsfewer hydrogen ions, making it
more acidic, but the fall in partial pressure of carbon
dioxide and the shift in chloride and bicarbonate ions
make the red blood cell less acidic.
(30:05):
The outward shift of water givesa smaller MCV and reduced
hematocrit. The oxygen dissociation curve
will shift to the left, that is bore effect.
(30:28):
The plasma concentration of chloride ion is higher in
arterial compared with venous blood.
Bicarbonate concentration is lower the role of carbon dioxide
(30:49):
in acid elimination. Every minute, 200 miles of
carbon dioxide is exhaled. This is the equivalent of 12 to
13 moles of hydrogen ions in 24 hours.
(31:12):
Urine pH varies from 4.5 to 8.0.Aph of 4.0 represents 10 raised
to the power of 4 millimoles perlitre of hydrogen ions.
(31:34):
Therefore, the passage of three litres of urine accounts for a
relatively small amount of hydrogen ion elimination in 24
hours. However, this includes the the
phosphate and sulphate ions thatcannot be converted to carbon
(31:58):
dioxide. Next, we move to Figure 5,
explaining the distribution of carbon dioxide in arterial and
venous blood. Kindly pause this recording to
go through Figure 5. Effects of apnea The total body
(32:27):
content of carbon dioxide including bicarbonate ion is 120
litres or 100 times that of oxygen.
If there is apnea and all the carbon dioxide is retained in
the body, the partial pressure of carbon dioxide will rise by
(32:50):
0.4 to 0.8 kilopascals per minute, that is 3 to 6
millimetres of mercury per minute.
Alveolar gas will rapidly equatewith venous blood giving an
(33:14):
alveolar partial pressure of carbon dioxide rise from 5.3 to
6.1 kilopascals and the partial pressure of oxygen fall from 14
to 5.3 kilopascals in one minute.
(33:37):
Therefore the patient becomes rapidly hypoxemic.
If the patient is pre oxygenatedwith oxygen 100%, the arterial
oxygen tension would remain above 13 kilopascals and 100%
(33:59):
saturation is maintained for several minutes AS250 meals per
minute of oxygen is used from a high partial pressure in the
lung. However, the arterial carbon
(34:20):
dioxide pressure will steadily rise after 5 minutes will
steadily rise after 5 minutes. It will be approaching 10
kilopascals with an associated fall in pH.
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