Elina_Physiology_Transport Of 02 And Co2 And The Regulation Of Ventilation

Front 1

Oxygen content = the concentration of oxygen in the blood, e.g., arterial blood

Back 1

20 volumes
% =20 volumes of o}.'"Ygen per 100 volumes of blood =20 mL of oxygen per 100 mL of blood
= 0.2 mL of oxygen per mL of blood.

Front 2

какое количество О2 находитсся в растворимом виде?

Back 2

Oxygen is not a very soluble gas in plasma; very little is present in this form. Thus, only a very
small amount of oxygen is delivered to the capillaries as dissolved oxygen

Front 3

Какое отношение мужду растворенным О2 и РО2?

Back 3

direct linear relationship between P02 and dissolved oxygen

When the P02 is 100 mm Hg, 0.3 mL 02 is dissolved in each 100 rnl. of blood (0.3 vol%).

Front 4

P02 is a force created by

Back 4

P02 is a force created by dissolved oxygen, which acts to keep Q2 on hemoglobin (Hb).

Front 5

Whether oxygen is attached to a site on Hb depends on

Back 5

the affinity of that site for oxygen and
the P02,


The greater the affinity of a site for oxygen, the lower the required POl to keep the
oxygen attached.

Front 6

Site4- 02

Back 6

02
attached when the minimal
P02 == 100mm Hg

systemic arterial blood =97% saturated

Front 7

Site 3 -02

Back 7

02
attached when the minimal
P02 =40 mrn Hg

systemic venous blood ;;;= 75% saturated
(resting state)

Front 8

Site 2- О2

Back 8

attached when the minimal
POz == 26 mm Hg

P50 for arterial blood. P50 is the POz
required for 50% saturation

Front 9

Site 1 - О2

Back 9

Site 1 - 02 usually remains attached under physiologic conditions. Under physiologic conditions,
only sites 2, 3, and 4 need to be considered.

Front 10

The number of mL of oxygen carried in each 100 mL of blood in combination with Hb
depends on

Back 10

The number of mL of oxygen carried in each 100 mL of blood in combination with Hb
depends on the Hb concentration [HbJ

Front 11

Each gram of Hb can combine with....О2?

Back 11

Each gram of Hb can combine with 1.34 mL of 02

1.34([HbJ) ;;;= 1.34(15) = 20 mL 0z1100 mL blood;;;= 20 vol%.

Front 12

if dissolved oxygen decreases, что происходит с О2 в Гемоглобине?

Back 12

if dissolved oxygen decreases, POz also decreases, and there is less force to keep
oxygen attached to Hb. Oxygen comes off Hb and dissolves in the plasma to maintain the flow
of oxygen to the tissues.

Front 13

Что произоходит при гигервентиляции с РО2?

Back 13

'Нyperventilation or supplementing the inspired air with additional oxygen in a normal indizidual
can significantly increase the Pa02 but with little effect on total oxygen content

Front 14

Oxygen-Hb Dissociation Curves
The following will shift the curve to the right:

Back 14

-increased CO2 (Bohr effect), -increased hydrogen
-ion (decrease pH),
-increased temperature,
- increased 2,3-diphosphoglycerate (2,3-DPG).

Front 15

Oxygen-Hb Dissociation Curves
will shift the curve to the left.

Back 15

снижение Temperature,
PC02 , 2,3-DPG, H+
Fetal hemoglobin

Front 16

Hb Concentration Effects
Anemia

Back 16

Anemia
Characterized by a reduced concentration of Hb in the blood.

Front 17

Hb Concentration Effects Polycythemia

Back 17

Polycythemia
Characterized by a higher than normal concentration of Hb in the blood.

Front 18

P50
In simple anemia and polycythemia, the P50 будет ли меняться?

Back 18

Pso
In simple anemia and polycythemia, the P50 does not change without tissue hypoxia; e.g., a paz
of 26 mm Hg will produce 50% saturation of arterial hemoglobin.

Front 19

Effects of Carbon Monoxide

Back 19

:arbon monoxide (CO) has a greater affinity for Hb than does oxygen (240 times greater). The
oartial pressure of CO in the blood is close to zero and all the CO molecules are attached to

Front 20

The
oartial pressure of CO in the blood is

Back 20

The
oartial pressure of CO in the blood is close to zero

Front 21

CO the 0rHb dissociation curve is shifted to the

Back 21

CO the 0rHb dissociation curve is shifted to the left and
carrying capacity is reduced.

Front 22

In anemia, hemoglobin is
arterial oxygen content is

Back 22

In anemia, hemoglobin is saturated but arterial oxygen content is depressed because of the
reduced concentration of hemoglobin

Front 23

In polycythemia, arterial oxygen content is

Back 23

In polycythemia, arterial oxygen content is above normal because of an increased hemoglobin
concentration

Front 24

In CO poisoning, arterial POz is oxygen saturation of hemoglobin is

Back 24

In CO poisoning, arterial POz is normal, but oxygen saturation of hemoglobin is depressed.

Front 25

Dissolved Carbon Dioxide

Back 25

Carbon dioxide is .24 times more soluble in blood than oxygen is. Even though the blood has a
PC02 of only between 40 and 47 mm Hg, about 5% of the total CO2 is carried in the dissolved
form.

Front 26

Carbamino Compounds

Back 26

Carbon dioxide reacts with terminal amine groups of proteins to form carbamino compounds.
The protein involved appears to be almost exclusively hemoglobin. About 5% of the total CO2
is carried as carbamino compounds. The attachment sites that bind CO2 arc different from the
sites that bind 02'

Front 27

Bicarbonate

Back 27

Bicarbonate
About 90% of the CO2 is carried as plasma bicarbonate.
Plasma contains no carbonic anhydrase; therefore, there can be no significant conversion of
COl to HC03- in this compartment.
Because deoxygenated Hb is a better buffer, removing oxygen from hemoglobin facilitates the
formation of bicarbonate in the red blood cells (Haldane effect).
To maintain electrical neutrality asHC03- moves into the plasma, Clmoves into the red blood
cell (chloride shift).
In summary, the bicarbonate is formed in the red blood cell but it is carried in the plasma
compartment.

Front 28

The relationship
between the РСО2 and the total CO2 content is

Back 28

The relationship
between the РСО2 and the total CO2 content is direct and nearly linear

Front 29

THE REGULATION OF ALVEOLAR VENTILATION

Back 29

The level of alveolar ventilation is driven mainly from the input of specific chernoreceptors to
the central nervous system. The stronger the stimulation of these receptors, the greater the level
of alveolar ventilation

Front 30

chernoreceptors receptors that respond to

Back 30

there are receptors that respond to pH, PCOl , and P02.

Front 31

wo groups of
receptors, and they are classified based upon their location.

Back 31

-Central Chemoreceptors
-Peripheral Chemoreceptors

Front 32

Central Chemoreceptors

Back 32

These receptors are located in the central nervous system-more specifically, close to the surface
of the medulla.
The receptors directly monitor and are stimulated by cerebrospinal fluid [H+l and CO2, The
hydration of CO2 and subsequent dissociation of H2C0 3 in the CSF generates H+. CSF H+ is
the stimulus to the central chemoreceptor.
Because the blood-brain barrier is freely permeable to CO2, the activity of these receptors
changes with increased or decreased systemic arterial PC02•
These receptors are very sensitive and represent the main drive for ventilation under normal
resting conditions at sea level.
Therefore, the main drive for ventilation is CO2 (H 1-) on the central chemoreceptors.

Front 33

Peripheral Chemoreceptors

Back 33

These receptors are found within small bodies at two locations:
Carotid bodies: near carotid sinus, afferents to eNS in glossopharyngeal nerve IX
Aortic bodies: near aortic arch, afferents to eNS in vagus nerve X
The carotid body is the most important peripheral chemoreceptor in humans. Because it
receives the most blood per gram of tissue in the body and is so small, it can meet all of its
metabolic requirements for 02 by utilizing the O2 that is dissolved in the blood. The peripheral
chemoreceptors are bathed in arterial blood, which they monitor directly

Front 34

These bodies have
two different receptors:

Back 34

1. H+le02 receptors
2 P02 receptors

Front 35

H+le02 receptors Peripheral Chemoreceptors

Back 35

These receptors are less sensitive than the central chemoreceptors, but they still contribute
to the normal drive for ventilation.
Therefore, under normal resting conditions at sea level, for all practical purposes, the
total drive for ventilation is CO2, mainly via the central chernoreceptors but with a small
contribution via the peripheral chernoreceptors

Front 36

P02 receptors Peripheral Chemoreceptors

Back 36

P02 receptors
The factor monitored by these receptors is P02 not oxygen content. Because they respond to
P02, they are actually monitoring dissolved oxygen and not oxygen on Hb. When systemic
arterial P02 is dose to normal (=100 mm Hg) or above normal, there is little if any stimulation
of these receptors. Thus, they do not contribute to our normal drive for ventilation.
They are strongly stimulated only by a dramatic decrease in systemic arterial P02• Under
these conditions, there is an increased drive for ventilation, and alveolar ventilation usually
increases. In most situations where the systemic arterial P02 is dramatically reduced,
the main drive for ventilation is the low P02 stimulation of the peripheral chemoreceptors.
Sensitivity to hypoxia increases with CO2 retention.
These receptors do not adapt.

Front 37

Abnormal Situation
Chronic hypoventilations

Back 37

Chronic hypoventilation
Though the PaC02 is increased, only the peripheral chemoreceptors are driving respiration.
Giving supplemental oxygen to these individuals and raising the arterial P02 dramatically can
raise arterial cal'

Front 38

Abnormal Situations
Anemia

Back 38

Anemia
Total O2 content is decreased, but the Pa02 is normal. Therefore, there is no ventilatory
response to this kind of hypoxia. Th is also applies to CO poisoning, and in addition, because of
the leftward shift in the oxy-Hb dissociation curve, it is life-threatening.

Front 39

The Central Respiratory Centers
Medullary centers

Back 39

Medullary centers
Site of the inherent rhythm for respiration.
Inspiratory center
Expiratory center

Front 40

For spontaneous breathing, an intact medulla must be connected to the

Back 40

For spontaneous breathing, an intact medulla must be connected to the diaphragm (via the
phrenic nerve). Thus a complete Cl or C2lesian will prevent diaphragmatic breathing but not
a complete C6 or lower lesion.

Front 41

Abnormal Breathing Patterns

Back 41

-Apneustic breathing:
-Biot's breathing:
-Cheyne-Stokes breathing:

Front 42

-Apneustic breathing:

Back 42

Apneustic breathing: prolonged inspirations alternating with a short period of expiration. This
pattern is attributed to the loss of the normal balance between vagal input and the pons-medullary
interactions. Lesions in patients with apneustic breathing are usually found in the caudal pons.

Front 43

Biot's breathing:

Back 43

Biot's breathing: irregular periods of apnea alternating with periods in which several breaths
of identical depth are taken. It is seen in patients with increased intracranial pressure and with
certain midbrain lesions.

Front 44

Cheyne-Stokes breathing:

Back 44

Cheyne-Stokes breathing: periodic type of breathing which has cycles of gradually increasing
depth and frequency followed by a gradual decrease in depth and frequency between periods of
apnea. It may result from midbrain lesions but also occurs in infants or during sleep, particularly
at high altitude

Front 45

UNUSUAL ENVIRONMENTS
High Altitude

Back 45

High Altitude
At high altitude, atmospheric pressure is reduced from 760 mm Hg of sea level. Because atmospheric

At high altitude, hypoxia can develop, resulting in increased circulating levels of erythropoietin.
Erythropoietin will increase red blood cell production and eventually cause an adaptive
polycythemia.
pressure is a factor that determines room air and alveolar P02, these two values are also
reduced. These two values are permanently depressed unless enriched oxygen is inspired.
Therefore, PA02 <100 mm Hg, Pa02 <100 mrn Hg, and the low arterial P02 will stimulate the
peripheral chernorcceptors and increase alveolar ventilation. At high altitude, then, the main
drive for ventilation changes from CO2 on the central chemoreceptors at sea level to a low P02
drive of the peripheral chemoreceptors, and hyperventilation ensues.

Front 46

UNUSUAL ENVIRONMENTS
High-Pressure Environment

Back 46

High-Pressure Environment
In a hyperbaric environmen t breathi ng room air (21% 02 and 79% N), the partial pressure
There are two prerequisites for the bends/caisson disease:
Breathing high-pressure nitrogen for a prolonged period of time
• Sudden decompression
The sudden decompression causes bubbles of nitrogen (emboli) in the bloodstream and tissues.
Treatment is recompression and a slow,gradual decompression
of 02 and N2 will increase in the alveoli and systemic arterial blood. The pressure of nitrogen
will also increase in other body compartments. The adverse effect of a high pal can be oxygen
toxicity. The high PN2 can cause nitrogen narcosis, but, more important, it can lead to the bends
(caisson disease).