Module 13 Trans

Module 13 Respiratory System: Pulmonary Gas Exchange & Regulation of Respiration
Ameril, Aritrangco, Barupathi, Dela Fuente, Escalante, Labial, Patacsil, Silagan, Vegiroutho
1. State the source of energy in order for diffusion of C. Total pressure - sum of the partial pressures
molecules to occur. - receives contribution from each gas, all directly proportional to its
Diffusion concentration
A. Definition - random motion of molecules in all directions *if not given, simply add the partial pressures calculated or given
through the respiratory membrane and adjacent fluids.
B. Occurrence in terms of respiratory physiology 4. Define partial pressure of a gas dissolved in water or in body
1. Rate tissues.
2. Source of energy - kinetic motion of molecules The gases dissolved in H2O or in body tissues also exert pressure.
case 1 - absolute 0o temp: no movement Reason: dissolved gas molecules are moving randomly and have
case 2 - free molecules: linear movement at high velocity kinetic energy
and continuous bouncing until they come in contact with ➔ when a gas dissolved in fluid encounters a surface such
other molecules as a cell membrane, it also exerts its own partial pressure
in the same way as a gas in the gas phase
➔ partial pressures of the separate dissolved gases are
designated the same as the partial pressures in the gas
state—i.e PO2, PCO2, PN2, PHe, and so on
5. State and briefly explain the factors that determine partial

pressure of a gas dissolved in a fluid.
5A. Concentration
1) chemistry - tells how much solute is dissolved in a solvent
- standard unit of concentration in chemistry is molarity (M)
- M = (molarity of solute) / liters of solution
2) biochemistry - measure of the amount of a
2. State the effect of concentration gradient on the net sub-component in a solution
diffusion of a gas in one direction. 3) pharmacology - refers to the strength of a pharmaceutical
Figure 40-1 preparation
- shows a gas chamber or solution of a certain gas with 2 5B. Solubility coefficient
ends: 1) high concentration; and 2) low concentration - physical or chemical attraction to H2O molecules (e.g CO2)
- net diffusion: 1) represented by the length difference in 1) if attracted: they can be dissolved without building up
the arrows; 2) occurs from high concentration to low partial pressure within the solution
concentration area 2) if repelled: high partial pressure develops, and fewer
- reason: distant molecules at the end A chamber will dissolved molecules
diffuse toward end B, than the other way around - these relationships are expressed by Henry's Law
- conclusion: rates of diffusion in both directions are
proportionately different 6. Briefly state and explain Henry’s Law.
3. Define partial pressure of a gas. Define the total pressure of

a mixture of gases.
A. *Pressure - caused by the impact of moving molecules against a
surface Solubility coefficient
The gas pressure acting on the surfaces of the respiratory passages A) given the following conditions:
and passages is proportional to the total force of impact striking 1) partial pressure is expressed in atmosphere (atm):
the surface in any given time. 1 atm pressure = 760 mm Hg
Conclusion: Pressure is directly proportional to the concentration of 2) concentration expressed in volume of gas
the gas molecules. dissolved in each volume of water
In respiratory physiology, the significant gas mixtures are: O2, N2, and B) for important respiratory gases at body temperature:
CO2.
B. Partial pressure
- of individual gases in a mixture are denoted by the symbols PO2,
PCO2, PN2, and so on
- rate of diffusion of each of these gases directly proportional to the
pressure caused by this specific gas alone
Application:
Air Composition: Based on the list, CO2 is 20x more soluble than O2.
1) approximate composition of 79% Nitrogen and 21% Oxygen; Explanation: PCO2 for a given concentration is less than 1/20 (5%) of
2) total pressure at sea level averages 760 mm Hg that exerted by O2.
0.79 * 760 mm Hg = 600.4 mm Hg ≈ 600 mm Hg
0.21 * 760 mm Hg = 159.6 mm Hg ≈ 160 mm Hg
7. Briefly explain how the difference in partial pressure of a gas ● Even before the air enters the alveoli, it becomes almost
in the gas phase in alveoli and the dissolved phase in totally humidified.
pulmonary blood affects the net diffusion of a gas. ● The PH2O at 37°C (N Body Temp) is 47 mm Hg, which is
also the PH2O in the alveolar air.
ADDITIONAL INFORMATION
➔ Because the total pressure in the alveoli cannot rise to more
than the atm pressure (760mm Hg) this water vapor simply
dilutes all the other gases in the inspired air.
➔ Humidification of the air dilutes the PO2 from 159 mm Hg in
atmospheric air to 149 mm Hg in the humidified air, and it
dilutes the PN2 from 597 mm Hg (atm air) to 563 mm Hg
(alveolar)
– Net diffusion is determined by the difference between two

partial pressures.
1) Net diffusion towards blood
- more molecules diffuse in the blood if partial pressure
in alveoli gas phase is greater
- true for O2
2) Net diffusion towards alveoli gas phase
- more molecules diffuses in the gas if partial pressure 10. State and briefly explain the factors affecting the rate of gas
of gas is greater in the dissolved state in blood diffusion in a fluid.
- true for CO2 Pressure Difference Causes Net Diffusion of Gases Through Fluids
➢ When the partial pressure of a gas is greater in one area, there will be
8. Briefly define the vapor pressure of water. State the factor net diffusion from the high-pressure area to low-pressure area.
➢ Molecules in the area of high pressure, because of their greater
affecting vapor pressure of water.
number, have a greater chance of moving randomly into the area of
DESCRIPTION
low pressure than do molecules attempting to go in the other
● When non-humidified air enters respiratory
direction. However, some molecules do bounce randomly from the
passageways, H20 evaporates from the surfaces of these
low-pressure area toward the high-pressure area.
passages and humidifies the air.
➢ Therefore, the net diffusion of gas (pressure difference for causing
● This results from the continually escape of H20 from the
diffusion) from the area of high pressure to the area of low pressure
passage surface into the gas phase. The partial pressure
that H20 molecules exert to escape is called the vapor is equal to:
pressure of the H20 . ○ the number of molecules bouncing in this forward direction
● [PH20], vapor pressure of H20 is 47 mm Hg (@ normal minus
body temp, 37°C (98.6°F)) the number bouncing in the opposite direction
FACTORS AFFECTING PH20 Quantifying Net Rate of Diffusion in Fluids.

● PH20 depends entirely on the TEMPERATURE of the SOLUBILITY OF GAS IN THE FLUID
H20. The greater the solubility of the gas, the greater the number of
molecules available to diffuse for any given partial pressure difference.
CROSS-SECTIONAL AREA OF FLUID
The greater the cross-sectional area of the diffusion pathway, the
greater the total number of molecules that diffuse.
DISTANCE THROUGH WHICH GAS MUST DIFFUSE
Conversely, the greater the distance the molecules must diffuse, the
longer it will take the molecules to diffuse the entire distance.
MOLECULAR WEIGHT OF GAS
9. Define humidification. Finally, the greater the velocity of kinetic movement of the molecules,
Humidification: which is inversely proportional to the square root of the molecular
● The process of adding H2O vapor/moisture/humidity into weight, the greater the rate of diffusion of the gas.
TEMPERATURE OF FLUID
air gas surface
In the body, the temperature remains reasonably constant and usually
Air Is Humidified in the Respiratory Passages
need not be considered. But in general terms, the greater the
● PH2O at 37°C (N Body Temp) is 47 mm Hg, which is also temperature of fluid, the faster the rate of diffusion of molecules due
the PH2O in the alveolar air. to increase molecular movement
● All these factors can be expressed in a single The alveolar walls are extremely thin, and between the alveoli is an
formula, as follows: almost solid network of interconnecting capillaries.
“Sheet” of flowing blood - due to extensiveness of capillary plexus
● in which:
■ D is the diffusion rate, 14. Define a respiratory membrane.
■ ΔP is the partial pressure difference between the two ends of the ● The alveolar gases are in very close proximity to the blood of
diffusion pathway,
the pulmonary capillaries.
■ A is the cross-sectional area of the pathway,
● Furthermore, gas exchange between the alveolar air and
■ S is the solubility of the gas,
■ d is the distance of diffusion, and pulmonary blood occurs through the membranes of all the
■ MW is the molecular weight of the gas. terminal portions of the lungs, not merely in the alveoli.
● All these membranes are collectively known as the respiratory
● The characteristics of the gas determine two factors of the membrane, also called the pulmonary membrane
formula—solubility, S and molecular weight, MW. Together, these two
factors determine the diffusion coefficient of the gas. It’s proportional to: 15. State the different layers of the respiratory membrane.
1. A layer of fluid containing surfactant that lines the alveolus and
reduces the surface tension of alveolar fluid
DIFFUSION COEFFICIENT: 2. The alveolar epithelium, composed of thin epithelial cells
● The relative rates at which different gases at the same partial pressure 3. An epithelial basement membrane
levels will diffuse are proportional to their diffusion coefficients. 4. A thin interstitial space between the alveolar epithelium and
○ Assuming that the diffusion coefficient for O2 is 1, the relative diffusion capillary membrane
coefficients for different gases of respiratory importance in the body 5. A capillary basement membrane that in many places fuses with
fluids are as follows: the alveolar epithelial basement membrane
6. The capillary endothelial membrane
16. State and briefly explain the factors affecting rate of gas
diffusion through the respiratory membrane.
a. Thickness of the membrane
● The thickness of the respiratory membrane occasionally
11. Briefly explain the difference in the compositions of alveolar increases. (ex: Fibrosis of Lungs)
air and atmospheric air. ● Because the rate of diffusion through the membrane is
● The Table 40-1 above (LO.9) shows that atmospheric air is inversely proportional to the thickness of the membrane, –
composed almost entirely of N2 and O2; it normally contains 2x thickness = interfere significantly with normal respiratory
almost no CO2 and little water vapor. exchange of gases.
● Alveolar air does not have the same concentrations of gases as
atmospheric air. There are several reasons for the differences. b. Surface area of the membrane
1. Alveolar air is only partially replaced by atmospheric air ● Can be greatly decreased by many conditions like:
with each breath. – Removal of an entire lung: decreases to ½ Normal
2. O2 is constantly being absorbed into the pulmonary – Emphysema: many alveoli coalesce plus
blood from the alveolar air. alveolar wall dissolution; alveolar chambers are larger than
3. CO2 is constantly diffusing from the pulmonary blood original alveoli, but total surface area of respiratory
into the alveoli. membrane is decreased 5x
4. Dry atmospheric air that enters the respiratory passages ● ⅓ or ¼ decrease in total surface area:
is humidified even before it reaches the alveoli. – Exchange of gases through the membrane is impeded to a
significant degree
12. Define a respiratory unit (or respiratory lobule). ● Even under resting conditions, and during competitive sports
13. State the composition of the respiratory unit. and other strenuous exercise, even the slightest decrease in
RESPIRATORY UNIT surface area of the lungs can be a serious detriment to
Composed of : respiratory exchange of gases.
1. Respiratory bronchiole
2. Alveolar ducts c. Diffusion coefficient of the gas in the substance of the
3. Atria and
membrane
4. Alveoli
● 300 million alveoli in 2 lungs ● The diffusion coefficient for transfer of each gas through
● Each alveoli : Diameter of 0.2 mm the respiratory membrane depends on the gas’s
● The alveolar walls are extremely thin, and between the alveoli solubility in the membrane and, inversely, on the square
is an almost solid network of interconnecting capillaries root of the gas’s molecular weight.
d. Partial pressure difference of the gas between the two sides 18. State the factors that can increase oxygen diffusing capacity
of the membrane during exercise.
● The pressure difference across the respiratory membrane is the ➔ During strenuous exercise where pulmonary blood flow and
difference between the partial pressure of the gas in the alveolar ventilation is greatly increased, O2 diffusing capacity
alveoli and the partial pressure of the gas in the pulmonary ↑ 3x under resting conditions.
capillary blood. ➔ Caused by:
● When partial pressure of a gas in the alveoli > pressure of the ◆ Opening of dormant pulmonary capillaries; ↑surface area for
extra dilation
gas in the blood, as is true for O2, net diffusion from the alveoli
◆ A better match between the ventilation of the alveoli and
to blood occurs. perfusion of the alveolar capillaries with blood
● When the pressure of the gas in the blood > partial pressure in 19. Briefly explain the concept of:
the alveoli, as is true for CO2, net diffusion from the blood to a. Ventilation-perfusion ratio
alveoli occurs. ➔ Quantitative concept determining the respiratory exchange
when there’s imbalance between alveolar ventilation and
17. Define the diffusing capacity of the respiratory membrane. alveolar blood flow
➔ Volume of gas that will diffuse through the membrane each ➔ Assumed that all alveoli are ventilated equally, and blood flow
through the alveolar capillaries is the same for each alveolus
minute for a partial pressure difference of 1 mm Hg
➔ Expressed as: VA/Q—where:
➔ For O2
*VA = alveolar ventilation(normal)
◆ Avg. for young man: 21 ml/min/mm Hg.
*Q=blood flow(normal)
◆ O2 diff. across respiratory membrane during normal
◆ Alveolar Oxygen and Carbon Dioxide Partial Pressures
quiet breathing ~11 mm Hg
When V˙ A/Q˙ Equals Zero
◆ Meaning: 11 x 21 = 230 ml of O2 diffusing through the
● No alveolar ventilation
respiratory membrane each minute.
● Normal venous blood:
➔ For CO2
PO2 40 mm Hg ; PCO2 45 mm Hg
◆ Has never been measured because:
◆ Alveolar Oxygen and Carbon Dioxide Partial Pressures
● CO2 diffuses through respiratory membrane so
When V˙A/Q˙ Equals Infinity
rapidly that average PCO2 pulmonary blood is not
● No capillary blood flow; no O2 to carry away or
very different from PCO2 in the alveoli
bring to alveoli
● —avg. diff. >1 mm Hg
● Normal inspired and humidified air:
◆ Diffusion coefficient CO2 is slightly more than 20x that
PO2 149 mm Hg; PCO2 0 mm Hg
of O2
◆ Gas Exchange and Alveolar Partial Pressures When V˙
● CO2 diffusing capacity under resting conditions
A/Q˙ Is Normal
~400 to 450 ml/min/mm Hg ; during exercise
● Normal alveolar ventilation and alveolar capillary
~1200 to 1300 ml/min/mm Hg
blood flow—O2 and CO2 exchange through
respiratory membrane is nearly optimal:
PO2 104 mm Hg; PCO2 40 mm Hg
b. Physiological shunt
➔ VA/Q is below normal results in inadequate ventilation for
O2 oxygenation of blood flow through alveolar capillaries
leading to a fraction of venous blood passing through
pulmonary capillaries not oxygenated which is then
called shunted blood.
➔ The total quantitative amount of shunted blood per
minute is called physiological shunt
where :
● QPS=physiological shunt blood flow per minute
● QT=cardiac output per minute
● CiO2=concentration of O2 in arterial blood if there is an
“ideal” VA/Q
● CaO2=measured concentration of O2 in arterial blood
● CvO2=measured concentration of O2 in the mixed
venous blood
❖ TRANSPORT OF OXYGEN IN ARTERIAL BLOOD

➢ About 98% of the blood that enters the left atrium from
the lungs has just passed through the alveolar capillaries
and has become oxygenated up to a PO2 of about 104 mm
Hg.
➢ Another 2% of the blood has passed from the aorta
through the bronchial circulation, which supplies mainly
the deep tissues of the lungs and is not exposed to lung
air.
➢ —is called shunt flow, blood is shunted past the gas
exchange areas
Normal shunt blood PO2: approx. 40 mm Hg
➢ Venous and mixture of blood - blood combines in the
∴The greater the physiological shunt, the greater the amount of pulmonary veins with oxygenated blood from alveolar
blood that fails to be oxygenated as it passes through the lungs capillaries
PO2 of blood entering left heart to aorta: 95 mm Hg
c. Physiological dead space
➔ When the ventilation of some of the alveoli is great but
alveolar blood flow is low
➔ Far more O2 available in alveoli than can be transported away
from the alveoli by the flowing blood
➔ Ventilation of alveoli is wasted; Anatomical dead space areas
are also wasted
➔ The sum of two types of wasted ventilation is called
physiological dead space
➔ Measured in lab via appropriate blood and expiratory gas
using Bohr equation
20. Briefly discuss the factors affecting the transport of oxygen

from the alveoli to the body tissues:
● Gases move via diffusion and the cause of movement is
partial pressure difference from first point to next.
● O2 diffuses from alveoli to pulmonary capillary because a. Partial pressure of oxygen
PO2 alveoli > PO2 pulmonary capillary
❖ Alveoli→Pulmonary capillaries: Initial pressure difference
● Other tissues of the body, higher PO2 in capillary blood
for O2 diffusion into pulmonary capillaries = 104 - 40 mm
than in tissues causes O2 diffusion to surrounding cells
Hg, or 64 mm Hg.
● Conversely, when O2 is metabolized in cells to form CO2
❖ Arterial blood: Shunt blood PO2= 104 mm Hg; 40 mm Hg
intracellular PCO2 rises, causing CO2 to diffuse into the
(leaving the lungs); 95 mm Hg (left heart→aorta)
tissue capillaries
❖ Peripheral capillaries→tissue fluid: PO2= 95 mm Hg;
● Transport of O2 and CO2 by the blood depends on both
interstitial fluid PO2= avg. 40 mm Hg
diffusion and flow of blood.
❖ DIFFUSION OF OXYGEN FROM THE ALVEOLI TO THE

PULMONARY CAPILLARY BLOOD
➢ Avg. Alveolus PO2 : 104 mm Hg;
venous blood PO2 : 40 mm Hg
➢ a large amount of O2 was removed from this blood as
it passed through the peripheral tissues.
b. Tissue blood flow rate

Increasing Blood Flow Raises Interstitial Fluid PO2
➢ ↑blood flow through a particular tissue, greater
quantities of O2 are transported, therefore PO2
becomes correspondingly higher
c. Rate at which the O2 is used by the tissues (Tissue 23. Briefly explain the oxygen-hemoglobin dissociation curve.
metabolism) - Figure 41-8 shows the O2-hemoglobin dissociation
Increasing Tissue Metabolism Decreases Interstitial Fluid PO2 curve, which demonstrates a progressive increase in the
➢ If cells use more O2 for metabolism than percentage of hemoglobin bound with O2 as blood PO2
normal, interstitial fluid PO2 is reduced. increases, called the percent saturation of hemoglobin.
- Because the blood leaving the lungs and entering the
systemic arteries usually has a PO2 of about 95 mm Hg,
It can be seen from the dissociation curve that the usual
O2 saturation of systemic arterial blood averages 97%.
- Conversely, in normal venous blood returning from the
peripheral tissues, the PO2 is about 40 mm Hg, and the
saturation of hemoglobin averages 75%.
∴tissue PO2 is determined by a balance between (1) the rate of O2

transport to the tissues in the blood, and (2) the rate at which the
O2 is used by the tissues.
21. Briefly explain the role of hemoglobin in oxygen transport.

- Normally, about 97% of the O2 transported from the
lungs to the tissues is carried in a chemical combination
with hemoglobin in the red blood cells.
- The remaining 3% is transported in the dissolved state in
the water of the plasma and blood cells. Thus, under
normal conditions, O2 is carried to the tissues almost
entirely by hemoglobin.
22. State the effect of partial pressure of oxygen in the

combination of oxygen and hemoglobin.
- The chemistry of hemoglobin points out that the O2
molecule combines loosely and reversibly with the heme
portion of hemoglobin.
- When PO2 is high, as in the pulmonary capillaries, O2
binds with hemoglobin, but when PO2 is low, as in the
tissue capillaries, O2 is released from hemoglobin.
- This is the basis for almost all O2 transport from the lungs
to the tissues. 24. State the Factors that shift the oxygen-hemoglobin
dissociation curve.
a. Blood pH
When the blood becomes slightly acidic, with the pH
decreasing from the normal value of 7.4 to 7.2, the
O2-hemoglobin dissociation curve shifts, on average,
about 15% to the right. Conversely, an increase in pH
from the normal 7.4 to 7.6 shifts the curve a similar
amount to the left.
b. CO2 concentration d. 2,3-biphosphoglycerate (BPG)
INCREASE CARBON DIOXIDE: DECREASE CARBON

SHIFT TO THE RIGHT AND DIOXIDE:
DOWNWARD SHIFT TO THE LEFT AND
UPWARD
● As the blood passes through ● Opposite effects occur in

the tissues, CO2 diffuses the lungs, where CO2
from tissue cells into the diffuses from the blood
blood. into alveoli.
● This diffusion increases the ● This diffusion reduces
blood PCO2, which in turn blood PCO2 and H+
raises blood H2CO3 (carbonic concentration, shifting the
acid) and H+ concentration. O2-hemoglobin - The normal BPG in the blood always keeps the
● These effects shift the dissociation curve to the O2-hemoglobin dissociation curve shifted slightly to the right.
O2-hemoglobin dissociation left and upward. - In hypoxic conditions that last longer than a few hours, the
curve to the right and ● Therefore, the quantity of quantity of BPG in the blood increases considerably, thus
downward, forcing O2 away O2 that binds with the shifting the O2-hemoglobin dissociation curve even farther to
from the hemoglobin and hemoglobin at any given the right.
therefore delivering alveolar PO2 becomes - This shift causes O2 to be released to the tissues at as much
increased amounts of O2 to considerably increased, as 10 mm Hg higher tissue O2 pressure than would be the
the tissues. thus allowing greater O2 case without this increased BPG.
transport to the tissues. - Therefore, under some conditions, the BPG mechanism can
be important for adaptation to hypoxia, especially to hypoxia
caused by poor tissue blood flow.
c. Blood temperature
25. Briefly explain the Bohr Effect.
- During exercise, several factors shift the dissociation

curve considerably to the right, thus delivering extra
amounts of O2 to the active, exercising muscle fibers.
- The exercising muscles, in turn, release large quantities of
CO2; this and several other acids released by the muscles
increase the H+ concentration in the muscle capillary
blood.
- In addition, the temperature of the muscle often rises 2°
to 3°C, which can increase O2 delivery to the muscle
fibers even more. A shift of the oxygen-hemoglobin dissociation curve to the right in
- All these factors act together to shift the response to increases in blood CO2 and H+ levels has a significant
oxygen-hemoglobin dissociation curve of the muscle effect by enhancing the release of O2 from the blood in the tissues
capillary blood considerably to the right. and enhancing oxygenation of the blood in the lungs. This is called
- This rightward shift of the curve forces O2 to be released the Bohr effect, which can be explained as follows:
from blood hemoglobin to the muscle at PO2 levels as - As the blood passes through the tissues, CO2 diffuses from
great as 40 mm Hg, even when 70% of the O2 has tissue cells → blood. This diffusion ↑ the blood Pco2, which in
already been removed from the hemoglobin. turn ↑ blood H2CO3 (carbonic acid) and H+ concentration.
- Then, in the lungs, the shift occurs in the opposite These effects shift the O2-hemoglobin dissociation curve to
direction, allowing extra amounts of O2 to be picked up the right and downward, forcing O2 away from the
from alveoli. hemoglobin and therefore delivering increased amounts of
O2 to the tissues.
- Exactly the opposite effects occur in the lungs, where CO2 Furthermore, as shown in Figure 41-6,
diffuses from the blood → alveoli. This diffusion reduces – Pco2 of the pulmonary capillary blood falls to almost exactly
blood Pco2 and H+ concentration, shifting the O2-hemoglobin equal the alveolar Pco2 of 40 mmHg before it has passed more
dissociation curve to the left and upward. than about one-third of the distance through the capillaries.
- Therefore, the quantity of O2 that binds with the hemoglobin – This is the same effect that was observed earlier for O2 diffusion,
at any given alveolar Po2 becomes considerably ↑, thus except that it is in the opposite direction.
allowing greater O2 transport to the tissues.
● Transport of CO2 in Blood

– Transport of CO2 by the blood is not nearly as problematic as
transport of O2 is because even in the most abnormal conditions,
CO2 can usually be transported in far greater quantities than can O2.
– However, the amount of CO2 in the blood has a lot to do with the
acid–base balance of the body fluids
– Under normal resting conditions, an average of 4 ml of CO2 are
transported from the tissues → lungs in each 100 ml of blood
26. Briefly discuss the factors affecting the transport of carbon

dioxide from the tissues to the alveoli:
● DIFFUSION OF CO2 FROM PERIPHERAL TISSUE CELLS INTO

CAPILLARIES AND FROM PULMONARY CAPILLARIES INTO Effect of Tissue Metabolism and Tissue Blood Flow Rate on
ALVEOLI Interstitial Pco2
– When O2 is used by the cells, virtually all of it becomes CO2 – Tissue capillary blood flow and tissue metabolism affect the
● This transformation increases the intracellular Pco2 Pco2 in ways exactly opposite to their effect on tissue Po2.
CO2 diffuses from the cells → capillaries → carried by
the blood →lungs → diffuses from the pulmonary
capillaries → alveoli → expired.
– At each point in the gas transport chain, CO2 diffuses in the

direction exactly opposite to the diffusion of O2.
– One major difference between diffusion of CO2 and of O2:
● CO2 can diffuse about 20 times as rapidly as O2
– Therefore, the pressure differences required to cause CO2
diffusion are, in each case, far less than the pressure differences
required to cause O2 diffusion.
● CO2 PRESSURES
1. Intracellular Pco2 = 46 mmHg
Interstitial Pco2 = 45 mmHg
Thus, there is only a 1 mmHg pressure differential – A decrease in blood flow from normal (point A) to ¼x Normal
(point B) increases peripheral tissue Pco2 from the normal value of
2. Pco2 of the arterial blood entering the tissues = 40 mmHg
45 mm Hg to an elevated level of 60 mm Hg.
Pco2 of the venous blood leaving the tissues = 45 mmHg
– Conversely, increasing the blood flow to 6x normal (point C)
Thus, the tissue capillary blood comes almost exactly to equilibrium
decreases the interstitial Pco2 from the normal value of 45 to 41
with the interstitial Pco2 of 45 mmHg
mm Hg, almost equal to the Pco2 in the arterial blood (40 mm Hg)
3. Pco2 of the blood entering the pulmonary capillaries at the entering the tissue capillaries.
arterial end = 45 mmHg – Note also that a 10-fold increase in tissue metabolic rate greatly
Pco2 of the alveolar air = 40 mmHg elevates the interstitial fluid Pco2 at all rates of blood flow, whereas
Thus, only a 5 mmHg pressure difference causes all the required decreasing the metabolism to ¼x Normal causes the interstitial
CO2 diffusion out of the pulmonary capillaries into the alveoli. fluid Pco2 to fall to about 41 mm Hg, closely approaching that of
the arterial blood, 40 mm Hg.
27. State the chemical forms in which CO2 is transported: – When a carbonic anhydrase inhibitor (e.g., acetazolamide) is
To begin the process of CO2 administered to an animal to block the action of carbonic
transport, CO2 diffuses out of the anhydrase in the RBCs
tissue cells in the dissolved ○ CO2 transport from the tissues becomes so poor that the
molecular CO2 form. tissue Pco2 may rise to 80 mm Hg instead of the normal
45 mm Hg
On entering the tissue capillaries, c. As carbaminohemoglobin
the CO2 initiates a host of almost Transport of CO2 in Combination With Hemoglobin and Plasma
instantaneous physical and Proteins
chemical reactions, shown in ● CO2 also reacts directly with amine radicals of the
Figure 41-13, which are essential hemoglobin molecule to form the compound
for CO2 transport. carbaminohemoglobin (CO2Hgb)
a. As dissolved CO2 ● Combination of CO2 and Hgb is a reversible reaction that
Small portion of the dissolved state of CO2 is transported to the occurs with a loose bond
lungs ○ CO2 is easily released into the alveoli, where the
RECALL: Pco2 is lower than in the pulmonary capillaries.
PCO2 (Venous Blood) = 45 mmHg ● A small amount of CO2 also reacts in the same way with
PCO2 (Arterial Blood) = 40 mmHg the plasma proteins in tissue capillaries.
Amount of CO2 dissolved in the fluid of the blood at :
● Reaction is much less significant for the transport of CO2
45 mmHg = 2.7 mL/dL (2.7 vol. percent)
○ The quantity of these proteins in the blood is
40 mmHg = 2.4 mL
only 1/4 as great as the quantity of Hgb.
■ Difference of 0.3 mL
Therefore, only 0.3 mL of CO2 is transported in the dissolved form ● The quantity of CO2 that can be carried from the
by each 100 mL of blood flow (7% of all CO2 that is normally peripheral tissues to the lungs by carbamino
transported) combination with hemoglobin and plasma proteins is
about 30% of the total quantity transported
b. As bicarbonate ion. ○ normally about 1.5 ml of CO2 in each 100 ml of
i. Role of carbonic anhydrase blood
Carbonic Anhydrase - Catalyzes the Reaction of CO2 With Water ● It is doubtful that under normal conditions this
in Red Blood Cells carbamino mechanism transports more than 20% of the
– Dissolved CO2 in blood reacts with water → carbonic acid total CO2.
● Reaction would occur much too slowly but with the carbonic
anhydrase inside the RBC, it catalyzes the reaction of CO2
and H2O which accelerates the reaction rate by 5000x
● Therefore, instead of requiring many secs or mins, reaction
occurs so rapidly in red blood cells that it reaches almost
complete equilibrium within a small fraction of a sec.
● This phenomenon allows tremendous amounts of CO2 to
react with the RBC H2O, even before the blood leaves the
tissue capillaries.
ii. Dissociation of carbonic acid Into bicarbonate

and hydrogen ions. Briefly discuss the changes in
blood acidity during CO2 transport
In a split second, carbonic acid formed in red cells (H2CO3)
dissociates into H+ and bicarbonate ions (H+ and HCO3 −). CARBON DIOXIDE DISSOCIATION CURVE
○ Most of the H+ ions combine with hgb in the RBC (hgb ● Depicts the dependence of total blood CO2 in all its
protein is a powerful acid–base buffer) forms on Pco2
○ Many of the HCO3− ions diffuse from the RBC→plasma ● NOTE:
while chloride ions diffuse into the RBC to take their place. ○ Normal blood Pco2:
■ 40 mmHg - arterial blood
– Diffusion is made possible by the presence of a special ■ 45 mmHg - venous blood
bicarbonate-chloride carrier protein in the RBC membrane that ○ Normal concentration of CO2 in blood (all its
shuttles these two ions in opposite directions at rapid velocities. form) - 50 volume percent
– Thus, the Cl- content of venous red blood cells is > arterial RBC, a ■ Only 4 volume percent is exchanged
phenomenon called the chloride shift. during normal transport of CO2
● Concentration
– Reversible combination of CO2 with H2O in RBC under the Rises to about 52 volume% as the blood
influence of carbonic anhydrase accounts for about 70% of the passes through the tissues
CO2 that is being transported from the tissues to the lungs. Falls to about 48 volume% as it passes through
the lungs
28. Explain the Haldane Effect – Normal Arterial blood pH: 7.41
HALDANE EFFECT -Venous blood (due to higher PCO2): 7.37 (More acidic)
● It is the reverse of Bohr effect which is the binding of O2 with -Change (fall) of 0.04 unit in venous blood due to
Hgb that tends to displace CO2 from the blood. increased CO2 in it.
● More important in promoting CO2 transport than the Bohr – Decrease in pH in the tissue blood (and in the tissues themselves)
effect which promotes O2 transport. ➢ during heavy exercise
● It displaces CO2 from the blood and into the alveoli in 2 ways: ➢ other conditions of high metabolic activity
1. The more highly acidic Hgb has less tendency to ➢ when blood flow through the tissues is sluggish
combine with CO2 to form carbaminohemoglobin, thus ➢ ph: 0.50 (about 12 times normal) thus causing significant
displacing much of the CO2 that is present in the tissue acidosis
carbamino form from the blood.
2. The increased acidity of the Hgb → release an excess of
H+ → these ions bind with HCO3− to form carbonic acid
→ dissociates into H2O and CO2 → CO2 is released from
the blood into the alveoli → into the air.
Demonstrates quantitatively the significance of the Haldane effect

on the transport of CO2 from the tissues to the lungs.
29. Briefly explain respiratory exchange ratio.

– Under normal resting conditions, only about 82% as much CO2 is
expired from the lungs as O2 is taken up by the lungs. The ratio of
CO2 output to O2 uptake is called the respiratory exchange ratio (R).
This figure shows small portions of two CO2 dissociation curves:

(1) when the Po2 is 100 mm Hg, which is the case in the blood
capillaries of the lungs; and
(2) when the Po2 is 40 mm Hg, which is the case in the tissue The value for R changes under different metabolic conditions:
capillaries.
● R rises to 1.00 when a person is using carbohydrates
– Point A shows that the normal Pco2 of 45 mm Hg in the tissues exclusively for body metabolism.
causes 52 volume% of CO2 to combine with the blood. ● R level falls to as low as 0.7 when a person is using fats
– On entering the lungs, the Pco2 falls to 40 mm Hg, and the Po2 exclusively for metabolic energy.
rises to 100 mm Hg.
– The reason for this difference is that:
– If the CO2 dissociation curve did not shift because of the Haldane *when O2 is metabolized with carbohydrates = one molecule
effect, the CO2 content of the blood would fall only to 50 volume %,
of CO2 is formed for each molecule of O2 consumed;
which would be a loss of only 2 volume% of CO2.
*when O2 reacts with fats = a large share of the O2 combines
– However, the ↑ Po2 in the lungs lowers the CO2 dissociation curve with H+ atoms from the fats to form H2O instead of CO2.
from the top curve to the lower curve of the figure, so the CO2 – For a person on a normal diet consuming average amounts of
content falls to 48 volume% (point B) which represents an additional
carbohydrates, fats, and proteins, the average value for R is
2 volume% loss of CO2.
considered to be 0.825.
– Thus, the Haldane effect approximately doubles the amount of
CO2 released from the blood in the lungs and approximately doubles
the amount of CO2 picked up in the tissues.
● Change in blood acidity during CO2 transport:

– The H2CO3 formed when CO2 enters the blood in
peripheral tissues decrease blood pH.
– However, reaction of this acid with acid-base buffers of the
blood prevents the H+ concentration from rising very much.
RESPIRATORY CENTER ● Inspiratory “Ramp” Signal

- The respiratory center is composed of several groups of neurons -> Begins weakly
located bilaterally in the medulla oblongata and pons of the brain -> Increases steadily in a ramp manner for about 2 seconds in
stem. normal respiration.
-> It then ceases abruptly for approximately the next 3 seconds,
(which turns off diaphragm & allows elastic recoil of lungs and
chest wall = expiration)
-> Next, the inspiratory signal begins again for another cycle
**This cycle repeats again and again, with expiration occurring in
between. Thus, the inspiratory signal is a ramp signal.
Two (2) qualities of inspiratory ramp are controlled, as follows:

1. Control of the rate of increase of the ramp signal so that
during heavy respiration, the ramp increases rapidly and
therefore fills the lungs rapidly.
30. State the three (3) major collections of neurons in the 2. Control of the limiting point at which the ramp
respiratory center. suddenly ceases - this is the usual method for controlling
the rate of respiration.
Three major collections of neurons: – That is, the earlier the ramp ceases, the shorter the
(1) Dorsal respiratory group, located in the dorsal portion of the duration of inspiration. This method also shortens the
medulla, which mainly causes inspiration. duration of expiration. Thus, the frequency of respiration
(2) Ventral respiratory group, located in the ventrolateral part of is increased.
the medulla, which mainly causes expiration.
(3) Pneumotaxic center, located dorsally in the superior portion of 32. Role of the pneumotaxic center in the dorsal superior portion
the pons, which mainly controls rate and depth of breathing. of the pons in respiration.
● Pneumotaxic center (Limits Inspiration duration and ↑RR)
31. The role of the dorsal respiratory group of neurons in the dorsal – Located dorsally in the nucleus parabrachialis of the upper
portion of medulla oblongata in respiration. pons, transmits signals to the inspiratory area.
– The primary effect of this center is to control the
● The dorsal respiratory group of neurons
“switch-off” point of the inspiratory ramp, thereby controlling
-extends most of the length of the medulla.
the duration of the filling phase of the lung cycle.
-most of its neurons are located in the nucleus of the
tractus solitarius (NTS).
33. Role of the ventral group of neurons in the ventrolateral part of
● Nucleus of the tractus solitarius (NTS) the medulla in respiration.
-is the sensory termination of both the vagal and the
● Ventral Respiratory Group of Neurons (Both Inspiration &
glossopharyngeal nerves, which transmit sensory signals
Expiration)
into the respiratory center from the following:
– Located on each side of the medulla, about 5 mm anterior
(1) peripheral chemoreceptors
and lateral to the dorsal respiratory group of neurons.
(2) baroreceptors
– Found in the nucleus ambiguus rostrally and the nucleus
(3) receptors in the liver, pancreas, and multiple
retroambiguus caudally.
parts of the gastrointestinal tract
(4) several types of receptors in the lungs. The function of this neuronal group differs from that of the dorsal
respiratory group in several important ways:
● Rhythmical Inspiratory Discharges From the Dorsal Respiratory
1. The neurons of the ventral respiratory group remain almost
Group
totally inactive during normal quiet respiration.
-The basic rhythm of respiration is generated mainly in the
2. The ventral respiratory neurons do not appear to participate
dorsal respiratory group of neurons.
in the basic rhythmical oscillation that controls respiration
-They emit repetitive bursts of inspiratory neuronal action
3. When the respiratory drive for increased pulmonary
potentials.
ventilation becomes >normal = respiratory signals “spill
over” into the ventral respiratory neurons from the basic
oscillating mechanism of the dorsal respiratory area.
4. Electrical stimulation of a few of the neurons in the ventral
group causes inspiration, whereas stimulation of others
causes expiration.
34. Hering-Breuer Inflation Reflex. Briefly discuss its role in

respiration.
● Hering-Breuer inflation reflex (Lung inflation signals limit of

inspiration)
- This mechanism affects inspiration in much the same way
as signals from the pneumotaxic center:
- When the lungs become overinflated → stretch
receptors → “switches off” the inspiratory ramp
→ stops further inspiration. ●
- Located in the muscular portions of the walls of the bronchi
c. Attenuating role of the kidneys on the stimulatory effect of
and bronchioles
CO2
- OVERSTRETCH OF LUNGS:
● Excitation of the respiratory center by CO2 is great the first
stretch receptors → vagus nn → dorsal respiratory
few hours after the blood CO2 first increases,
group of neurons
● but then it gradually declines over the next 1 to 2
- This reflex also increases the rate of respiration, as is true days, decreasing to about 1/5 the initial effect.
for signals from the pneumotaxic center ● Part of this decline results from renal readjustment of the H+
. concentration in the circulating blood.
● CONTROL OF OVERALL RESPIRATORY CENTER ACTIVITY ● The kidneys achieve this readjustment by increasing
Chemical Control of Respiration the blood HCO3−, which binds with H+ in the blood and
CSF to reduce their concentrations.
- O2, in contrast, does not have a major direct effect on the
● But, even more importantly, over a period of hours, the
respiratory center of the brain in controlling respiration. Instead, HCO3− also
it acts almost entirely on peripheral chemoreceptors located in – slowly diffuses through the blood–brain and
the carotid and aortic bodies, and these chemoreceptors in turn blood–CSF barriers and
transmit appropriate nervous signals to the respiratory center for – combines directly with H+ adjacent to the respiratory
control of respiration. neurons as well, thus reducing the H+ back to near
normal.
● A change in blood CO2 concentration therefore has a potent
35. Effect of CO2, excess H+, and O2 on chemosensitive area of
acute effect on controlling respiratory drive but only a weak
the respiratory center. chronic effect after a few days’ adaptation.
a. Briefly describe the chemosensitive area of the
respiratory center beneath the medulla’s ventral surface d. Effect of O2 on the sensor neurons in the chemosensitive area
● The hemoglobin-oxygen buffer system delivers almost
● Chemosensitive Area of the Respiratory Center Beneath the
exactly normal amounts of O2 to the tissues, even when the
Medulla’s Ventral Surface pulmonary Po2 changes from a value as low as 60 mm Hg up
- Chemosensitive area is located bilaterally, lying only to a value as high as 1000 mm Hg(or <1/2-normal to as high
0.2 mm beneath the ventral surface of the medulla. as 20x or more than normal)
- This area is highly sensitive to changes in either blood ● However for CO2, both the blood and tissue Pco2 change
Pco2 or H+ concentration, and it in turn excites the inversely with the rate of pulmonary ventilation; thus,
other portions of the respiratory center ○ CO2 is the major controller of respiration, not O2.
● Changes in O2 concentration have virtually no direct effect on
b. Briefly state the effect CO2 and excess H+ on the sensor the respiratory center—although O2 changes do have an
neurons in the chemosensitive area indirect effect, acting through the peripheral chemoreceptors.
● This peripheral chemoreceptor mechanism responds O2 when
● CO2 AND H+ (Direct Control of Respiratory Center Activity) it falls too low, mainly below a PO2 of 70 mm Hg.
● The sensor neurons in the chemosensitive area are
especially excited by H+; in fact, it is believed that H+ may 36. Effect of O2, CO2, and excess H+ on the peripheral
be the only important direct stimulus for these neurons. chemoreceptor system.
However, H+ ions do not easily cross the blood–brain a. Peripheral chemoreceptor system
barrier. ● Most of the chemoreceptors are in the carotid bodies. But
● CO2 has little direct effect in stimulating the neurons in few are also in the aortic bodies. A very few are located
the chemosensitive area, it does have a potent indirect elsewhere in association with other arteries of the thoracic
effect. and abdominal regions.
● It has this effect by reacting with the H2O of ● Carotid bodies are located bilaterally in the bifurcations
the tissues to form carbonic acid, which of the common carotid arteries. Their afferent nerve
dissociates into H+ and HCO3−; the H+ then fibers → Hering’s nerves → glossopharyngeal nerves →
have a potent direct stimulatory effect on dorsal respiratory area of the medulla.
respiration
● Aortic bodies are located along the arch of the aorta;

their afferent nerve fibers → the vagi → dorsal
medullary respiratory area.
● They are especially important for detecting changes in O2 in
the blood, although they also respond to a lesser extent to
changes in CO2 and H+. Blood flow through these bodies is
extreme, 20x the weight of the bodies themselves per
minute.
● Therefore, the percentage of O2 removed from the flowing
blood is virtually zero, which means that the
– The red curves were measured at a blood pH of 7.4,
chemoreceptors are exposed at all times to arterial blood, not
These curves were recorded at different levels of arterial
venous blood, and their Po2 values are arterial Po2 values.
Po2—40, 50, 60, and 100 mm Hg. For each of these curves, the
Pco2 was changed from lower to higher levels. Thus, represents
b. Role of O2 in respiratory control via the peripheral
the combined effects of alveolar Pco2 and Po2 on ventilation.
chemoreceptor system – The green curves were measured at a pH of 7.3.
● When the oxygen concentration in the arterial blood – The curves would be displaced to the right at higher pH and
falls below normal, the chemoreceptors become displaced to the left at lower pH.
strongly stimulated. This effect is demonstrated in
Figure 42-5, d. Phenomenon of “Acclimatization”
Mountain climbers have found that when they ascend a
mountain slowly, over a period of days rather than a period of
hours, they breathe much more deeply and therefore can
withstand far lower atmospheric O2 concentrations than when
they ascend rapidly
● The reason for acclimatization is that within 2 to 3 days,
the respiratory center in the brain stem loses about 80%
of its sensitivity to changes in Pco2 and H+.
● Therefore, the excess ventilatory blow-off of CO2 that
normally would inhibit an increase in respiration fails to
occur, and low O2 can drive the respiratory system to
higher alveolar ventilation than under acute conditions.
which shows the effect of different levels of arterial Po2 on the ● Instead of the 70% increase in ventilation that might
rate of nerve impulse transmission from a carotid body. occur after acute exposure to low O2, the alveolar
– Note that the impulse rate is particularly sensitive to ventilation often increases by 400% to 500% after 2 to
changes in arterial Po2 in the range of 60 mm Hg down to 30 3 days of low O2.
mm Hg, a range in which Hgb saturation with O2 decreases
rapidly. 37. briefly discuss interrelationship between chemical and
nervous factors in controlling respiration during exercise
– Carotid body glomus cell
oxygen sensing. When the NERVOUS FACTOR CHEMICAL FACTORS
Po2 decreases below around
60 mmHg, potassium Sends nervous signals Occasionally, the nervous respiratory
channels close, causing cell to stimulate the control signals are too strong or too
depolarization, opening of respiratory center by weak- CHEMICAL FACTOR then
calcium channels, and almost the proper plays the role in the final adjustment
increased cytosolic calcium amount to supply the of respiration required to keep the O2
ion concentration. This extra O2 required for and CO2 and H+ concentrations of
stimulates transmitter exercise and to blow off the body fluids as nearly normal as
release ( [ATP] is likely the extra CO2 possible
most important), which
activates afferent fibers that
send signals to the central INTERRELATIONSHIP BETWEEN CHEMICAL AND NERVOUS
nervous system (CNS) and FACTORS IN CONTROLLING RESPIRATION DURING EXERCISE
stimulate respiration.
The lower curve shows

c. Composite effects of PCO2 , pH, and PO2 on alveolar changes in alveolar
ventilation during one
ventilation
minute of exercise------
● two families of curves representing the combined effects of Pco2 while the upper curve shows
and Po2 on ventilation at two different pH values. changes inarterial PCO2.
NERVOUS FACTOR CHEMICAL FACTOR NEUROGENIC CONTROL OF VENTILATION DURING

EXERCISE MAY BE PARTLY A LEARNED RESPONSE
The brain provides an After 30 to 40 seconds, the
“anticipatory” stimulation of amount of CO2 released into With The brain becomes progressively more able
respiration at the onset of the blood from the active repeated to provide the proper signals required to
exercise, causing extra muscles approximately periods keep the blood PCO2 at its normal level
alveolar ventilation even matches the increased rate of of
before it is necessary---and ventilation, and the arterial PCO2 exercise Also, cerebral cortex is involved in this
forges the ventilation ahead returns essentially to normal, learning because of experiments that block
of the buildup of blood CO2. even d the exercise continues only the cortex also block the learned
response
38. Briefly explain the role of the following factors in respiration

INTERRELATIONSHIP BETWEEN CHEMICAL AND NERVOUS
FACTORS IN CONTROLLING RESPIRATION DURING OTHER FACTORS THAT AFFECT RESPIRATION
EXERCISE
PULMONARY Action
IRRITANT RECEPTORS
·
Located in the · Initiates coughing and sneezing
epithelium of · May also cause bronchial
trachea, bronchi and constriction in persons with
bronchioles diseases such as asthma and
emphysema
J RECEPTORS ACTION
A few sensory nerve They are stimulates when;

endings in the - Pulmonary capillaries
alveolar walls in become engorged with
juxtaposition to the blood or when
pulmonary capillaries pulmonary edema
occurs in condition such
The lower curve is the effect of different levels of arterial PCO2
as congestive heart
on the alveolar ventilation when the body is at rest (not
failure
exercising)
Function:
Their excitation may give the person a
The upper curve shows the approximate shift of this
feeling of dyspnea
ventilatory curve caused by neurogenic drive from the
respiratory center that occurs during heavy exercise
ACTION
The point indicated on the two curves shows the arterial PCO2
Depresses and inactivates the
first in the resting state and then in the exercising state
respiratory center
Note in both cases that the PCO2 is at the normal level of
Example:
40 mmHg
Brain concussion- damages the brain
tissues swell, compressing the cerebral
NERVOUS FACTOR CHEMICAL FACTOR
arteries against the cranial vault and
BRAIN EDEMA thus partially blocking the cerebral
Shifts the curve about it has stimulatory effect on
blood supply
20-fold in the upward ventilation at a PCO2 value
direction, so ventilation greater than 40 mm Hg and a
TREATMENT
almost matches the rate of depressant effect at a PCO2
CO2 release, thus keeping the value less than 40 mm Hg
- Intravenous injection of a
arterial PCO2 near its normal
hypertonic solution such as
value
mannitol solution (can temporarily
relieve)----- and osmotically
remove some of the fluids of the
brain.
OVERDOSAGE OF ACTIONS 2 SEPARATE CONDITIONS THE

ANESTHETICS AND DAMPING FACTORS CAN BE
NARCOTICS OVERRIDDEN AND CSB DOES
OCCUR:
· The most prevalent cause of
respiratory depression and When a long delay occurs for
respiratory arrest transport of blood from the lungs to
Example: the brain, , changes in CO2 and O2 in
1. Sodium pentobarbital the alveoli can continue for many more
2. Halothane seconds than usual. Under these
3. Morphine conditions, the storage capacities of
4. Opioids the alveoli and pulmonary blood for
these gases are exceeded; then, after a
PERIODIC ACTION few more seconds, the periodic
BREATHING respiratory drive becomes extreme and
Cheyne- Stokes breathing begins. This
An abnormality of Person breathes deeply for a short type of Cheyne- Stokes breathing
respiration occurs in interval and then breathes slightly or often occurs in patients with severe
several disease not at all for an additional interval, with cardiac failure because blood flow is
conditions the cycle repeating itself over and over slow, thus delaying the transport of
blood gases from the lungs to the
CHEYNE-STOKES ACTION brain. In patients with chronic heart
BREATHING failure, Cheyne- Stokes breathing can
sometimes occur on and off for
Characterized by Mechanism: months.
slowly waxing and When a person overbreathes, thus
waning respiration blowing off too much CO2 from the A second cause of Cheyne- Stokes
occurring about pulmonary blood while at the same breathing is increased negative
every 40 to 60 time increasing blood O2, it takes feedback gain in the respiratory control
seconds several seconds before the epithelium areas, which means that a change in
of the trachea, bronchi, and blood CO2 or O2 causes a far greater
bronchioles is supplied with sensory change in ventilation than normally.
nerve endings called pulmonary irritant
receptors that are stimulated by many
factors.
The brain damage often turns off the
By this time, the person has already respiratory drive entirely for a few
over ventilated for an extra few seconds, and then an extra- intense
seconds. increase in blood CO2 turns it back on
with great force. Cheyne- Stokes
Therefore, when the over ventilated breathing of this type is frequently a
blood finally reaches the brain prelude to death from brain
respiratory center, the center becomes malfunction. Typical records of changes
depressed to an excessive amount, at in pulmonary and respiratory center
which point the opposite cycle Pco2 during Cheyne- Stokes breathing
begins—that is, CO2 increases, and O2 are shown in Figure 42-12.
decreases in the alveoli.
Again, it takes a few seconds before the Note that the Pco2 of the pulmonary
brain can respond to these new blood changes in advance of the Pco2
changes. When the brain does respond, of the respiratory neurons. However,
the person breathes hard once again the depth of respiration corresponds
and the cycle repeats with the Pco2 in the brain, not with the
Pco2 in the pulmonary blood where
the ventilation is occurring.
SLEEP APNEA ACTIONS of the pharynx due to excessive fat

masses in the neck. In a few individuals,
Apnea means · Occasional apneas occur sleep apnea may be associated with
absence of during normal sleep, but nasal obstruction, a very large tongue,
spontaneous in persons with sleep enlarged tonsils, or certain shapes of
breathing. apnea, the frequency the palate that greatly increase
and duration are greatly resistance to the flow of air to the lungs
increased, with episodes during inspiration.
of apnea lasting for 10
Patients affected by seconds or longer and
central sleep apnea occurring 300 to 500 TREATMENT OF OBSTRUCTIVE
may have decreased times each night. SLEEP APNEA
ventilation, even
when they are awake, · Sleep apneas can be 1 surgery to remove excess fat tissue at
although they are caused by obstruction of the back of the throat (a procedure
fully capable of the upper airways, called uvulopalatopharyngoplasty),
normal voluntary especially the pharynx, remove enlarged tonsils or adenoids, or
breathing. or by an impaired central create an opening in the trachea
nervous system (tracheostomy) to bypass the
During sleep, their respiratory drive obstructed airway during sleep; and
breathing disorders
usually worsen, CAUSES OF “OBSTRUCTIVE” SLEEP 2) nasal ventilation with continuous
resulting in more APNEA positive airway pressure (CPAP).
frequent episodes of
apnea that decrease “CENTRAL” SLEEP APNEA
Po2 and increase Blockage of the Upper Airway.
Pco2 until a critical CAUSES:
level is reached that - Occurs when the neural
eventually stimulates The muscles of the pharynx normally drive to respiratory
respiration. keep this passage open to allow air to muscles is transiently
flow into the lungs during inspiration. abolished
During sleep, these muscles usually
relax, but the airway passage remains DISORDERS THAT CAN CAUSE
open enough to permit adequate CESSATION OF THE VENTILATORY
airflow. DRIVE DURING SLEEP INCLUDE
damage to the central respiratory

Some people have an especially centers or abnormalities of the
narrow passage, and relaxation of these respiratory neuromuscular apparatus.
muscles during sleep causes the
pharynx to close completely so that air
cannot flow into the lungs. In some cases, sleep apnea may be
caused by a combination of obstructive
The periods of apnea and labored and central mechanisms. This “mixed”
breathing are repeated several hundred type of sleep apnea is estimated to
times during the night, resulting in account for approximately 15% of all
fragmented restless sleep. sleep apnea cases, whereas pure
“central” sleep apnea accounts for less
Therefore, patients with sleep apnea than 1% of cases. The most common
usually have excessive daytime cause of sleep apnea is obstruction of
drowsiness, as well as other disorders, the upper airway.
including increased sympathetic
activity, high heart rate, pulmonary and THESE TRANSIENT INSTABILITIES OF
systemic hypertension, and a greatly RESPIRATION CAUSE RESTLESS
elevated risk for cardiovascular disease. SLEEP AND CLINICAL FEATURES
SIMILAR TO THOSE OBSERVED IN
PEOPLE WITH OBSTRUCTIVE SLEEP
Obstructive sleep apnea usually occurs APNEA.
in older obese personsin whom there is
increased fat deposition in the soft
tissues of the pharynx or compression

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Module 13 Respiratory System: Pulmonary Gas Exchange & Regulation of Respiration

5. State and briefly explain the factors that determine partial

3. Define partial pressure of a gas. Define the total pressure of

– Net diffusion is determined by the difference between two

FACTORS AFFECTING PH20 Quantifying Net Rate of Diffusion in Fluids.

❖ TRANSPORT OF OXYGEN IN ARTERIAL BLOOD

20. Briefly discuss the factors affecting the transport of oxygen

❖ DIFFUSION OF OXYGEN FROM THE ALVEOLI TO THE

b. Tissue blood flow rate

∴tissue PO2 is determined by a balance between (1) the rate of O2

21. Briefly explain the role of hemoglobin in oxygen transport.

22. State the effect of partial pressure of oxygen in the

b. CO2 concentration d. 2,3-biphosphoglycerate (BPG)

INCREASE CARBON DIOXIDE: DECREASE CARBON

● As the blood passes through ● Opposite effects occur in

- During exercise, several factors shift the dissociation

● Transport of CO2 in Blood

26. Briefly discuss the factors affecting the transport of carbon

● DIFFUSION OF CO2 FROM PERIPHERAL TISSUE CELLS INTO

– At each point in the gas transport chain, CO2 diffuses in the

ii. Dissociation of carbonic acid Into bicarbonate

Demonstrates quantitatively the significance of the Haldane effect

29. Briefly explain respiratory exchange ratio.

This figure shows small portions of two CO2 dissociation curves:

● Change in blood acidity during CO2 transport:

RESPIRATORY CENTER ● Inspiratory “Ramp” Signal

Two (2) qualities of inspiratory ramp are controlled, as follows:

34. Hering-Breuer Inflation Reflex. Briefly discuss its role in

● Hering-Breuer inflation reflex (Lung inflation signals limit of

● Aortic bodies are located along the arch of the aorta;

The lower curve shows

NERVOUS FACTOR CHEMICAL FACTOR NEUROGENIC CONTROL OF VENTILATION DURING

38. Briefly explain the role of the following factors in respiration

A few sensory nerve They are stimulates when;

OVERDOSAGE OF ACTIONS 2 SEPARATE CONDITIONS THE

SLEEP APNEA ACTIONS of the pharynx due to excessive fat

damage to the central respiratory

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