Gas Exchange and Alveolar Ventilation

Gas Exchange and Alveolar Ventilation

Objectives At the end of this session students should be able to
1.Define dead space, physiological and anatomical 2.Define partial pressure and fractional concentration as they apply to gases in air. 3. List the normal airway, alveolar, arterial, and mixed venous PO2 and PCO2 values. 3. List the normal arterial and mixed venous values for O2 saturation, [HCO3-], and pH.

4. Be able to estimate the alveolar oxygen partial pressure (PAO2) using the simplified form of the alveolar gas equation 5.Name the factors that affect diffusive transport of a gas between alveolar gas and pulmonary capillary blood. 6. Understand diffusion limited and perfusion limited gas exchange. 7.Define oxygen diffusing capacity.

Dead space Regions of the respiratory system that contain air but are not exchanging O2and CO2with blood are considered dead space. Anatomic dead space Airway regions that, because of inherent structure, are not capable of O2and CO2exchange with the blood. Includes the conducting zone, which ends at the level of the terminal bronchioles. The size of the anat VD in mL is approximately equal to a person’s weight in pounds. (Thus a 150-lb individual has an anatomic dead space of 150 mL.)

Alveolar dead space(alv VD)
Refers to alveoli containing air but without blood flow in the surrounding capillaries. An example is a pulmonary embolus Physiologic dead space total dead space in the lung system (anatVD+alvVD)

This is called the Bohr dead space equation, named after the physiologist Christian Bohr.

VENTILATION Total Ventilation/minute volume or minute ventilation
total volume of air moved in or out (usually the volume expired) of the lungs per minute.

Alveolar Ventilation Represents the air delivered to the respiratory zone(include the alveoli, alveolar sacs, alveolar ducts, and respiratory bronchioles)per breath.

Increases in the Depth of Breathing:
There will be equal increases in total and alveolar ventilation per breath, since dead space volume is constant Increases in the Rate of Breathing Increased rate causes increased ventilation of dead space and alveoli.

A woman has a respiratory rate of 18, a tidal volume of 350 mL, and a dead space of 100 mL. What is her alveolar ventilation? a. 4.0 L b. 4.5 L c. 5.0 L d. 5.5 L e. 6.0 L

Gas laws Boyle's law: when temperature is constant, pressure (P) and volume (V) are inversely related Dalton's law: the partial pressure of a gas in a gas mixture is the pressure that the gas would exert if it occupied the total volume of the mixture in the absence of the other components. Henry's law : that the concentration of a gas dissolved in a liquid is proportional to its partial pressure. Boyle’s law At a given temperature, the product of pressure times volume is constant. P1V1 = P2V2 Dalton’ law of Partial Pressures Px = PB x F for dry gas or Px = [PB-PH2O] x F for gas saturated with water vapor where PX =Partial pressure of gas (mm Hg) PB =Barometric pressure (mm Hg) Ph2o =Water vapor pressure at 37°C (47 mmHg) F =Fractional concentration of gas (no units) Henry’s Law for concentrations of dissolved gases Henry's law deals with gases dissolved in solution (e.g., in blood). Both O2 and CO2 are dissolved in blood (a solution) en route to and from the lungs. An important point is that at equilibrium, the partial pressure of a gas in the liquid phase i.e. solution equals the partial pressure in the gas phase. Thus, if alveolar air has a PO2 of 100 mm Hg, then the capillary blood that equilibrates with alveolar air also will have a PO2 of 100 mm Hg.

Henry's law is used to convert the partial pressure of gas in the liquid phase to the concentration of gas in the liquid phase (e.g., in blood). Where; Cx =Concentration of dissolved gas (mL gas/100 mL blood) and not the gas present in blood in bound form like bound to hemoglobin or plasma protein. Px =Partial pressure of gas (mmHg) Solubility =Solubility of gas in blood (mL gas/100 mL blood/mmHg)

Partial pressure of a gas in inspired air

COMPOSITION OF AIR Partial pressure-gas Ambient air Humidified air
Alveolar air Expired air P O2 158mm 149mm 104mm 120mm P CO2 0.3mm 40mm 28mm P H2O 5.7mm 47mm P N2 596mm 563mm 573mm 565mm Inspiration brings ambient air to the alveoli, where O2 is taken up and CO2 is excreted. Alveolar ventilation thus begins with ambient air. Ambient air is a gas mixture composed of N2 and O2, with minute quantities of CO2, argon, and inert gases. The composition of a gas mixture can be described in terms of either gas fractions or the corresponding partial pressure. Because ambient air is a gas, it obeys the gas laws. Atmospheric air or INSPIRED AIR is humidified in the air passages before reaching the Alveoli. In the Alveoli O2 is absorbed & CO2 is added Expired air is a mixture of Alveolar air & dead space air. Therefore the composition of Inspired air, Humidified air, Alveolar air & Expired air are different.

Alveolar–Blood Gas Exchange

The O2 tension at the mouth can be altered in one of two ways-by changing the fraction of O2 or by changing barometric (atmospheric) pressure. Thus, ambient O2 tension can be increased through the administration of supplemental O2 and is decreased at high altitude

Factors affecting alveolar pCO2
Metabolic Rate An increase in arterial Pco2 results in respiratory acidosis (pH <7.35), whereas a decrease in arterial Pco2 results in respiratory alkalosis (pH >7.45). Hypercapnia is defined as an elevation in arterial Pco2, and it is secondary to inadequate alveolar ventilation (hypoventilation) relative to CO2 production. Conversely, hyperventilation occurs when alveolar ventilation exceeds CO2 production, and it decreases arterial Pco2 (hypocapnia).

Factors affecting alveolar pCO2 2. Alveolar Ventilation
Hyperventilation Hypoventilation inappropriately elevated level of alveolar ventilation, and pACO2 is depressed. inappropriately depressed level of alveolar ventilation, and pACO2 is elevated.

Factors affecting alveolar pO2
The Alveolar Gas Equation

The Effect of pACO2 on pAO2

RESPIRATORY MEMBRANE 1)fluid lining alveolus 2)alveolar epithelium
3)epith basement membrane 4)interstitial space 5)Capillary basement membrane 6)capillary endothelial cell

alveolar–blood gas transfer: Fick law of diffusion
Structural Features That Affect the Rate of Diffusion. A- area , T- thickness Factors That Are Specific to Each Gas Present D- diffusion coefficient, P1-P2 = pressure diff THICKNESS Any factor that increases thickness of membrane 2-3 times will decrease significantly diffusion of gases eg a)Pulmonary edema b) pulmonary fibrosis SURFACE AREA a)When total surface area is decreased to 1/3 or 1/4 of normal, exchange of gases is decreased even at rest eg a) Emphysema b)Removal of one lung

FACTORS DETERMINING DIFFUSION-DIFFUSION COEFFICIENT
DIFFUSION COEFFICIENT=S/√MW Depends on 1) Solubility in water 2)Molecular Weight Though CO2 has greater molecular weight than O2 it is 20 times more soluble in water than O2. CO2 > O2> N2 Therefore CO2 diffuses 20 times more rapidly than O2. O2 Diffuses 2 times more rapidly than N2

Diffusing Capacity of the Respiratory Membrane
In practice, surface area, thickness, and the diffusion coefficient can be combined to yield a constant that describes the lung’s diffusing capacity (DL) for gas. Gas flow across the barrier can then be estimated from: Volume of a gas that will diffuse through the membrane each minute for a partial pressure difference of 1mmHg Q- Conditions that increase Diffusion capacity and conditions that decrease Diffusion capacity

DIFFUSION-LIMITED AND PERFUSION-LIMITED GAS EXCHANGE
Gas exchange across the alveolar/pulmonary capillary barrier is described as either diffusion-limited or perfusion-limited. Diffusion-limited gas exchange means that the total amount of gas transported across the alveolar-capillary is limited by the diffusion process. In these cases, as long as the partial pressure gradient for the gas is maintained, diffusion will continue along the length of the capillary. The equilibrium is not achieved. Perfusion-limited gas exchange means that the total amount of gas transported across the alveolar/capillary membrane is limited by blood flow (i.e., perfusion) through the pulmonary capillaries. In perfusion-limited exchange, the pressure gradient is not maintained, and in this case, the only way to increase the amount of gas transported is by increasing blood flow. Equilibrium is achieved.

Hb does not bind N2O(nitrous oxide), so blood and alveolar partial pressures for N2O equilibrate in <100 ms .Modest changes in barrier architecture have little effect on net uptake. Instead, net N2O uptake is tied to flow. - transfer of this gas is perfusion limited - Increased blood flow will increase gas transfer - This is very soluble in biological tissues and diffuses rapidly. - Capillary pressure for this gas rises rapidly, and Pc=PA - Because there is no pressure gradient, no diffusion occurs after about .1 sec - Fresh blood entering the capillary has not yet equilibrated and can still take up this gas.

Perfusion-Limited Gas Exchange
the transport of N2O across the alveolar/pulmonary capillary barrier PAN2O is constant, and PaN2O is assumed to be zero at the beginning of the pulmonary capillary. Thus, initially, there is a very large partial pressure gradient for N2O between alveolar gas and capillary blood, N2O rapidly diffuses into the pulmonary capillary. Because all of the N22O remains free in blood, all of it creates a partial pressure. Thus, the partial pressure of N2O in pulmonary capillary blood increases very rapidly and is fully equilibrated with alveolar gas in the first one fifth of the capillary. Once equilibration occurs, there is no more partial pressure gradient and, therefore, no more driving force for diffusion. Net diffusion of N2O then ceases, although four fifths of the capillary still remain to be travelled by blood. O2 (under normal conditions) In the first case, a trace amount of nitrous oxide (laughing gas), a common dental anesthetic, is breathed. Nitrous oxide (N2O) is chosen because it diffuses across the alveolar-capillary membrane and dissolves in the blood, but does not combine with hemoglobin

Blood traverses the length of a pulmonary capillary in ∼0.75 s at rest. Equilibration of O2 between alveolar gas and blood occurs within a fraction of this time, so uptake is not normally limited by the rate at which O2 diffuses across the exchange barrier Under normal conditions ,capillary pressure of this gas reaches alveolar pressure of this gas about 1/3 of the distance through the capillary (After HGB is saturated). Therefore under normal conditions transfer is perfusion limited. With exercise, the time blood spends in the capillary is reduced, and this gas is now limited by diffusion limitation.

Perfusion-limited O2 transport
In the lungs of a normal person at rest, O2 transfer from alveolar air into pulmonary capillary blood is perfusion-limited. PAO2 is constant at 100 mm Hg. At the beginning of the capillary, PaO2 is 40 mm Hg, reflecting the composition of mixed venous blood. There is a large partial pressure gradient for O2 between alveolar air and capillary blood, which causes diffusion into the capillary. As O2 is added to pulmonary capillary blood, PaO2 increases. The gradient for diffusion is maintained initially because O2 binds to hemoglobin, which keeps the free O2 concentration in blood and the partial pressure low. Equilibration of O2 occurs about one third of the distance along the capillary, at which point PaO2 becomes equal to PAO2, and unless blood flow increases, there can be no more net diffusion of O2. Thus, under normal conditions, transport is perfusion-limited. Another way of describing perfusion-limited O2 exchange is to say that pulmonary flow determines net O2 transfer. Thus, increases in pulmonary blood flow (e.g., during exercise) will increase amount of O2 transported, and decreases in pulmonary blood flow will decrease the total amount transported

During maximal exercise, however, cardiac output increases, and capillary transit time decreases to <0.4 s. Blood may exit the capillary before being fully O2 saturated .O2 uptake is now considered to be diffusion limited because exchange has been limited by the rate at which O2 diffuses across the blood–gas interface

Diffusion-limited O2 transport
In certain pathologic conditions (e.g., fibrosis) and during strenuous exercise, transfer becomes diffusion limited. Fibrosis: In fibrosis the alveolar wall thickens, increasing the diffusion distance for gases across the wall and decreasing DL which slows the rate of diffusion of O2 and prevents equilibration of O2 between alveolar air and pulmonary capillary blood. In these cases, the partial pressure gradient for O2 is maintained along the entire length of the capillary, converting it to a diffusion-limited process (although not as extreme as in the example of CO). At the end of the pulmonary capillary, equilibration has not occurred between alveolar air and pulmonary capillary blood (PaO2 is less than PAO2), which will be reflected in a decreased PaO2 in systemic arterial blood and decreased PvO2 in mixed venous blood.

O2 diffusion along the length of the pulmonary capillary in normal persons and persons with fibrosis. A, at sea level and B, at high altitude.

O2 transport at high altitude
Ascent to high altitude alters some aspects of the O2 equilibration process. At high altitude, barometric pressure is reduced, and with the same fraction of O2 in inspired air, the partial pressure of O2 in alveolar gas also will be reduced. PAO2 is reduced to 50 mm Hg, compared the normal value of 100 mm Hg. Mixed venous PO2 is 25 mm Hg (as opposed to the normal value of 40 mm Hg). Therefore, at high altitude, the partial pressure gradient for O2 is greatly reduced compared with sea level. Even at the beginning of the pulmonary capillary, the gradient is only 25 mm Hg (50 mm Hg - 25 mmHg) instead of the normal gradient at sea level of 60 mm Hg (100 mm Hg - 40 mm Hg). This reduction of the partial pressure gradient means that diffusion of O2 will be reduced, equilibration will occur more slowly along the capillary, complete equilibration will be achieved at a later point along the capillary (two-thirds of the capillary length at altitude, compared with one third of the length at sea level). The final equilibrated value for PaO2 is only 50mmHg because PAO2 is only 50 mm Hg (it is impossible for the equilibrated value to be higher than 50 mm Hg). The equilibration of O2 at high altitude is exaggerated in a person with fibrosis. Pulmonary capillary blood does not equilibrate even by the end of the capillary, resulting in values for PaO2 as low as 30 mm Hg, which will seriously hamper O2 delivery to the tissues.

Carbon monoxide uptake: Hb binds CO with an affinity that is ∼240 times greater than that for O2. In practice, this means CO molecules bind to Hb as fast as they can diffuse across the exchange barrier, and alveolar CO never has the chance to equilibrate with plasma CO Blood pressure of this gas rises very slowly because it is bound to Hgb, with very little dissolved. -Capillary pressure of this gas does not approach the Alveolar pressure of this gas. - Partial pressure gradient is maintained throughout the time the blood is in the capillary. Diffusion continues throughout this time. - Transfer of this gas is limited by diffusivity (diffusion limited), surface area, and thickness of the wall. A diffusion limitation such as this might be offset by increasing the pressure gradient driving diffusion or by increasing the DL for CO (DLCO).

Diffusion-Limited Gas Exchange
Examples Diffusion-Limited Gas Exchange the transport of CO across the alveolar/pulmonary capillary barrier net diffusion of CO into the pulmonary capillary depends on the magnitude of the partial pressure gradient, is maintained because CO is bound to hemoglobin in capillary blood. Recall that only free, dissolved gas causes a partial pressure. Thus, CO does not equilibrate by the end of the capillary. In fact, if the capillary were longer, net diffusion would continue indefinitely, or until equilibration occurred. the transport of O2 during strenuous exercise and in pathologic conditions such as emphysema and fibrosis.

Carbon Monoxide: A Gas that is Always Diffusion Limited
measuring the volume of carbon monoxide absorbed in a short period and dividing this by the alveolar carbon monoxide partial pressure, one can determine accurately the carbon monoxide diffusing capacity.

11. A patient inspired a gas mixture containing a trace amount of carbon monoxide and then held his breath for 10 sec. During breath holding, the alveolar PCO averaged 0.5 mm Hg and CO uptake was 10 mL/min. What is his pulmonary diffusing capacity (DLCO)? (A) 2.0 mL/min per mm Hg (B) 5.0 mL/min per mm Hg (C) 10 mL/min per mm Hg (D) 20 mL/min per mm Hg (E) 200 mL/min per mm Hg D

Transport of Oxygen and carbon dioxide

Learning objectives At the end of this session students should be able to Define oxygen partial pressure (tension), oxygen content, and percent hemoglobin saturation as they pertain to blood. Interpret an oxyhemoglobin dissociation curve (hemoglobin oxygen equilibrium curve)

Learning objectives Show how the oxyhemoglobin dissociation curve is affected by changes in blood temperature, pH, PCO2, and 2,3-DPG. List the forms in which carbon dioxide is carried in the blood. Identify the percentage of total CO2 transported as each form. Interpret the carbon dioxide dissociation curves for oxy- and deoxyhemoglobin. Describe the interplay between CO2 and O2 binding on hemoglobin that causes the Haldane effect.

Oxygen uptake in the lungs

O2 Transport in blood

Dissolved form: Henry's law deals with gases dissolved in solution (e.g., in blood). Both O2 and CO2 are dissolved in blood (a solution) en route to and from the lungs. An important point is that at equilibrium, the partial pressure of a gas in the liquid phase i.e. solution equals the partial pressure in the gas phase. Thus, if alveolar air has a PO2 of 100 mm Hg, then the capillary blood that equilibrates with alveolar air also will have a PO2 of 100 mm Hg.

The interaction is reversible and is an oxygenation rather than oxidation. DeoxyHb has a relatively low affinity for O2, but each successive O2-binding event produces a conformational change within the protein that incrementally increases the affinity of the other sites

Combined form with hemoglobin

Molecular basis of the sigmoid shape

Association: Mixed-venous blood arrives at an alveolus with a Po2 of 40 mm Hg but an O2 saturation of ∼75%. The cooperative nature of O2 binding to Hb means that the single unoccupied heme group has a very high affinity for O2. This allows the site to capture O2 as fast as it can diffuse across the blood–gas interface, simultaneously maintaining a steep pressure gradient for O2 diffusion across the exchange barrier even as equilibration with alveolar gas occurs. Note that the plateau region of the O2 dissociation curve begins at a Po2 of around 60 mm Hg .In practice, this ensures that saturation still occurs if PAo2 is suboptimal (i.e., 60 mm Hg), either because ventilation is impaired or when cardiac output is increased to the point where perfusion becomes limiting. Dissociation: Once blood arrives at a tissue, Hb must release bound O2 and make it available to mitochondria. Transfer is facilitated by the steepness of the pressure gradient between blood and mitochondria, which maintain a local Po2 of ∼3 mm Hg. Hb begins releasing O2 at a Po2 of 60 mm Hg and delivers ∼60% of total as Po2 falls to 20 mm Hg. Each O2 dissociation event lowers the affinity of the remaining heme groups for bound O2, so that if a tissue’s metabolic rate is very high and its need for O2 is increased, unloading occurs with increased efficiency.

Diffusion of oxygen from a tissue capillary to the cells
Diffusion of oxygen from a tissue capillary to the cells. (Po2 in interstitial fluid = 40 mm Hg, and in tissue cells = 23 mm Hg.)

Pulse oximetry Hb changes color from dark blue to bright red when O2 binds, which makes it possible to monitor arterial O2-saturation levels using noninvasive pulse oximetry. A light-emitting probe is attached to a finger or ear, then the relative amounts of saturated and desaturated Hb is calculated from the amount of light absorbed at 660 nm and 940 nm, respectively.

The blood of a normal person contains about 15 grams of hemoglobin in each 100 milliliters of blood, and each gram of hemoglobin can bind with a maximum of 1.34 milliliters of oxygen. There-fore, 15 times 1.34 equals 20.1 On average, the 15 grams of hemoglobin in 100 milliliters of blood can combine with a total of almost exactly 20 milliliters of oxygen if the hemoglobin is 100 per cent saturated On passing through the tissue capillaries, this amount is reduced, on average, to milliliters (Po2of 40 mm Hg, 75 per cent saturated hemoglobin). Thus, under normal conditions, about 5milliliters of oxygen are transported from the lungs to the tissues by each 100 milliliters of blood flow.

Co-efficient of O2 utilisation

Rightward shifts: Metabolism generates heat and CO2 and acidifies the local environment. All three changes reduce Hb’s O2 affinity and cause it to unload O2. The liberated O2 keeps free (dissolved) O2 levels high and maintains a steep pressure gradient between blood and mitochondria even as blood’s O2 stores are being emptied. 2,3-Diphosphoglycerate: 2,3-Diphosphoglycerate (2,3-DPG) is synthesized from 1,3-DPG, which is an intermediate in the glycolytic pathway. 2,3-DPG is abundant in RBCs, its concentration rivaling that of Hb. 2,3-DPG binds preferentially to the deoxygenated form of Hb and stabilizes it, thereby reducing its O2 affinity .The Hb–O2 dissociation curve shifts to the right, and O2 is unloaded. 2,3-DPG and its effects on O2 affinity is a constant in blood, unlike the effects of temperature, CO2, and H+, which typically remain localized to an active tissue.

Chronic hypoxemia caused by pathologic changes in lung function or living at high altitude stimulates 2,3-DPG production. Increased 2,3-DPG levels shift the Hb–O2 dissociation curve even further to the right, which increases the tissue’s accessibility to available O2 .Although 2,3-DPG does reduce the efficiency of O2 loading by Hb in the lungs, the effects are minor and more than offset by the beneficial effects of assisting O2 delivery to tissues If HbA is stripped of 2,3-DPG, its O2-dissociation curve resembles that of HbF. Storing blood causes 2,3-DPG concentrations to decline over the course of a week, causing a leftward shift in the dissociation curve .Although RBCs replenish lost 2,3-DPG within hours to days of transfusion, giving a critically ill patient large volumes of 2,3-DPG–depleted blood presents some difficulties because such blood does not readily give up its O2.

HbF’s increased O2 affinity compared with the adult form (HbA) reflects the fact that γ-globins bind 2,3-DPG very weakly. 2,3-DPG normally stabilizes the deoxygenated form of HbA and reduces its affinity. HbF’s inability to bind 2,3-DPG favors O2 loading at low partial pressures.

Aerobic metabolism generates CO2 and causes tissue Pco2 to rise
Aerobic metabolism generates CO2 and causes tissue Pco2 to rise. CO2 binds to terminal globin amino groups and decreases Hb’s O2 affinity. The Hb–O2 dissociation curve shifts to the right, and O2 is unloaded. CO2 also dissolves in water to yield free acid, which promotes further O2 unloading via the Bohr effect

BOHR EFFECT The PH of the blood falls as its CO2 content increases

CO is formed by combustion of hydrocarbons
CO is formed by combustion of hydrocarbons. Common sources of exposure include automobile exhaust, poorly ventilated heating systems, and smoke. Carboxyhemoglobin comprises up to ∼3% of total Hb in nonsmokers, increasing to 10%–15% in smokers

CO poisoning

CO poisoning CO decreases O2 bound to hemoglobin and also causes a left shift of the O2-hemoglobin dissociation curve. CO binds to hemoglobin with an affinity that is 250 times that of O2 to form carboxyhemoglobin. the presence of CO decreases the number of O2-binding sites available on hemoglobin. Reduces O2 content of blood and O2 delivery to tissues

Use the following diagram of oxyhemoglobin saturation curves

What is the P50of the oxyhemoglobin curve labeled A in the diagram. a
What is the P50of the oxyhemoglobin curve labeled A in the diagram? a. 80 mmHg b. 60 mmHg c. 40 mmHg d. 30 mmHg e. 20 mmHg Which of the following conditions is most likely to shift the above oxyhemoglobin curve from A to B? a. Increased temperature b. Exercise c. Acclimatization to high altitude d. Hyperventilation e. Metabolic acidosis

Which of the following conditions causes a decrease in arterial O2 saturation without a decrease in O2tension? a. Anemia b. Carbon monoxide poisoning c. A low V/Q ratio d. Hypoventilation e. Right-to-left shunt

Which one of the above oxyhemoglobin saturation curves was obtained from fetal blood? a. A b. B c. C d. D e. E

Which one of the above oxyhemoglobin saturation curves was obtained from blood exposed to carbon monoxide? a. A b. B c. C d. D e. E

TRANSPORT OF CARBON DIOXIDE

In the tissues, CO2 is produced from aerobic metabolism
In the tissues, CO2 is produced from aerobic metabolism. CO2 then diffuses across the cell membranes and across the capillary wall, into the red blood cells by simple diffusion, driven by the partial pressure gradient for CO2. Carbonic anhydrase is found in high concentration in red blood cells. It catalyzes the hydration of CO2 to form H2CO3. In the red blood cells, H2CO3 dissociates into H+ and HCO3-. The H+ remains in the red blood cells, where it will be buffered by deoxyhemoglobin, and the HCO3- is transported into the plasma in exchange for Cl- (chloride) i.e. chloride shift. H+ is buffered by deoxyhemoglobin. Deoxyhemoglobin is a better buffer than oxyhemoglobin. The bicarbonate that is formed in the red blood cell is carried in the plasma compartment. All of the reactions described here occur in reverse in the lungs. H+ is released from its buffering sites on deoxyhemoglobin, HCO3 - enters the red blood cells in exchange for Cl-. H+ and HCO3- combine to form H2CO3, and H2CO3 dissociates into CO2 and H2O. The regenerated CO2 and H2O are expired by the lungs

The H+ released during HCO3− formation remains trapped in RBCs by the cell membrane, which is relatively impermeable to cations. This might be expected to lower intracellular pH, but H+ accumulation occurs at the precise moment that Hb is releasing O2 and undergoing a conformational change that favors H+ binding. As noted above (i.e., the Bohr effect), H+ binding actually facilitates O2 unloading by shifting the Hb–O2 dissociation curve to the right and reducing Hb’s affinity for O2. Virtually all of the acid excess caused by loss of HCO3− to the plasma is buffered by Hb. With intracellular H+ kept low by Hb and the Cl−-HCO3− exchanger keeping HCO3− low, the reaction catalyzed by CA remains biased in favor of increased H+ and HCO3− formation. The CO2-carrying capacity of blood increases as a result.

Transport of Carbon dioxide
Dissolved Carbon Dioxide 5% of the total CO2 content of blood Carbon dioxide is 20 times more soluble in blood than oxygen is. Carbamino Compound Carbon dioxide reacts with terminal amine groups of proteins(Hb) to form carbamino compounds. The protein involved appears to be almost exclusively hemoglobin and this binding is responsible for Bohr effect. Reversly, O2 bound to Hb changes its affinity for CO2, such that when less O2 is bound, the affinity of hemoglobin for CO2 increases called the Haldane effect. About 5% of the total CO2 is carried as carbamino compounds. The attachment sites that bind CO2 are different from the sites that bind O2.

BOHR EFFECT The PH of the blood falls as its CO2 content increases

Bicarbonate About 90% of the CO2 is carried as plasma bicarbonate. In order to convert CO2 into bicarbonate or the reverse, carbonic anhydrase (CA) enzyme must be present. Plasma contains no carbonic anhydrase; therefore, there can be no significant conversion of CO2 to HCO3- in this compartment.

All of the reactions described here occur in reverse in the lungs.
H+ is released from its buffering sites on deoxyhemoglobin, HCO3 - enters the red blood cells in exchange for Cl-. H+ and HCO3- combine to form H2CO3, and H2CO3 dissociates into CO2 and H2O. The regenerated CO2 and H2O are expired by the lungs

REVERSED CHLORIDE SHIFT

. The degree of Hgb saturation with O2 has a major effect on the CO2 dissociation curve. Although O2 and CO2 bind to Hgb at different sites, deoxygenated Hgb has greater affinity for CO2 than oxygenated Hgb does. Thus, deoxygenated blood (venous blood) freely takes up and transports more CO2 than oxygenated arterial blood does. The deoxygenated Hgb more readily forms carbamino compounds and also more readily binds free H+ ions released during the formation of HCO3-. The effect of changes in oxyhemoglobin saturation on the relationship of CO2 content to Pco2 is referred to as the Haldane effect and is reversed in the lung when O2 is transported from the alveoli to red blood cells. This effect is illustrated by a shift to the left in the CO2 dissociation curve in venous blood as compared with arterial blood

Gas Exchange and Alveolar Ventilation

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