this unit covered a few basic biochemical ideas about the way that oxygen and carbon dioxide are transported by the blood. oxygen is mainly transported in the bound form to hemoglobin, oxyhemoglobin, and thus the uptake and release of oxygen to and from the blood is governed by the oxyhemoglobin saturation curve, a sigmoidal shaped curve which describes the relative saturation of oxygen for a given PO2. this graph ties in with the previous lecture on gas exchange, in which we covered all the PO2 and PCO2s for the atmosphere, arteries, body tissues, and veins. looking at these numbers using the dissociation curve, we find that at the arterial PO2 of 95 mmHg, hemoglobin is ~97% saturated and at the venous PO2 of 40 mmHg, hemoglobin is ~70% saturated -- this difference in saturation represents oxygen's unloading from the blood. we then look at factors that can shift the dissociation curve to the right (essentially saying that for a given partial pressure, hemoglobin affinity for oxygen has decreased). these factors are: increased H+ production, which causes conformational changes in hemoglobin that reduces its affinity to oxygen, increased temperature, and increased 2,3-DPG, which competes for O2 binding sites on Hb.
carbon dioxide is transported as a dissolved gas (7%), bound to hemoglobin (23%), but mainly in the form of bicarbonate ion (70%). this conversion to bicarbonate is facilitated by carbonic anhydrase, which converts dissolved CO2 into carbonic acid, H2CO3, which then dissociates into H+ and bicarbonate ion, HCO3-. this reaction is important because it also is the common pathway which describes the mechanism for both the bohr and the haldane effect. the bohr effect can be summed up as: increased CO2 production in body tissues and uptake into the blood facilitates O2 release into tissues. this occurs when CO2 is converted to carbonic acid, and thus H+ and bicarbonate-- the H+ binds to hemoglobin and as described above decreases its affinity for O2, allowing it to be released into the tissues. the haldane effect is the opposite: increased O2 uptake in the lungs facilitates CO2 release. this happens because O2 binds to hemoglobin and causes the release of H+ protons, which then combine with bicarbonate and form carbonic acid, which is converted back into CO2 via carbonic anhydrase, which is then released into the air.
questions
1. what are the ways in which O2 is transported in the blood and the relative percentage of each?
2. what is the saturation level of hemoglobin in arterial blood?
3. what is the saturation level of hemoglobin in venous blood?
4. what would the saturation level of hemoglobin be if PO2 was at 160mmHg, the atmospheric PO2?
5. what are three factors that can shift the hemoglobin saturation curve to the right?
6. what are the ways in which CO2 is transported in the blood and the relative percentage of each?
7. describe the formation of bicarbonate ion from dissolved CO2.
8. what is the enzyme that catalyzes the formation of carbonic acid?
9. what is the "chloride shift"?
10. describe the bohr effect.
11. describe the haldane effect.
answers
1. 3% as a dissolved gas, 97% bound to hemoglobin.
2. ~97%
3. 70%
4. >99%
5. decreased pH, increased temperature, increased concentration of 2,3-DPG
6. 7% as a dissolved CO2 gas, 23% bound to hemoglobin, 70% as bicarbonate ion.
7. dissolved CO2 + H2O -> H2CO3 (carbonic acid) -> H+ and bicarbonate ion.
8. carbonic anhydrase.
9. Cl- moving into cells to balance the H+ that is being dissociated from carbonic acid.
10. the bohr effect refers to hemoglobin's decreased affinity for O2 in the tissues which is caused by the increase in H+ concentration which binds to hemoglobin and changes its conformation. the increased H+ concentration in the tissues is due to higher CO2 levels from metabolism, which is converted into carbonic acid, which dissociates into H+ and bicarbonate. in short: increased CO2 in the tissues causes decreased hemoglobin affinity for O2.
11. the haldane effect is analogous to the bohr effect except in the reverse order; increased O2 in the lungs causes CO2 to be released from the blood.
Showing posts with label gas exchange. Show all posts
Showing posts with label gas exchange. Show all posts
Saturday, December 6, 2008
Saturday, November 29, 2008
organ systems: gas exchange
this unit is the second of dr. kaminski's guest lecture on respiration and looks at the mechanism for gas exchange in the lungs and body tissues. the first section is an introduction to the rules governing gas exchange in general. gas exchange in the lungs is a study of the diffusion of gases, which depends on several factors: anatomical features of the lung (area of the surface that the gas can diffuse across, and distance it has to traverse), chemical characteristics of the gas itself (solubility coefficient, molecular weight), and the partial pressures / concentration gradient of the gases. the first two factors do not govern gas exchange behavior because they are relatively static, but the partial pressures of the gases are dynamic and are the driving force behind gas exchange. the diffusion equation can thus be represented by d=P*(A/D)*(S/sqrtMW), which collapses to d=P*constant.
the partial pressures of the different gases are in turn influenced by several factors: the natural mixing and exchange of gases that occurs during ventilation (a complete change of air takes more than 10 breaths), humidification of the air in the alveoli in which higher H2O partial pressure displaces others, ventilation characteristics (the rate and depth of breathing), and the flow of O2 into the blood and the flow of CO2 out from the blood. the partial pressure's relationship to ventilation is further explored- for O2, when O2 consumption is decreased, or ventilation is increased, then PO2 in the alveoli increases. for CO2, if ventilation is decreased or CO2 production is increased, then PCO2 in the alveoli is increased.
we then look at another aspect of gas exchange, the ventilation perfusion ratio. this is a ratio of the air that is coming into the alveoli vs. the blood that is coming in to exchange gas. if the V/Q ratio is high, this indicates that airflow is high but blood flow is inadequate, which results in physiologic dead space (as opposed to anatomical dead space, which is basically the upper airways that do not take place in gas exchange) and subsequent shriveling of alveoli. if the V/Q ratio is low, this generally indicates an obstructed airway, which can result in "shunting" of deoxygenated blood back into the heart to be pumped back into the body. one of the body's strategies to deal with a low V/Q ratio is to vasoconstrict the blood going to the affected areas, which diverts the blood to working alveoli and reduces the amount of blood that is shunted.
the unit also looks at the whole cycle of gas exchange in relation to partial pressures, starting in the atmosphere, into the lungs, into the body tissues, and back out into the lungs and atmosphere. the general rule of thumb is that gas will flow from a region of higher to lower partial pressure. the atmospheric pressure is 760mmHg, out of which 79% is N2, 21% is O2, and ~0% is CO2, yielding a PO2 of 160mmHg and a PCO2 of roughly 0. following O2 first: when air comes into the alveoli, it drops from 160mmHg to 105mmHg because it is transported into the blood which has a lower PO2 of 40mmHg. however, due to the shunting of deoxygenated blood described above, the PO2 in the arteries drops an additional ~10mmHg to 95mmHg. when it reaches the capillaries, it flows out into the extracellular matrix, which has a PO2 of 40mmHg, then into the body tissue cells, which have a PO2 of ~25mmHg, and finally into the mitochondria, which have the lowest PO2 of ~5mmHg. the venous blood is left with a PO2 of 40mmHg and returns to the lungs to restart the cycle.
CO2 starts with a negligible partial pressure in the atmosphere, but in the alveoli PCO2 rises to 40mmHg after accepting CO2 from venous blood. arterial blood has the same PCO2 and as the blood flows into the body tissues, the higher PCO2 of 45mmHg causes CO2 to be loaded into the blood. although this difference in partial pressure is much less than that of O2 (compare O2's ~50mmHg difference to CO2's ~5mmHg difference), it is adequate due to CO2's high solubility and diffusibility (20 times that of oxygen). the venous blood contains 45mmHg PCO2, which causes it to unload CO2 into the alveoli, which has the lower 40mmHg PCO2.
questions
1. what is air composed of? what is the breakdown in terms of mmHg?
2. describe the change of H2O partial pressure when air enters the alveoli.
3. describe CO2's solubility and diffusibility.
4. what are the three factors that diffusion of a gas depends on? which of these factors are relatively static and which are dynamic?
5. what are the two factors in lung histology that affect gas diffusion?
6. what are the four barriers that gas must traverse in the alveoli?
7. what are some anatomical factors that could lower gas exchange?
8. what are the two factors in gas solubility that affect gas diffusion?
9. what is henry's law in relation to gas exchange?
10. what is the complete diffusion equation using all factors mentioned previously? what does it collapse down to and why?
11. describe the changes in partial pressures of CO2 and O2 when gas goes from the atmosphere into the lungs.
12. what are the five factors that influence partial pressures of gases in the lungs?
13. describe the relationship of alveolar PO2 to ventilation rate and O2 consumption rate.
14. describe the relationship of alveolar PCO2 to ventilation rate and CO2 production rate.
15. what is the PCO2 and PO2 in the arteries, body tissues, and veins?
16. what is the ventilation perfusion ratio?
17. what happens with a low ventilation perfusion ratio?
18. what happens with a high ventilation perfusion ratio?
19. what are normal values for V, Q and the ratio?
20. how do different areas of the lung differ in the V/Q ratio?
21. what is a mechanism that reduces the need for physiologic shunting with a low V/Q ratio?
22. oxygenation happens in...
23. describe the oxygenation of body tissues in terms of partial pressure.
24. describe the diffusion of CO2 into the blood in terms of partial pressure.
answers
1. 79% N2, 21% O2-- 600mmHg N2, 160mmHg O2.
2. H2O partial pressure jumps from basically zero to 47mmHg.
3. CO2 is much more soluble in water than O2, and 20X more diffusable.
4. lung histology/anatomy, concentration gradient/partial pressure of the gas, and solubility of the gas. only the concentration gradient/partial pressure is dynamic and is the main vehicle for gas exchange.
5. area of diffusion (larger area, more diffusion), distance that gas diffuses (more distance, less diffusion)
6. type 1 pneumocyte cells, basement membrane of type 1 cell, basement membrane of capillary, type 1 capillary.
7. damaging or thickening of the alveolar wall, extra fluid or material in the alveoli.
8. molecular weight (sqrt(MW)) and solubility coefficient (S).
9. dissolved gas = solubility X partial pressure
10. D= (P*A*S)/(d*sqrt(MW)). it collapses down to D=P because the A/d and S/MW terms are relatively constant.
11. in atmosphere, CO2=0 and O2=160. in lungs, CO2=40 and O2=105.
12. the mixture of fresh vs. old air in the lungs which contain different proportions of gases (takes ~15 breaths to completely exchange air), humidification of air which causes H2O partial pressure to rise and all others to fall, O2 diffusion into capillaries, CO2 diffusion into the lungs, and ventilation characteristics.
13. alveolar PO2 is proportional to ventilation rate and inversely proportional to O2 consumption.
14. alveolar PCO2 is inversely proportional to ventilation rate and proportional to CO2 production.
15. in arteries, PO2 is 95mmHg and PCO2 is 40mmHg. in body tissues PO2 is 40mmHg and PCO2 is 45mmHg. in veins PO2 is 40mmHg and PCO2 is 45mmHg.
16. the ratio of the flow of air in the alveoli to the blood flow in the alveolar capillaries.
17. this can occur when the airways become blocked, not allowing any air to flow into the alveoli. in this case, the deoxygenated blood is shunted past the non functional alveoli and joins the normal oxygenated blood.
18. this can occur when the blood flow to an alveoli is obstructed, causing the pressures inside the alveoli to match the atmospheric pressure (since there is no gas exchange), forming physiological dead space (as opposed to anatomical).
19. V=4.2, Q=5, V/Q=0.84
20. the top part of the lung has lower blood pressure and therefore a higher V/Q ratio, which can cause collapse of some alveoli (from the creation of the physiologic dead space). lower part of the lung has higher hydrostatic blood pressure and therefore a lower V/Q ratio, which can lead to the shunting described above. the middle part generally has a good V/Q ratio. during exercise, the increased blood pressure and flow causes a more even and efficient V/Q ratio.
21. if the airflow is obstructed in a certain area of the lung, the pulmonary blood vessels can vasoconstrict and redirect the blood flow to unaffected areas, reducing the need for shunting of the blood.
22. the first third of the capillary space.
23. the O2 diffuses from regions of higher to lower PO2. arterial blood has a PO2 of 95mmHg, and when the blood reaches the capillaries, it diffuses out into the extracellular matrix which has a PO2 of ~40mmHg. from there, it enters body tissue cells, which have a lower PO2 of ~25mmHg, and inside the cell diffuses into the mitochondria, which has the lowest PO2 of ~5mmHg.
24. arterial blood has a PCO2 of 40mmHg. when it reaches the capillaries, it is loaded with more CO2 from the body tissues, which have a PCO2 of 45mmHg. although the gas exchange only happens within 1 sec and with a max pressure differential of 5mmHg, gas exchange is still effective due to CO2's huge solubility (20X that of O2)
the partial pressures of the different gases are in turn influenced by several factors: the natural mixing and exchange of gases that occurs during ventilation (a complete change of air takes more than 10 breaths), humidification of the air in the alveoli in which higher H2O partial pressure displaces others, ventilation characteristics (the rate and depth of breathing), and the flow of O2 into the blood and the flow of CO2 out from the blood. the partial pressure's relationship to ventilation is further explored- for O2, when O2 consumption is decreased, or ventilation is increased, then PO2 in the alveoli increases. for CO2, if ventilation is decreased or CO2 production is increased, then PCO2 in the alveoli is increased.
we then look at another aspect of gas exchange, the ventilation perfusion ratio. this is a ratio of the air that is coming into the alveoli vs. the blood that is coming in to exchange gas. if the V/Q ratio is high, this indicates that airflow is high but blood flow is inadequate, which results in physiologic dead space (as opposed to anatomical dead space, which is basically the upper airways that do not take place in gas exchange) and subsequent shriveling of alveoli. if the V/Q ratio is low, this generally indicates an obstructed airway, which can result in "shunting" of deoxygenated blood back into the heart to be pumped back into the body. one of the body's strategies to deal with a low V/Q ratio is to vasoconstrict the blood going to the affected areas, which diverts the blood to working alveoli and reduces the amount of blood that is shunted.
the unit also looks at the whole cycle of gas exchange in relation to partial pressures, starting in the atmosphere, into the lungs, into the body tissues, and back out into the lungs and atmosphere. the general rule of thumb is that gas will flow from a region of higher to lower partial pressure. the atmospheric pressure is 760mmHg, out of which 79% is N2, 21% is O2, and ~0% is CO2, yielding a PO2 of 160mmHg and a PCO2 of roughly 0. following O2 first: when air comes into the alveoli, it drops from 160mmHg to 105mmHg because it is transported into the blood which has a lower PO2 of 40mmHg. however, due to the shunting of deoxygenated blood described above, the PO2 in the arteries drops an additional ~10mmHg to 95mmHg. when it reaches the capillaries, it flows out into the extracellular matrix, which has a PO2 of 40mmHg, then into the body tissue cells, which have a PO2 of ~25mmHg, and finally into the mitochondria, which have the lowest PO2 of ~5mmHg. the venous blood is left with a PO2 of 40mmHg and returns to the lungs to restart the cycle.
CO2 starts with a negligible partial pressure in the atmosphere, but in the alveoli PCO2 rises to 40mmHg after accepting CO2 from venous blood. arterial blood has the same PCO2 and as the blood flows into the body tissues, the higher PCO2 of 45mmHg causes CO2 to be loaded into the blood. although this difference in partial pressure is much less than that of O2 (compare O2's ~50mmHg difference to CO2's ~5mmHg difference), it is adequate due to CO2's high solubility and diffusibility (20 times that of oxygen). the venous blood contains 45mmHg PCO2, which causes it to unload CO2 into the alveoli, which has the lower 40mmHg PCO2.
questions
1. what is air composed of? what is the breakdown in terms of mmHg?
2. describe the change of H2O partial pressure when air enters the alveoli.
3. describe CO2's solubility and diffusibility.
4. what are the three factors that diffusion of a gas depends on? which of these factors are relatively static and which are dynamic?
5. what are the two factors in lung histology that affect gas diffusion?
6. what are the four barriers that gas must traverse in the alveoli?
7. what are some anatomical factors that could lower gas exchange?
8. what are the two factors in gas solubility that affect gas diffusion?
9. what is henry's law in relation to gas exchange?
10. what is the complete diffusion equation using all factors mentioned previously? what does it collapse down to and why?
11. describe the changes in partial pressures of CO2 and O2 when gas goes from the atmosphere into the lungs.
12. what are the five factors that influence partial pressures of gases in the lungs?
13. describe the relationship of alveolar PO2 to ventilation rate and O2 consumption rate.
14. describe the relationship of alveolar PCO2 to ventilation rate and CO2 production rate.
15. what is the PCO2 and PO2 in the arteries, body tissues, and veins?
16. what is the ventilation perfusion ratio?
17. what happens with a low ventilation perfusion ratio?
18. what happens with a high ventilation perfusion ratio?
19. what are normal values for V, Q and the ratio?
20. how do different areas of the lung differ in the V/Q ratio?
21. what is a mechanism that reduces the need for physiologic shunting with a low V/Q ratio?
22. oxygenation happens in...
23. describe the oxygenation of body tissues in terms of partial pressure.
24. describe the diffusion of CO2 into the blood in terms of partial pressure.
answers
1. 79% N2, 21% O2-- 600mmHg N2, 160mmHg O2.
2. H2O partial pressure jumps from basically zero to 47mmHg.
3. CO2 is much more soluble in water than O2, and 20X more diffusable.
4. lung histology/anatomy, concentration gradient/partial pressure of the gas, and solubility of the gas. only the concentration gradient/partial pressure is dynamic and is the main vehicle for gas exchange.
5. area of diffusion (larger area, more diffusion), distance that gas diffuses (more distance, less diffusion)
6. type 1 pneumocyte cells, basement membrane of type 1 cell, basement membrane of capillary, type 1 capillary.
7. damaging or thickening of the alveolar wall, extra fluid or material in the alveoli.
8. molecular weight (sqrt(MW)) and solubility coefficient (S).
9. dissolved gas = solubility X partial pressure
10. D= (P*A*S)/(d*sqrt(MW)). it collapses down to D=P because the A/d and S/MW terms are relatively constant.
11. in atmosphere, CO2=0 and O2=160. in lungs, CO2=40 and O2=105.
12. the mixture of fresh vs. old air in the lungs which contain different proportions of gases (takes ~15 breaths to completely exchange air), humidification of air which causes H2O partial pressure to rise and all others to fall, O2 diffusion into capillaries, CO2 diffusion into the lungs, and ventilation characteristics.
13. alveolar PO2 is proportional to ventilation rate and inversely proportional to O2 consumption.
14. alveolar PCO2 is inversely proportional to ventilation rate and proportional to CO2 production.
15. in arteries, PO2 is 95mmHg and PCO2 is 40mmHg. in body tissues PO2 is 40mmHg and PCO2 is 45mmHg. in veins PO2 is 40mmHg and PCO2 is 45mmHg.
16. the ratio of the flow of air in the alveoli to the blood flow in the alveolar capillaries.
17. this can occur when the airways become blocked, not allowing any air to flow into the alveoli. in this case, the deoxygenated blood is shunted past the non functional alveoli and joins the normal oxygenated blood.
18. this can occur when the blood flow to an alveoli is obstructed, causing the pressures inside the alveoli to match the atmospheric pressure (since there is no gas exchange), forming physiological dead space (as opposed to anatomical).
19. V=4.2, Q=5, V/Q=0.84
20. the top part of the lung has lower blood pressure and therefore a higher V/Q ratio, which can cause collapse of some alveoli (from the creation of the physiologic dead space). lower part of the lung has higher hydrostatic blood pressure and therefore a lower V/Q ratio, which can lead to the shunting described above. the middle part generally has a good V/Q ratio. during exercise, the increased blood pressure and flow causes a more even and efficient V/Q ratio.
21. if the airflow is obstructed in a certain area of the lung, the pulmonary blood vessels can vasoconstrict and redirect the blood flow to unaffected areas, reducing the need for shunting of the blood.
22. the first third of the capillary space.
23. the O2 diffuses from regions of higher to lower PO2. arterial blood has a PO2 of 95mmHg, and when the blood reaches the capillaries, it diffuses out into the extracellular matrix which has a PO2 of ~40mmHg. from there, it enters body tissue cells, which have a lower PO2 of ~25mmHg, and inside the cell diffuses into the mitochondria, which has the lowest PO2 of ~5mmHg.
24. arterial blood has a PCO2 of 40mmHg. when it reaches the capillaries, it is loaded with more CO2 from the body tissues, which have a PCO2 of 45mmHg. although the gas exchange only happens within 1 sec and with a max pressure differential of 5mmHg, gas exchange is still effective due to CO2's huge solubility (20X that of O2)
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