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)
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