this is the last unit in dr. kaminski's guest lecture on respiration and talks about the control and regulation of respiration. it focuses on the "respiratory group", which is an area in the upper medulla and contains four different groupings of neurons: the dorsal respiratory group, the ventral respiratory group, the pneumotaxic center, and the chemisensitive area. the dorsal group contains motor neurons which innervate the muscles involved in inspiration ("inspiratory neurons") as well as afferent sensory neurons. most of the impetus for inspiration comes from the dorsal respiratory group. during normal restful breathing, these neurons fire to stimulate the inspiratory muscles, and expiration occurs due to relaxation of the muscles and elastic recoil of the ribcage. in vigorous, more ribcage based breathing, the ventral respiratory center gets stimulated as well, which has inspiratory as well as expiratory neurons-- this causes both the inspiratory muscles to be activated during inspiration (external intercostals, SCM, scalenes, etc) as well as the expiratory muscles during expiration (rectus abdominis and internal intercostals).
we then look at the different factors that can affect this rhythm. the pneumotaxic center inhibits the neurons of the dorsal and ventral respiratory center, specifically causing the amplitude of the "inspiratory ramp signal" to decrease. this causes more shallow, rapid breathing. the central chemoreceptor (of the "chemosensitive area") detects levels of H+ in the cerebrospinal fluid-- H+ in the CSF is directly representative of CO2 levels because the only H+ that is beyond the blood brain barrier is that which is produced from the dissociation of carbonic acid, which is formed from CO2. if H+ levels rise, the chemosensitive area stimulates the dorsal inspiratory neurons to increase the ramp signal. peripheral chemoreceptors are a secondary chemical feedback system and are located near the aorta and carotid artery and measure O2 levels -- if PO2 falls below 100mmHg, they also activate the dorsal respiratory group.
a couple other ways in which ventilation can be regulated: via stretch receptors in the lungs, which inhibit the dorsal inspiratory neurons if the pressure from inspiration becomes too great-- this is called the hering breuer reflex. conscious control of breathing from higher brain centers can bypass the respiratory group completely and innervate the thoracic muscles directly.
questions
1. where is the "neurogenesis" of the respiratory drive?
2. what is the "respiratory control center" and where is it located?
3. what are the different neuronal groupings of the respiratory control center?
4. describe the dorsal respiratory group.
5. describe the ventral respiratory group.
6. describe the pneumotaxic center.
7. describe the chemosensitive area.
8. within the respiratory control center, where does the main respiratory drive come from?
9. describe how the inspiratory neurons control breathing.
10. describe the effect of the pneumotaxic center on the depth of breathing.
11. describe what happens in the respiratory center during vigorous breathing.
12. what are the three factors that can modify the ventilation cycle?
13. describe how the higher brain centers modify the ventilation cycle.
14. what is the hering breuer reflex?
15. where is the central chemoreceptor and what does it measure?
16. why does the central chemoreceptor measure H+ levels?
17. what does the central chemoreceptor stimulate?
18. describe the peripheral chemoreceptors.
answers
1. the medullary centers
2. a set of neuronal groupings that are found in the upper medulla and pons.
3. dorsal respiratory group, ventral respiratory group, pneumotaxic center, chemosensitive area.
4. contains inspiratory neurons and afferent sensory neurons.
5. contains both inspiratory and expiratory neurons.
6. inhibits the inspiratory neurons of the respiratory groups.
7. wired into the dorsal inspiratory neurons, has neurons that are sensitive to the chemistry of CSF.
8. inspiratory neurons of the dorsal respiratory group.
9. inspiratory neurons have a rhythm in the form of a "ramp signal" that signals the diaphragm. the faster the inspiratory neurons fire, the more the diaphragm is stimulated to contract via the phrenic nerve.
10. the pneumotaxic center inhibits inspiratory neurons and thus greater pneumotaxic activity facilitates shallow, rapid breathing.
11. during vigorous breathing, the ventral inspiratory and expiratory neurons get activated and both the inspiratory and expiratory muscles get activated.
12. voluntary override by higher centers of the brain, physical input from stretch receptors in the lung, evaluation of blood chemistry.
13. corticospinal and corticobulbar tracts connect directly to lower motor neurons of thoracic musculature, bypassing the respiratory control center.
14. when stretch receptors in the lung are activated by inspiration and inhibit the inspiratory neurons of the dorsal respiratory group.
15. in the "chemosensitive area" on the ventral surface of the medulla.
16. H+ is representative of CO2 levels since CO2 converts into carbonic acid, which dissociates into H+ and bicarbonate. furthermore, H+ does not cross the blood brain barrier, so it is directly representative of CO2.
17. the dorsal respiratory group.
18. the peripheral chemoreceptors are the aortic and carotid bodies, which sense O2 levels and begin firing if O2 levels fall below 100mmHg, stimulating the dorsal respiratory group.
Showing posts with label respiration. Show all posts
Showing posts with label respiration. Show all posts
Sunday, December 7, 2008
Thursday, December 4, 2008
histology: the respiratory system
this section traces the passage of air from the trachea to the capillaries in the alveolus. the trachea is the largest tube in the respiratory system which is bolstered by 20 or so cartilage rings and smooth muscle. it has a PSCC epithelium with goblet cells and tracheal glands in the submucosa. the trachea then branches into the brochi, which have smatterings of cartilage and are like smaller versions of the trachea. bronchioles (from organ systems: primary for each lung, secondary for each lobe, tertiary for each bronchopulmonary segment) have no cartilage, and epithelium which begins to transition from PSC to simple columnar. terminal bronchioles are the last section of the airway that does not take place in gas exchange, and they have simple columnar epithelium with no goblet cells. next comes the respiratory bronchioles, where gas exchange begins to take place, which have simple cuboidal epithelium and the beginnings of alveoli protruding out from the walls. these transition into alveolar ducts, which are basically smaller respiratory bronchioles with simple squamous epithelium and many alveolar sacs. finally, the air reaches the alveolar sac, which is the end of the passageway.
between the alveolar sacs is the interalveolar septum, where gas exchange with blood actually takes place. this border is lined with type 1 and 2 pneumocytes, involved in gas exchange and surfactant secretion, respectively. thus, in order to reach the blood, gas has to diffuse through: type 1 pneumocyte cell, type 1 pneumocyte basement membrane, endothelial basement membrane, endothelial cell. also between the interalveolar septum are some fibroblasts, alveolar phagocytes, and a scant CT matrix called the zona diffusa.
questions
1. describe the passage of air from the trachea to the alveoli.
2. describe the physical support of the trachea
3. describe the layers of the trachea.
distinguishing characteristics of:
4. bronchi...
5. bronchiole...
6. terminal bronchiole...
7. respiratory bronchiole...
8. alveolar duct...
9. alveolar sac...
10. what are the two alveolar surfaces formed by epithelia?
11. what is inside the interalveolar septa?
12. describe the barrier between blood and air in the alveoli.
answers
1. trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.
2. ~20 cartilage rings with smooth muscle (trachealis) spanning the posterior openings.
3. PSCC in mucosa with goblet cells, sometimes diffuse lymphatic tissue. submucosa of CT and tracheal glands. hyaline cartilage layer, then adventitia.
4. fragmented hyaline cartilage, PSCC with goblet cells.
5. smooth muscle but no cartilage, PSCC to simple columnar epithelium with goblet cells.
6. simple columnar, cilia but no goblet cells. clara cells secrete lipoprotein surfactant.
7. beginning of gas exchange; alveoli begin to protrude through walls. simple cuboidal epithelium with no cilia.
8. like a smaller respiratory bronchiole with many alveolar sacs.
9. terminal room of alveoli at ends of ducts, simple squamous epithelium.
10. type 1 pneumocytes which allow for gas exchange and type 2 pneumocytes which secrete surfactant.
11. CT matrix called zona diffusa, fibroblasts, alveolar phagocytes, capillaries. zone fiber phago cap
12. pneumocyte, pneumocyte basement membrane, endothelium basement membrane, endothelium.
between the alveolar sacs is the interalveolar septum, where gas exchange with blood actually takes place. this border is lined with type 1 and 2 pneumocytes, involved in gas exchange and surfactant secretion, respectively. thus, in order to reach the blood, gas has to diffuse through: type 1 pneumocyte cell, type 1 pneumocyte basement membrane, endothelial basement membrane, endothelial cell. also between the interalveolar septum are some fibroblasts, alveolar phagocytes, and a scant CT matrix called the zona diffusa.
questions
1. describe the passage of air from the trachea to the alveoli.
2. describe the physical support of the trachea
3. describe the layers of the trachea.
distinguishing characteristics of:
4. bronchi...
5. bronchiole...
6. terminal bronchiole...
7. respiratory bronchiole...
8. alveolar duct...
9. alveolar sac...
10. what are the two alveolar surfaces formed by epithelia?
11. what is inside the interalveolar septa?
12. describe the barrier between blood and air in the alveoli.
answers
1. trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.
2. ~20 cartilage rings with smooth muscle (trachealis) spanning the posterior openings.
3. PSCC in mucosa with goblet cells, sometimes diffuse lymphatic tissue. submucosa of CT and tracheal glands. hyaline cartilage layer, then adventitia.
4. fragmented hyaline cartilage, PSCC with goblet cells.
5. smooth muscle but no cartilage, PSCC to simple columnar epithelium with goblet cells.
6. simple columnar, cilia but no goblet cells. clara cells secrete lipoprotein surfactant.
7. beginning of gas exchange; alveoli begin to protrude through walls. simple cuboidal epithelium with no cilia.
8. like a smaller respiratory bronchiole with many alveolar sacs.
9. terminal room of alveoli at ends of ducts, simple squamous epithelium.
10. type 1 pneumocytes which allow for gas exchange and type 2 pneumocytes which secrete surfactant.
11. CT matrix called zona diffusa, fibroblasts, alveolar phagocytes, capillaries. zone fiber phago cap
12. pneumocyte, pneumocyte basement membrane, endothelium basement membrane, endothelium.
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)
Tuesday, November 25, 2008
organ systems: pulmonary ventilation
pulmonary ventilation is the first unit in dr. kaminski's guest lecture on the physiology of respiration. it reviews the mechanisms for breathing and introduces a slew of terminology and ideas with which we can analyze the process of respiration. the first part was the review of the mechanics of breathing, which occurs when the pleura is expanded via the lowering of the diaphragm and the raising / expansion of the ribcage. the muscles involved in raising the ribcage are the external intercostals, sternocleidomastoid, scalenes, and serratus anterior while the muscles involved in lowering the ribcage are the rectus abdominis and the internal intercostals. the forces that are at play in the thoracic region are then looked at: the elastin in the alveoli causes it to collapse inward, countered by the elasticity of the ribcage pushing outward. the surface tension of water on the inside of the alveoli draws it inward, countered by the surfactant that is secreted in the alveoli which reduces surface tension. finally, the negative pressure (less than atmospheric) in the pleural cavity draws the lungs outward and the pleura inward.
the idea of respiratory work is then introduced. in mechanics, work = force x distance, and in respiration this is analogous to work = intrapleural pressure x displaced air. the total work of inspiration is the idealized work if all the energy of inspiration is converted directly into air movement. tissue resistance work is the work done to move the ribcage, muscles, bones, cartilage, etc. airway work is the work done to move the air itself and is analogous to the "resistance" of Q=P/R, especially in the sense that increasing or decreasing the radius of brochi has a huge effect on airway resistance and thus work. tissue resistance + airway work represents the deviation from the idealized compliance work-- these two factors create the delay after the pleura expands, before the increasingly negative pressure in the intrapleural cavity causes the lungs to expand.
the free work of expiration is the idealized work from expiration minus the tissue resistance and airway work. maybe the most important term in this section is the total work of breathing, which is the sum of the work from inspiration and expiration (and is graphically represented by the area between the two curves).
next we look at the different terms given to the breakdown of lung capacity. total lung capacity is the total air possible in the lung and is generally ~5500mL. of this, ~1000mL is untouched by respiration and is called the residual volume. what's left is the vital capacity, which is generally 4500mL. the vital capacity is made up of the tidal volume, inspiratory reserve volume, and expiratory reserve volume. the tidal volume represents the volume of air that comes in and out of the lungs during normal breathing, generally 500mL. the inspiratory reserve is the amount you can breathe in after the tidal volume, which is generally 3000mL. the expiratory reserve is the amount you can breathe out after the tidal volume, generally 1000mL. some factors that can influence vital capacity-- anatomy can play a role in that a larger body size or shape can increase VC while abnormalities like scoliosis or lung paralysis can decrease VC. physiology plays a role in that muscle strength or exertion can increase VC while decreased compliance or bronchoconstriction can reduce VC.
the last set of terms that are introduced seem to be more geared toward measurement of respiratory function. forced vital capacity represents the time it takes to exhale the vital capacity, while forced expiratory volume represents the volume or percentage of vital capacity that is exhaled within a unit time, generally 1 or 3 seconds. the FEV (1sec) for a normal, young adult is 80-90% of the vital capacity. forced expiratory flow is a measure of the flow rate during the middle of the exhalation of the vital capacity. minute respiratory volume is the volume of fresh air that is actually being exchanged in the lungs, and is analogous to cardiac output -- represented by breathing rate x tidal volume. minute alveolar volume is the same, except looking at the fresh air that is being exchanged specifically in the alveoli. finally, anatomical dead space is the volume of air from respiration that does not take place in gas exchange.
questions
1. what are the two mechanisms for respiration?
2. what are the muscles that raise the ribcage?
3. what are the muscles that lower the ribcage?
4. restful breathing is mostly ___ while vigorous breathing is mostly ___.
5. describe the force dynamics operating in the thoracic cavity due to elasticity, surface tension, and negative intrapleural pressure.
6. what is compliance, tissue resistance, and airway work?
7. what is the total work of inspiration?
8. what is the free work of expiration?
9. what is the "total work of breathing"?
10. what proportion of total body work is the work of breathing?
11. tidal volume...
12. inspiratory reserve volume...
13. expiratory reserve volume...
14. vital capacity...
15. residual volume...
16. total lung volume...
the factors that influence vital capacity:
17. normal anatomical factors...
18. normal physiological factors...
19. abnormal anatomical factors...
20. abnormal physiological factors...
21. what is forced vital capacity?
22. what is forced expiratory volume?
23. what is a normal value (percentage of vital capacity) of 1 second FEV for healthy, young, people?
24. what is forced expiratory flow?
25. what is minute respiratory volume?
26. what is minute alveolar volume?
27. what is anatomical dead space?
answers
1. diaphragm lowering and raising, ribcage raising and lowering.
2. external intercostals, parasternal internal intercostals, scalenes, sternocleidomastoid, serratus anterior
3. rectus abdominis, internal intercostals.
4. diaphramatic, rib-cage based.
5. elastin in alveolar septa causes inward recoil while elasticity in ribs and chest promotes outward expansion. water on inner surface of alveoli causes inward force, surfactant produced by alveoli counters this surface tension. negative intrapleural pressure causes alveoli to expand and chest/ribs to shrink.
6. in the respiratory system, the W=F x D equation is translated into W=Pressure X air displacement. compliance work represents the ideal work done if all energy is converted into air movement. tissue resistance work is the work done to move the bones, muscles, cartilage, etc. airway work is the work done to move the air itself and is analogous to the "R" in the Q=P/R from hemodynamics.
7. the combination of compliance, tissue resistance, and airway work.
8. the compliance work from expiration minus the tissue and airway work from expiration.
9. the work of the entire breathing cycle (the area inside the inspiration / expiration curves)
10. ~3%, no more than 5% even in heavy exercise.
11. the regular amount of air ventilated per breath, generally ~500mL
12. amount of air that can be inhaled after tidal volume, ~3000mL
13. amount of air that can be exhaled after tidal volume, ~1000mL
14. expiratory reserve + tidal volume + inspiratory reserve ~4500mL
15. amount of air still in lungs after complete exhalation, ~1000mL
16. vital capacity + residual volume, ~5500mL
17. larger body size or type increases VC
18. muscle strength or vigor of effort increases VC
19. kyphosis, scoliosis, respiratory paralysis lowers VC
20. pulmonary congestion, reduced compliance (asthma, bronchitis, etc.) lowers VC
21. time it takes to get the vital capacity out.
22. the amount of vital capacity exhaled in a given unit of time, which includes tissue resistance and airway work.
23. 90-100% of VC
24. average flow during the middle part of the FVC
25. tidal volume X respiratory rate (analagous to cardiac output), generally ~6L/min
26. the amount of fresh air that is reaching the alveoli
27. the air that filled the airways but does not participate in gas exchange, generally ~150mL
the idea of respiratory work is then introduced. in mechanics, work = force x distance, and in respiration this is analogous to work = intrapleural pressure x displaced air. the total work of inspiration is the idealized work if all the energy of inspiration is converted directly into air movement. tissue resistance work is the work done to move the ribcage, muscles, bones, cartilage, etc. airway work is the work done to move the air itself and is analogous to the "resistance" of Q=P/R, especially in the sense that increasing or decreasing the radius of brochi has a huge effect on airway resistance and thus work. tissue resistance + airway work represents the deviation from the idealized compliance work-- these two factors create the delay after the pleura expands, before the increasingly negative pressure in the intrapleural cavity causes the lungs to expand.
the free work of expiration is the idealized work from expiration minus the tissue resistance and airway work. maybe the most important term in this section is the total work of breathing, which is the sum of the work from inspiration and expiration (and is graphically represented by the area between the two curves).
next we look at the different terms given to the breakdown of lung capacity. total lung capacity is the total air possible in the lung and is generally ~5500mL. of this, ~1000mL is untouched by respiration and is called the residual volume. what's left is the vital capacity, which is generally 4500mL. the vital capacity is made up of the tidal volume, inspiratory reserve volume, and expiratory reserve volume. the tidal volume represents the volume of air that comes in and out of the lungs during normal breathing, generally 500mL. the inspiratory reserve is the amount you can breathe in after the tidal volume, which is generally 3000mL. the expiratory reserve is the amount you can breathe out after the tidal volume, generally 1000mL. some factors that can influence vital capacity-- anatomy can play a role in that a larger body size or shape can increase VC while abnormalities like scoliosis or lung paralysis can decrease VC. physiology plays a role in that muscle strength or exertion can increase VC while decreased compliance or bronchoconstriction can reduce VC.
the last set of terms that are introduced seem to be more geared toward measurement of respiratory function. forced vital capacity represents the time it takes to exhale the vital capacity, while forced expiratory volume represents the volume or percentage of vital capacity that is exhaled within a unit time, generally 1 or 3 seconds. the FEV (1sec) for a normal, young adult is 80-90% of the vital capacity. forced expiratory flow is a measure of the flow rate during the middle of the exhalation of the vital capacity. minute respiratory volume is the volume of fresh air that is actually being exchanged in the lungs, and is analogous to cardiac output -- represented by breathing rate x tidal volume. minute alveolar volume is the same, except looking at the fresh air that is being exchanged specifically in the alveoli. finally, anatomical dead space is the volume of air from respiration that does not take place in gas exchange.
questions
1. what are the two mechanisms for respiration?
2. what are the muscles that raise the ribcage?
3. what are the muscles that lower the ribcage?
4. restful breathing is mostly ___ while vigorous breathing is mostly ___.
5. describe the force dynamics operating in the thoracic cavity due to elasticity, surface tension, and negative intrapleural pressure.
6. what is compliance, tissue resistance, and airway work?
7. what is the total work of inspiration?
8. what is the free work of expiration?
9. what is the "total work of breathing"?
10. what proportion of total body work is the work of breathing?
11. tidal volume...
12. inspiratory reserve volume...
13. expiratory reserve volume...
14. vital capacity...
15. residual volume...
16. total lung volume...
the factors that influence vital capacity:
17. normal anatomical factors...
18. normal physiological factors...
19. abnormal anatomical factors...
20. abnormal physiological factors...
21. what is forced vital capacity?
22. what is forced expiratory volume?
23. what is a normal value (percentage of vital capacity) of 1 second FEV for healthy, young, people?
24. what is forced expiratory flow?
25. what is minute respiratory volume?
26. what is minute alveolar volume?
27. what is anatomical dead space?
answers
1. diaphragm lowering and raising, ribcage raising and lowering.
2. external intercostals, parasternal internal intercostals, scalenes, sternocleidomastoid, serratus anterior
3. rectus abdominis, internal intercostals.
4. diaphramatic, rib-cage based.
5. elastin in alveolar septa causes inward recoil while elasticity in ribs and chest promotes outward expansion. water on inner surface of alveoli causes inward force, surfactant produced by alveoli counters this surface tension. negative intrapleural pressure causes alveoli to expand and chest/ribs to shrink.
6. in the respiratory system, the W=F x D equation is translated into W=Pressure X air displacement. compliance work represents the ideal work done if all energy is converted into air movement. tissue resistance work is the work done to move the bones, muscles, cartilage, etc. airway work is the work done to move the air itself and is analogous to the "R" in the Q=P/R from hemodynamics.
7. the combination of compliance, tissue resistance, and airway work.
8. the compliance work from expiration minus the tissue and airway work from expiration.
9. the work of the entire breathing cycle (the area inside the inspiration / expiration curves)
10. ~3%, no more than 5% even in heavy exercise.
11. the regular amount of air ventilated per breath, generally ~500mL
12. amount of air that can be inhaled after tidal volume, ~3000mL
13. amount of air that can be exhaled after tidal volume, ~1000mL
14. expiratory reserve + tidal volume + inspiratory reserve ~4500mL
15. amount of air still in lungs after complete exhalation, ~1000mL
16. vital capacity + residual volume, ~5500mL
17. larger body size or type increases VC
18. muscle strength or vigor of effort increases VC
19. kyphosis, scoliosis, respiratory paralysis lowers VC
20. pulmonary congestion, reduced compliance (asthma, bronchitis, etc.) lowers VC
21. time it takes to get the vital capacity out.
22. the amount of vital capacity exhaled in a given unit of time, which includes tissue resistance and airway work.
23. 90-100% of VC
24. average flow during the middle part of the FVC
25. tidal volume X respiratory rate (analagous to cardiac output), generally ~6L/min
26. the amount of fresh air that is reaching the alveoli
27. the air that filled the airways but does not participate in gas exchange, generally ~150mL
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