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 organ systems I. Show all posts
Showing posts with label organ systems I. Show all posts
Sunday, December 7, 2008
Saturday, December 6, 2008
organ systems: gas transport
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.
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.
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
Tuesday, November 18, 2008
organ systems: respiratory system anatomy I
this lecture describes the basic anatomy of the lungs and thoracic area and goes over the basics for the mechanics of breathing. the first part deals with lung anatomy. the right and left lungs are divided into upper and lower lobes by oblique fissures, and the right has a middle lobe that is delineated by the horizontal fissure. in the left lung, the lingula is a protuberance that is homologous to the right middle lobe and is formed by the cardiac notch. the lungs are further divided into 10 "bronchopulmonary" segments, which are functional units that are separated by connective tissue septa. air comes into the lungs first through the trachea, which then branches into primary, secondary, and tertiary bronchi, which branch off into the right and left lungs (primary), individual lobes (secondary), and individual bronchopulmonary segments (tertiary). the root of the lung is called the hilum and contains the pulmonary arteries, veins, nerves, and lymph nodes. within the bronchopulmonary segment, pulmonary arteries snake down the center, supplying oxygenated blood, while the pulmonary veins collect deoxygenated blood and follow the intersegmental CT septa.
next we look at the mechanics of breathing. the pleura is introduced as the bursa that surrounds the lungs and reduces friction. much like the pericardium, it has a parietal and visceral layer and is filled with a lubricating fluid. the visceral layer in this case adheres to the lungs and the parietal layer adheres to the diaphram, pericardium, and thoracic cage. the space between the visceral and parietal pleura is called the pleural cavity and is the space in which the lungs can expand into during inspiration. a couple of pathologies related to the pleura are mentioned: pleurisy is inflammation of the pleura, causing the visceral and parietal layers of the pleura to fuse together and not allow the lung any room to expand. pneumothorax is the filling of the pleura with liquid, which causes the lungs to collapse.
the structure of the ribs is looked at: ribs 1-7 are "true ribs" and insert directly into the sternum, ribs 8-10 are "false ribs" and insert onto the costal margin, and ribs 10-12 are "floating ribs" which do not insert on bone or cartilage. the ribs origin has two types of joints: costovertebral joints, which are the joints between the heads of the ribs and the articular facets of two adjacent vertebras, and costotransverse joints, which are the joints between the transverse processes of the vertebrae and the tubercle of the ribs. these joints allow the ribs to be pulled up and out, allowing the thoracic cage to increase its transverse (from side to side) as well as anterior-posterior diameters, the first step in inspiration. the external intercostal and parasternal intercostal muscles lift the ribs as the diaphram pulls the pleura downward, producing negative (below atmospheric) pressure in the pleura, which expands the lung and begins inspiration. expiration can occur passively, in which the lungs elastically recoil and the inspiration muscles relax, or actively, in which the abdominal muscles pull the ribs back out and the diaphragm pushes back upwards.
questions
1. what is the advantage of the separation of the lungs into lobes via fissures?
2. what are the upper and lower lungs separated by?
3. what is the right middle lobe formed by?
4. what is the lingula formed by and what is it homologous to?
5. what is the apex of the lung called and where does it extend to?
6. what is the root of the lung called and what does it contain?
7. describe the role of the trachea in maintaining an open airway.
8. describe the subdivision of the bronchi in relation to their location/function in the lung.
9. what is one important role of elastic tissue and smooth muscle in the lungs?
10. describe the symmetry of the primary bronchi.
11. what are bronchopulmonary segments and how many are there?
12. describe the locations of the pulmonary arteries, veins, and lymphatics in a bronchopulmonary segment.
13. describe the organization of lymph drainage in the lungs.
14. what does lymph from the lung often contain?
15. describe the location and function of the bronchial arteries and veins.
16. what effects do parasympathetic nerves have on the lungs?
17. what effect do the sympathetic nerves have on the lungs?
18. what is the pleura?
19. what does the parietal pleura adhere to?
20. what is the pleural cavity?
21. what are the costodiaphragmatic and costomediastinal recesses?
22. what is pleurisy?
23. what is pneumothorax?
24. describe the costovertebral joints.
25. describe the costotransverse joints.
26. describe the costosternal joints.
27. what are "true ribs"?
28. what are "false ribs"?
29. what are "floating ribs"?
30. describe the actions required for inspiration.
31. what are the two diameters increased during the movement of the ribs during inspiration?
32. what are the accessory muscles involved in raising of the ribs?
33. what is the diaphram and what goes through it?
34. what is the phrenic nerve and what does it innervate?
35. what is passive vs. active expiration?
origins and insertions for...
36. external oblique
37. internal oblique
38. transversus abdominis
39. rectus abdominis
40. how do the abdominal muscles aid in respiration?
41. how do the abdominal muscles move the vertebral column?
42. what do the intercostal nerves innervate and where do they originate on the spinal column?
answers
1. separation promotes more uniform expansion of the lungs, allows the upper lobes to "expand unimpeded".
2. the oblique fissure
3. the horizontal fissure
4. the cardiac notch, homologous to the right middle lobe.
5. called the cupola, and extends into neck above the 1st rib
6. called the hilum, location of passage of bronchi, pulmonary artery and vein, nerves, and lymph nodes.
7. the trachea contains cartilage rings that maintain patency, and the trachealis muscle maintains wall tension.
8. primary bronchi branch off into each lung, secondary bronchi branch off into each lobe, tertiary bronchi branch off into each bronchopulmonary segment.
9. facilitating passive expiration
10. the right primary bronchi extends down straighter than the left, allowing particulates to flow into right lung more easily.
11. there are 10 bronchopulmonary segments and they are functional units of the lung separated by CT septa and filled with tertiary bronchi.
12. the pulmonary artery flows down the middle of the segment, the pulmonary vein flows near the intersegmental CT septa, and the lymphatics follow the veins.
13. superficial and deep plexuses drain into the bronchopulmonary nodes in the hilum of the lungs.
14. lymph from the lung often contains lung macrophages which have injested carbon particles.
15. the bronchial arteries branch off of the aorta and supply the lung tissue with oxygenated blood. the bronchial veins drain deoxygenated blood from the lung tissue and follow the intercostal veins to the azygos veins.
16. the vagus nerve causes bronchoconstriction and activates mucus glands
17. bronchodilation
18. the bursa that surrounds the lungs that has a parietal and visceral layer.
19. thoracic cage, diaphragm, pericardium
20. the space in between the visceral and parietal layers that is filled with a viscous lubricating fluid.
21. the spaces in between the visceral and parietal layers of pleura into which the lung expands.
22. inflammation of the pleura that may lead to adhesions between pleural layers, limiting lung movements.
23. entry of fluid between the visceral and parietal layers of pleura causes collapse in lung.
24. joints between the head of the ribs and the facets of two adjacent vertebral bodies, with ligaments radiating outward from rib
25. joints between tubercle of the rib and transverse processes of vertebrae, with costotransverse ligaments.
26. ribs that articulate with the sternum via costal cartilage.
27. ribs 1-7, articulate directly onto sternum
28. ribs 8-10, articulate onto costal cartilage of ribs above
29. ribs 11,12, do not attach to sternum or costal cartilage.
30. the external and parasternal internal intercostal muscles raise the ribs, and the diaphragm lowers
31. the anterior poster and the transverse diameters
32. serratus posterior, levator costarum, SCM, scalenes
33. a ring of muscle around a central tendon attached along the costal margin. penetrated by IVC, aorta, esophagus
34. nerve that originates in C3,4,5, innervates fibrous pericardium, diaphragm, pancreas, gall bladder.
35. passive expiration comes from the relaxation of the inspiration muscles and the elastic recoil of the lungs. active expiration comes from abdominal muscles pulling down on the ribs, as well as pushing the diaphram upwards to collapse the lungs.
36. O: lower 8 ribs, I: iliac crest, pubis, linea alba
37. O: iliac crest, I: costal margin, linea alba, symphysis pubis
38. O: costal margin, iliac crest, I: linea alba
39. O: symphysis pubis, I: costal margin, cartilage of ribs 5,6,7
40. the rectus abdominus and obliques depress ribs during expiration
41. the rectus abdominus flexes and the obliques abduct and rotate.
42. they innervate the intercostal muscles (T1-T12) and the abdominal muscles (T6-L1)
next we look at the mechanics of breathing. the pleura is introduced as the bursa that surrounds the lungs and reduces friction. much like the pericardium, it has a parietal and visceral layer and is filled with a lubricating fluid. the visceral layer in this case adheres to the lungs and the parietal layer adheres to the diaphram, pericardium, and thoracic cage. the space between the visceral and parietal pleura is called the pleural cavity and is the space in which the lungs can expand into during inspiration. a couple of pathologies related to the pleura are mentioned: pleurisy is inflammation of the pleura, causing the visceral and parietal layers of the pleura to fuse together and not allow the lung any room to expand. pneumothorax is the filling of the pleura with liquid, which causes the lungs to collapse.
the structure of the ribs is looked at: ribs 1-7 are "true ribs" and insert directly into the sternum, ribs 8-10 are "false ribs" and insert onto the costal margin, and ribs 10-12 are "floating ribs" which do not insert on bone or cartilage. the ribs origin has two types of joints: costovertebral joints, which are the joints between the heads of the ribs and the articular facets of two adjacent vertebras, and costotransverse joints, which are the joints between the transverse processes of the vertebrae and the tubercle of the ribs. these joints allow the ribs to be pulled up and out, allowing the thoracic cage to increase its transverse (from side to side) as well as anterior-posterior diameters, the first step in inspiration. the external intercostal and parasternal intercostal muscles lift the ribs as the diaphram pulls the pleura downward, producing negative (below atmospheric) pressure in the pleura, which expands the lung and begins inspiration. expiration can occur passively, in which the lungs elastically recoil and the inspiration muscles relax, or actively, in which the abdominal muscles pull the ribs back out and the diaphragm pushes back upwards.
questions
1. what is the advantage of the separation of the lungs into lobes via fissures?
2. what are the upper and lower lungs separated by?
3. what is the right middle lobe formed by?
4. what is the lingula formed by and what is it homologous to?
5. what is the apex of the lung called and where does it extend to?
6. what is the root of the lung called and what does it contain?
7. describe the role of the trachea in maintaining an open airway.
8. describe the subdivision of the bronchi in relation to their location/function in the lung.
9. what is one important role of elastic tissue and smooth muscle in the lungs?
10. describe the symmetry of the primary bronchi.
11. what are bronchopulmonary segments and how many are there?
12. describe the locations of the pulmonary arteries, veins, and lymphatics in a bronchopulmonary segment.
13. describe the organization of lymph drainage in the lungs.
14. what does lymph from the lung often contain?
15. describe the location and function of the bronchial arteries and veins.
16. what effects do parasympathetic nerves have on the lungs?
17. what effect do the sympathetic nerves have on the lungs?
18. what is the pleura?
19. what does the parietal pleura adhere to?
20. what is the pleural cavity?
21. what are the costodiaphragmatic and costomediastinal recesses?
22. what is pleurisy?
23. what is pneumothorax?
24. describe the costovertebral joints.
25. describe the costotransverse joints.
26. describe the costosternal joints.
27. what are "true ribs"?
28. what are "false ribs"?
29. what are "floating ribs"?
30. describe the actions required for inspiration.
31. what are the two diameters increased during the movement of the ribs during inspiration?
32. what are the accessory muscles involved in raising of the ribs?
33. what is the diaphram and what goes through it?
34. what is the phrenic nerve and what does it innervate?
35. what is passive vs. active expiration?
origins and insertions for...
36. external oblique
37. internal oblique
38. transversus abdominis
39. rectus abdominis
40. how do the abdominal muscles aid in respiration?
41. how do the abdominal muscles move the vertebral column?
42. what do the intercostal nerves innervate and where do they originate on the spinal column?
answers
1. separation promotes more uniform expansion of the lungs, allows the upper lobes to "expand unimpeded".
2. the oblique fissure
3. the horizontal fissure
4. the cardiac notch, homologous to the right middle lobe.
5. called the cupola, and extends into neck above the 1st rib
6. called the hilum, location of passage of bronchi, pulmonary artery and vein, nerves, and lymph nodes.
7. the trachea contains cartilage rings that maintain patency, and the trachealis muscle maintains wall tension.
8. primary bronchi branch off into each lung, secondary bronchi branch off into each lobe, tertiary bronchi branch off into each bronchopulmonary segment.
9. facilitating passive expiration
10. the right primary bronchi extends down straighter than the left, allowing particulates to flow into right lung more easily.
11. there are 10 bronchopulmonary segments and they are functional units of the lung separated by CT septa and filled with tertiary bronchi.
12. the pulmonary artery flows down the middle of the segment, the pulmonary vein flows near the intersegmental CT septa, and the lymphatics follow the veins.
13. superficial and deep plexuses drain into the bronchopulmonary nodes in the hilum of the lungs.
14. lymph from the lung often contains lung macrophages which have injested carbon particles.
15. the bronchial arteries branch off of the aorta and supply the lung tissue with oxygenated blood. the bronchial veins drain deoxygenated blood from the lung tissue and follow the intercostal veins to the azygos veins.
16. the vagus nerve causes bronchoconstriction and activates mucus glands
17. bronchodilation
18. the bursa that surrounds the lungs that has a parietal and visceral layer.
19. thoracic cage, diaphragm, pericardium
20. the space in between the visceral and parietal layers that is filled with a viscous lubricating fluid.
21. the spaces in between the visceral and parietal layers of pleura into which the lung expands.
22. inflammation of the pleura that may lead to adhesions between pleural layers, limiting lung movements.
23. entry of fluid between the visceral and parietal layers of pleura causes collapse in lung.
24. joints between the head of the ribs and the facets of two adjacent vertebral bodies, with ligaments radiating outward from rib
25. joints between tubercle of the rib and transverse processes of vertebrae, with costotransverse ligaments.
26. ribs that articulate with the sternum via costal cartilage.
27. ribs 1-7, articulate directly onto sternum
28. ribs 8-10, articulate onto costal cartilage of ribs above
29. ribs 11,12, do not attach to sternum or costal cartilage.
30. the external and parasternal internal intercostal muscles raise the ribs, and the diaphragm lowers
31. the anterior poster and the transverse diameters
32. serratus posterior, levator costarum, SCM, scalenes
33. a ring of muscle around a central tendon attached along the costal margin. penetrated by IVC, aorta, esophagus
34. nerve that originates in C3,4,5, innervates fibrous pericardium, diaphragm, pancreas, gall bladder.
35. passive expiration comes from the relaxation of the inspiration muscles and the elastic recoil of the lungs. active expiration comes from abdominal muscles pulling down on the ribs, as well as pushing the diaphram upwards to collapse the lungs.
36. O: lower 8 ribs, I: iliac crest, pubis, linea alba
37. O: iliac crest, I: costal margin, linea alba, symphysis pubis
38. O: costal margin, iliac crest, I: linea alba
39. O: symphysis pubis, I: costal margin, cartilage of ribs 5,6,7
40. the rectus abdominus and obliques depress ribs during expiration
41. the rectus abdominus flexes and the obliques abduct and rotate.
42. they innervate the intercostal muscles (T1-T12) and the abdominal muscles (T6-L1)
Saturday, November 15, 2008
11.12.08 organ systems: cardiovascular development 2
this is the second lecture in the cardiovascular development series and focuses on development of prenatal circulation and the transition to post natal circulation. it starts with where we left off with the last lecture, looking at the development of the larger structures in the heart, like the aortic arch being formed from the truncus arteriosus, forming the aorta on the left. the left recurrent laryngeal nerve is underneath the aorta and the right recurrent laryngeal nerve is underneath the right subclavian artery.
then we go back to some possible defects in structural development in the BC/TA trunk. when the spiral aortic-pulmonary septum forms from the endocardial cushion, there are several possibilities for abnormal development. these are: lack of septum altogether, called persistent truncus arteriosus, lack of a spiral in the septum, causing transposition of the aorta and pulmonary trunks, and an unequal divide in the trunk, causing one of the trunks to be bigger than the other. the tetralogy of fallot is a condition that combines the unequal divide with a VSD, resulting in right ventricular hypertrophy (induced by the pulmonary stenosis) as well as "aortic override".
finally, we look at the development of fetal circulation on a larger scale, as it interacts with its placenta. the trophoblast that is embedded in the endometrium differentiates into two layers: the syncytiotrophoblast, which contains spiralling maternal blood vessels and interstitial spaces, and the cytotrophoblast, which has "choroinic villi" that extend into the interstitial spaces and contain the fetal blood vessels. we then shift over to look at the difference between pre and post natal circulation, which is mainly in prenatal's use of shunts which divert blood from the liver and lungs. the ductus venous diverts blood from the liver, the ductus arteriosus and foramen ovale divert blood from the lungs, instead going directly back into circulation, which apparently "reduces oxygenated blood" in the lower limbs. two more random facts: blood supply from umbilical cord and vena cava remain in separate streams when entering the right atrium. the right ventricle and pulmonary trunk receives more deoxygenated blood and the left ventricle receives more oxygenated blood.
then we go back to some possible defects in structural development in the BC/TA trunk. when the spiral aortic-pulmonary septum forms from the endocardial cushion, there are several possibilities for abnormal development. these are: lack of septum altogether, called persistent truncus arteriosus, lack of a spiral in the septum, causing transposition of the aorta and pulmonary trunks, and an unequal divide in the trunk, causing one of the trunks to be bigger than the other. the tetralogy of fallot is a condition that combines the unequal divide with a VSD, resulting in right ventricular hypertrophy (induced by the pulmonary stenosis) as well as "aortic override".
finally, we look at the development of fetal circulation on a larger scale, as it interacts with its placenta. the trophoblast that is embedded in the endometrium differentiates into two layers: the syncytiotrophoblast, which contains spiralling maternal blood vessels and interstitial spaces, and the cytotrophoblast, which has "choroinic villi" that extend into the interstitial spaces and contain the fetal blood vessels. we then shift over to look at the difference between pre and post natal circulation, which is mainly in prenatal's use of shunts which divert blood from the liver and lungs. the ductus venous diverts blood from the liver, the ductus arteriosus and foramen ovale divert blood from the lungs, instead going directly back into circulation, which apparently "reduces oxygenated blood" in the lower limbs. two more random facts: blood supply from umbilical cord and vena cava remain in separate streams when entering the right atrium. the right ventricle and pulmonary trunk receives more deoxygenated blood and the left ventricle receives more oxygenated blood.
11.11.08 organ systems: cardiovascular development 1
this unit covers some basic ideas in early cardiovascular development. the first section focuses on the development of blood and blood vessels: blood production starts mainly in the yolk sac and moves to the liver/spleen, then to the bone marrow during development and involves differentiation of hemangioblast cells. these cells are derived from mesenchymal cells and triggered by the growth factor FGF to differentiate into blood cell precursors, hematopoetic stem cells, or blood vessel (capillary) walls, which then converge into larger and larger vessels. VEGF is a growth factor that stimulates nearby mesenchyme cells to differentiate into smooth muscle or pericyte cells.
the next sections describe the early structural development of the heart. the formation of the heart chambers begins when the endocardial cushion forms in the middle of the heart via a fusion of projections of tissue from the anterior and posterior walls. in the atriums, the primary septum is formed with a secondary foramen, and the secondary septum is formed with a foramen ovale. in the prenatal heart, blood flows from the right atrium, into the foramen ovale, through the primary septum, directly into the left atrium, bypassing the lungs. (this is the second "shunting" we've learned about- the first being the ductus arteriosus) in the post natal heart, the pressure from the pulmonary artery in the left atrium causes the primary septum to close and fuse with the secondary, creating the fossa ovalis. the ventricles are partitioned when the muscular and the membranous aspects of the interventricular septum join, closing up the interventricular foramen. finally, the endocardial cushion projects a spiral aortic pulmonary septum that projects into the bulbus cordis / truncus arteriosus vessel and separates it into the aortic and pulmonary trunks. the points of fusion between the bulbus cordis and truncus arteriosus becomes the semilunar valves.
we then look at some defects possible in the development of these structures. in the atriums, atrial septal defect can occur, called probe patent formation, when there is an imperfect adhesion between the primary and secondary septums. in the ventricles, VSD can occur when the membranous aspect of the interventricular septum does not close completely.
the next sections describe the early structural development of the heart. the formation of the heart chambers begins when the endocardial cushion forms in the middle of the heart via a fusion of projections of tissue from the anterior and posterior walls. in the atriums, the primary septum is formed with a secondary foramen, and the secondary septum is formed with a foramen ovale. in the prenatal heart, blood flows from the right atrium, into the foramen ovale, through the primary septum, directly into the left atrium, bypassing the lungs. (this is the second "shunting" we've learned about- the first being the ductus arteriosus) in the post natal heart, the pressure from the pulmonary artery in the left atrium causes the primary septum to close and fuse with the secondary, creating the fossa ovalis. the ventricles are partitioned when the muscular and the membranous aspects of the interventricular septum join, closing up the interventricular foramen. finally, the endocardial cushion projects a spiral aortic pulmonary septum that projects into the bulbus cordis / truncus arteriosus vessel and separates it into the aortic and pulmonary trunks. the points of fusion between the bulbus cordis and truncus arteriosus becomes the semilunar valves.
we then look at some defects possible in the development of these structures. in the atriums, atrial septal defect can occur, called probe patent formation, when there is an imperfect adhesion between the primary and secondary septums. in the ventricles, VSD can occur when the membranous aspect of the interventricular septum does not close completely.
11.11.08 organ systems: capillaries
this lecture is a brief overview of capillaries and their filtration and absorptive functions. the first section describes the physical characteristics of capillaries and the three major types of capillaries: continuous, fenestrated, and discontinuous. continuous is found in the skin, muscle, lungs, CNS, and connective tissue, and contain small clefts that pass water and small solutes, but not proteins. fenestrated capillaries have a more extensive pore network, up to 10 times larger than continuous, and are found in the renal glomeruli, exocrine ducts, and the choroid plexus. discontinuous capillaries have huge holes which let proteins and rbc pass and are located in the spleen, liver, and bone marrow.
the next section delves into the details about capillary absorption/filtration. starling forces are the balance of hydrostatic and oncotic forces. hydrostatic forces are basically created from the transmural pressure from the fluid flow, and oncotic pressure is created by the osmotic pressure across the endothelium from the proteins inside the capillaries. the starling force equation describes the net flow of fluid either in or out of the capillary according to the interaction of these two forces: V=K[(Pc-Pi)-Ï€(pc-pi)]. as the fluid flows down the length of the vessel, hydrostatic force gradually decreases (force lost to maintaining pressure of vessel?) and eventually becomes less than the oncotic pressure, causing the net flow to go from filtration to absorption (NFP describes the filtration pressure and NAP describes the absorption pressure)
a few more random details about capillaries are thrown in: the interstitial space around capillaries is composed of collagen, proteoglycans (hyaluronic acid gel), and rivulets of free fluid. capillary growth happens via pseudopods that are extended into surrounding CT, in response to nearby tissue O2 demand or injury.
lymph is then introduced: the remaining 10% of the extravasated interstitial fluid that is not reabsorbed by the venous sections of capillaries. lymphatics reabsorb fluids and proteins, absorbed into terminal lymphatics via the hydrostatic pressure in the interstitial fluid. lymph is transported through lymph vessels through valves, mediated by smooth muscle that is innervated by the sympathetic nervous system. the deep lymph layer runs alongside the aorta and the superficial lymph layer runs along the veins and coalesces into the axillary, cervical, and inguinal nodes. lymph drains back into the venous system, via either the thoracic drain, which collects from the lower 3/4 of the body, and the right lymphatic drain, which drains the upper right 1/4. both drain into the subclavian and internal jugular veins.
the last section describes some pathologies related to interstitial fluid buildup, otherwise known as edema. these pathologies involve either an excess hydrostatic pressure or a deficient oncotic pressure, which both cause excess filtration or deficient reabsorption (leading to fluid buildup) the first type mentioned is venous edema, which occurs because of excess hydrostatic pressure in the lower limbs due to occlusion or CHF. the second type is hypoalbuminemic enema, which is when the lack of proteins in the capillaries reduces the encotic pressure inside, leading to reduced reabsorption. the third type is inflammatory edema, when protein leaks out into the interstitial space, raising its encotic pressure and thereby reducing absorption. the last is lymphatic edema, where uptake into the lymph vessels is blocked by infection or damage.
the next section delves into the details about capillary absorption/filtration. starling forces are the balance of hydrostatic and oncotic forces. hydrostatic forces are basically created from the transmural pressure from the fluid flow, and oncotic pressure is created by the osmotic pressure across the endothelium from the proteins inside the capillaries. the starling force equation describes the net flow of fluid either in or out of the capillary according to the interaction of these two forces: V=K[(Pc-Pi)-Ï€(pc-pi)]. as the fluid flows down the length of the vessel, hydrostatic force gradually decreases (force lost to maintaining pressure of vessel?) and eventually becomes less than the oncotic pressure, causing the net flow to go from filtration to absorption (NFP describes the filtration pressure and NAP describes the absorption pressure)
a few more random details about capillaries are thrown in: the interstitial space around capillaries is composed of collagen, proteoglycans (hyaluronic acid gel), and rivulets of free fluid. capillary growth happens via pseudopods that are extended into surrounding CT, in response to nearby tissue O2 demand or injury.
lymph is then introduced: the remaining 10% of the extravasated interstitial fluid that is not reabsorbed by the venous sections of capillaries. lymphatics reabsorb fluids and proteins, absorbed into terminal lymphatics via the hydrostatic pressure in the interstitial fluid. lymph is transported through lymph vessels through valves, mediated by smooth muscle that is innervated by the sympathetic nervous system. the deep lymph layer runs alongside the aorta and the superficial lymph layer runs along the veins and coalesces into the axillary, cervical, and inguinal nodes. lymph drains back into the venous system, via either the thoracic drain, which collects from the lower 3/4 of the body, and the right lymphatic drain, which drains the upper right 1/4. both drain into the subclavian and internal jugular veins.
the last section describes some pathologies related to interstitial fluid buildup, otherwise known as edema. these pathologies involve either an excess hydrostatic pressure or a deficient oncotic pressure, which both cause excess filtration or deficient reabsorption (leading to fluid buildup) the first type mentioned is venous edema, which occurs because of excess hydrostatic pressure in the lower limbs due to occlusion or CHF. the second type is hypoalbuminemic enema, which is when the lack of proteins in the capillaries reduces the encotic pressure inside, leading to reduced reabsorption. the third type is inflammatory edema, when protein leaks out into the interstitial space, raising its encotic pressure and thereby reducing absorption. the last is lymphatic edema, where uptake into the lymph vessels is blocked by infection or damage.
11.10.08 organ systems: vascular regulation
this unit talks about the two types of vascular regulation: intrinsic and extrinsic. intrinsic regulation has several mechanisms which either vasodilate or vasoconstrict. metabolic vasodilators are generated in response to low flow or O2, and induce the vessel to dilate, which increases flow and washes the metabolite away. myogenic constriction is contraction of smooth muscle around vascular walls in response to increased transmural pressure, a sort of stabilizing counterforce. nitric oxide is another vasodilator that is derived from arginine and released from endothelial walls. finally, endothelin is a vasoconstrictor which is upregulated in hypertension. all of these mechanisms represent the vessel being stimulated by local events and auto-adjusting vessel diameter so as to increase or decrease local pressure.
contrast this with extrinsic control, which is more of a top down, executive level approach which monitors and maintains blood flow to individual organs or body parts, ensuring that increased blood flow to one does not take away from another. it "senses" mean arterial pressure by way of baroreceptors, which are essentially stretch transducers in the aortic arch and carotid sinuses. these baroreceptors then route out to the medulla, in the solitary nucleus (or NTS-- nucleus, the solitary?), and then to the nucleus ambiguus and the caudal ventrallateral medulla. the nucleus ambiguus innervates the heart parasympathetically via the vagus nerve, while the CVLM continues to the RVLM, the rostral ventrallateral medulla, which is the pacemaker of sympathetic activity and projects down to sympathetic preganglionic neurons in the spinal cord, which project out to the heart. this network of sensory and efferent neurons are influenced by the following brain structures: hypothalamus and pituitary, and the motor and limbic systems.
baroreceptors are the eyes and ears of the extrinsic regulatory system, while the autonomic nervous system are the hands that effect change in the vessels to maintain homeostasis. the sympathetic nervous system has a major role in the extrinsic regulation of blood vessels: the rate at which the post-ganglionic sympathetic neurons fire directly influences the contraction of the smooth muscle around the vessels and thus vasodilation or constriction can be adjusted simply by firing rate of neurons. norepinephrine binding to alpha receptors has the effect of vasoconstriction, and vasodilating when binding to beta receptors. the parasympathetic nervous system vasodilates when muscarinic receptors are innervated.
the last idea that this lecture talked about it is that of heart rate variability, or of the larger patterns of heart rate frequencies. when plotted out over time and analyzed by frequency groups, heart rate can be broken down into three frequencies: high frequency heart rate, which is mainly controlled by parasympathetic ("beat by beat control") and represents rapid changes due to arrhythmia or increased pulmonary circulation during inspiration. the "low" frequency band, called mayer waves, is caused by feedback rhythms created by baroreceptors, as well as sympathetic / vagal activity. the "very low" frequency waves are due to very slow changes in TPR and thermoregulation.
contrast this with extrinsic control, which is more of a top down, executive level approach which monitors and maintains blood flow to individual organs or body parts, ensuring that increased blood flow to one does not take away from another. it "senses" mean arterial pressure by way of baroreceptors, which are essentially stretch transducers in the aortic arch and carotid sinuses. these baroreceptors then route out to the medulla, in the solitary nucleus (or NTS-- nucleus, the solitary?), and then to the nucleus ambiguus and the caudal ventrallateral medulla. the nucleus ambiguus innervates the heart parasympathetically via the vagus nerve, while the CVLM continues to the RVLM, the rostral ventrallateral medulla, which is the pacemaker of sympathetic activity and projects down to sympathetic preganglionic neurons in the spinal cord, which project out to the heart. this network of sensory and efferent neurons are influenced by the following brain structures: hypothalamus and pituitary, and the motor and limbic systems.
baroreceptors are the eyes and ears of the extrinsic regulatory system, while the autonomic nervous system are the hands that effect change in the vessels to maintain homeostasis. the sympathetic nervous system has a major role in the extrinsic regulation of blood vessels: the rate at which the post-ganglionic sympathetic neurons fire directly influences the contraction of the smooth muscle around the vessels and thus vasodilation or constriction can be adjusted simply by firing rate of neurons. norepinephrine binding to alpha receptors has the effect of vasoconstriction, and vasodilating when binding to beta receptors. the parasympathetic nervous system vasodilates when muscarinic receptors are innervated.
the last idea that this lecture talked about it is that of heart rate variability, or of the larger patterns of heart rate frequencies. when plotted out over time and analyzed by frequency groups, heart rate can be broken down into three frequencies: high frequency heart rate, which is mainly controlled by parasympathetic ("beat by beat control") and represents rapid changes due to arrhythmia or increased pulmonary circulation during inspiration. the "low" frequency band, called mayer waves, is caused by feedback rhythms created by baroreceptors, as well as sympathetic / vagal activity. the "very low" frequency waves are due to very slow changes in TPR and thermoregulation.
11.09.08 organ systems: hemodynamics part II
this lecture introduces one major idea in hemodynamics; venous return and its influence on CO. venous pressure is explained to be caused by three factors: contraction of skeletal muscle during movement which squeezes blood up a series of valves, venoconstriction, and thoracic pressure from breathing. venous pressure in turn affects CO by increasing the end diastolic volume and hence the stroke volume and hence the cardiac output. the venous pressure's relationship to cardiac output follows the frank starling law (although i thought this applied to the active tension curve, but i guess not) and is pictured as an ascending curve in the graph of cardiac output vs. venous pressure.
the "cardiac function" is then introduced as a secondary mechanism that affects / is affected by venous flow / cardiac output. as cardiac output increases, blood is drawn from the veins into the arteries, thereby reducing venous pressure. as cardiac output decreases, equilibrium between the pressures of arteries and veins is reached and more blood is pooled into the veins due to the higher compliance; venous pressure is increased. thus, this relationship is pictured by a curve that descends on the same output vs. venous pressure graph.
the intersection of the two curves represents the equilibrium point, the specific venous pressure and cardiac output that the body has reached as a balance of the two functions. these curves can both be shifted due to different factors: for example, increasing the contractility or heart rate will shift the ascending (frank starling) curve, while vasoconstriction or decreasing vascular resistance will shift the descending curve upwards. both of these actions can potentially shift the cardiac output upwards, and the most efficient increase in cardiac output is created from the combination of increased contractility plus decreased vascular resistance.
the "cardiac function" is then introduced as a secondary mechanism that affects / is affected by venous flow / cardiac output. as cardiac output increases, blood is drawn from the veins into the arteries, thereby reducing venous pressure. as cardiac output decreases, equilibrium between the pressures of arteries and veins is reached and more blood is pooled into the veins due to the higher compliance; venous pressure is increased. thus, this relationship is pictured by a curve that descends on the same output vs. venous pressure graph.
the intersection of the two curves represents the equilibrium point, the specific venous pressure and cardiac output that the body has reached as a balance of the two functions. these curves can both be shifted due to different factors: for example, increasing the contractility or heart rate will shift the ascending (frank starling) curve, while vasoconstriction or decreasing vascular resistance will shift the descending curve upwards. both of these actions can potentially shift the cardiac output upwards, and the most efficient increase in cardiac output is created from the combination of increased contractility plus decreased vascular resistance.
11.08.08 organ systems: vascular physiology and hemodynamics part 1
this was a long introduction to the more intricate details of blood flow dynamics. the beginning of the lecture introduced the larger structures of the circulatory system: the major arteries and aortas: the aortic arch, which branches into the braciocephalic, left common carotid, and left subclavian, with the braciocephalic branching off into the right subclavian and right common carotid. the thoracic aorta, which has intercostal, brachial, and esophageal branches. finally, the abdominal aorta, which has a visceral branch that is divided into the renal, suprarenal, and the GI branch, as well as a common iliac and femoral artery. other details of larger architecture: the right pulmonary artery goes underneath the aortic arch. the ligamentum arteriosum is the vestigial remains of the ductus arteriosum in the developing heart, which shunted blood from the pulmonary artery directly to the aorta, past the non-functioning lungs. the superior vena cava is a combination of the right and left brachiocephalic veins, which are each a convergence of the right and left internal jugular and subclavian veins.
we then zoom in and look at the smaller architecture of arteries, arterioles, capillaries, veins and venules. arteries have three layers, a tunica intima which has endothelium, sub endothelial CT, and an internal elastic lamina. tunica media is the middle layer with smooth muscle and external elastic lamina. tunica adventitia is the outermost layer, with fibrocollagen. arterioles have extensive smooth muscle (which, as it is explained later, helps create a large resistance which causes the largest pressure drop in the circulatory system), running 1-5 layers deep in the tunica media with less fibrous tissue in the tunica intima and adventitia. capillaries are described as the place for nutrient exchange, either through the membrane for lipid soluble solutes such as gas, or through the extensive pore network for water soluble solutes. veins and venules have thinner walls and less elastin, allowing them to function as a reservoir for the blood, containing up to 64% of the circulating blood.
then we shift to blood flow dynamics and begin with a simple equation describing blood flow: Q=P/R. blood flow equals pressure gradient divided by vascular resistance. blood flow is essentially cardiac output, which is stroke volume times heart rate, and is regulated by neural and endocrine systems. resistance is related to vascular resistance and is regulated by metabolic and neurohumoral systems. pressure is described as an "emergent property" which arises from the interaction of flow and resistance. which seems like just a fancy way of saying P=Q*R. pressure difference is then defined as Paorta-Pvenacava, but since Pvenacava is negligible, P=Paorta. we later find out that Paorta is essentially mean arterial pressure (the formal definition / estimation of which is diastolic pressure plus 1/3 of the difference between systolic and diastolic pressure). thus the most useful, applicable form of this flow equation seems to be (cardiac output) = (mean arterial pressure) / (vascular resistance)
several more terms are introduced in the discussion of blood flow. resistance is elucidated in the poiseuille equation as being proportional to the viscosity of the blood and length of the vessel while being inversely proportional to the radius^4. velocity is the measure of flow taking into account surface area; it can also be described as the speed at which the blood flows along the length of the vessel (as opposed to the flow, which does not account for this). capillaries have the greatest total surface area, making the velocity of blood drop considerably, allowing time for nutrient exchange. viscosity is used as a segue into the idea of laminar flow, which occurs as a result of blood/blood friction and also blood/vessel wall friction, causing the velocity to be greatest in the center of the vessel. finally, turbulence is described as proportional to the reynold's number, which is proportional to diameter of the vessel, density of blood, and velocity, and inversely proportional to the viscosity.
there are a few different aspects of blood pressure that are looked at in this last section. the first is the act of taking blood pressures via a sphygmanometer, which can measure systolic and diastolic pressure by listening for the pressure at which the korotkow sound appears, which represents the turbulence caused by the systolic pressure briefly opening up the occluded brachial artery. the diastolic pressure can then be determined when the korotkow sounds disappear, since the artery will be continuously open when diastolic pressure is slightly greater than the pressure of the cuff. the second is the idea of the two different types of blood pressure on the microscopic level: pressure that arises from blood/blood interaction, going along the length of the vessel, is described as perfusion pressure and is related to kinetic energy. the blood pressure that arises from blood/vessel wall interaction is called transmural pressure and is related to potential energy (in this case stored as pressure in the arteries).
the next aspect of pressure that is looked at is the pulse pressure, which is defined as the difference between the systolic and diastolic pressures, and as such is directly related to both stroke volume and compliance. we learn that in healthy circulation, there is a certain level of compliance in the aortas which allows for some of the stroke volume to be effectively "stored" in the arteries during systole, and the pressure created from this storage allows blood to flow in the capillaries even during diastole. in contrast, in arterial dysfunction involving low compliance, the stroke volume translates directly into the capillaries, not allowing for any additional flow during diastole. this is displayed graphically on the pressure vs. stroke volume graph, in which compliance is a line with a positive slope; where decreased compliance increases the slope of the compliance line, thereby increasing systolic pressure and reducing diastolic pressure. finally, three pathologies relating to pulse pressure are described: artherioscerlosis is a disease in which the arteries have lower compliance, causing higher systolic pressure and therefore larger pulse pressure. hypothyroidism and aortic stenosis are both diseases in which the stroke volume is reduced, which also leads to an reduced pulse pressure.
we then zoom in and look at the smaller architecture of arteries, arterioles, capillaries, veins and venules. arteries have three layers, a tunica intima which has endothelium, sub endothelial CT, and an internal elastic lamina. tunica media is the middle layer with smooth muscle and external elastic lamina. tunica adventitia is the outermost layer, with fibrocollagen. arterioles have extensive smooth muscle (which, as it is explained later, helps create a large resistance which causes the largest pressure drop in the circulatory system), running 1-5 layers deep in the tunica media with less fibrous tissue in the tunica intima and adventitia. capillaries are described as the place for nutrient exchange, either through the membrane for lipid soluble solutes such as gas, or through the extensive pore network for water soluble solutes. veins and venules have thinner walls and less elastin, allowing them to function as a reservoir for the blood, containing up to 64% of the circulating blood.
then we shift to blood flow dynamics and begin with a simple equation describing blood flow: Q=P/R. blood flow equals pressure gradient divided by vascular resistance. blood flow is essentially cardiac output, which is stroke volume times heart rate, and is regulated by neural and endocrine systems. resistance is related to vascular resistance and is regulated by metabolic and neurohumoral systems. pressure is described as an "emergent property" which arises from the interaction of flow and resistance. which seems like just a fancy way of saying P=Q*R. pressure difference is then defined as Paorta-Pvenacava, but since Pvenacava is negligible, P=Paorta. we later find out that Paorta is essentially mean arterial pressure (the formal definition / estimation of which is diastolic pressure plus 1/3 of the difference between systolic and diastolic pressure). thus the most useful, applicable form of this flow equation seems to be (cardiac output) = (mean arterial pressure) / (vascular resistance)
several more terms are introduced in the discussion of blood flow. resistance is elucidated in the poiseuille equation as being proportional to the viscosity of the blood and length of the vessel while being inversely proportional to the radius^4. velocity is the measure of flow taking into account surface area; it can also be described as the speed at which the blood flows along the length of the vessel (as opposed to the flow, which does not account for this). capillaries have the greatest total surface area, making the velocity of blood drop considerably, allowing time for nutrient exchange. viscosity is used as a segue into the idea of laminar flow, which occurs as a result of blood/blood friction and also blood/vessel wall friction, causing the velocity to be greatest in the center of the vessel. finally, turbulence is described as proportional to the reynold's number, which is proportional to diameter of the vessel, density of blood, and velocity, and inversely proportional to the viscosity.
there are a few different aspects of blood pressure that are looked at in this last section. the first is the act of taking blood pressures via a sphygmanometer, which can measure systolic and diastolic pressure by listening for the pressure at which the korotkow sound appears, which represents the turbulence caused by the systolic pressure briefly opening up the occluded brachial artery. the diastolic pressure can then be determined when the korotkow sounds disappear, since the artery will be continuously open when diastolic pressure is slightly greater than the pressure of the cuff. the second is the idea of the two different types of blood pressure on the microscopic level: pressure that arises from blood/blood interaction, going along the length of the vessel, is described as perfusion pressure and is related to kinetic energy. the blood pressure that arises from blood/vessel wall interaction is called transmural pressure and is related to potential energy (in this case stored as pressure in the arteries).
the next aspect of pressure that is looked at is the pulse pressure, which is defined as the difference between the systolic and diastolic pressures, and as such is directly related to both stroke volume and compliance. we learn that in healthy circulation, there is a certain level of compliance in the aortas which allows for some of the stroke volume to be effectively "stored" in the arteries during systole, and the pressure created from this storage allows blood to flow in the capillaries even during diastole. in contrast, in arterial dysfunction involving low compliance, the stroke volume translates directly into the capillaries, not allowing for any additional flow during diastole. this is displayed graphically on the pressure vs. stroke volume graph, in which compliance is a line with a positive slope; where decreased compliance increases the slope of the compliance line, thereby increasing systolic pressure and reducing diastolic pressure. finally, three pathologies relating to pulse pressure are described: artherioscerlosis is a disease in which the arteries have lower compliance, causing higher systolic pressure and therefore larger pulse pressure. hypothyroidism and aortic stenosis are both diseases in which the stroke volume is reduced, which also leads to an reduced pulse pressure.
10.28.08 organ systems: the heart, part 4
this lecture is the fourth and last in the series about the heart and accordingly looks at some of the larger ideas related to heart contractility, analyzing the cardiac cycle mechanically and graphically. the first main section was an in depth look at the entire heart cycle, displaying all events graphically in a pressure vs. time format. the second section was a mishmash of definitions mainly centered around the pressure/tension vs. length and active vs. passive tension relationships which were described in the muscle lectures and now applied to the heart in all its glory. the third section skipped back and looked at the mechanisms for contractility, specifically what enhanced and what decreased it. the fourth section was a look at the heart cycle within the context of the pressure vs. length graph and graphically demonstrated (similar to the way economics display disturbances to the supply/demand graphs) how different factors could influence the different measures of heart output, most important being stroke volume and work.
although he started with the overview of the heart cycle i think it's better to look at the contractility mechanisms first because it's a smoother transition from the previous material. we know from previous lectures that sympathetic post-ganglionic neurons innervate the SA, AV and myocardium using catecholamine neurotransmitters and adrenergic receptors. this section describes two mechanisms by which the sympathetic neurons accomplish greater contractility and relaxation (=faster heartrate). the metabotropic beta receptors on the nodes and heart facilitate the synthesis of the second messenger cAMP, which then phosphorylates a protein kinase which performs two actions: 1) phosphorylates membrane protein / ion channel which increases permeability of Ca2+, thereby increasing intracellular levels of Ca2+ available for contraction mechanism. 2) phosphorylates phospholamban, which acts to aid the sarcoplasmic reticulum in the reuptake of Ca2+, thereby speeding up relaxation of the cardiac muscle.
the second mechanism for sympathetic stimulation of the heart is with cardiac glycosides, which work by: inhibiting the Na/K pump, which leaves more Na+ ions in the cell, which reduces the concentration gradient and therefore the action of the Ca/Na ion exchanger, which leaves more Ca2+ in the cell to catalyze contraction. on the other hand, the parasympathetic neurons have two ways of de-stimulating the myocardium -- first is via an axo-axonic synapse to the sympathetic axon, which decreases the amount of sympathetic catecholamine NT released. the more direct mechanism is by decreasing cAMP synthesis on the post synaptic side, which will block the stimulation pathways described above.
the overview of the heart cycle is looked at in more depth than the first lecture mentioned: late ventricular diastole, where the blood is passively led into the heart via incoming venous pressure (either from the vena cava's or the pulmonary vein). atrial systole, which is an extra contraction of the atrium in times of stress, duress, or exercise, and is one last extra push of blood into the ventricle before the next phase: the pressure in the ventricle has now equalled and just begun to exceed that of the incoming venous / atrial pressure, so the AV valve (bicuspid or tricuspid) closes to prevent backflow and the ventricle is now a sealed container. the ventricle now undergoes isovolumic contraction, where it is squeezing against its fixed volume of blood in order to overcome the pressure in the aorta walls. once it gets up to this pressure, the semilunar valves open up and the blood starts rushing through the aortas during isotonic contraction, where the blood volume in the ventricle is decreasing via ejection but force of contraction is relatively constant. in reality, it is more of an auxotonic contraction, because the force of contraction changes significantly by the change in length of muscle fiber, first increasing, then decreasing. at a certain point, the pressure from the blood column in the aortas exceeds that of the ventricles, and the semilunar valves close back up. the emptied ventricles are now back to being a sealed, fixed volume, and needs to release pressure isovolumically in order to restart the diastole process. it contracts until the pressure drops down to below the atriums and the AV valves open up and incoming venous blood starts passively filling the thing back up.
the next section looks at the heart cycle within the context of the active/passive tension curve for the ventricles. the idea being that during diastolic filling, the passive stretching forces of the ventricle walls are at work and thus the passive tension curve can determine the point at which the filling pressure equals the venous pressure, causing the valves to close. and during systolic ejection, the active tension curve is at work, so this provides both a view of the maximum possible contractility at a certain fiber length (if the ventricle needed to contract against a higher aortic pressure), as well as the point at the end of systole at which the maximum active force equals the aortic pressure, which closes the semilunar valves back up. displaying the heart cycle graphically can be handy in terms of displaying two key measures of cardiac output: the stroke volume and internal/external cardiac work.
we look at different ways that the heart contractility can be affected. an increase in contractility will shift the active tension curve: this is essentially saying that for a given fiber length, the myocardium has the ability to contract more strongly. this means that during systolic ejection, the ventricle can maintain higher forces for shorter fiber lengths, meaning that the point at which the aortic pressure overcomes the ventricular will come later, thereby increasing the stroke volume. increasing the preload (as in, increasing the pressure of the incoming venous blood) will lengthen the time it takes before the AV valves are shut due to backpressure, which will increase the stroke volume. increasing compliance (inverse of elasticity) shifts the passive tension curve downwards and has the same effect as the last one. increasing the afterload (the pressure in the aortas that the ventricles have to overcome) will cause the semilunar valves to close earlier (because at the higher pressure of systolic ejection, the maximum force of the ventricles that can match the aortic pressure is reached earlier, at a longer fiber length), decreasing the stroke volume.
finally, two random facts about the graphs are thrown in. auxotonic contraction was already covered above. cardiac work is split into two categories: external work, which is the stroke volume times the height of isovolumic contraction, and internal work, which is graphically estimated to be the triangle formed by the beginning portion of the active tension curve and the isovolumic relaxation.
although he started with the overview of the heart cycle i think it's better to look at the contractility mechanisms first because it's a smoother transition from the previous material. we know from previous lectures that sympathetic post-ganglionic neurons innervate the SA, AV and myocardium using catecholamine neurotransmitters and adrenergic receptors. this section describes two mechanisms by which the sympathetic neurons accomplish greater contractility and relaxation (=faster heartrate). the metabotropic beta receptors on the nodes and heart facilitate the synthesis of the second messenger cAMP, which then phosphorylates a protein kinase which performs two actions: 1) phosphorylates membrane protein / ion channel which increases permeability of Ca2+, thereby increasing intracellular levels of Ca2+ available for contraction mechanism. 2) phosphorylates phospholamban, which acts to aid the sarcoplasmic reticulum in the reuptake of Ca2+, thereby speeding up relaxation of the cardiac muscle.
the second mechanism for sympathetic stimulation of the heart is with cardiac glycosides, which work by: inhibiting the Na/K pump, which leaves more Na+ ions in the cell, which reduces the concentration gradient and therefore the action of the Ca/Na ion exchanger, which leaves more Ca2+ in the cell to catalyze contraction. on the other hand, the parasympathetic neurons have two ways of de-stimulating the myocardium -- first is via an axo-axonic synapse to the sympathetic axon, which decreases the amount of sympathetic catecholamine NT released. the more direct mechanism is by decreasing cAMP synthesis on the post synaptic side, which will block the stimulation pathways described above.
the overview of the heart cycle is looked at in more depth than the first lecture mentioned: late ventricular diastole, where the blood is passively led into the heart via incoming venous pressure (either from the vena cava's or the pulmonary vein). atrial systole, which is an extra contraction of the atrium in times of stress, duress, or exercise, and is one last extra push of blood into the ventricle before the next phase: the pressure in the ventricle has now equalled and just begun to exceed that of the incoming venous / atrial pressure, so the AV valve (bicuspid or tricuspid) closes to prevent backflow and the ventricle is now a sealed container. the ventricle now undergoes isovolumic contraction, where it is squeezing against its fixed volume of blood in order to overcome the pressure in the aorta walls. once it gets up to this pressure, the semilunar valves open up and the blood starts rushing through the aortas during isotonic contraction, where the blood volume in the ventricle is decreasing via ejection but force of contraction is relatively constant. in reality, it is more of an auxotonic contraction, because the force of contraction changes significantly by the change in length of muscle fiber, first increasing, then decreasing. at a certain point, the pressure from the blood column in the aortas exceeds that of the ventricles, and the semilunar valves close back up. the emptied ventricles are now back to being a sealed, fixed volume, and needs to release pressure isovolumically in order to restart the diastole process. it contracts until the pressure drops down to below the atriums and the AV valves open up and incoming venous blood starts passively filling the thing back up.
the next section looks at the heart cycle within the context of the active/passive tension curve for the ventricles. the idea being that during diastolic filling, the passive stretching forces of the ventricle walls are at work and thus the passive tension curve can determine the point at which the filling pressure equals the venous pressure, causing the valves to close. and during systolic ejection, the active tension curve is at work, so this provides both a view of the maximum possible contractility at a certain fiber length (if the ventricle needed to contract against a higher aortic pressure), as well as the point at the end of systole at which the maximum active force equals the aortic pressure, which closes the semilunar valves back up. displaying the heart cycle graphically can be handy in terms of displaying two key measures of cardiac output: the stroke volume and internal/external cardiac work.
we look at different ways that the heart contractility can be affected. an increase in contractility will shift the active tension curve: this is essentially saying that for a given fiber length, the myocardium has the ability to contract more strongly. this means that during systolic ejection, the ventricle can maintain higher forces for shorter fiber lengths, meaning that the point at which the aortic pressure overcomes the ventricular will come later, thereby increasing the stroke volume. increasing the preload (as in, increasing the pressure of the incoming venous blood) will lengthen the time it takes before the AV valves are shut due to backpressure, which will increase the stroke volume. increasing compliance (inverse of elasticity) shifts the passive tension curve downwards and has the same effect as the last one. increasing the afterload (the pressure in the aortas that the ventricles have to overcome) will cause the semilunar valves to close earlier (because at the higher pressure of systolic ejection, the maximum force of the ventricles that can match the aortic pressure is reached earlier, at a longer fiber length), decreasing the stroke volume.
finally, two random facts about the graphs are thrown in. auxotonic contraction was already covered above. cardiac work is split into two categories: external work, which is the stroke volume times the height of isovolumic contraction, and internal work, which is graphically estimated to be the triangle formed by the beginning portion of the active tension curve and the isovolumic relaxation.
10.24.08 organ systems: the heart, part 2
this lecture, second in the series of the heart, introduced the finer details of heart contraction and the nervous system's influence over it. the first broad section was about the general components of the action potential mechanism in the hearts. cardiac muscle is introduced as an intermediate between skeletal and smooth muscle, in that it has similarities to both (striations similar to skeletal, cell size similar to smooth). the general mechanism of cardiac muscle contraction and relaxation is then described; induced by the SA and AV nodes, which both produce differently shaped AP curves, and propagating throughout the atriums, ventricles, and purkinje fibers.
the molecular mechanism is described as well: Na+ channels initiate the AP and immediately deactivate. Ca2+ plays a crucial role in promoting a longer during AP and in the actual contraction mechanism. L-type channels have a plateau like permeability curve, representing Ca2+ ions flowing in for a long duration (~150ms), which keeps the AP depolarized for much longer (this is also aided by the decrease in outward K+ flux). inside the cell, Ca+ stimulates further release of intracellular calcium from the sarcoplasmic reticulum, which provides the Ca2+ that is mainly used in the muscle contraction. the actual contraction mechanism is nearly (or completely?) identical to skeletal muscle -- Ca2+ binds to troponin, etc. etc.
the nodes are looked at in further detail. the SA node is the sinoatrial node, which is the primary pacemaker of the heart, because its frequency of depolarization is the fastest. the AV node is a conducting pathway between the atria and ventricles, and is slower due to the relative lack of gap junctions, and this allows the delay in contraction between the atria and ventricles. in the nodes, AP's are initiated by fast T-type Ca2+ channels, which are not affected by Ca2+ blockers, have no long plateau (due to the lack of the slow L-type channels), and spontaneously, autorhythmically depolarize due to the actions of the "funny" Na+ channels, which are activated by hyperpolarization and K+ flux.
finally, we zoom out and look at the overall hierarchy of nervous control over the heart, which starts all the way up in the upper brain structures and trickles down to the autonomic nervous system via the sympathetic and parasympathetic neurons. the main differences between the sympathetic vs. parasympathetic control over the heart are elucidated. the sympathetic preganglionic neurons originate in T1-5 of the spinal cord and innervate the neurons in the autonomic ganglia. the postganglionic neurons project to the heart via the cardiac plexus, stimulating the beta1 receptors on the nodes and myocardium, using NE and E as neurotransmitters. the effect on the SA node is to increase heart rate while the effect on the AV node is to increase conductivity (decrease latency?). the sympathetic innervation also uses second messengers to activate the "funny" Na channels.
the parasympathetic nervous system effect on the heart starts with the preganglionic neurons, which route out to the heart via the cardiac plexus, whatever that is, and the post ganglionic neurons innervate the nodes (but not the myocardium). the receptors used are muscarinic receptors, with ACh as the NT and with plenty of ACh esterase in the receptor areas. the vagus nerve (the name of the parasympathetic nerve), by means of directly opening K+ channels on the SA node, using g-proteins but without any second messengers such as cAMP, thereby allows greater outflow of K+ and therefore a lower membrane potential, and therefore a harder time reaching the threshold potential, thereby reducing the heartrate.
the molecular mechanism is described as well: Na+ channels initiate the AP and immediately deactivate. Ca2+ plays a crucial role in promoting a longer during AP and in the actual contraction mechanism. L-type channels have a plateau like permeability curve, representing Ca2+ ions flowing in for a long duration (~150ms), which keeps the AP depolarized for much longer (this is also aided by the decrease in outward K+ flux). inside the cell, Ca+ stimulates further release of intracellular calcium from the sarcoplasmic reticulum, which provides the Ca2+ that is mainly used in the muscle contraction. the actual contraction mechanism is nearly (or completely?) identical to skeletal muscle -- Ca2+ binds to troponin, etc. etc.
the nodes are looked at in further detail. the SA node is the sinoatrial node, which is the primary pacemaker of the heart, because its frequency of depolarization is the fastest. the AV node is a conducting pathway between the atria and ventricles, and is slower due to the relative lack of gap junctions, and this allows the delay in contraction between the atria and ventricles. in the nodes, AP's are initiated by fast T-type Ca2+ channels, which are not affected by Ca2+ blockers, have no long plateau (due to the lack of the slow L-type channels), and spontaneously, autorhythmically depolarize due to the actions of the "funny" Na+ channels, which are activated by hyperpolarization and K+ flux.
finally, we zoom out and look at the overall hierarchy of nervous control over the heart, which starts all the way up in the upper brain structures and trickles down to the autonomic nervous system via the sympathetic and parasympathetic neurons. the main differences between the sympathetic vs. parasympathetic control over the heart are elucidated. the sympathetic preganglionic neurons originate in T1-5 of the spinal cord and innervate the neurons in the autonomic ganglia. the postganglionic neurons project to the heart via the cardiac plexus, stimulating the beta1 receptors on the nodes and myocardium, using NE and E as neurotransmitters. the effect on the SA node is to increase heart rate while the effect on the AV node is to increase conductivity (decrease latency?). the sympathetic innervation also uses second messengers to activate the "funny" Na channels.
the parasympathetic nervous system effect on the heart starts with the preganglionic neurons, which route out to the heart via the cardiac plexus, whatever that is, and the post ganglionic neurons innervate the nodes (but not the myocardium). the receptors used are muscarinic receptors, with ACh as the NT and with plenty of ACh esterase in the receptor areas. the vagus nerve (the name of the parasympathetic nerve), by means of directly opening K+ channels on the SA node, using g-proteins but without any second messengers such as cAMP, thereby allows greater outflow of K+ and therefore a lower membrane potential, and therefore a harder time reaching the threshold potential, thereby reducing the heartrate.
10.15.08 organ systems: the heart, part 1
this lecture introduces the basic layout of the heart and begins to talk about blood flow dynamics. blood flows in through the inferior and superior vena cava into the right atrium, which uses its pectinate muscles and vestigial auricle to contract and squeeze the blood through the tricuspid valve into the right ventricle. while the tricuspid is open it is stabilized by chordae tendonae, which are tendons that are attached to the papillary muscles, which contract during the valve opening in order to stabilize. when the right ventricle contracts, it goes out of the pulmonary semi-lunar valve, which leads to the pulmonary vein, which leads to the lungs.
the now oxygenated blood comes back through the pulmonary artery into the left atrium, and is then let into the left ventricle via the bicuspid (or mitral) valve. once in the left ventricle, it is squeezed out through the aortic semi lunar valve into the aorta, in order to irrigate all the capillaries of the body.
systole is the expulsion of blood from the heart and diastole is the filling of the heart. the first heart sound comes from systole of the ventricles, where the atrioventricular cusps are shut closed due to the pressure from contraction. diastole is the second heart sound, which is the sound of the semilunar valves closing back up under the retrograde pressure of the column of blood in the aortas, which fill the sinuses behind the cusps of the SLV and shut it.
the coronary artery is the blood supply to the heart muscle itself. the left is split into the anterior descending and the circumflex, and the right is split into the posterior descending and the marginal. coronary bypass is when a piece of thoracic artery (for thick arteries like the anterior descending) or saphenous veins (for thin arteries like the marginal) is grafted in as a shunt to bypass any "occlusion", which is a site of blockage or damage.
the now oxygenated blood comes back through the pulmonary artery into the left atrium, and is then let into the left ventricle via the bicuspid (or mitral) valve. once in the left ventricle, it is squeezed out through the aortic semi lunar valve into the aorta, in order to irrigate all the capillaries of the body.
systole is the expulsion of blood from the heart and diastole is the filling of the heart. the first heart sound comes from systole of the ventricles, where the atrioventricular cusps are shut closed due to the pressure from contraction. diastole is the second heart sound, which is the sound of the semilunar valves closing back up under the retrograde pressure of the column of blood in the aortas, which fill the sinuses behind the cusps of the SLV and shut it.
the coronary artery is the blood supply to the heart muscle itself. the left is split into the anterior descending and the circumflex, and the right is split into the posterior descending and the marginal. coronary bypass is when a piece of thoracic artery (for thick arteries like the anterior descending) or saphenous veins (for thin arteries like the marginal) is grafted in as a shunt to bypass any "occlusion", which is a site of blockage or damage.
10.13.08 organ systems: neurotransmitters
this lecture introduces neurotransmitters and neuropeptides, the receptors that bind them, the actions they produce, and what role they play in the autonomic nervous system. the first section introduces neurotransmitters and synapse terminology, indicating that the object of focus in this lecture is the specific type of neurotransmitter and receptor that is involved in the synapse.
the second section gives an overview of the nervous system, specifically the peripheral nervous system and the distribution of neurons throughout the body. the differences between the parasympathetic and sympathetic nervous systems are summarized, mainly being that they produce different results in the organs that they innervate (stimulation vs. relaxation), originate in different areas of the spinal cord, and also have ganglia in different locations (autonomic ganglia or adrenal medulla for sympathetic and closer to the organs for parasympathetic).
the third section introduces the different types of ANS neurotransmitters that are dealt with in this lecture, with the two broad categories being cholinergic and catecholamine. the main cholinergic neurotransmitter is acetylcholine and it is associated with nicotinic and muscarinic receptors, which are differentiated by their location; neurons / skeletal muscle for nicotinic, and body tissue / CNS neurons for muscarinic. the other broad category of neurotransmitter is catecholamines, which include dopamine, norepinephrine, and epinephrine. a later slide describes the chain of synthesis of these three NT's from tyrosine: tyrosine to L-dopa to dopamine to norepinephrine to epinephrine.
nicotinic receptors are looked at in greater detail, first starting with the phenomenon of excitatory post synaptic potential's, also called end-plate potentials in these neuromuscular junctions between the post synaptic neuron and the skeletal muscle cell. this is caused when the release of acetyl choline causes an increase in the permeability of the ionotropic Na+ and K+ channels, causing a net influx of positive ions and therefore a depolarization of the membrane. the location is on the dendrite, and an example includes that of glucose.
muscarinic receptors, on the other hand, are not covered in much detail in terms of their physiology. they are found in the parasympathetic postganglionic synapses and associated with acetylcholine. two examples are given of muscarinic receptor action: the vagus nerve innervating the heart's SA node, the pacemaker, and hyperpolarizing the membrane by opening the K+ channels directly. the other example is stimulating smooth muscle contraction via IP3.
the next few slides deal with norepinephrine and epinephrine and their receptors, alpha and beta. not much physiology is covered here either, except to say that alpha receptors regulate Ca++ and K+ channels and beta receptors regulate smooth muscle, cardiac, and metabolism. beta 1 and 2 are also responsive to drugs, such as ephedra (Ma Huang), Propranolol, and amphetamines (ie: cocaine).
neuropeptides are then introduced as a different type of neurotransmittter, one that is synthesized and packaged into larger vescicles in the cell body, transported to the axon, and are released only with higher frequency stimulation (translating into higher concentration gradients of intracellular calcium), at which point they are co-released with other neuropeptides and create a longer lasting effect than neurotransmitters. neuropeptides act at much lower concentrations than neuotransmitters.
the last two slides are a huge chart of the entire peripheral nervous system, showing the somatic, parasympathetic and sympathetic divisions, the neurotransmitters secreted and receptors used in each synapse, and the end target of innervation. the somatic nervous system shows a single axon (motorneuron) going to the skeletal muscle, releasing ACh into the neuromuscular junction (NMJ) and picked up by a nicotinic receptor. the sympathetic nervous system shows one preganglionic cell synapsing in the autonomic ganglia with ACh and nicotinic receptors, with one of the post ganglionic branches going to smooth muscle, using norepinephrine and alpha/beta receptors, and the other branch going to the sweat glands with a muscarinic receptor and ACh neurotransmitter. the adrenal medulla is also part of the sympathetic, being innervated using ACh and releasing hormones (mainly epinephrine) directly into the bloodstream. the last branch is the parasympathetic, which uses muscarinic receptors and acetyl choline and goes to smooth muscle, cardiac muscle, and glands.
some larger thoughts about this chart: ACh and nicotinic receptors are always used in the synapses between pre and postganglionic neurons. alpha and beta receptors are only used in the sympathetic nervous system for smooth muscle and glands. muscarinic receptors are only used in the parasympathetic postganglionic synapses and the sweat glands of the sympathetic.
the second section gives an overview of the nervous system, specifically the peripheral nervous system and the distribution of neurons throughout the body. the differences between the parasympathetic and sympathetic nervous systems are summarized, mainly being that they produce different results in the organs that they innervate (stimulation vs. relaxation), originate in different areas of the spinal cord, and also have ganglia in different locations (autonomic ganglia or adrenal medulla for sympathetic and closer to the organs for parasympathetic).
the third section introduces the different types of ANS neurotransmitters that are dealt with in this lecture, with the two broad categories being cholinergic and catecholamine. the main cholinergic neurotransmitter is acetylcholine and it is associated with nicotinic and muscarinic receptors, which are differentiated by their location; neurons / skeletal muscle for nicotinic, and body tissue / CNS neurons for muscarinic. the other broad category of neurotransmitter is catecholamines, which include dopamine, norepinephrine, and epinephrine. a later slide describes the chain of synthesis of these three NT's from tyrosine: tyrosine to L-dopa to dopamine to norepinephrine to epinephrine.
nicotinic receptors are looked at in greater detail, first starting with the phenomenon of excitatory post synaptic potential's, also called end-plate potentials in these neuromuscular junctions between the post synaptic neuron and the skeletal muscle cell. this is caused when the release of acetyl choline causes an increase in the permeability of the ionotropic Na+ and K+ channels, causing a net influx of positive ions and therefore a depolarization of the membrane. the location is on the dendrite, and an example includes that of glucose.
muscarinic receptors, on the other hand, are not covered in much detail in terms of their physiology. they are found in the parasympathetic postganglionic synapses and associated with acetylcholine. two examples are given of muscarinic receptor action: the vagus nerve innervating the heart's SA node, the pacemaker, and hyperpolarizing the membrane by opening the K+ channels directly. the other example is stimulating smooth muscle contraction via IP3.
the next few slides deal with norepinephrine and epinephrine and their receptors, alpha and beta. not much physiology is covered here either, except to say that alpha receptors regulate Ca++ and K+ channels and beta receptors regulate smooth muscle, cardiac, and metabolism. beta 1 and 2 are also responsive to drugs, such as ephedra (Ma Huang), Propranolol, and amphetamines (ie: cocaine).
neuropeptides are then introduced as a different type of neurotransmittter, one that is synthesized and packaged into larger vescicles in the cell body, transported to the axon, and are released only with higher frequency stimulation (translating into higher concentration gradients of intracellular calcium), at which point they are co-released with other neuropeptides and create a longer lasting effect than neurotransmitters. neuropeptides act at much lower concentrations than neuotransmitters.
the last two slides are a huge chart of the entire peripheral nervous system, showing the somatic, parasympathetic and sympathetic divisions, the neurotransmitters secreted and receptors used in each synapse, and the end target of innervation. the somatic nervous system shows a single axon (motorneuron) going to the skeletal muscle, releasing ACh into the neuromuscular junction (NMJ) and picked up by a nicotinic receptor. the sympathetic nervous system shows one preganglionic cell synapsing in the autonomic ganglia with ACh and nicotinic receptors, with one of the post ganglionic branches going to smooth muscle, using norepinephrine and alpha/beta receptors, and the other branch going to the sweat glands with a muscarinic receptor and ACh neurotransmitter. the adrenal medulla is also part of the sympathetic, being innervated using ACh and releasing hormones (mainly epinephrine) directly into the bloodstream. the last branch is the parasympathetic, which uses muscarinic receptors and acetyl choline and goes to smooth muscle, cardiac muscle, and glands.
some larger thoughts about this chart: ACh and nicotinic receptors are always used in the synapses between pre and postganglionic neurons. alpha and beta receptors are only used in the sympathetic nervous system for smooth muscle and glands. muscarinic receptors are only used in the parasympathetic postganglionic synapses and the sweat glands of the sympathetic.
10.13.08 organ systems: metabotropic transmission
here's the first summary that i tried this semester:
this lecture introduces the concept of metabotropic transmission, which is essentially when membrane receptor proteins set off chains of reactions of proteins and enzymes which then mediate a cell response which is generally longer lasting, more amplified than that of ionotropic receptors. g proteins are the single most important transducer molecule in that they are the first intermediate which set off the chain reactions. they are energized by GTP and can affect ion channel permeability, create second messengers, and regulate protein transcription.
second messengers are then detailed, with an emphasis on cAMP, its synthesis and its actions. cAMP is synthesized when g proteins stimulate adenyl cyclate to make cAMP from ATP. the total cAMP in the cell is a summation of the stimulatory and inhibitory activity of g-proteins. cAMP then stimulates enzyme protein kinases, which then can have a plethora of effects on the cell. specific examples: affect excitability of cell by affecting permeability of non gated K+ channels. convert glycogen to glucose in the liver. release fatty acids from adipose cells. etc. etc.
the other two second messengers talked about in this lecture are IP3 and DAG. the synthesis pathway is: g proteins stimulate PLC to cleave PIP into IP3 and DAG. IP3 is responsible for Ca+ release in smooth muscle cells and DAG is responsible for cell growth and proliferation.
the last main concept in this lecture is the regulation of gene transcription and ion channel permeability (up and down regulation) by g-proteins. the former is accomplished by protein kinases stimulating CREB, which is a translational activator. the latter is accomplished by cAMP stimulating protein kinases to interact with transcription factors which then produce proteins that interact with the protein channels on a long term basis (contrast this with the way that g proteins sometimes directly bind to ion channels)
this lecture introduces the concept of metabotropic transmission, which is essentially when membrane receptor proteins set off chains of reactions of proteins and enzymes which then mediate a cell response which is generally longer lasting, more amplified than that of ionotropic receptors. g proteins are the single most important transducer molecule in that they are the first intermediate which set off the chain reactions. they are energized by GTP and can affect ion channel permeability, create second messengers, and regulate protein transcription.
second messengers are then detailed, with an emphasis on cAMP, its synthesis and its actions. cAMP is synthesized when g proteins stimulate adenyl cyclate to make cAMP from ATP. the total cAMP in the cell is a summation of the stimulatory and inhibitory activity of g-proteins. cAMP then stimulates enzyme protein kinases, which then can have a plethora of effects on the cell. specific examples: affect excitability of cell by affecting permeability of non gated K+ channels. convert glycogen to glucose in the liver. release fatty acids from adipose cells. etc. etc.
the other two second messengers talked about in this lecture are IP3 and DAG. the synthesis pathway is: g proteins stimulate PLC to cleave PIP into IP3 and DAG. IP3 is responsible for Ca+ release in smooth muscle cells and DAG is responsible for cell growth and proliferation.
the last main concept in this lecture is the regulation of gene transcription and ion channel permeability (up and down regulation) by g-proteins. the former is accomplished by protein kinases stimulating CREB, which is a translational activator. the latter is accomplished by cAMP stimulating protein kinases to interact with transcription factors which then produce proteins that interact with the protein channels on a long term basis (contrast this with the way that g proteins sometimes directly bind to ion channels)
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