First the primary functions of the respiratory system are to
1. Exchange gases between the atmosphere and the blood.
2. Homeostatic regulation of pH through the regulartion of CO2
3. Protection from inhaled patholgens and irritating substances
Quick overview of exchanges and transport. The first exchange is the atmosphere to the lungs. CO2 out, O2 in. The second is from the lungs to the blood, or the blood back to the lungs. O2 in and CO2 out respectively. The last exchange is from the blood to cells, or cells to blood, and again O2 into the cells and CO2 out of the cells into the blood stream.
17-2 a and b
This is the conducting system of passages or airways that lead from the environment to the exchange surface of the lungs. Divided into the upper and lower tract. The upper tract is the nasal cavity, pharynx and larynx. The lower respiratory tract is the trachea, two bronchi, their branches and the lungs. This is also called the thoracic portion because it is in the thorax.
The thorax/chest cavity is bound by bones of the spine and rib cage with their appropriate muscles. The diaphragm is located on the bottom. Two sets of intercostal muscles connect 12 pairs of ribs. The sternocliodmastoids and the scalenes run from the head and neck to the sternum and first two ribs. As seen in the picture, the muscles used for inspiration are the external intercostals, the scalenes, the diaphragm and the sternocleidomastoids. The muscles used for expiration are the abdominal muscles and the internal intercostals.
17-c and d
The lungs themselves consist of light and spongy tissue whose volume is mostly occupied by air filled spaces. The right lung has three lobes called the superior lobe, the middle lobe and the inferior lobe and the left lung has 2 lobes, the superior lobe and the inferior lobe.
This picture helps to orient how everything fits together. The lungs are in two individual pleural membranes which are double membrane sacs containing several layers of elastic connective fluid and many capillaries.
The pleural membranes act as a sac to surround the lungs. The opposing layers of this sac are held by a thin film of pleural fluid which is only a couple mL. The result is similar to an air filled balloon surrounded by water . This serves two purposes 1) so that the opposing membranes can slide across one another and 2) It holds the lungs tight against the thoracic wall and holds them stretched in a partially inflated state.
17-2 e and f
This shows the dividing of the airways as they get deeper into the longs. It goes from the trachea, to the primary bronchus, then the secondary bronchus and then the bronchiole and lastly the aveoli which are enlarged here. The divisions of the bronchi are about 2-11 times, and the divisions of the bronchioles is about 12-23 more times.
As is says, each cluster of aveoli are surrounded by elastic fibers and a network of capillaries which are necessary for gas transport between the blood and alveoli.
17-2 g and h
The alveolous itself is comprised a single layer of epithelium. The two types are the type I cell for gas exchange, the type II cell to synthesize surfactant which helps to ease the expansion of the lungs during breathing. Also around the alveoli are the avelolar macrophages which eat up all the foreign material. Also you can see parts of the capillaries imbedded into the cell. This will all make a little more sense later.
In this last picture you can see how the gas exchange happens. Next to the alveolus is the capillary and gas is exchanged across this boarder.
Boyleıs Law helps to show how the lungs work. We know that when chest decreases in volume, the pressure increases, which would push air out, and when the chest increases with volume, pressure decreases and pulls air in. This movement of air is called bulk flow b/cthe entire gas mixture is moving rather than merely one or two gas species.
The job of the upper airways and the bronchi are not simply to allow air in, but to also make it ready for the alveoli. First the warm the air to about 37 degrees C so that the alveoli will not be damaged. Second, they moisten the air to 100% humidity so that when the air reaches the epithelium it will not dry them out. Lastly they filter foreign material which is seen here. The mucus is secreted by goblet cells in the epithelium and the cilia beat upwards moving the mucus conintuously towards the pharynx and then it is swallowed. This is called the mucus escalator. The mucus also contains many immunoglobins which disable many pathogens.
A single respiratory cycle consists of an inspiration followed by an expiration. During inspiration, the thoracic volume increases when the external intercostals, scalene muscles and the sternocleidomastoid muscles contract pulling the ribs up. At the same time the diaphragm flattens out to let the lungs at the base to extend. The degree to which all of these muscles contributes in relaxed breathing is not exactly known, but for sake of brevity they are known as the inspiration muscles. Then the diaphragm relaxes the muscles relax which make one exhale.
In the book atm is 0 mm Hg.
This figure shows the different ways of measuring the respiratory cycle. The first is through alveolar pressures. At time 0, between inspiration and expiration, the alveolar pressure is equal to that of the atm. Time 2 alveolar pressure is less than atm pressure b/c we are inhaling. Time 3, it is equal because the lungs are equalized with the atm, and at time 4 it is greater that the atm pressure because the volume in the lungs is becoming less and so air flow reverses out of the lungs. Graph of C is self-explainitory. When we inhale our volume increases, exhale-decreases.
In the second graph the interpeural pressure changes as well. Normally the interpleuralpressure is sub atm and the two pleural membranes are held by the pleural fluid. Think of when you put a little water between two glass panes. You can slide them back and forth, but it isnıt easy to take them apart. This is the same idea. Anyway, the membranes force the lungs to expand into the larger volume of the thoracic cavity. However, the elastic recoil of the lungs gives an extra pull that wants the lungs to recoil into their smaller state. This gives the negative pressure. Also you can see when the pleural membrane is pierced in a condition called pneumothorax the lung deflates like a balloon. So the chest wall can expand, but the lung is stuck in its recoiled state because air was allowed to rush inbetween the membranes and separate them. To correct this, one must suck all of the air out with a pump and try to seal the hole.
So returning to the graph, one can judge respirations by intrapleural pressure. First, at point 0, it is the resting pressure of the intraplueral membrane. Then as inspiration continues, the pleural membrane keeps expanding the lungs against the lungs preferred recoiled state. So, because the force of the lungs to recoil is even greater than before, the intrapleural pressure becomes even more negative. (Questions?? ) this is a little hard to visualize.
Much of the resistance in the lungs has been thought to have been caused by surface tension created by a thin fluid layer between the alveolar cells and the air. Water molecules within the alveoli cause this surface tension. Because it is such a thin layer, it takes on a bubble identitiy in which the H-bonds between the water molecules are very strong. Because of this, the law of LaPlace can be used to describe the pressure. *On picture* The smaller bubble has a much greater pressure. So, when put into the alveoli situation, the surface can be covered in fluid and create a strong surface tension which will make it harder to expand. However, surfactants created by the Type II cells disrupt the cohesive forces between the molecules and make the surface tension in the smaller alveoli less than that in the larger alveoli. With lower surface tension, less work is needed to expand.
Ok, so how do we test lung or pulmonary function? One way is with a spirometer which you will work with in lab today. These can be used to diagnostically test for asthma, emphysema, and chronic bronchitis. This machine measures different lung volumes and these volumes are compared with the averages to see where the problems lie.
The different volumes are shown on this graph. First is the tidal volume. This is where if you breathe quietly, the amount of air that goes in or out. Next is the expiratory reserve volume. This is where after relaxing exhaling, you go further and exhale as much as you possibly can. Next is the inspiratory reserve volume, and this is where you take in as much additional air as you possibly can. Then there is the residual volume, where even after maximal expiration, there is still about 1.2 L of air left in your lungs. Most of this is due to the fact that the lungs are held to the thoracic wall by the pleural fluids.
On the other side of the graph we see lung capacities. The vital capacity is the sum of the inspirational reserve volume expiratory reserve volume and the tidal volume. Vital capacity represents the maximum amount of air that can be moved in and out of the lungs. Other important capacities are the inspiratory capacity which is the sum of the tidal volume and then inspiratory reserve volume, the functional capacity which si the sum of the expiratory reserve volume and the residual volume, and lastly the total lung capacity which is everything added together.
In this picture we are assuming, using table 17-4, which I highly suggest you look at, which shows the effects of breathing patterns on alveolar ventilation, that the total pulmonary ventilation is 500 ml/breath, and the alveolar ventilation is 350 mL/breath. So, starting at the end of inspiration when the lungs have as much air as they can take, we have 150 mL of dead space filled with fresh air (in the bronchi and trachea). The tidal volume of 500 mL is exhaled first the fresh air comes out first, then the used air comes out second. So, although 500 mL is exhaled, only 350 mL of it is stale air. At the end of the expiration, that 150 mL of dead space is filled with stale air. Then we inhale again and 500 mL of fresh air enter the body. This pushes the 150 mL of stale air back into the alveoli followed by 350 mL of new fresh air. Over all, although we inhale 500 mL of fresh air, only 200 mL of it actually makes it to the alveoli. L
Different types of breathing can dramatically effect alveolar ventilation. Table 17-4
Shows hypoventilation versus hyperventilation. Hyperventilation is when you have too much O2 and too high O2 pressure in the alveoli, while hypoventilation is when the CO2 pressure is too high and there is not enough O2.
Shows the regulation of capillaries due to the amount of O2 in the alveoli. If the alveoli have lots of O2, and another does not, then blood is directed in that way by local mechanisms.
Diffusion of gases in the respiratory system follows this path. Oxygen is exchanged at the aveoli, transported through the pulmonary circulation to the heart, and then transported by the systemic circulation to be exchanged at the cells, and then CO2 is exchanged at the cells into the blood stream, it is transported through the systemic circulation to the heart, and then through the pulmonary circulation to the lungs and then CO2 is exchanged at the aveoli.
Simple diffusion of gases follows Fickıs Law of Diffusion in which
Diffusion aSurface Area X Concentration Gradient
Membrane Thickness X Membrane Resistance
Assume Membrane Resistance is constant
Also from general rules of diffusion, Diffusion is most rapid under short distances.
18-2 Solubility of gases
When gas is placed directly in contact with water, and there is a pressure gradient, the gas molecules move from one phase to the other. If the gas pressure is higher in the water phase, then they will move to the air, and vice versa. The movement of gas molecules is directly proportional to three factors. 1) thre pressure gradient of the individual gas, 2) the solubility of the gas and 3) temperature of the system. If a gas is very soluble, the large portions of the gas will dissolve in the water at low pressures. If a gas is not very soluble then even at high pressure much of the gas may not dissolve. Partial pressure of gas in solution= the amount of gas that dissolves in the solution at any given pressure. So letıs look at this figure. In the figure we have 100 mm Hg O2 added to water. We let the oxygen dissolve. After it has dissolved we see that there is the same amount of pressure of O2 in the water as there is in the atm. That means they are in equilibrium, although the concentrations are not equal, and it is seen that O2 is not very soluble. On the other hand looking at CO2 it is seen that under the same conditions, CO2 is much more soluble.
In general the gas laws state that gases will flow from regions of high partial pressure to regions of low partial pressure. This provides the reasoning for what is seen here. First for the oxygen diffusion, as the oxygen depleted blood comes up to the alveoli it is at 40 mmHg, which the alveoli is at 100 mm Hg. Then as the blood passes, the partial pressure even out, so that the blood has the same partial pressure as the alveoli. Then as it hits the peripheral tissues, it diffuses across to a lower partial pressure. For CO2 the same thing happens, just in reverse. So as the blood approaches the alveoli, it has a CO2 partial pressure of 46 mm Hg and the alveoli have a partial pressure of 40 mm Hg, and then the blood gives off its CO2 to the alveoli. And the same for the peripheral tissues. As the blood flows by with a lower CO2 partial pressure, the CO2 in the tissues diffuse across to the blood.
Type I capillary cells and the capillary endothelium create the barrier that O2 must diffuse across. Normally diffusion distances are small because cells are thing and there is little or no interstitial fluid between the two cell layers. In addition, oxygen and CO2 are water and lipid soluble so it creates an environment where gas exchange can happen rapidly. In addition, blood flow through the pulmonary capillaries is slow, and diffusion can reach equilibrium in less than a second, so there is ample time for the gases to diffuse across their respective barriers.
Oxygen is transported two ways, one directly through blood plasma, and two through hemoglobin. Hemoglobin is the oxygen binding protein in red blood cells that binds reversibly to oxygen. In the lungs, where oxygen concentration is high, hemoglobin binds to O2 At the cells where O2 concentration is low, hemoglobin gives up the oxygen. Hemoglobin is necessary because O2 is only slightly soluble in liquids as we saw before. More than 98% of our oxygen is transported by hemoglobin.
In ³a² it shows O2 transport without hemoglobin. Look at the total carrying capacity, which is the sum of the O2 in the plasma and the O2 held by the hemoglobin. As you can see, with the hemoglobin working at 50% with decreased O2, it still is more efficient than full O2 without any hemoglobin.
This is the binding curve, or the dissociation curve of oxygen-hemoglobin. Percent saturation refers to the percentage of available binding sites that are bound to oxygen. If all binding sites of hemoglobin are bound to oxygen it is 100% saturated. At normal alveolar oxygen levels, 98% of the hemoglobin is bound to O2. Around where the PO2 is about 60 mmHg, the binding affinity of O2 to hemoglobin seems to begin to drop dramatically. The steep slope as it goes down the curve shows that it is releasing O2.
The binding affinity of O2 onto hemoglobin is different at different temperatures, pHıs and Metabolites. In A, it is seen that is pH rises, the curve shifts up, showing that O2 binds to hemoglobin better at higher pHıs. However, it also shows that at 40 mm Hg, where cells typically are, hemoglobin at 7.2 releases more O2 to the cells than that at 7.6. Then for temperature, as the temperature decreases, the binding affinity for O2 on hemoglobin increases. Lastly, it is seen that as the PCO2 rises, the binding affinity for hemoglobin to oxygen decreases.
Changes in hemoglobin structure also affect binding affinity. Here it is seen that the fetal hemoglobin has a much stronger binding affinity than that of the maternal hemoglobin. The hemoglobin in fetuses has a unique protein chain for two of its subunits and enhances the abiligy of fetal hemoglobin to bind to oxygen in its low oxygen environment.
This is a summary of the slides prior which talked about the total O2 content of the arterial blood. I would review this for the quiz as a check list to see if everything makes sense.
Moving CO2 out. Elevated CO2 causes a pH disturbance called acidosis. Also abnormally high pH levels depress the central nervous system function causing confusion, coma, or death. So CO2 must be removed by the lungs. Although CO2 is more soluble in liquids than O2 only 7% of it is carried in the form of dissolved CO2. 93% of it diffuses into red blood cells where 70% of it is converted to the bicarbonate ion, which is seen here. I think we did this in either MCB, or Cell Structure, so I am not going to get too specific. Basically there are two reasons why this is important, 1) It provides additional means by which carbon dioxide can be transported from cell to lungs and 2) the bicarbonate created is able to act as a buffer for metabolic acids, thereby stabilizing pH. You will have to know this more for Bodeıs class, but for this, know that the products of creating bicarbonate are first carbonic anhydrase makes CO2 and water into carbonic acid. Then carbonic acid goes to bicarbonate and Hb-H plus a chloride shift which brings a chloride into the red blood cell and puts a bicarbonate out. The H that the hemoglobin picked up helps to maintain the pH, and when CO2 levels are too high, it cannot take that H and it causes a condition known as respiratory acidosis.
Then when at the lungs, the processes reverse. Plasma CO2 falls because it diffuses to the alveoli, which allows CO2 to diffuse out of red blood cells, which upsets the equilibrium of CO2 bicarbonate levels and the removal of CO2 causes the removal of H from the hemoglobin. The chloride shift reverses and Cl is pumped out of the rbc and HCO3 is pumped back in. HCO3 binds with H and then the carbonic acid is converted into water and CO2 by CA and CO2 diffuses out.
A good review of transport and diffusion.
Basic ideas of respiration control
1. Respiratory neurons in the medulla control inspiration and expiration
2. Neurons in the pons modulate ventilation
3. The rhythmic pattern of breathing asrises from a network of spontaneously discharging neurons
4. Ventilation is subject to modulation by various chemical factors and by higher brain centers.
The figure shows what controls what. The dorsal respiratory group controls the inspirational muscles and the ventral respirational group controls the muscles that are used for expiration.
The carotid and aortic chemoreceptors are sensitive to PO2, PCO2, and pH. When specialized cells called glomus cells are triggered by decreases in PO2 or pH or increases in PCO2, the trigger a reflex to increase ventilation. (Know this.. do not memorize pathway).
The most important chemical controller of ventilation is CO2 mediated through central receptors located in the medulla. When arterial PCO2 increases, CO2 moves across the blood brain barrier and activates the central chemoreceptors. Well kind of. The chemoreceptors actually respond to the increase in H that is created in the spinal fluid after the blood brain barrier where CO2 is converted into bicarbonate and an H. This tells the brain to increase ventilation.
Summary of what happens.
Acknowledgement – This lecture was first put together by Chris Hawkins, 2005 TA.
Quiz questions from 2005 relating to this lecture, integrative physiology and lab
1. List 2 of the 4 primary functions of the respiratory system.
1. Exchange gases between the atmosphere and the blood.
2. Homeostatic regulation of pH through the regulartion of CO2
3. Protection from inhaled patholgens and irritating substances
2. The right lung has __3___(fill in number) lobes and the left lung has ____2____ lobes.
3. Give one reason for the existence of the pleural membrane.
1) so that the opposing membranes can slide across one another and
2) It holds the lungs tight against the thoracic wall and holds them stretched in a partially inflated state.
4. When the volume of a gas decreases, its pressure _____increases______.
5. Which muscles are responsible for inspiration (there are 4).
external intercostals, the scalenes, the diaphragm and the sternocleidomastoids
6. When you inhale, the interpleural pressure increases or decreases?
7. What is the name of the substance that disrupts surface tension within the alveoli?
8. The maximum amount of air that can be moved in our out of the lungs is the vital capacity_______.
9. True or false: Eventually all the air in our lungs is replaced by fresh air.
10. True or false: When we have too much CO2 in our system we hyperventilate.---throwing out! (Badly worded)
11. Simple diffusion of gases follows ____Flicks_(ficks) (typo from sheet.. I corrected it on my harddrive, but not Dr. Starks)__ law of diffusion and what is the equation?
Diffusion = Surface Area X Concentration Gradient
Membrane Thickness X Membrane Resistance
12.How is most oxygen transferred through the circulatory system to the cells?
through the use of hemoglobin
13. How is most CO2 transferred through the circulatory system back to the lungs?
As Bicarbonate (HCO3)-
14. When someone (or you) breathed into a plastic bag, how did your respiration (time and depth) change?
Depth decreases, time decreases
15. In the medulla what exactly do the chemoreceptors respond to, to know that carbon dioxide levels are too high?
Increase in H+ ion.
Final exam questions from 2005 relating to this outline, interactive physiology and lab
a) scalenes and external intercostals
b) abdominal muscles and internal intercostals
c) abdominal muscles and external intercostals
d) scalenes and internal intercostals
e) scalenes and abdominal muscles
Because air was allowed between the two pleural membranes and they can no
Longer hold the lung against the thoracic wall
Warm the air
Take foreign materials out of the air
Moisten the air
So surface tension in the alveoli does not develop
Resistance within the airway
a. Arterioles constrict __c__ Low PCO2
b. Arterioles dilate __a___Low PO2
c. Bronchioles constrict __d___High PCO2
d. Bronchioles dilate __b___High PO2
This page was last revised 7/13/06