HL Mechanics of Breathing 10_24a PDF

RESPIRATORY PHYSIOLOGY The role of the respiratory system is 1) to make oxygen available to the body (to be transported to all cells by the cardiovascular system) and 2) to remove carbon dioxide from the blood (which got there by diffusion from metabolizing...

RESPIRATORY PHYSIOLOGY The role of the respiratory system is 1) to make oxygen available to the body (to be transported to all cells by the cardiovascular system) and 2) to remove carbon dioxide from the blood (which got there by diffusion from metabolizing cells). We will cover what is needed in order to accomplish these tasks: 1) Pulmonary ventilation (the act of bringing air into the lungs and then expelling gases from the lungs); 2) Gas diffusion between the alveoli and the blood; 3) Transport of oxygen and carbon dioxide in the blood; 4) Regulation of breathing; and 5) Special topics involving respiration. That’s a lot to cover in a short period of time, so let’s get started: Pulmonary Mechanics and Anatomy: Air, like anything else we’ve talked about, moves from high pressure to low pressure. In the case of breathing, we want air to initially move into the lungs, and then later to exit the lungs. The pressure of air outside our body is Atmospheric Pressure (the weight of air molecules pressing down on other air molecules due to their attraction by gravity). In essence, we are walking around each day under a very tall column of air pushing down on us. That is atmospheric pressure, and it varies depending on where we are located within the atmosphere. If we climb a mountain, the column of air above us is less than what was above us at sea level. Therefore, atmospheric pressure decreases with altitude. 1 Atmosphere Mt. Everest = 760 mm Hg 29,000 feet  = 253 mm Hg Sea Level  The pressure of air “inside” our body is Alveolar Pressure. NOTE: The alveoli are small sacs within the lungs where gas exchange with blood occurs. The gas found in the alveoli is in direct contact with atmospheric air by way of the respiratory passages. Therefore, alveolar gas (or alveolar air) is not technically inside our body because it has not passed through a layer of cells yet. When we inhale we have air moving from the atmosphere into our lungs. This means that when air is entering our mouth and moving toward the alveoli atmospheric pressure (Patm) must be greater than alveolar pressure (Palv). When we exhale a breath, alveolar pressure must be greater than atmospheric to cause air to move from the alveoli to the atmosphere. Patm > P Alv PAlv > Patm Inhale Exhale Now, The atmosphere is a big thing, and not apt to change pressure very readily (and certainly not at our command). Alveolar volume is much more manageable, and contained within our chest. So, we will accomplish respiration by alternately decreasing (to inhale) and then increasing (to exhale) alveolar pressure. We alter alveolar pressure by changing the volume within the thoracic cage. This area contains the lungs (which in turn contain the alveoli) and is comprised of the ribs, internal intercostal muscles between ribs, external intercostal muscles between ribs, and the diaphragm. Note the presence of three groups of skeletal muscles, indicating that we will be changing thoracic volume using skeletal muscle contraction. PAtm Chest cavity increases PAtm External in volume, pulling intercostals outward on alveoli and pull ribs PAlv reducing the gas upward and pressure within them. PAlv outward Air enters alveoli until pressures are equal. Diaphragm contracts Let’s take a breath now: In order for atmospheric air to reach the alveoli it must flow through the respiratory passages. It first enters the nose or mouth, passes through the pharynx (which is a passageway for both food and air) and then passes through the glottis to enter the larynx. The glottis is the gateway for air only, with food moving instead into the esophagus. The glottis can be open or closed, depending on whether we are attempting to inhale air or swallow food. From the glottis, air moves through the larynx (where the vocal cords are located) and into the trachea. The trachea then bifurcates, giving rise to multiple bronchi of smaller diameter. The bronchi also bifurcate, giving rise to multiple smaller diameter passages called bronchioles. It is the bronchioles that eventually empty into the alveoli – dead end sacs of air that comprise much of the volume of the lungs. NOTE: As mentioned a moment ago, the glottis can be open or closed. When the glottis is closed it is a high resistance barrier to air movement into or out of the lungs. Picture taking a breath, closing your glottis and then trying to exhale. Pressure in your lungs increases, but air is not expelled. This is called a Valsalva Maneuver, something that is performed every morning by millions of constipated individuals! The point here is that when the glottis is open, air will move from high to low pressure through the glottis. If the glottis is open and air is NOT moving, then the pressure in the alveoli must be equal to atmospheric pressure. So, if air is moving in or out, there is an imbalance between atmospheric and alveolar pressures, and no movement indicates the pressures are equal. Closed glottis Open glottis PAtm PAtm PAlv PAlv Okay, now we’re ready to inhale. Start by exhaling your current breath and pause for a moment with your glottis open (Isn’t it neat that you can do this stuff during an exam!). Air isn't moving, so just before we inhale we must have: PAtmosphere = PAlveoli. As we now inhale we have air moving from the atmosphere into the alveoli. This must be because we now have a new situation, where: PAtmosphere > PAlveoli. Air moves from the high pressure toward the low pressure, from the atmosphere into the lungs. Patm = PAlv Patm > P Alv At rest after exhaling Inhale: Open glottis Patm stays constant Ready to inhale PAlv decreases as lungs expand How did the alveolar pressure fall below atmospheric pressure when they were equal just a moment ago? Alveolar pressure falls because we increase the volume inside the thoracic cage. Initially, as this volume increases there is the same volume of air inside the alveoli – meaning that there are the same number of gas molecules there as were there a moment ago – yet the volume these gas molecules now occupy is larger than before. This causes a drop in alveolar pressure. The moment alveolar pressure becomes minutely lower than atmospheric pressure, gas molecules will begin to move into the alveoli to equilibrate the two pressures once again. Try closing your glottis and inhaling. Feel the “suction” in your throat as air is sucked toward the lower pressure in the lungs but can’t enter due to the closed glottis? Well, air will continue moving from the atmosphere into the lungs as long as we continue to expand the volume of the thoracic cavity. When we stop expanding the thoracic cavity air moving into the alveoli will rapidly cause an equilibration of atmospheric and alveolar pressures, and air will stop moving into our lungs because once again PAtmosphere = PAlveoli. How did we increase the volume of the thoracic cage? By skeletal muscle contraction: During normal breathing in the resting state of a healthy individual the volume of thoracic cage is increased by contraction of the diaphragm and the simultaneous contraction of the external intercostal muscles. At rest, the diaphragm is bowed up into the thoracic cage. When the diaphragm contracts, it “straightens out”, removing the bowing into the thorax and thereby increasing the volume of the thorax. At the same time the external intercostal muscles begin to contract. Their contraction pulls the ribs upward and anteriorly, causing the ribs to project outward (rather than their resting state, where they angle downward and posteriorly). This causes the chest wall to move outward, away from the spine (increasing the distance between sternum and spine by about 20%). The sternocleidomastoid, anterior serrati and scaleni muscles also assist with this movement. Side view PAtm of ribs PAtm PAlv PAlv The expansion of the chest cavity pulls the lungs outward, expanding alveolar volume and decreasing alveolar pressure, and atmospheric air enters to equilibrate the pressures of the two compartments (atmosphere and alveoli). There, we have inhaled! Now what about exhaling? In the normal quiet and healthy individual exhalation is accomplished by relaxing the inspiratory muscles, which will act to decrease the volume of the chest cavity – increasing alveolar pressure. Side view PAtm PAtm of ribs PAlv PAlv Alveolar pressure increases, forcing air Relax contracting diaphragm out of the and external intercostals lungs Actually, the relaxation of the inspiratory muscles causes the lungs to pull inward on the chest wall. This is because there is substantial elasticity in the lungs (a good idea given that they are constantly being stretched and then compressed). This is much like stretching a rubber band, and then having the elastic recoil of the rubber band pull it back to its resting state when you remove the tension that you placed on it. So, elastic recoil causes the volume of the alveoli to decrease (and the pressure on the gas inside the alveoli to increase). Air then flows from the high pressure (alveoli) to the lower pressure (atmosphere) and we exhale. Elastic recoil pulls alveoli (and therefore the lungs) inward. This increases PAlv Alveolar Pressure to PAlv greater than Atmospheric pressure What if we aren’t just quiet and resting? In situations which promote heavy breathing (I’m thinking exercise here – like walking up 10 steps – but you can come up with other visions if you wish!) inhalation will continue as described above, but we must augment elastic recoil to help us to exhale rapidly enough to get ready for the next breath. In this case, exhalation is aided by the contraction of: 1) the internal intercostal muscles (which pull the sternum down toward its resting position); 2) the abdomnal recti muscles (which pull downward on the lower ribs); and 3) abdominal muscles (which force the organs of the abdomen upward into the diaphragm). These contractions help to decrease thoracic cavity volume more rapidly than by passive relaxation. This causes the air pressure in the alveoli to increase more rapidly, and therefore a more rapid expulsion of air from the lungs because of the greater pressure difference that is produced. Let’s go back to the elasticity of the lung, and the lung’s relationship to the chest wall: The lungs are NOT firmly attached to the interior of the chest wall. Rather, the lungs are always held in a partially inflated state by negative pressure “sucking” the lungs up against the chest wall. So, there is a space between the lungs and the chest wall that is sucking the lungs outward. This space is called the intrapleural space, and it contains pleural fluid (which will help lubricate shifting of the lungs against the chest wall during inhalation and exhalation). NOTE: The pleural fluid is constantly being pumped into the lymphatic drainage from the lungs, producing and maintaining the suction. Lungs (are pulled inward Chest wall (wants to - want to collapse) spring outward) Intrapleural space (Contains pleural fluid and a negative pressure - due to suction produced by lungs pulling inward and chest wall pulling outward, and constant lymphatic drainage Normally you would not see any “space” per se, but you could measure the negative pressure that Relative Pressures (Glottis open): exists between the chest wall and the lungs. What is “negative pressure”? Well, if we were going Patm = 0 cm H2O to compare one pressure to another, and use one pressure as the baseline, we would best choose atmospheric pressure as being our relative value of 0. When we have exhaled and are about to inhale but there is no air currently moving, then the pressure difference Palv = 0 cm H2O NOTE: We between the alveoli and wouldn’t atmosphere would be 0. At that actually see same time, if we recorded the space here in pressure in the intrapleural space the normal we would find that pressure was healthy about 5 cm H2O more negative person than the atmosphere – hence the Intrapleural Pressure idea that the pressure is negative. = -5 cm H2O NOTE: What’s this “5 cm H2O” mean? This is a measure of pressure, just like measuring blood pressure in mm Hg. It is telling us that the pressure in the intrapleural cavity could support a column of water that is 5 cm less tall than the column of water that the atmosphere could support. Since water is less dense than mercury, water is used for expressing smaller pressure differences (e.g. 5 cm H2O is approximately equal to 3.5 mm Hg). The pressures of the two columns are the same: = 3.5 mm Hg = 5.0 cm H2O In fact, the lowest possible energy state for the lung is to be deflated (allowing the elasticity to be totally relaxed - like letting go of a rubber band). We can accomplish this by allowing the negative pressure in the intrapleural space to equilibrate with atmospheric pressure. This can be accomplished by poking a hole in either the chest wall or the lung itself. As air enters the intrapleural space (because it is drawn by the negative pressure) the lungs will undergo further elastic recoil and further deflation. This situation is called a pneumothorax (fancy term) or on the street – a collapsed lung. Patm = 0 cm H2O Palv = Air Palv = 0 cm H2O 0 cm H2 O Intrapleural Pressure Intrapleural Pressure = 0 cm H2O = -5 cm H2O  Let’s look at the pressure changes which occur during a respiratory cycle: Once again we’ll start after just having exhaled and there is no air moving through our airways. This means that alveolar pressure is equal to atmospheric pressure (and that the intrapleural, or transpulmonary, pressure is –5 cm H2O). Inspiration is initiated by contraction of the diaphragm and the external intercostal muscles. As the volume of the chest cavity begins to expand it will be pulling against the elasticity tending to collapse the lungs. Therefore, the first thing we are likely to record is a drop in the pleural pressure, from –5 toward –7.5 cm H2O. This increased negativity pulls more firmly outward on the lungs, causing them to expand some. Patm = 0 cm H2O Palv = Palv = 0 cm H2O 0 cm H2O - 5 cm H2O intrapleural pressure - 7.5 cm H2O intrapleural pressure As they expand it is causing the volume of each alveolus to increase. The increase in alveolar volume (prior to any air entering) means that alveolar pressure begins to drop. Initially there was no difference between alveolar and atmospheric pressure, but now alveolar pressure becomes transiently negative relative to atmospheric (by about –1 cm H2O maximum). This is all the pressure difference that is necessary for air to begin flowing into the lungs and preventing a further negative pressure from developing in the alveoli. As air enters, the lungs expand and the increased number of gas molecules in the enlarged alveoli means that alveolar pressure begins to equilibrate with the atmosphere. Air enters the alveoli, flowing from high to low pressure: Palv = From Atmospheric Palv = ( 0 cm H2O) to - 1 cm H2O Alveolar (-1 cm 0 cm H2O H2O) - 7.5 cm H2O intrapleural pressure - 5 cm H2O intrapleural pressure This continues until we stop expanding chest volume. At this point our diaphragm and external intercostals are contracting as firmly as they will during this respiratory cycle. Once the chest cavity stops expanding the air entering through the mouth and nose will quickly cause equilibration of pressure between the atmosphere and alveoli. Once the pressures are equal we have finished inhaling our breath. Now we have equal pressures in the alveoli and atmosphere, and the pleural pressure is as negative as we will see at any point in the cycle (-7.5 cm H2O). To reach this point about 2 seconds has passed, and the –1 cm H2O pressure difference in the alveoli has caused about 500 ml of air to enter the lungs.  Now we exhale: The diaphragm and external intercostals relax (and, if need be, we also have contraction of the internal intercostals and abdominal muscles). This causes the chest wall to begin moving back toward its resting position, meaning that it is no longer pulling outward on the intrapleural space as greatly as before. Pleural pressure starts to become less negative, changing from –7.5 cm H2O back toward –5 cm H2O. This means that the intrapleural space is no longer “sucking” outward on the lungs as much, and elastic recoil of the lungs begins. As the lungs return back to their lower energy state there is an increase in alveolar pressure such that alveolar pressure now is greater than atmospheric pressure by about +1 cm H2O. Now air will begin moving from the alveoli back to the atmosphere, and we exhale 500 ml of air in 2-3 seconds. Air exits the alveoli, flowing from high to Palv = low pressure: Palv = + 1 cm H2O From Alveolar 0 cm H2O ( +1 cm H2O) to Atmospheric (0 cm H2O) - 5 cm H2O intrapleural pressure - 5 cm H2O intrapleural pressure One more thing to note: The difference between the pleural pressure and the alveolar pressure is called the transpulmonary pressure (I call it the intrapleural pressure). Transpulmonary pressure is a measure of lung elasticity, and the greater the transpulmonary pressure the greater the elastic force acting to collapse the lungs. So what? It turns out that the elasticity of the lungs only accounts for about 1/3 rd of lung compliance. About 2/3rd’s of the force tending to collapse the lungs is due to surface tension. Why is there surface tension in the lungs? In order to facilitate gas diffusion across the alveoli we first need to get the gas into solution. This means that we need to have at least some water inside the alveoli. Normally there is a very thin layer of water lining the interior of the alveoli. This water layer is what produces surface tension. Lowest energy state Surface tension H2O H2O H2O H2O H2O H2O H2O H2O H2O H O H2O Surface H2O H2O H2O 2 tension H2O H O H O H2O 2 2 tends to collapse Higher energy states alveoli If you remember way back to Biochemistry, you may recall that water stabilizes itself (goes to a lower possible energy state) when surrounded by other water molecules. This provides hydrogen and electrostatic bonding between water molecules. Unfortunately, this also means that each water molecule wants to totally surround itself with other water molecules in order to be maximally stabilized. In the thin layer of water coating the alveoli, all of those molecules on the gas-water interface are only partially surrounded by water. Lowest energy state Surface tension H2O H2O H2O H2O H2O H2O H2O H2O H2O Surface H2O H2O H O H2O H2O 2 tension H2O H O H O H2O 2 2 tends to collapse Higher energy states alveoli The water molecules on the surface act to pull other water molecules around them – pulling inward on the alveolus. This is the surface tension which is tending to collapse the lung. The water in the alveolus will be at its lowest possible energy state if the entire alveolus is filled with water. Unfortunately, that would mean that fresh air couldn’t enter the alveolus. So, we’re left with the need for the water and must work harder to breath (overcoming the tendency of that water to collapse our lungs). We do have something working in our favor though, the chemical called surfactant, which acts to decrease surface tension – and, therefore, decreasing the force necessary to keep the lungs inflated. Surfactant is a mixture of phospholipid (in particular dipalmitoyl lecithin – the key “active ingredient”), surfactant apoproteins and ions (in particular calcium). Surfactant is secreted into the alveolus by Type II alveolar epithelial cells, and it greatly reduces surface tension by interfering with interactions between water molecules. The presence of the surfactant on the water surface decreases surface tension by 50-90% compared to what would exist if surfactant were not present. H2O H2O H2O H2O H O H2O H2O H2O 2 H2OH O H2O H2O H2O 2 H2O H2O H2O H2O H2O Without surfactant With surfactant The most likely time to hear about problems with surfactant are in premature infants. Surfactant synthesis and secretion begin late in gestation. Therefore, premature infants have limited surfactant production, and surface tension is much greater than in the normal healthy adult. In addition, the alveolar diameter in infants is smaller in the adult, meaning that even with surfactant the pressure tending to collapse the alveolus is much greater than in the larger adult alveolus (Collapse Pressure = [(2)(Surface Tension)]/Radius). Without surfactant to help reduce the collapse pressure these premature infants must work very hard to be able to inflate their lungs. This leads to the situation called newborn respiratory distress syndrome. One final note about surfactant: When we inhale we increase alveolar diameter. This increased diameter decreases collapse pressure (see above), but simultaneously “dilutes” the surfactant present by distributing it over a greater water surface area. When we exhale, the diameter of the alveolus decreases but the surfactant concentration on the surface increases (because the surface area for surfactant distribution is decreased). These two component – radius and surfactant – effects help to assure that collapse pressure never gets too large or too small. S S S S S S S S S S S S S S S S S S S S S S S S A couple of times now I have mentioned the “work” of breathing. Yes, it takes energy to get oxygen to make more energy. In a normal, healthy adult, the work of breathing (primarily contracting skeletal muscles for air movement) accounts for about 3-5% of total body energy consumption – not a bad trade-off, like paying a 3-5% sales tax. Interestingly, if a person has restricted airways (such as with asthma) this percentage increases because the muscles must work harder in order to accomplish the same amount of gas movement. During heavy exercise the amount of energy expended in breathing can reach 50% of total body energy consumption (This is more like federal income taxes!). This high percentage becomes a limiting factor in the intensity of exercise that we can attain. Cool! (Not that I’ve ever approached that level) Pulmonary Volumes: You can’t talk about respiratory physiology without talking about lung volumes and capacities. These are measures of the amount of air existing in the lungs at different times, or which can be moved into or out of the lungs in different situations. For instance, exhale a breath. There is still a volume of air left in your lungs. That volume is referred to as the Functional Residual Capacity (FRC), and it is about 2.3 liters in an “average” young adult male. It consists of the Expiratory Reserve Volume (ERV = 1,100 ml) and the Residual Volume (RV = 1,200). So, ERV + RV = FRC. The expiratory reserve volume is the amount of air that you can blow out after having exhaled a normal breath. The residual volume is the air that is left in your lungs after you have exhaled as much air as you possibly can. Functional Residual Volume (1.2 liters) Residual Capacity Expiratory Reserve (1.1 liters) (1.2 liters) Tidal Volume (0.5 liters) Another volume to know is the Tidal Volume (TV). Tidal volume is the amount of air that you inhale and exhale during a normal breath, typically about 500 ml. After having taken a normal breath you can still inhale additional air if needed. The additional air that can be inhaled is about 3 liters and is called the Inspiratory Reserve Volume (IRV = 3,000 ml). The total amount of air which can be inhaled just after exhaling a normal breath (IRV + TV) is called the Inspiratory Capacity (IC), and is about 3.5 liters.  That leaves us with two final physical volumes: 1) The combination of the ERV + TV + IRV = Vital Capacity (VC). To get an idea of vital capacity simply inhale as deeply as possible, and then exhale as much as possible. The volume exhaled is your vital capacity, about 4,600 ml (4.6 liters) in our average young adult male. 2) Even after exhaling there is still the residual volume of air left in the lungs (which we can never get out), so the total amount of air that can possibly be held in the lungs (called Total Lung Capacity – TLC) is equal to VC + RV = 5.8 liters. Residual Volume (1.2 liters) Total Expiratory Reserve (1.1 liters) Lung Vital Capacity Capacity Tidal Volume (0.5 liters) (4.6 liters) (5.8 liters) Inspiratory Reserve (3.0 liters) This is all very rewarding to us guys, but what would the volumes and capacities be for women? Basically, just take the values listed for men and reduce them by 25-30%. This is generally necessary because most textbooks have been written by men! Larger people and trained athletes tend to have greater volumes than those listed. I have no idea how to estimate the volumes of trained athletic female dwarves. A spirometer can be used to measure and/or calculate most of the volumes and capacities named above. A spirometer just requires the person to perform the tasks described above and then exhaling into a collection cylinder. One volume which can’t be measured in this way is the residual volume.  To estimate the residual volume of the lungs one could use the helium dilution method: The patient exhales normally and then inhales from a filled spirometer containing air and helium of known concentration and volume. As the patient continues re-breathing from the spirometer there is an equilibration of the “pure” air of the original functional residual capacity and the helium/air mix in the spirometer. Then, just measure the final concentration of the helium to determine the FRC: FRC = { CiHe – 1} ViSpir CfHe Where: FRC = Functional Residual Capacity CiHe = Initial concentration of helium in the spirometer CfHe = Final concentration of helium in the spirometer ViSpir = Initial volume of gas in the spirometer Once the FRC is calculated you can estimate RV by subtracting: RV = FRC – ERV Some relationship equations to remember: VC = IRV + TV + ERV VC = IC + ERV TLC = VC + RV TLC = IC + FRC FRC = ERV + RV  Now that we have a grasp of the physical volumes of the lung we can move on to the minute respiratory volume and alveolar ventilation. The minute respiratory volume is the volume of air per minute which is inhaled. Thus, it is simply the tidal volume times the respiratory rate: VI = (TV)(Respiratory Rate) = (500 ml)(12) = 6 liters/min This value tells us how much air we breath in per minute, but we have another problem: If with each breath we inhale 500 ml of fresh air, a significant part of that fresh air never reaches our lungs – it gets into our mouth and trachea but doesn’t reach the alveoli. Therefore, a portion of each tidal volume doesn’t get to the gas exchanging structures and is instead occupying the “Dead Space”. Sure, 500 milliliters of air enters the alveoli with each breath, but the initial air entering the alveoli when we inhale is air which had just been trapped in the dead space when we exhaled our previous breath. The dead space volume is about 150 ml (and gets slightly larger as we age), so only about 350 ml of fresh air (along with the 150 ml from the dead space) enters the alveoli with each new breath. The dead space described above is the anatomical dead space, accounting for the volume of air present in the airways leading up to the alveoli. In addition to this there is something called the physiological dead space. This accounts for the volume of air which enters alveoli where gas exchange is limited or absent due to compromised blood flow to that region. In the healthy person this volume is negligible, but it can be very significant (up to 1-2 liters in volume) in disease states where perfusion and ventilation are not matched. For instance, in chronic obstructive lung disease (such as emphysema in a person who smokes) one problem that develops is the gradual destruction of alveolar walls – producing in essence abnormally large alveoli. They get a bigger share of ventilation, yet have decreased gas exchange capability with nearby blood vessels. Therefore, perfusion is insufficient to meet ventilation, and there is an increase in the physiological dead space. This results in poorer oxygenation of the blood. Normal small alveolus Normal large alveolus Fused alveoli in Emphysema Now back to minute volumes: We have just seen that the true value of each breath is the fresh air which reaches the alveoli for gas exchange: Volume reaching alveoli = Tidal Volume – Dead Space Volume = VT – VD If we then multiply this volume (~350 ml) times the respiratory rate we have the volume of fresh air reaching the alveoli each minute – The alveolar minute volume, abbreviated VA: VA = (Freq)(VT – VD) = (12)(500-150) = 4,200 ml/min It is alveolar ventilation which plays a major role in determining partial pressures of oxygen and carbon dioxide in alveoli (and, therefore, in blood).