EP2 - Mechanics Of Breathing | Anaesthetic Primary Topic | Respiratory Physiology | CT10

Hello and welcome back to Counterten. Today we will continue talking about respiratory physiology and go through work of breathing. There are seven learning objectives for this topic as per Mac95 that we will discuss and then have a look at some of the past SAQs and exam reports. So let's get started. Now the first LO to cover is discuss the structure of the chest wall and diaphragm and the implications for respiratory mechanics. This is actually quite a tricky LO to actually cover and to begin before we get into the muscles we have to understand why we're breathing and how we breathe. So to understand that we have to understand that for breathing to occur we need a gradient of pressure and this relates back to Boyle's law. Boyle's law will state that for a fixed temperature the volume of gas is inversely proportional to the pressure exerted by that gas. What that means in simple terms is that if you increase volume you decrease pressure. If you imagine your lungs that when they expand the pressure inside them decreases this creates a pressure gradient between the outside being the atmospheric pressure and the inter alveolar pressure. This pressure gradient then allows the flow of air in and then this gets reversed when we expire. So what we're trying to do in terms of our chest and our lungs is we're trying to increase our chest wall expansion. We're trying to increase our anterior posterior diameter of our chest wall. We're trying to increase our transverse diameter of our chest wall all to increase the volume inside that lung so that we can decrease the pressure, create a gradient for air to flow in and that decrease in pressure in the gradient is only very very very tiny. Atmospheric pressure is 760 millimeters of mercury. The gradient that's needed is only a difference of one millimeter of mercury to allow air to come into the lungs and then the reverse to get the air out of the lungs. So for this to occur we can then think about respiration as muscles of inspiration and muscles of expiration. Inspiration normally is an active process and expiration is normally a passive process. When we think about any muscle that we're trying to describe in a short answer question we can divide it into five basic components. So when you're describing a muscle think about its basic structure, its relationships to other structures, its innovation, its blood supply and then what it actually does so its function and you can change the order of that depending on how you like it or how you like to think about it. So when we use those five components and then we can use that to incorporate and describe the diaphragm. So the basic structural anatomy of the diaphragm is that it's a thin sheet of skeletal muscle. It's oval in shape or dome shaped. It has two different types of muscle fibers. There's type one muscle fibers and type two muscle fibers. The type one muscle fibers are the slow twitch muscle fibers which are important in being fatigue resistance. So they can last for longer and work for longer and type two muscle fibers are those fast acting muscle fibers that are good for short action. The importance of that is that when we're neonates the distribution of proportion of type one fibers is much lower. So that's why neonates have an increased propensity to develop respiratory failure. When we talk about the relationship of the diaphragm we can say that it's located in the lower six ribs. It attaches to the vertebral bodies posteriorly, the zippy sternum anteriorly and it descends one to two centimeters down with quite inspiration and then we take a forceful inspiration it can go down as far as 10 centimeters and that's usually an important MCQ that usually comes up quite repeatedly. The other relationship that's important with the diaphragm is that it's unique that it has three openings. It has an opening for the aorta at T12, the esophagus at T10 and then the vena cava at T8 and you can remember that as the vena cava having eight letters and the esophagus depending on the way you spell it has 10 letters in it. The other obvious relationships is that above the diaphragm is the lungs and below the diaphragm is the abdominal contents so it separates that and that can be incorporated into your function. When we then talk about the innovation we'll know the common saying C345 keep the diaphragm alive and mainly it's your C4 and this is through your phrenic nerve so this is your e-fran pathway controlling your motor function of your diaphragm and there's bilateral phrenic nerves there's a left and a right. The blood supply of the diaphragm can be thought about as above the diaphragm and below the diaphragm. Above the diaphragm it's done by the internal thoracic artery and below the diaphragm is done by the inferior phrenic artery and then they drain into the inferior vena cava and the superior renal veins. Finally the most important thing is the function of the diaphragm so what we spoke about at the start is important with the diaphragm it does all those main actions that increase the lung volume so in terms of respiration it increases the chest wall elevation it causes increase in transverse diameter increase in the AP diameter and also it has other additional functions that you need to mention to for a well-rounded answer it separates the abdominal and thoracic content it's important in vomiting and in other reflexes such as coughing it is important in your lower esophageal sphincter tone and it's also important with other things such as urination and defecation. Now talking about other muscles of inspiration an important one that you must also remember is the external intercostal so the external intercostal and the internal intercostal kind of oppose each other's actions the external intercostal is sloped down and inferiorly and when it contracts it lifts the chest wall up in a bucket handle motion and this is important on inspiration and on expiration the internal intercostal do the opposite so they're sloped the opposite way and that's why they're important with expiration. Now normally the external intercostals are not really required it was quiet breathing remember the diaphragm is the most important it's doing about 80 percent of our breathing at any time we're doing just normal quiet breathing. There are other accessory muscles and these can be thought about as your sternocleidomastoid your serratus anterior your trapezius your pec major and all these if you really forget are just trying to do those main three actions they're trying to cause their chest wall elevation they're trying to increase the transverse diameter they're trying to increase the AP diameter and all of them might not do all three of those they might do one or another. Now in terms of expiration we've said it's a passive process normally and that the most important muscles of expiration when we actually try to do it actively are the abdominal muscles they push up against the diaphragm decreasing the volume of your lungs and now all of a sudden you're reversing that pressure gradient so that airflow flows out from the lungs. Additionally we have these internal intercostal muscles we also have the latissimus dorsi the serratus posterior the quadratus lumborum and other muscles that are trying to do the opposite action and again they're trying to just decrease the AP diameter decrease the transverse diameter and cause a decrease in the chest wall elevation so those three things are the most important things in terms of thinking about muscles of respiration and again the real aim of respiration is what's happening between that pressure gradient from outside in the atmosphere and inside the alveoli and what the way the pressure gradient goes determines if you're going to be inspiring or expiring. Now moving on to our second learning objective which is describe the properties of surfactant and relate these to its roles and influencing respiratory mechanics. When you think about surfactant you have to think back to what the lung is. The lung is a big elastic body and there's a few factors involved in making sure that elastic body works well. One of those factors is making sure we reduce surface tension. Other property of the lung is the elasticity of the lung and we'll talk about that when we talk about compliance. So when we talk about surface tension surface tension can be defined as the force acting across an imaginary line one centimeter long in the surface of a liquid and that force is measured in dimes and people love that definition and especially asking that definition in a viva setting. Why does surface tension occur? Well it occurs because between the molecules of the liquid and molecules of the gas there is attraction forces and the attraction forces between liquid molecules is stronger than the attraction forces between the liquid and gas molecules and what that means in simple terms is that the liquid molecules want to come closer to each other and because those are the most strongest form of attraction those the way that the liquid molecule can be closest to each other is being in a spherical shape because it's the smallest surface area for the volume and therefore it's the closest that the liquid molecules can be to each other because their attraction forces are stronger so the liquid to liquid attraction forces is stronger than the liquid to gas attraction forces. The next thing to understand is that there's pressure inside that liquid air bubble and that pressure can be described as Laplace's law. Laplace's law is not unique to the alveoli but it's unique to any hollow structure or any hollow viscera so it can be applied to the alveoli it can be applied to the heart it can be applied to the blood vessels and it can also be applied to hollow viscera such as your bowel. Laplace's law describes that pressure is equal to four times the tension divided by the radius and on the numerator that you will see different numbers being used sometimes you'll see two sometimes you'll see four and the different numbers reflect what are we actually calculating with that Laplace's law. Four is used if we're using both the inside and the outside surface when we're calculating the pressure two is used when we're only using one surface of the inside so typically when we talk about the alveoli Laplace's law will be described as pressure is equal to two times the tension over the radius so if the tension remains constant so the numerator remains constant if we take an alveoli which has a big radius and a small radius the alveoli with the small radius will have a higher pressure therefore it'll have a higher tendency to collapse and that's where surfactant comes in to decrease the tendency of alveoli to collapse that is one role of surfactant it's not the only role but we'll discuss the other roles as well so surfactant is produced by type two alveoli cells there's rapid turnover of surfactant and the half life of surfactant is around about 15 to 30 hours it's produced in the fetus at approximately 24 weeks of gestation to 28 weeks of gestation and that's why in a preterm infant that's born surfactant is given the content of surfactant is that it's mainly a phospholipid 90% of it is a lipid and the most important phospholipid is the DPPC molecule the DPPC molecule is an amphipathic molecule and what that means is that it has dual traits it has a hydrophobic tail which is the dipalmetol part which lies in the alveoli gas so the hydrophobic meaning that it doesn't like water it has a hydrophilic head which likes water with the choline group and this lies within the alveolar wall itself the other components of surfactant within the lipids there's the DPPC and then there's also the phosphodiol glycerol together they make up 90% of the lipid component but then the remaining 10% of surfactant is made up of surfactant associated proteins and a small amount of carbohydrates the best way to describe how surfactant works is thinking about it like acting like a detergent it's reducing the attraction forces between the water and water molecules next to each other and the way it does that it inserts that hydrophilic head into that water molecule on the alveolar wall and then this repels the water molecules from being attracted to each other and therefore reduces the tendency of that alveolar to collapse and decreases the pressure inside that alveolar the arrangement of the surfactant molecule and the DPPC molecule is absolutely key to understand and you have to understand that it's that ampipathic molecule with a hydrophilic head and a hydrophobic tail the other important thing with surfactant is that when the alveolar are small the surfactant molecules are closer together and therefore they have a stronger effect at reducing the surface tension when the alveolar are larger the surfactant molecules are further away from each other and therefore the ability to reduce surface tension is reduced and this is one of the reasons why the lung displays hysteresis hysteresis is the difference that we see in the pressure volume curve of the lung on inspiration and expiration it's not the only reason that there is hysteresis but it's an important reason why there is hysteresis and we know that surfactant is not the only reason for hysteresis because in west's you can find a diagram that shows that the lung still has hysteresis if it's been inflated just with saline and no air and that is an important diagram to note especially in the viver setting the other roles of surfactant to mention is that it helps to improve the lung compliance and therefore decrease work of breathing it helps to decrease the tendency for pulmonary edema and keep the alveolar dry and the reason is quite simple because of the hydrophobic tail that likes to repel water out from the alveolar and within the alveolar itself so it just has the gas in there and tries to take the water out it helps to equalize the pressure between large and small alveolar and therefore stabilize alveolar and decrease aterelectasis and then the final thing of surfactant is that production of hysteresis and in saying that the important thing to understand is that surfactant's ability to reduce surface tension is greater when the alveolar are smaller so therefore the surfactant molecules are closer to each other increasing its repelling action and a decreased repelling action when the alveolar are larger at a larger lung volume so this flows in quite nicely into the next LO talking about the elasticity of the lung which is defined compliance static dynamic specific and relate this to the elastic properties of the lung this LO also overlaps with the next LO which is describe the elastic properties of the chest wall and plot the pressure volume relationships of the lung chest wall and the total respiratory system so compliance can be defined as the change in volume over change in pressure and when we think about the lungs this is the change in pressure regarding the transpulmonary pressure it's measured in mils per centimetres of water and the normal human lung compliance is 200 mils per centimetres of water what compliance is telling us is the ease of distensibility of stretching the lung it's the reciprocal of elastins which is the tendency of the lung to recoil back and so compliance is the opposite to elastins within compliance we can break this down into static compliance dynamic compliance and specific compliance static compliance is the change in volume over change in pressure when there is no airflow and the lung is at a fixed volume dynamic compliance is when there is airflow and because there's airflow there's always going to be increased resistance therefore dynamic compliance will always be lower than static compliance and specific compliance is the compliance which is measured independent of lung volumes so it's comparing the compliance of a neonate compared to an adult compared to an elderly patient and it's taking into account the functional residual capacity and the total compliance and that number is super small it's 0.05 it's the same in neonates compared to adults so how do you measure static compliance now to measure static compliance there can't be any airflow so the basic concept is that you get the subject to breathe in a fixed amount of volume and then hold their breath at that volume and you measure the compliance at that time there's gradual turns taken to inhale a fixed volume and relax against the closed glottis usually for around about 10 seconds the pressure at the mouth is recorded and then the pressure at the distal esophagus is recorded and the reason we measure the distal esophagus is that this is thought to be approximating the intraplural pressure so it's measuring that trans pulmonary pressure gradient this is plotted across a graph and on that graph you have intraplural pressure on the x-axis and on the y-axis you have the lung volume and this gives you the typical hysteresis curve that you see in very simple terms the static compliance of the lung is a function of its elasticity and the surface tension in the alveoli dynamic compliance is a bit more complex than static compliance only because it takes into account airflow because it takes into account airflow there's only two points where you can measure dynamic compliance and those are the points where there's end inspiration and end expiration at that point you measure the mouth pressure and this is thought to be the same as alveolar pressure because there's no gas flow occurring now you can measure dynamic and static compliance on an anesthetized patient anytime when they're on a ventilator and the way you do that is that if you're measuring static compliance you would just take the tidal volume and divide that with the plateau pressure minus the peep and if you're measuring dynamic compliance you would just take the tidal volume and divide that by the peak inspiratory pressure minus the peep now technically these wouldn't be giving you just lung compliance because it would be taking into account chest wall compliance as well and therefore you'd be getting total respiratory lung compliance in terms of numbers to remember static compliance is 200 mils per centimetres of water and dynamic compliance is less than that and it can be variable in different texts some will say between 50 to 100 mils per centimetres of water so the common question that comes up is what are the factors that affect lung compliance and the main factors that affect lung compliance are the lung volume so compliance is decreased at very high lung volumes and at very low lung volumes so on extremes of lung volumes compliance is decreased and this relates back to that hysteresis curve at FRC compliance is thought to be the greatest so lung size also affects compliance the larger the lung the more the compliant the more compliant the lung is and this is also evident in the compliance measured in adults compared to neonates and you can think about this is relating back to the Laplace's law and adult compliance we've said is around about 200 mils per centimetres of water and neonates can be as small as five the age also affects the compliance so compliance normally increases as we get older because of the structural changes in the decrease in elastin so now the lung becomes easier to expand however the elastin of the lung decreases so factoring is another important factor in changing lung compliance and this relates back to surface tension posture is another important factor so when you're supine you have a decrease in your thoracic volume this leads to you having a decrease in your functional residual capacity pushing your hysteresis curve or your pressure volume curve to the left and therefore you have a decrease in your lung compliance compared to when you're standing up that lung compliance is improved so with that you have the effect of gravity compliance is best in the lower part of the lung compared to the apices of the lung when you're standing up and this again relates to where it lies on the hysteresis curve there are other minor factors that also affect compliance so this is the pulmonary blood volume so if you increase total pulmonary blood volume you will get more stiffer lung because of the venous congestion they're harder to expand and then you have the effect of disease states so this is separate to the effect of aging leading to a change in elastin with disease states you can have stiffer lungs due to fibrosis leading to a decrease in lung compliance or emphasmatus changes leading to an improved lung compliance then if you were to ask about factors that affect dynamic lung compliance you would put in all those factors and then add in factors that affect airway resistance and then this would be talking about bronchial smooth muscle tone now when we talk about compliance a term that we've mentioned quite a few times is hysteresis these two go hand in hand with each other when we think about hysteresis we think about hysteresis as the lung displaying time-dependent elastic behaviors there's four causes of these time-dependent elastic behaviors these are recruitment and derecruitment the effect of alveolar surface tension the concept of stress relaxation and then the redistribution of gas better known as the pendulum effect the recruitment derecruitment is essentially thinking about the lung in the fact that if you have a collapsed alveolar it takes a lot of energy for you to open up that alveolar compared to an alveolar that's already open we've spoken about surface tension before when we talked about surfactant the stress relaxation component is essentially the loss of energy of any kind of parent karma when it's stretched and the way you think about it is that if you imagine a spring that is pulled to its maximum length the tension in it will decline despite you holding it at its maximum length so because of that constant tension you get a decrease in energy with time which is just a normal form of loss of energy and then finally there's the pendulum effect this is just explaining that gas will differentially go from fast alveolar to slow alveolar in simple terms when alveolar expiring some of them expire really quickly and then those that expire really quickly will then redistribute their gas into slow alveolar which are still expiring slowly and those are the four overall causes of the time-dependent elastic behaviors of the lung that together lead to hysteresis if you were asked what's the major one you would say surface tension and the role of surfactant now let's look at the respiratory compliance as a whole we've spoken about lung compliance but respiratory compliance as a whole consists of lung compliance and chest wall compliance when you're actually figuring out what the total respiratory compliance is when you add those two compliances together they have to be added as a reciprocal so the lung compliance is 200 mils per centimetres of water and chest wall compliance is the same 200 mils per centimetres of water but when we add them we have to add them as a reciprocal so one over 200 and this leads to the total respiratory compliance being 100 mils per centimetres of water and that's where we get that number from our body is always trying to have a balance of respiratory compliance our lungs are trying to collapse back in because they're elastic and our chest wall is trying to open back out because they want to bow out because of their bony structures so consistently these two factors are trying to fight each other and at a certain point those two factors need to equal each other where they're balanced between what's trying to pull out and what's trying to pull in and where their balance is known as the functional residual capacity and that's why compliance is thought to be the greatest at functional residual capacity at this mark there is five centimetres of water that's pulling out and five centimetres of water that's pulling in and those two are equal so this is the equilibrium point the factors that affect the chest wall compliance can be thought about those that increase chest wall compliance or decrease chest wall compliance there's not many factors that will try to increase chest wall compliance you can have collagen disorders you can have change in posture when you're upright or prone but there are a lot more factors that decrease chest wall compliance and this can be anatomical differences so when we're elderly we can have ossified cartilage which decreases our chest wall compliance compared to when we're neonates we have the cartilaginous ribs which are more compliant to open up then other factors that decrease chest wall compliance so again posture so when we're super and we're causing restriction of our chest wall when we have any paralysis of our chest wall if we have any kind of disease states like obesity kyphosis pregnancy and pregnancy is unique because it decreases chest wall compliance but it doesn't change lung compliance and then we have other things like external causes of decreasing chest wall compliance like burns that will cause you to have scarring of the tissue so when you understand that total respiratory compliance is chest wall compliance plus lung compliance what you must then try to memorize is the satian pressure volume curve for the lung and the chest wall and this graph is hard to describe in a podcast setting but it's something that you need to look at and just have a look at what the key important numbers are the important numbers to note would be the minimum value the point where the chest wall and the lung compliance are equal so this would be at FRC and the point where the total lung compliance overtakes the lung compliance which is approximately around about 75 percent of total lung compliance and this is because chest wall compliance finally becomes positive from being negative below that value before I can't recommend looking at this graph enough and you can find a beautiful drawing of it in west's moving on we have our next learning objective which is discuss the fast and slow alveoli including the concept of time constants now time constant is just the way to describe a time course for an exponential process in a time constant one time constant refers to the time taken for an exponential process to be 63 percent complete while three time constants refers to it being 95 percent complete compare this with half-life where you require around about four to five half-lifes to have the process complete by 95 percent now a time constant can be described as the time is equal to the resistance times the compliance the resistance being the resistance to filling so that airway resistance and the compliance being the compliance of the alveoli normally resistance is two centimeters of water per liter per second and the normal compliance of the whole respiratory system as we've said previously is a hundred mils per centimeter of water so the normal time constant for an alveoli is 0.2 of a second so for an alveoli to be completely filled or emptied it would take three time constants which would be 0.6 of a second we can divide alveoli into slow and fast alveoli depending on how fast they are in terms of their time constant speed so alveoli have differences within different regions of the lungs at the apex of the lung the alveoli compliance is reduced and this is reflected in our hysteresis curve being a plateau shape at the top at high lung volumes also at the apices there is increased diameter of our alveoli so the resistance is lower so there's disparity between fast alveoli at the top of the lungs versus slow alveoli at the base of the lungs now normally this disparity is very small and in healthy individuals it doesn't really equate to any kind of clinical difference but when we get into a disease state that's when the concept of alveoli speed difference comes in so if we take a clinical manifestation as an example in a desired alveoli I say it takes three times longer for it to empty what we then see is that we get the development of the pendulough effect and this is that the fast alveoli will empty very quickly and slow alveoli will slowly empty during expiration and the gas from the fast alveoli will redistribute to these slow alveoli's causing a decrease in the measured expiratory volume leading to an overall decrease in the dynamic lung compliance and this is what the pendulough effect describes and that's how it relates back to being one of the four key time dependent elastic properties of the lung that cause hysteresis now another clinical example is say we're looking at a capnography trace with a patient who has asthma this heterogeneity of alveoli speed leads to a change in our n-title CO2 trace we get a slow uprise to the n-title CO2 leading to a typical shark fin appearance and this is because of the difference in speed due to the changing in resistance in compliance due to a disease state so again the difference in fast and slow alveoli does occur normally however in normal conditions where people are healthy the effect is minimal it's more exacerbated in a disease state and therefore can lead to vq mismatching other ways we can measure the difference in fast and slow alveoli is also to look at peak pressures compared to plateau pressures the next learning objective is describe the work of breathing this tends to be a favorite of many examiners for vivas and also for short answer questions and that's because it's easy to get confused with lots of different graphs you have to know for this topic now when we think about work of breathing we have to define firstly what work is work is the amount of energy spent during breathing it's measured in joules and one joule is the energy needed to move one liter of gas through 10 centimeters of water pressure gradient work is equal to the force times displacement or the distance so in simple terms work is the energy you put into the system to move something for ventilation it can be measured by the pressure that's generated to cause a change in volume so therefore we can say that work is equal to a pressure times volume and that's where we get the pressure volume curve if we want to go back and think about how do we get work equaling pressure times volume we can take pressure as an example pressure is the force applied over an area so p is equal to f divided by a if we times both the numerator and the denominator by distance so force times distance and area times distance what we get is the numerator becomes work because work is equal to force times distance and the denominator becomes volume because area times distance will give you a volume and that's how that circles back in to work is equal to pressure times volume now in a normal healthy patient the normal work of breathing is 0.35 joules per liter or approximately 2.4 joules per minute i would just remember one of those numbers so that i can plug that in very quickly for one of my for my saq we've already spoken about initially that a normal ventilation in spiritually muscles do all the work and normally expiration is a passive process so when we think about work there's two components of work there's the elastic work and then there's a non-elastic work and these will be called different things in different texts but i just keep it very simple so elastic work is essentially the work that's needed to overcome the inward elastic recall force of the lungs and the inward force of the surface tension on the alveoli the elastic work is approximately 65 percent of the total work that's done and this is work done against the elastic forces and this work done against the elastic forces is stored as potential energy and it's used to overcome the non-elastic work forces during expiration the non-elastic work can be divided into two components so in total non-elastic work is approximately 35 percent of the total work and in some texts you will find that elastic and non-elastic work is referred to as 50 50 60 40 but i have here 65 to 35 percent non-elastic work the two components are airway resistance which is the main component which is 80 percent of that non-elastic work and then tissue resistance which is 20 percent tissue resistance is very simple to understand it's just the force of the different pleura sliding across each other so it's the lung pleura and the chest wall pleura sliding across each other and the diaphragm also sliding across with the abdomen organs causing friction that leads to a loss of energy airway resistance work is also simple to understand this is just the airway resistance encountered on inspiration on and on expiration so how can we describe normal worker breathing within normal worker breathing no matter what you will have to encounter non-elastic forces when you're inspiring and expiring because there's going to be air movement there's going to be resistance work done on inspiration and on expiration and there's going to be that tissue resistance work done no matter what with the sliding of tissues then elastic work is only encountered on inspiration and that's to try and expand the lungs so what happens is you get this typical graph which shows on the x-axis intra pleural pressure and on the y-axis you have the volume or the volume of the lung as you breathe in you do work to overcome the elastic forces and you do work to overcome the non-elastic forces those two combined are plotted as your total work done on inspiration the work done to overcome the elastic forces is then stored and that work is then used or that stored potential energy is used to help then do the work of the non-elastic forces on expiration normally that work stored is more than enough than what's needed to do those non-elastic forces on expiration however in disease states that's when we start to use our accessory muscles so when we start to use up all that stored potential energy we start to then use up our accessory muscles to breathe and expiration becomes a active process so take for example we have a patient with asthma they have increased airway resistance so their total amount of non-elastic forces or non-elastic work done has increased dramatically both on inspiration on expiration now on expiration they don't have enough stored potential energy to make expiration a passive process they have to use their active muscles to expire out so what can we do to compensate for that well we can do different ventilation strategies we know that if we take an asthmatic patient and we increase their respite even further we're only going to make their work of breathing and their non-elastic forces even worse so what we do is we slow down the respite to reduce the total amount of times they're breathing and we might also increase their tartar volume so they have more stored energy available for use when they're expiring on the opposite spectrum say you have a patient with restrictive lung disease now for them the main energy use is going to be trying to expand the lungs so elastic forces are going to take up a lot of energy so what we can do is give them small tartar volumes so they're not using as much of their elastic energy and then we can compensate for the minute ventilation decrease by slightly increasing their respite we don't want to increase their respite too much because they might still have increase in airway resistance but what we want to try to do is minimize the elastic energy they use and decrease their tartar volumes another example of a patient group where the elastic forces may not be optimized is neonates neonates have a decrease in surfactant and this can lead to an decrease in their ability to expand their lungs and so for them we might decrease their tartar volume to help decrease the elastic forces or the energy needed with elastic forces overall the respiratory system as a whole is not very efficient at all the majority of the energy despite our best use is wasted as heat and we can calculate that by calculating the total amount of energy that we use on inspiration being the elastic and non-elastic forces and then minusing that away from the total amount of energy we use on expiration mainly being the non-elastic forces because remember the lung naturally wants to recline back in so we're not using any elastic forces normally with expiration and whatever we haven't used is the wasted energy so then we can then describe the efficiency of the work of breathing and the normal efficiency is that it's only five to ten percent efficient so 90 percent of the energy is being wasted the normal cost of breathing as per the oxygen requirement is approximately three mils a minute of oxygen itself this is approximately one percent the total amount of oxygen consumption in your body so there's two graphs that you have to know really well when we talk about work of breathing there's that initial graph that talks about inter pleural pressure over volume and has energy use in inspiration and expiration and then there's the graph that looks at respite over work of breathing and it looks at non-elastic work and elastic work and total work with three different separate lines and what it shows is that if you increase your respite you will increase your non-elastic work and when you decrease your respite you will decrease your non-elastic work and when you increase your tidal volume you increase the elastic work and when you decrease your tidal volume you decrease your elastic work and unfortunately those are just graphs you have to stare at until they kind of just click now the final learning objective in mechanics of breathing is describe the altered lung mechanics in common disease states this is a very clinical learning objective that we will discuss indirectly as we cover more LOs with our respiratory topic so we're going to move on and talk about some of the past SAQs and examiner reports from questions that came up with mechanics of breathing now the most common SAQs they get asked are either going to be on compliance or on work of breathing the important thing to recognize is that any question that gets asked on compliance you need to read very carefully and figure out whether it's asking about respiratory compliance lung compliance or chest wall compliance the last question that was asked on compliance was in 2020 in the second sitting where they were asked to discuss respiratory system compliance and outline factors that affected so this is a loaded question where they want information about the chest wall compliance the lung compliance potentially some increase information a little bit of information about hysteresis and then really good definitions so the examiner report here stated that they wanted a really good definition of compliance the composition of compliance of the respiratory system like we've spoken about the different types of compliance within each of these different forms of compliance so within lung compliance you have static compliance and dynamic compliance and don't forget about specific compliance as well and the factors that increase and decrease compliance there was credit given if you were able to talk about measurements methods with regards to static and dynamic compliance an explanation of hysteresis explain the concepts of slow and fast alveoli and the effects of anesthesia on respiratory compliance reading this examiner report what i think is important is nailing the basic points you can quickly give a definition of compliance and you can quickly list the different factors that affect lung and chest wall compliance you probably don't have enough time to talk about hysteresis but what you want to do is try to tie in this question to some clinical applications or clinical disease states and compliance lends itself very easily to be tied into restrictive lung disease emphysema and asthma as three very easy examples that you can incorporate into factors that affect compliance and this is different to other saqs where there are specifically for lung compliance when you get asked specifically for lung compliance you want to make sure you give a good definition between the difference between static compliance dynamic compliance and specific compliance and you need to have time built in in your answer to talk about hysteresis as well you want to note in your answer when you're talking about hysteresis that there's the time dependent behaviors of the lungs and if you have time at the end you can then incorporate the measurement of compliance with static compliance remember they're using a subject who's breathing in from frc they're breathing in a fixed volume and they're relaxing against the closed glottic and there's a pressure reading taken at the mouth and then also in the distilosophagus to get the intraplural pressure this gives us the transpulmonary pressure so the alveolar pressure and the intraplural pressure and then we can calculate the compliance however dynamic compliance measurement can only be done at the end of expiration or the end of inspiration and if you have time enough to cover those important concepts with compliance questions i think you will score a good mark other comment sqs from worker breathing have been to describe the determinants of worker breathing and an adult human at rest now this question hasn't been asked post 2013 but has been asked four times before 2013 and to answer this question again you would just start off with the basics of defining what work is defining the different types of work being elastic and non-elastic what those components of work are and why the work is generated with elastic and non-elastic work drawing in your diagram which is key for elastic and non-elastic work and then taking in the clinical examples and that's pretty much what the examiner reports wanted they wanted you to be able to know that work is pressure times volume and the unit to measure this is in joules that inspiratory work overcomes both the elastic and resistant forces that non-elastic work consists of overcoming airway resistance and those viscous forces or the tissue resistant forces talking about the potential energy required during work and how it's used on inspiration and expiration drawing that pressure volume diagram looking specifically at pressure on the x-axis and then lung volume on the y-axis and then dividing that into work done on inspiration and expression and those can be either combined graph or individual graphs and then additionally talking about how if you had time the contribution of the components of worker breathing clinical applications and then the oxygen costs of work and the efficiency of worker breathing from the other remaining sq's from worker breathing we had in 2008 explained the concept of time constant and relate these to fast and slow alveoli so that's a carbon copy of the LO but there have been a few sq's that haven't been asked in the ansky exam yet but have been asked in the kikum exam related to some of the LO's and mechanics of breathing and the main one that hasn't been asked before is the anatomy of the diaphragm and describing the function of the diaphragm in respiration the kikum answer followed that basic structure of having those five points the basic anatomy of the diaphragm the relationship of the diaphragm to other structures the innovation the blood supply and then the function of the diaphragm and clearly when you talk about function you want to relate that function into respiration because that was specifically asked in the question that completes a very heavy topic mechanics of breathing and there are a few important takeaway points firstly we're understanding mechanics of breathing it's understanding why breathing occurs and how breathing occurs in terms of creating a gradient from outside to inside our lungs then the importance of surfactant in the role that it plays in its specific molecular structure which allows it to have hydrophobic and hydrophilic properties how that then relates itself into talking about hysteresis and lung compliance talking about different types of lung compliance when we talk about dividing into lung compliance chest wall compliance and total respiratory compliance and then finally understanding that work of breathing as a concept requires elastic work and non-elastic work and this ties into the properties of the lungs which is that it's an elastic tissue and then this is the main cause of elastic work of breathing and then that there's airflow occurring when there's breathing and this is the main cause of non-elastic work so thank you so much for listening and until next time good luck with your studying and we'll be back talking about gas volumes and gas exchange next time