Pulmonary Structure and Function

hello and welcome to structure and function of the pulmonary system in this section we're going to be talking about pulmonary alterations and what kind of things you can expect to see in your patient when your patient has altered respiratory function let's start out with a little quiz surfactant coats the inner surface of the alveoli and is it a increases the work of breathing B increases lung elasticity C contains antibodies or D prevents alveolar collapse during expiration correct answer is D prevents alveolar collapse during expiration so surfactant decreases the surface area the amount of tension that's on that alveolus so the alveolus can stay open even when the patient is exhaling next we'd like to trace a molecule of oxygen from the atmosphere to the lungs which answer has the respiratory structures that the oxygen passes through in the correct order is it a the fair Nick's the esophagus the bronchioles the bronchi in a vowel or sacs or is it B the larynx the trachea the bronchi the bronchioles the alveolar sacs and the alveoli or is it C the trachea the bronchi alveolar sacs in the pleural cavity or is it d the bronchi the trachea alveolar ducts bronchioles and alveoli our correct answer is letter B it's the Lennox the trachea the bronchi bronchioles alveolar ducts and then the alveoli so this is the normal process that air is going to move through in order to get down to the alveoli so that it can be absorbed into the body and we can get oxygen to the tissues where we need it which of the following mechanisms causes air to move into the lung during passive inspiration is it a lifting of the ribcage by the accessory muscles of inspiration or B muscular contraction the diaphragm or C dilation of the primary bronchi or D an increase in intrapleural pressure our correct answer of course is B muscular contraction of the diaphragm with passive inspiration we don't have to do all the work of using the accessory muscles so we're just relying on the muscular contraction of the diaphragm to pull air into the lung now having dilation of the primary bronchi is not going to be the thing that causes inspiration dilation of the primary bronchi would just allow air to move in and out of the lungs a little bit better and an increase in intrapleural pressure will actually probably cause the patient to have less air moving in and out of the lung because we're kind of compressing the lung remember the pleural area is outside of the lung surrounding the lung by the chest wall this question is asking about the covering of the lungs covering the lungs is a serous membrane called E is it a visceral peritoneum B parietal perineum C visceral pleura are deep riedel pleura okay so this one should be fairly easy at least we can start to eliminate some of the incorrect answers when we pick C visceral pleural okay so obviously a and B would be wrong because it's talking about peritoneum so that's in the abdomen and we're talking about covering it along so we're talking about a pleura and we want to know whether it's the visceral or parietal pleura in this question in this case it's the visceral pleura that is covering the lungs so let's take a look at the structures of the pulmonary system as error moves into the mouth you know I think a lot of this stuff is kind of taken for granted when we breathe in and out we're not thinking about air moving through our upper Airways down through the trachea moving through the bronchi and down finally to the alveoli we're just thinking about taking a breath all right but air has to move first into the airways now what we consider the airways to be really is all the way from the nose and mouth all the way down to right before the alveoli so those alveolar ducts are going to be part of this process so we have our Airways and that's going again from the picture all the way from the nose and mouth down the trachea into the bronchi into the bronchioles into those alveolar ducts to get the oxygen down to the alveoli next we have our pulmonary circulation now we're going to talk about this in a little bit more depth later on the difference between the pulmonary and the bronchial circulation that's occurring in the lungs the pulmonary circulation is going to the lung to become oxygenated next we have our chest wall protecting the whole thing and providing that elastic recoil it's going to help to open along now if you think of the lung as being like a balloon there's two ways we can open it up we can push air into the balloon and blow it open or we could grab the balloon from the outside and pull it open what happens in the patient's body is going to be pulling the balloon from the outside in order to pull air into the balloon that's the normal process that occurs if we put somebody on mechanical ventilation then it's like blowing up a balloon so that's a whole different process but our normal spontaneous ventilation is going to be like pulling on the outside of the balloon in order to inflate the balloon our lungs have different lobes to them so on the right hand side we have three lobes and we can see that illustrated here in this picture there's an upper and middle middle and a lower lobe on the right now the left lobe only has two it has an upper and a lower lobe on the left side we also have segments within those lobes and then we have lobules which are also included within those lobes separating out the lung into different areas certain structures of the pulmonary system are considered to be conducting Airways because they are moving air through the respiratory tract down through the lung we have our upper airway which includes the nasal pharynx in the oral pharynx so the nasal pharynx obviously breathe into your nose that's going in through the nasal pharynx now breathe in through your mouth that's going in through the oral fare and exo-k they're both going to connect together in the back of your mouth that your throat is where they're going to connect together but we can breathe through the nose or breathe through the mouth either way we're going to get air down into the lungs the Lenox is going to connect these two upper Airways the nasal pharynx and the oral four and X together and then connect those things to the trachea the trachea is the big windpipe that we talked about and in fact you can feel it in your neck if you feel the center of your neck you can feel something that feels kind of hard and ribbed there that is your trachea the trachea goes down into the upper part of the chest and separates into two bronchi the bronchi are what is actually going to feed each one of those lungs and the bronchi will break down into the bronchioles and eventually down into the alveolar ducts now beyond the conducting Airways now we have the Airways we consider to be the gas exchange Airways in other words these are the Airways that are way down deep in there that are right by the alveoli and these are the Airways that are actually going to be conducting right to the alveolus to cause gas acceding to occur so we have our respiratory bronchioles we have our alveolar ducts but the alveoli themselves are going to be the actual gas exchange mechanisms and here we have two different types of cells that make up the alveoli that's going to be the type 1 alveolar cells they provide structure to the alveolus so that's what helps to build that nice round little alveolus and then we have our type 2 cells which produce surfactant surfactant is the secretion that is made in order to help keep that lvls open so it helps to decrease the surface area of the surface tension rather of the alveolus so the alveolus will stay open it's kind of like protecting a bubble and if we can protect the surface tension on that it'll stay a bubble longer it's only when that surface tension is broken that the bubble is going to burst so let's say that you're doing the dishes and you have soap in the water and you have a whole bunch of bubbles that are forming there and you get this nice big bubble that forms now if you come up and you pop it with your finger you broke the surface tension and then that will cause obviously the bubble to burst we don't want our alveoli to burst so we have surfactant in there that's going to reinforce the surface tension so that they will be more likely to stay open and be productive all right well that's all well and good but when it really comes down to it I've got to see a visual in order to be able to put this together in my mind so maybe this is helpful to you and what this is illustrating here is the Airways coming all the way down from the trach yet we're breaking out into the bronchi and you see we have our two major branches of rocaille there the one is kind of going up any error and then we have our one coming down here to the right so the one going up in here would be going to the left lung the one coming straight down or more of a straight kind of a pattern is to the right one of the things that we talked about in some of our different disease processes is the processor the idea that the right brachii is straighter than the left bronchi and that is a situation where the patient may have more of a risk for aspiration and things like that anyway what is helpful to me about this diagram is being able to see how the respiratory tract is dividing and in fact before we get down to the alveolar ducts that respiratory tract is going to divide 25 times so you see lots and lots of divisions here all those little bifurcations occurring all the way down there until we get all the way down to the alveolus so we have our trachea our bronchi we then have our sub segments or bronchi the non-respiratory and the respiratory sections of it and then the alveolar ducts going to our alveoli so you can see we go way down here so now if your patient has got fluid that is stuck in their alveoli you can see it's going to be a long trip to get that back up so if we can't reabsorb it through the vasculature it's going to be a long trip getting that stuff so somebody may have a lot of gurgling in their chest or something like that because they've got mucus in there or they've got some secretions that have built up in their lung it's going to take a lot of work to move that all the way back up to the trachea where the patient can then expectorate that secretion as I mentioned before there are two different circulatory systems in the lung we have our pulmonary circulation this is the circulation that is going to the long to become oxygenated it has a lower pressure it's coming from the right side of the heart it has a lower pressure it's just going to the lung becoming oxygenated then going over the left side of the heart to be pumped to the body our other circulatory system is the bronchial circulation it originates from the aorta and is going to the lung to provide oxygen to the lungs so this is the thing that's going to actually give the lung the oxygen it needs in order to be able to carry out its functions so we can't rely on the pulmonary circulation it's going there uh knocks ajaita so we can't rely on the pulmonary circulation to provide enough oxygen for the lung to work so we have to rely on a separate circulatory system called a bronchial circulation now the reason why this distinction may be important would be if we have somebody who has a condition like a pulmonary embolism in a pulmonary embolism we have an emboli that's stuck in the pulmonary circulation not in the bronchial circulation so the lungs are still being perfused the way they normally would but we have a block of our pulmonary circulation and that leads to a ventilation/perfusion mismatch there's a problem between our ventilation and our perfusion in the lung as opposed to if we were to have an embolus in the bronchial circulation we would end up with having decreased perfusion and as we learned before decreased perfusion leads to ischemia injury and necrosis so we'd actually have necrotic damage occurring to the lung now bronchial emboli are really much more rare than having a pulmonary emboli the reason for this is the bronchial emboli would have to be coming from the left side of the heart as opposed to having an embolus that's going to the lung which is coming from the peripheral circulation now somebody isn't getting up and moving around a whole lot they may have an obstruction or they may have a emboli form thrombosed form in the venous circulation which is then mobilized back to the lung and blocks the pulmonary circulation which is a pulmonary embolus where the rubber hits the road is in the alveolar capillary membrane this is the membrane between the alveolus okay so just think of that bubble not alveolus bubble there and then we have a network like a big net of capillaries over top that alveolus now between the alveolus and that network of capillaries there is a membrane it's called the alveolar capillary membrane this is where gas exchange occurs it goes through that membrane so that we can have oxygen going to the bloodstream Co to come back out into the lungs that means that if we had changes in that membrane we would have difficulty and oxygenating and we'd have difficulty in eliminating co2 now what we're looking at here is an alveolus and there's actually parts of three alveoli here but you see the alveolus right in this center of your screen and then we have two blood vessels two capillaries that are going around that alveolus now in reality we don't have too big vessels like that going around the Ovilus we have a whole network of vessels going around the alveolus but this helps to show helps to demonstrate the process of what's going on so in our alveolus we're going to have air coming in and out air is coming in and out of that alveolus and really what it's doing is it's not coming in and out so much as it's circulating air is circulating in in lvls because the air is moving in and out of the lungs therefore oxygen is able to move across our alveolar capillary membrane into the bloodstream so move over to the little cutout here on the right where it's showing that we have the alveolus on the left and the blood vessel the capillary on the right now you see oxygen is passing from the alveolus into the capillary and co2 is passing from the capillary back into the alveolus so this is where the gas exchange takes place however if we get a problem in this alveolar capillary memory for example what if fluid were to start to form in between those two membranes in between those two functional areas the alveolus in the capillary then we would start to move those two pieces further away from each other and we would have a harder time getting oxygen across the membrane and co2 across the membrane so there's actually this membrane there's actually a little space in between and fluid could collect there which could impede the patient's gas exchange the bronchial circulation as I mentioned before is part of our systemic circulation comes off of the aorta and is going to then directly perfuse the lungs it doesn't participate in gas exchange in any way but it does help in our respiratory process by warming up and moistening the inspired air it does this by having vessels that are close to the surface of our Airways so that the warmth of the blood it can warm the air that's coming in and can also provide some amount of moisture to that air so that we don't get dry air hitting the alveolus other functional areas include the chest wall on the pleural the chest wall is going to be the skin the ribs etcetera so it's going to be the thing that's actually providing the structure the framework is the skeleton to the chest itself so this is the piece that's holding that chest together and making its shape and giving it some structure then we have the pleura and the pleura is inside of the chest wall and the pleura is going to provide an area first of all for negative pressure to exist and also some fluid in that pleural space is going to keep the lung from rubbing up against the chest wall three main functions of the pulmonary system include ventilate the alveoli so we need to get oxygen down to the alveoli we need to remove co2 from the alveoli diffuse gases in and out of the blood so that's a function down there of the alveoli and the alveolar capillary membrane and to perfuse the lungs so that the body receives oxygen so there's our bronchial circulation piece well of course one function of the pulmonary system is ventilation a vent station is the process of moving air so this is the mechanical movement of air in and out of the lungs which is going to circulate the air that is in the alveoli kind of envision this is the air in the room where you're sitting right now the air in that room does not get removed and replaced every time the air conditioner or the furnace kicks on instead what happens is that air conditioner furnace just simply circulates the air that is already present so it's not sucking all the air out and replacing it instead it's just simply circulating the air that is there this is ventilation so ventilation is merely circulating the air that happens to be present ventilation is controlled by neural chemical control from the respiratory center so there's a number of areas in the body where the respiratory center is going to control your amount of ventilation and let me just give you a couple examples so we have different areas of the body that can sense that we need to have an increase in ventilation for example there are sensors in some of our big muscle groups into big joint areas that if we're doing exercise in that area they're going to stimulate an increase in respiration because the assumption is being made that you're producing more co2 so if you're doing a lot of work let's say that you're either running or maybe you're doing some squats or something like that where you're working on the big leg muscles and muscles of the back etc when you're doing that kind of an exercise the body senses that there's going to be a lot of co2 produce as a result of metabolism and then of course we have to get rid of that co2 and the co2 is going to be getting rid of bided lungs so we need to make sure that we have an adequate amount of ventilation in addition of course there is also respiratory centers in the brain that are going to be able to sense that we need to eliminate co2 or to increase the amount of oxygen in the blood so getting a little bit more specific in the lung we have these receptors and there's three different types that we're going to be talking about the irritant receptors the stretch receptors and the J receptors irritant receptors are receptors in your lung are going to respond to irritants so for example let's say that you happen to be walking down the street and a bus drives by and blows this big cloud of black smoke up in your face and you happen to inhale part of it you're probably going to cough that's an irritant receptor the long sense that oh my gosh we have an irritant in the lung coughed to get rid of it okay so that's what the irritant receptor does next we have our stretch receptors they're going to tell you hey stop inhaling so if you were to take a really really really deep breath you're going to find that as soon as you get to a certain point it's going to start to become uncomfortable the stretch receptors are saying hey enough were full we don't need to go anymore so this is the thing that tells us either to take a breath a bigger breath or a smaller breath so that we're maintaining a normal lung function so it works on both ends - if we're not stretching it enough we're going to start to get some stimulation - thirdly we have the J receptors J receptors respond to fluid so if your patient is developing some pulmonary edema the J receptors are initiated the J receptors respond and say okay we have fluid in here and we need to do something about it that's going to be first of all irritating to the body so it's going to increase the patient's respiratory rate secondly it may cause the patient also to COFF to try to eliminate that fluid that is starting to collect and along we also have our chemo receptors those are central chemoreceptors like those in the brain and in the aortic arch carotid bodies and places like that where we have large chemo receptors we also have peripheral chemoreceptors that's what I was talking about before when you're starting to do those big muscle exercises your body you start breathing faster you're not breathing faster because you need more oxygen all of a sudden you're breathing faster because the body is anticipating that you need to get rid of more co2 so in order to do all of this breathing we have to have a certain amount of musculature that is moving the lung moving the chest wall etc so that we can have adequate breathing so our major muscles of inspiration are going to be the diaphragm the diaphragm drops and flattens out and it's going to pull down on the lung and make the lung expand then we have the external intercostals the external intercostals are between our ribs and those are going two contractors are going to make the chest wall expand we also have accessory muscles of inspiration so those are going to be both up in the sternal the mastoid area so that's in the sternum area and up toward the clavicles and we also have in the back the top part of the back so we're talking about like the shoulders and back muscles here those are not real good muscles of respiration you know if you were to just right now use your shoulders and upper back and chest muscles to try to breathe it's not going to be very efficient however if somebody normal muscles of respiration aren't doing the trick they're not getting enough oxygen in or enough co2 out then we have to implement those in order to be able to have normal respiration we can also use our abdominal muscles and the internal intercostal muscles as additional accessory muscles for expiration the alveolar surface tension is going to be a function of the amount of surfactant we have so if we don't have an adequate amount of surface tension the alveoli will collapse and then we won't have adequate ventilation of the lung we won't be able to ventilate the area that actually does all the work the elastic properties of long are going to be comprised of two different things the compliance of the lung which refers to how much elasticity the lung has in general just take for example a rubber band now you have a nice brand-new rubber band right out of the box real nice and stretchy and elastic but let's say you've got a really old rubber band you found laying around somewhere and you pull on that thing and it stretches a little bit in breaks see it doesn't have the same kind of elastic recoil it doesn't have the same kind of compliance and elasticity that it used to have so we need to have that elasticity and that recoil of the lungs to in order to have adequate ventilation and breathing our airway resistance is going to affect how patients breathe so if there's too much airway resistance we're not going to get air in and out of the lungs and then the work of breathing is another one of the components the work of breathing refers to how much work the person needs to do in order to be able to breathe let me give you an example right now if you're sitting and listening to this your work of breathing is not very high however if you were to start and go out and start running your work of breathing would become much more have you ever done exercise to the point where you feel like you're out of breath that's a lot of work or breathing if you want a little bit more information about the mechanics of breathing you might want to check out this YouTube video take a moment now and check yourself can you describe three functions of the respiratory center of the brain what are the three types of long receptors and how do the functions of the central and peripheral chemoreceptors differ take a moment to pause the recording right now and answer those questions for yourself so one of your questions was what are those central and peripheral chemoreceptors so here we have some examples some pictures here giving you some ideas about all the different controls over our respiratory center and over our respiration so first of all we have the cerebrum itself we have our actual brain that's having some control and those are our central chemoreceptors they're going to respond to an increase in acid and an increase in co2 we also have our peripheral chemoreceptors that respond to an increase in acid and increase in co2 and a decrease in oxygen our muscles of respiration there's going to be a positive or negative effect upon them depending upon what the peripheral and central chemoreceptors find our stretch receptors will control how deep that respiration goes and then we also have proprio receptors that are going to have some effect on our muscles of respiration as well so again just to review some of the different controls we've talked about already chemo receptors are going to be based upon acid concentration in the central system and also about an increase in our co2 which will cause an increase in acid concentration so in the central system it's going to be the medulla peripheral system it's going to be the core artery's we also have mechanical receptors that are going to be stimulated by irritants by stretching by alveolar wall distortion or by stretch receptors just when you thought that this whole process now was extremely complicated let's throw in some more see we have our neural chemical control of ventilation here at the top that's the respiratory center the central and peripheral chemoreceptors that we've already talked about we also have our mechanics of breathing that are going to be controlled by our major muscles our accessory muscles it's to some extent the along elasticity so if our lung is not very elastic or compliant we're not going to be able to have good mechanics of breathing our airway resistance will play into this remember those patients who have COPD and asthma will have more problems moving air in and out of the lung and that will affect our mechanics our breathing our alveolar surface tension will also affect our mechanics our breathing and then the work of breathing affects the mechanics of breathing so this is some of this stuff is kind of like you know what comes first the chicken or the egg the work of breathing goes up because we have decreased lung elasticity the work of breathing goes up because we have less airway or we have we more airway resistance so you can see how some of this stuff kind of just falls together work of breathing typically does not go up just independent of having anything else happen in the patient our gas transport so the distribution of ventilation and perfusion oxygen transport in our carbon dioxide transport remember ventilation and perfusion are two entirely different things you're going to hear those two phrases put together a lot what ventilation refers to is the movement of air in and out of the lung that's ventilation movement of air in and out of the lung perfusion is the gas exchange across the alveolar capillary membrane so two entirely different things we can have perfectly normal ventilation and have disrupted ventilation I'm sorry disrupted perfusion and we could have a problem in too long so we can have normal ventilation disrupted perfusion there's a problem we can have disrupted ventilation normal perfusion there's a problem so it doesn't have to be both things that are affected it could be one thing or the other that's affected and still going to cause problems in oxygenating our patient our control of our pulmonary circulation pulmonary circulation is controlled by their own little receptors in the pulmonary circulation l okay so in other words there are a number of things that are going to make that pulmonary circulation have some changes in its vasculature one thing could be the amount of perfusion pressure we're getting at the alveolar capillary membrane and another thing is going to be our oxygenation so the patient's oxygen level is low that's going to stimulate vasoconstriction and along in an attempt to try to improve perfusion however usually it just leads to a further decrease in perfusion four steps the gas transport we have to ventilate the lungs then we get diffusion of oxygen from the alveoli to the capillary blood then we get perfusion of the systemic capillaries with oxygenated blood and the diffusion of oxygen from the systemic capillaries to the cells so can you see those four distinct processes anything that happens with any one of these processes is going to affect how much oxygen gets to the patient cells so we have to be paying attention to each and every one of these four steps in order to assure that our patient is getting enough oxygen to the tissues conversely we have the opposite process occurring with co2 co2 is going to diffuse from the tissues back into the systemic capillaries from the systemic capillaries back into the systemic circulation then to the alveoli and then be ventilated out of the lungs well it really would be a good idea to have enough oxygen getting to the body and enough co2 removed from the body so we need to have some mechanism by which we're going to measure these things and we usually refer to this as being a blood gas and we've already talked about how to analyze blood gases but we didn't really talk much about the measurement we're getting from our blood gas when we measure on our blood gas we're talking about these measurements in terms of partial pressure so you may have seen that written somewhere before that the P and po2 stands for the partial pressure of oxygen in the blood so po2 so the measurement of gas is looked at from the aspect of how much pressure the partial pressure the barometric pressure or in relationship to the barometric pressure that we have in the vasculature and that's what we're talking about so the po2 co2 when we're talking about po2 and we're talking about pco2 we're talking about the partial pressure and that's the pressure that it's exerting in the capillary as a kind of as a function of our barometric pressure and the amount of oxygen or co2 that is present so let's follow through our respiratory and our circulatory system with our partial pressures and see what happens to the pressure of oxygen and co2 as we move through our system so we start out with a po2 and I'm starting at the left top side of your diagram with the inspire to air with our po2 of 159 let's find low po2 down so we're inhaling a po2 of 159 from our air that goes down the trachea down through all the Airways finally gets down to the alveolus you see now we have a po2 of 104 left two reasons for that we lost some of our partial pressure going through the Airways the other mechanism is that some of that po2 is already diffusing across the alveolar capillary membrane to get into the blood so we're losing some of it that way so the po2 in the alveolus is about 104 now the po2 returning to the right side of the heart so you go over to the very left side of your diagram there from the heart and systemic circulation we have appeal to a 40 so that 40 is coming into the pulmonary artery where it meets 104 obviously diffusion is going to be the diffusion gradient is going to be from the 104 over to the 40 right because particles go to where there's less particles so the particles the po2 goes over to where there's less po2 and it's going to increase the amount of po2 in that pulmonary capillary now on the pulmonary vein end that's going back to the heart you see we have a po2 of 100 why not 104 geez we had 104 in the alveolus why can't we get 104 coming back to the heart again we have this process of perfusion going on back and forth so we're not going to have enough time to fully get the benefit of all of that po2 that's in the alveolus again remember the blood is moving as it goes past this alveolus it's not sitting there it doesn't come there I mean this diagram makes it look very nice okay the blood just came and sat there and waited for perfusion to occur that's not what's happening in real life what's happening is that blood is moving through that capillary so it's trying it's like trying to get on and off of a moving train if a train is moving past the station and we got a whole bunch of people that need to get off it's unlikely everybody's going to get off at that station when the train is moving if the train were stopped obviously everybody could get off so this is the reason why we're not able to access all of that po2 that's in the alveolus so we're over on the right side of the diagram now where it says to heart and systemic circulation now we have a po2 of 100 get on there to the tissues and at the tissue level the tissues are going to use that po2 and they're going to suck up about 40 millimeters of mercury of that po2 and send 40 I'm sorry I said I must have said they're wrong they're going to suck up about 60 of that po2 and send 40 back to the right side of the heart so if you take a look at the diagram hopefully that's going to give you a better idea as to why all these values are different in different places gas transport is dependent upon the distribution of ventilation and perfusion so the gravity and alveolar pressure we're going to have an effect as will the ventilation perfusion ratio our oxygen transport is going to be dependent upon the diffusion across that alveolar capillary membrane so we have to have good diffusion we can't have stuff sitting in that alveolar capra membrane that might be interfering with how well we get gas transport our determinants of arterial oxygenation include how well that oxygen is able to bind to hemoglobin and there are things that interfere with that and our oxygen saturation we'll talk more about those two concepts in a moment oxyhemoglobin Association and dissociation by way of the oxyhemoglobin dissociation curve you carbon dioxide is also transported from the tissues back to the lungs to be eliminated carbon dioxide transport is first dissolved in the blood and may be buffered by bicarbonate or our carb carb amino acids they may also be buffering our carbon dioxide and its way back out of the lung we can also have this thing called a Haldane effect and there is some debate about how that works and what kind of effect that's going to have on our oxygen so I'm not going to really talk about that at this point that may be something that you're probably going to learn more about in your critical-care courses and it's probably not something that we want to touch out at this remember that the pulmonary circulation is the circulation going to the lung that is going to actually have the perfusion get oxygen and drop off our co2 so very important that we have good pulmonary circulation our pulmonary circulation is going to have some of its own controls so two major controls that will affect our pulmonary circulation include hypoxia hypoxia is going to cause vasoconstriction in the lung now that's not necessarily helpful so when we get vasoconstriction in the lung we're going to have decreased perfusion of the lung and if the patient's already hypoxic that may not be a very helpful type of event acidosis will also cause vasoconstriction in our patient may not be very helpful either if the patient is acidotic because they're in shock from a lack of oxygen to the tissues there's a number of tests that you're going to hear referred to when we talk about testing your patients pulmonary function that includes spirometry spirometry we have the patient take a deep breath in as deep as they can and blow it out as hard and fast as they can the purpose of spirometry is to test how much volume they can get into their lungs and how fast they can get it back out this tells us a lot about restrictive air diseases and also about airway diseases so to tell us a lot about their total function of the lung we can also use a diffusion capacity which tells us about the diffusion capability across at alveolar capillary membrane we can look at the patient's functional residual capacity and their residual volume and total lung capacity these are things that are again done with spirometry in with our pulmonary function tests one test we already talked about was the arterial blood gas which tells us about the patient po2 Oh two saturation so that does tell us about some oxygenation components of the lung and also about co2 removal lastly we can do our chest x-ray and chest CTS which will give us more information about the structural components as to what's happening in the lung you additional blood studies include arterial blood gases also checking the hemoglobin level you know if the hemoglobin is low we're not going to be able to carry as much oxygen to tissue the body we can check a pulse oximetry pulse oximetry is a device you put onto the finger and it measures how much oxygen is balancing hemoglobin but keep in mind there's a lot of things that could be wrong with pulse oximetry first of all it's peripheral and it measures everything that's bound to hemoglobin including carbon monoxide nitric oxide and other kinds of substances so it's a good monitoring tool it's not a good diagnostic tool if you think your patient really has a respiratory problem they need a blood gas sputum studies so we have the patient obtain a sputum sample Koff that stuff up and then we're going to send it down to the lab and they're going to look at it to find out if there's something growing in there any particular kind of bacteria etc and then what kind of antibiotics it might be susceptible to so that we can treat it appropriately we can check for tuberculosis by doing our PPD test in which of course everybody's probably familiar with because you have to do that for clinical compliance as we age there is a loss of elastic recoil that occurs there's stiffening in the chest wall there can be alterations in gas exchange as a result of the loss of elastic recoil and stiffening in the chest wall there's an increase in our flow resistance as a result of the loss of elastic recoil and stiffening and decreased exercise tolerance as a result of all of the above so these changes that occur as a result of aging can decrease our patient's ability to be able to tolerate exercise and to have good gas exchange this diagram is showing the differences in lung capacities of the normal lung and the aging lung and primarily one of the things you're going to see here is that there is a much bigger residual volume that's the very bottom there the much bigger residual volume in the aging lung which means there's more air stuck in along all the time so that's going to move everything up that means we have less inspiratory reserve so we don't have as much ability to be able to confidence when there's needs for type of exercise etc signs and symptoms of pulmonary disease include dyspnea dyspnea is also called difficulty breathing now difficulty breathing is a subjective sensation now we can look at somebody we can say that their respiratory rate is very high and they're struggling to breathe but this feeling of dismay is a subjective sensation that the patient has it doesn't always correlate with what we're finding objectively people can feel when something's happening in there long before it's going to be expressed through changes in any of our objective measures so pay attention when the patient tells you that they have this feeling feel like I can't catch my breath pay attention to that because dis Mia is an early sign that your patient has a respiratory problem we can further differentiate dyspnea down into orthopnea orthopnea is a condition where the patient is difficulty breathing when they're laying down you hear this a lot about people at night when they go to bed and they say I have to sleep on two or three or four pillows in order to be able to breathe okay when you hear that they've got to sleep on two or three or four pillows in order to be able to breathe you've got to be thinking of orthopnea that they can't lay flat and that could be a number of reasons it could be a cardiac condition so there's lots of different things that could be causing that we also have our peroxisome own nocturnal dyspnea so the client wakes up in the middle of the night not able to breathe this is very common and people who have asthma asthma is often expressed most commonly or most often at night and there's reasons for this there is a circadian rhythm a 24-hour rhythm to our hormones in the body so a cortisol and epinephrine norepinephrine etc there's a 24-hour cycle to those so in the middle of the night we have the lowest levels of epinephrine norepinephrine and cortisol which means our bronchi are going to relax they're going to become smaller and the patient's going to have more difficulty with breathing some of our abnormal breathing patterns include Kussmaul respirations kuzmin's respirations are a very deep rapid expressions and in fact here it also refers to them as hyper Nia so this means the patient is breathing very fast cheyne-stokes respiration czar a condition where the patient is breathing fast and deep and then starts to slow down and have very shallow or maybe even no respirations at all for a short time then deep rapid respirations again the one you're going to see most often is tachypnea which simply means the patient has a rapid breathing rate in fact you have experienced this many many times in your life you've had Tekkit Nia every time you exercise you have tachypnea when we're looking for it and calling it abnormal is when the patient is not exercising and they have tachypnea that would be abnormal so the person's at rest and they're still unable to catch their breath one of the ways that we can assess for problems that are occurring in the patient's lung is to listen to lung sounds so you're going to get your stethoscope out and you're going to listen to your patients lung sounds and what we're going to expect to hear is one of three different types of sounds a wheeze rhonchi or crackles or the crackles are also called rowels crackles are going to be a soft sound that you hear at the end of inspiration and you're going to hear that in the basis in the back so you're going to cepe tarring crackles at the end of inspiration and it's going to be at the basis in the back rhonchi are going to be kind of more of a bubbly sound that's heard throughout inspiration and throughout expiration that's in the upper Airways caused by secretions in those Airways then we have wheezing occurring wheezing is a high-pitched musical sound that occurs usually first on expiration because the Airways are smaller during expiration and then later on inspiration as the disease process progresses our pulmonary disease can be classified according to a number of different criteria whether it's acute or chronic obstructive or restrictive infectious are not infectious and whether it's caused by an alteration in the lung or the heart so we may have classifications according to those things dyspnea has multiple causes remember again is that subjective sensation and again we can break it down into those two different subcategories hyperventilation is a condition that occurs when the patient is breathing faster than they need to this is going to cause the patient to blow off co2 this may be a good thing in certain situations but we can have hyperventilation occur with a patient who has a head injury so they're hyperventilating they're in respiratory center is saying hey we need to breathe faster when they really don't pain and anxiety so you know somebody who's anxious tends to breathe faster and they can tend to blow off their co2 this can lead to a hyperventilation syndrome so bad in fact that we need to take the little paper bag and put it in front of their face so that they stop blowing off that co2 and they can stop that hyperventilation syndrome hypoventilation on the other hand is a situation where we have inadequate alveolar ventilation and hypercapnia and our co2 will increase this can lead to a high per capita Kress per Ettore failure where the patient just stops breathing because the co2 level gets so high alterations in mechanics and neurologic function are going to be our primary reasons why the patient has hypo ventilation other signs and symptoms we're going to look for include cough okay so we're going to look for that coffin that patient that's a protective reflex trying to get rid of that junk out of the lungs so that the patient is then able to have normal functioning healthy lungs hemoptysis is a situation where the patient is spitting up coughing up blood now this is a difficult situation because a lot of times people will say I'm vomiting blood when in fact they're actually coughing it up out of their lung or they may say it the other way around I'm coughing up blood and when actually they vomited it or maybe it dripped down from their sinuses so you do need to do a little bit of Investigation here and find out exactly what's going on however if your patient does have a history of lung cancer or maybe they have a severe inflammation or infection of the lung it's very possible they could have bloody sputum and that's not an abnormal thing is just part of the disease process cyanosis is a bluish discoloration around the mouth and the mucous membranes it's caused by desaturated blood so we have a decrease in amount of hemoglobin that's into blood and we're seeing that through the skin typically you're going to see that in the mucous membranes first so that bluish color is called cyanosis pain could be a sign of symptom of a pulmonary condition and abnormal sputum so changes in the color and the consistency of our sputum indicates that there could be a pulmonary problem if a patient has a condition that causes a chronic hypoxia so the patient's chronically hypoxic what can happen is we can get a hypertrophy of the capillary network in the nail bed and that causes clubbing where the tip of the finger tends to expand outward and it turns into kind of a club so you look at the early stage there that's more of a normal-looking nail and you move on down to the severe and you can see how the tip of the finger has become very bulbous and that's the result of this hypertrophy of the vasculature well obviously a very severe sign symptom problem that we have with pulmonary problems is going to be hypoxemia there's reduced oxygen getting to the tissues of the body and this can cause the patient to have some severe ischemic injury and necrotic damage to tissues of the body oxygen delivery is a problem with the alveoli so we want to take a look and see if the patient has an adequate oxygen content coming in and whether or not we're having good ventilation of the alveoli in order to try to deal with a ventilation/perfusion mismatch that's causing this hypoxemia the diffusion part could be a real issue here as well where we have an imbalance between the amount of diffusion that's occurring through our alveolar capillary membrane so oxygen can't get across that barrier and co2 can't get backed out so the diffusion of oxygen is also an important component in Mabel in our ability to be able to maintain a normal type of oxygenation in the blood stream well thank you for joining me for the structure and function of the pulmonary system in is part two we're going to talk about pulmonary disorders so let's move on to part two and find out more about what happens when patients have alterations of their structure and function and they develop pulmonary disorders thanks for joining me this time and until next time bye now you

Channel: David Woodruff

Views: 23,080

Rating: 4.8606963 out of 5

Keywords: Nursing education, nursing, nursing student, Pathophysiology, Respiratory, Pulmonary

Id: jb6BOt-xHbk

Length: 53min 11sec (3191 seconds)

Published: Mon Jun 03 2013