Ventilation is the movement of air into and out of the lungs, governed by the relationship: airflow = pressure difference / airway resistance. Key factors include alveolar pressure, atmospheric pressure, and airway diameter, which is primarily influenced by cartilage, connective tissue, and smooth muscle tone. Spirometry measures lung function through parameters like forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), distinguishing between obstructive diseases (like asthma and COPD, where airflow is impaired) and restrictive diseases (where capacity is limited). Anatomical dead space (~150ml) reduces alveolar ventilation efficiency, making deep breathing more effective than shallow breathing.
Deep Dive
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Deep Dive
Ventilation [Sunday Slides]Added:
hey everyone it's me welcome back to another episode of physiology 2.
especially for you in this video the topic will be ventilation and that means we're going to be looking at airflow and the factors associated to airflow so for example the pressure difference and Airway resistance is what we will cover in this video first we're going to look at spirometry because that is the measurement of airflow and I'm gonna just play the first minute of this video which will illustrate spirometry in a practical way and we'll show you some clinical applications so I'm just going to play the first minute roughly and then I will move on to the next slides spirometry is a simple non-invasive test that measures the amount of air a person can breathe out and the amount of time required to do so therefore spirometry is used to detect and monitor respiratory diseases spirometry is performed with an instrument called the spirometer that can measure the airflow or the air volume that a patient can mobilize in the lungs spirometers can be classified in two types large Bellows or rolling seal spirometers usually only available in pulmonary Laboratories smaller handheld devices often with electronic calibration systems that are portable and can be used in Primary Care the device is usually connected to a computer that transforms the signals received into a volume time curve graph and values the spirometric values are obtained with a forced expiration by the patient that measures the most important parameters of lung function these are the forced vital capacity or fvc which is the maximum volume of air that can be exhaled during a forced expiration after a maximal inspiration all right that was just the first minute please watch the remaining of the video yourself to get a nice idea and some great examples what we will look at for now is a normal spirogram and what you can see here is a list of eight different volumes all important and definitely for any physio my advice is always please know your numbers so respiratory numbers but also numbers related to exercise physiology heart rate cardiac output as we will discuss in later videos those numbers are essential for you to easily diagnose whether a number is normal or abnormal or maybe a measurement is slightly off so for spirometry title volume inspiratory Reserve volume Etc should be known to you in the book of vendor you can clearly find the explanations and also the normal values so please study them so that you know your numbers and you can work with them later on airflow is all about physics so again High School physics definitely will come in handy and what you see in this formula right here is that airflow is defined or can be calculated as the pressure difference divided by resistance so in simple English if the pressure difference goes up the flow will go up if the resistance goes up the flow will go down so here you can see the alveolar pressure and here the atmospheric pressure so if you're able to create a lower alveolar pressure compared to the atmospheric pressure you have a positive pressure difference or at least a pressure difference that will allow air to flow into the lungs and then depending on the diameter mainly the resistance is a factor that will finally complete the determination of the airflow more examples later on in a normal situation unless someone is growing and you follow someone over time the length of the tube especially the upper Airways is not really going to change the tube radius is going to change so you can say that the direct influence or the direct factor that influences the resistance is the diameter of the Airways and normally especially the upper Airways are kept open by several structures which will make sure that the resistance is as low as possible and that is done for example by cartilage but also by just the fact that the whole system is more or less or the lungs are glued to the chest wall and also some connective tissue especially in the bigger upper Airways we'll make sure that the Airways will remain open in order for the diameter to be as wide as possible and therefore the resistance to be relatively low but for example during a forceful expiration the intrapleural pressure can actually cause the radii of the Airways to decrease and if the radius of the tube decreases the formula in the previous slide showed you that the flow or the resistance will go up and therefore the flow will go down and especially if the Airways would collapse the flow would be dramatically impaired and sometimes even brought completely to zero in case of a complete collapse of the upper Airways but that's only in an abnormal situation normally the resistance is relatively small well besides these physical factors your Airway resistance can also be influenced by hormones and the immune system and the two examples in this slide illustrate what both factors could do epinephrine as related to the sympathetic nervous system will cause a relaxation of the smooth muscle that is normally contracted around the upper Airways and that relaxation will cause the radii of the Airways to increase which will decrease the resistance and makes airflow easier leco trains for example would do the opposite if they cause the smooth muscle tissue to contract that will constrict the Airways will decrease the diameter and that will then increase the resistance especially in the diagnostic process not always done by physios but at least something a physio should be able to understand in a diagnostic process you can separate obstructive issues from restrictive issues quite easily through spirometry because in an obstructive disease so with a patient with an obstructive problem like COPD air flow is impaired but vital capacity could still be normal in a restrictive situation the airflow is not really affected but it is the capacity that is decreased well for you at any time you can increase or decrease your minute ventilation consciously but you can basically do that in different ways you could either increase your tidal volume just by increasing the volume per breath or you can upgrade the frequency by just taking more breaths per second but although the the product the minute ventilation of those two factors might be the same what is really important is the alveolar ventilation and that's what you can see on the next slides minute ventilation is not the same as alveolar ventilation and ultimately alveolar ventilation is really what will make the difference in this video that I'm going to play for you just now there's no sound attached I will show you with some numbers what the difference is between these different breathing strategies so have a look so what you can see here is an example where you're breathing with 12 breaths per minute and a tighter volume of 500 milliliters and that will give you a minute ventilation of 6 000 that's what you can see here so six liters if you would then look at the amount of what we call dead space ventilation you can see that from each 500 milliliters of vital volume you would have to subtract 150 milliliters of dead air and that is basically the amount of air that's trapped in the upper Airways and the air that is left after the previous expiration so the LV of alveolar ventilation is actually 4.2 liters per minute in this example I'm going to play it again and then the numbers will change so you will see how that will affect the minute ventilation all right so what you see here is a minute ventilation that is still 6000 on the left hand side but that is now done with a higher frequency and a lower tidal volume and then the end result here is that the net alveolar ventilation is a lot less so it's only 4.2 liters of alveolar ventilation and that is because the same 150 milliliters of dead air needs to be subtracted from that to 50 and that will leave you with less alveolar ventilation even though the minute ventilation was exactly the same finally let's jump to the last example if you do the opposite in terms of your strategy you would now take very deep breaths and that is done with only a small a low frequency you could still reach the same minute ventilation of six liters but here then you can see that because of the relatively small impact of the Dead Space you will still be left with 5.1 liters of fresh alveolar ventilation so you see in this animation with these numbers that the strategy definitely has a big impact now in the previous in the next slides starting with this one you can see in a static picture what I was just showing you in the video before so the amount of anatomical Dead Space is 150 milliliters and that means that every breath that you take you basically are first breathing in the dead air that was still left from the previous expiration so from 500 milliliters you would have to subtract 150 and that will leave you with 350 of fresh alveolar ventilation per breath now in this table you can see an even more extreme situation where first again we can start with subject C that has the same values as you you saw in the previous video where with a low volume sorry with a high volume but a low frequency you can end up with 6 liters per minute as minute ventilation and that then results in 5.1 liters per minute of alveolar ventilation if you breathe a little bit more with a normal tidal volume of 500 and you do so with 12 breaths per minute you would still have 6 000 milliliters so 6 liters of minute ventilation but because you're now basically breathing in 12 times this 150 milliliters you're left with 4.2 liters per minute again during rest or even during exercise that would be still more than enough but here's an example of someone that is really hyperventilating meaning breathing with a very very small title volume very shallow breathing and if the title volume would actually be the same as the Dead Space effectively you can see here with the numbers you're exchanging zero fresh air so shallow breathing is definitely very inefficient because of the impact of the Dead Space so one of the take-home messages especially the one for this video would be that taking a deep breath is beneficial because of the impact of the Dead Space that is drastically reduced and in a previous video I already explained to you what the impact is on the release of surfactant so for two reasons taking a deep breath is definitely a good idea so what about the clinical application well in this course we're going to focus on just two obstructive examples asthma and COPD both will have an increased Airway resistance the underlying pathology though will be different asthma you will see that the radius of the Airways is reduced and that will cause an increase in the resistance the reason for this reduced radius is a chronic inflammation that will trigger smooth muscle contraction and that could be triggered also by for example exercise or other chemicals pollution or a pollen hay fever for example is also a trigger that could cause the smooth muscles to contract restricting the diameter or constricting the airflow and therefore increasing the resistance in a graph or in a picture here you can see how the smooth muscle tissue is relatively relaxed here on the left hand side but if for whatever reason the smooth muscle tissue is activated it will really cause a constriction of the Airways which will reduce the diameter and increase the resistance in order to treat this you could either try and Target the inflammation for example by drugs that would cause a reduction of the inflammation or you could try to just focus directly on the smooth muscle contraction for instance by chemicals that are related to epinephrine or similar to epinephrine and that would widen the Airways lower the resistance and lower the symptoms COPD is different because COPD is also an obstructive disease but it is not caused by this excess or extra smooth muscle activity CPD is actually an umbrella term so we have to always separate the emphysema component and the bronchitis component if we're trying to explain the physiology of the pathology so with emphysema basically your lungs will look more like plastic bags instead of elastic balloons which means that they can actually collapse a little bit easier which will be especially problematic in a expiration and even more in a forceful expiration because the Airways could easily collapse chronic bronchitis on the other hand is all about excess mucus production that would literally cause an obstruction obstruction because of the mucus that will lower the diameter of the airway to to flow through chronic as you can see right here so here it's not hard to imagine that if normally this would be the diameter right now with the extra mucus effectively the diameter is maybe even half and that will definitely increase the resistance dramatically for the cross-sectional area you can see here a normal cross-sectional area with a large pathway and right here because of the mucus definitely a significantly reduced pathway so if the diameter goes down the resistance will dramatically go up in emphysema here you can see that all these little alveoli seem to have merged together a little bit so effectively it means that the Airways are not as elastic of of these small balloons anymore but it's more like a plastic bag that I mentioned earlier and that will cause the Airways to more easily collapse during a forceful or at least somewhat forceful expiration and thereby dramatically decreasing again the diameter of the airflow during expiration and also increasing dramatically the resistance if you want to know more about COPD then definitely I can recommend you to watch this video I'm not going to play it inside this video for now but definitely it's a good example of the different components of COPD and definitely a good preparation for next year when CPD and cardiac patients are actually part of our courses at ESP as mentioned before the difference between obstructive and restrictive problems can be measured by spirometry so again obstruction means airflow is limited whereas with a restriction it is the capacity that is limited these are just a few examples of obstructive and restrictive problems in this course we're not going to cover the restrictive category but we've just mentioned asthma and COPD as an example of an obstructive pathology but definitely I would encourage you to look up more and definitely later on in clinical internships or also in second year ESP courses you can expect different pathologies inside your cases so it's good to realize in which category a pathology will fall so that you can make a better diagnosis and also better treatment plan and that brings me to the last part of this video so before the end of this video I just want to illustrate a few clinical practice examples in the COPD guidelines for example you can see quite a few outcome measures that are directly related to what we're covering in this video and in the rest of this course and definitely also it will be interesting for you to look into the different interventions based on the advice from the guideline and see if these videos already helped you to make more sense out of what you can do as a physio with this patient's category to already give you some examples for next year here's a few graphs that illustrate how spirometry can help in the diagnostic process and maybe later on also in the evaluation of your interventions these clinical graphs will not be part of this exam for physiology too but definitely are interesting for the future so what you can see is a so-called flow volume curve where you see that different pathologies will come with different curves so depending on the curve that you measure for your patients or that you see in the patient file you can already draw some conclusions about either it being restrictive or obstructive or anything else so if you're interested please have a look so that you're fully prepared for next year and definitely for any potential cases that you may encounter during your internship for example finally this course in this video is related to spirometry and one of the most common measures in clinical practice are the fev1 the forced expiratory volume in one second because it would give you an indication of the obstruction and also the type of obstruction the fvz is the first vital capacity is actually giving you a overall indication of the obstruction and you will see in many guidelines that the so-called typhenol index is used to categorize the patients and the severity by looking at this ratio just have a look and hopefully later on everything will make sense that was it for this video I thank you very much for watching and I really hope to see you soon in the next one
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