Transcription
We'll start this part of the lecture with an important concept we need to discuss, the dead space in airways. In fact, a large portion of airways is considered dead space. This dead space can be divided into two types.
First, there's normal or anatomical dead space. In this region, gas exchange is not intended to occur. It extends from the nasal cavity down to the respiratory bronchioles. In a typical person, this space is about 100 to 150 ml. It can also be estimated theoretically by multiplying the ideal body weight by two, not the current body weight, but the ideal one. Of course, you, dear listener, you may have already right now the ideal body weight.
So, but the second type is physiological dead space. This essentially is the anatomical dead space plus alveoli where gas exchange does not occur. Under normal conditions, there may be a few such alveoli, for example, at the apex of the lungs where ventilation, as we discussed, is less effective. However, in various respiratory and severe illnesses, the physiological dead space can increase significantly.
And now for some practical thinking, let's take a look at this image. You probably heard of or maybe even tried this activity called snorkeling. As you can see, in order for a person to breathe, there is a tube attached to the mask. This tube in this situation also becomes part of the dead space. And maybe not now, but in childhood, you might have thought about how to make this activity even cooler that if you took a longer tube, you could dive deeper underwater. For example, you might think about taking a long vacuum cleaner hose and using it to dive deeper underwater. But, well, here I have to disappoint you quite quickly. Very soon, you would run out of usable air and the situation would end rather badly. The reason is that this dead space also becomes far too large and too long for the lungs to handle. In that case, the air would just be moving back and forth in the tube without actually bringing in fresh oxygen-rich air from the outside.
And now, I will support this whole story with some formulas. First, we have minute ventilation. Similar to cardiac output in the heart, this is the volume of air exchanged in the lungs per minute. We calculate it by taking the tidal volume, which is the normal breathing volume obtained, for example, from spirometry, and we will talk about this in a minute, and multiplying this tidal volume by respiratory rate.
There is another important parameter we need to consider also, alveolar ventilation. The definition sounds similar and also the formula is quite similar, but for this calculation, we must first subtract the dead space from the tidal volume and only then multiply by the respiratory rate. This gives us then the volume of air that actually reaches the alveoli per minute, and this is what truly matters because we are interested in the part of air that actually allows oxygen to enter the blood. Now, if you look at the formula, you can quickly realize that alveolar ventilation to occur at all, the dead space must not be equal to the tidal volume. If they were equal, the subtraction would result in zero, and therefore the alveolar ventilation would be zero. This means that dead space can never be as large as the tidal volume. In other words, as dead space increases, alveolar ventilation decreases. And that's why a snorkel increases dead space, and in a very long tube, air simply moves back and forth without effective exchange in the alveoli.
In medicine, this principle is very important in the design of respiratory equipment. For example, in anesthesia, when a mask is applied to a patient, it is crucial that the dead space is as small as possible, and this is something you can literally write down now in your notebooks and underline. Medical respiratory devices must have minimal dead space, and this is extremely important.
Then, let me show you another image. Here you can see a medical device with a very long tube. At first glance, this may seem like the opposite of what I just explained, because I said that the tubing should be as short as possible to minimize dead space. But here, there is a different mechanism involved. As you can see, there are actually two tubes. This means that air flows in through one tube and out through the other tube. Because of this, the dead space is not determined by the length of these tubes, since inhalation and exhalation occur through separate pathways. And there is also a valve system that controls the direction of air flow here. And as a result, the additional dead space in this setup is limited mainly to the mask itself. And as you can imagine, the volume of the mask is relatively small.
So, this was a brief overview of dead space. Now, let's talk about some other parameters. One of the most important lung volume parameters in physiology is the vital capacity of the lungs. The vital capacity is the maximum amount of air that a person can exhale after taking a maximal inhalation. In other words, a person inhales as deeply as possible and then exhales as much air as possible. This is measured and then compared with normal values. In a healthy adult, the average vital capacity is about 4 L, typically ranging from 3 to 5 L. Well, in generally, it should not be much lower than 3 L, but in trained individuals, it can reach 6 L or more.
The vital capacity is made up of three volumes, which are listed here. And plus, there's another additional volume in lungs that never leaves actually the lungs. This remaining air is called the residual volume. It's similar to the heart where you have residual volume of blood never leaving the heart. Because also the lungs never completely collapse, there is always some air left inside.
So, the first component of vital capacity is my before-mentioned tidal volume. This is the amount of air that a person normally inhales and exhales during regular breathing. On average, this is about 500 ml, so half a liter. The next two volumes go beyond normal breathing. The inspiratory reserve volume is the additional amount of air that can be inhaled after a normal inhalation. So, this is quite substantial, on average about 2.5 liters, could be also 3 liters. Similarly, the expiratory reserve volume is the amount of air that can still be exhaled after a normal exhalation. And this is slightly smaller, about 1 liter.
Now, pay attention also here, I'm using words inhale, exhale, but very often in physiology and medicine, some other terms are used. Inspiration for inhalation and expiration for exhalation. Now, but whatever you use actually doesn't matter. More importantly, that you know which process is which, of course.
Then, back to volumes. As I mentioned earlier, there's also this residual volume, the air that never leaves the lungs. And this is also somewhere about 1 liter, even after maximal exhalation. Well, unfortunately, these values are quite important and must be known for the exam because they are part of normal reference parameters for patients.
Vital capacity is measured using a device called spirometer, and the method is known as spirometry. This whole process of spirometry may remind you a bit of blowing into a breathalyzer because the idea is somewhat similar. The patient blows into a tube and sensors then record the amount of air either exhaled or inhaled as it passes through the device. These volumes, that is the amount of air moved, are typically recorded electronically, usually on a computer connected to the spirometer. This system, together with the specialized software, registers both inhalation and exhalation.
So, what does a classic spirometry result look like? You can see an example here. I have also marked all the lung volumes, which I mentioned before. First of all, the tidal volume is about as you heard, plus minus 500 ml. So, this represents normal inspiration and expiration. In this graph, the upward curves represent inhalation, and the downward curves represent exhalation. Here, the patient has been asked to breathe normally twice, and on the third attempt, the patient is asked to inhale as deeply as possible, which represents the inspiratory reserve volume. Though, be careful, we measure this above the normal tidal volume, because the tidal volume is always part of normal breathing, and it is already included in the graph baseline. After that, the exhalation occurs. The patient is again asked to breathe normally, inhale, exhale, inhale, and then perform a maximal exhalation. Similarly, the expiratory reserve volume is measured starting from the end of normal exhalation. This process may be repeated several times to obtain more accurate measurements, but unfortunately, as I told you, the residual volume cannot be measured with spirometry, because it is the air that remains in the lungs. We can only estimate it, and usually, as I said, it's around 1 L.
Finally, where do we see vital capacity on this graph? It is represented by the total range between maximal inhalation and maximal exhalation. In other words, vital capacity is the sum of tidal volume, inspiratory reserve volume, and expiratory reserve volume. And as mentioned earlier, residual volume is not included in vital capacity because it cannot be measured with spirometry. However, there is another parameter actually called total lung capacity. That would be all of this part. So, everything together. And total lung capacity does include the residual volume. So, vital capacity plus this residual volume. To calculate total lung capacity, we either measure residual volume using other methods like nitrogen washout or helium dilution, or we just estimated that it is 1 L and added to the vital capacity.
So, from this, it is clear that vital capacity is influenced by diseases, but even without pathological factors, there are several variables that affect it in all individuals. First, gender. In general, men tend to have a slightly larger vital capacity. Then comes age. As with many physiological functions, vital capacity gradually decreases with age. Height is also important. Taller individuals usually have a greater vital capacity. Body weight also plays a role. Excess weight tends to reduce vital capacity. Another important factor is respiratory muscle strength and training. And this is not limited to sports alone, by the way. Of course, athletes typically have a higher vital capacity, but it can also be increased through other activities that train breathing, such as singing or professions that rely heavily on voice use. Practices like yoga can also help improve vital capacity. On the other hand, factors such as smoking clearly reduce lung vital capacity. However, the most important determinant is the elasticity of lung tissue. This depends on the amount and function of such pro- teins as elastic fibers in the lungs, which allow this organ to expand effectively and take in air. Lung elasticity is also closely related to age, and as mentioned earlier, tends to decline over time. It can also be reduced prematurely by factors such as smoking, exposure to polluted or harmful environments, and of course, by various pathological conditions, such as serious infectious diseases.
Okay, let's continue, and next in our list are dynamic lung parameters. The first one is maximum voluntary ventilation. It is defined as the volume of air that would be exchanged in the lungs in 1 minute if a person were breathing as deeply and as rapidly as possible. Pay close attention to the wording here. It says would be exchanged, not is exchanged. That's because this describes a theoretical not something a person can actually sustain. No one can, or rather should, breathe that intensely for a full minute. If someone tried, after about 15 to 20 seconds, they would start feeling dizzy, and the body would essentially say, "That's enough." Continuing such intense breathing, which is called hyperventilation then, could lead to loss of consciousness. And that's probably not what we aim for during breathing exercises, right? This happens because although oxygen is essential for energy production, too much oxygen can disturb blood chemistry leading to vascular reactions and even fainting.
So, returning to lung function, maximum voluntary ventilation is measured using a clever method. The patient is asked to hyperventilate for only 10 until 15 seconds and the result is then extrapolated to 1 minute. This gives the theoretical maximal ventilation then. For women it is usually 50 to 100 liters per minute, for men approximately 100 to 150 liters per minute. Although other sources may show slightly higher values. I have seen also mentioned that for females it could be 80 to 120 liters per minute and in males 140 to 180 liters per minute. So, don't be surprised if numbers vary in other source materials. Maximum voluntary ventilation reflects the reserve capacity of the respiratory system. So, for example, during physical activity, like when you have to run after a bus.
The second parameter here mentioned in my slide is peak expiratory flow or PEF. You can think of it as how fast you can blow out a candle. It represents the maximum air flow achieved during exhalation. The most important thing here is the normal value. It should be at least 70% of the predicted value because given every patient's age, gender, height and so on, every patient will have a predicted value individually. So, if it is lower, it may indicate to respiratory obstruction. Unlike basic spirometry values, PEF usually requires either a more advanced spirometer or some other specific measurement device. And then the result is displayed on a flow-volume curve, which shows how quickly airflow reaches its peak during exhalation. And I will show you the flow-volume curve in a few minutes. So, if you ever want to know how powerfully you can blow out a candle, PEF is the parameter you're looking for.
Next, we have vital capacity again, which is also assessed together with dynamic lung parameters. However, this vital capacity is often marked with the letter F. So, on measurement devices, you will frequently see FVC, meaning forced vital capacity. This refers to vital capacity measured during forced breathing, or more precisely during maximum ventilatory effort. Since the exhalation is performed forcefully, this measurement value is usually slightly lower than the normal vital capacity obtained during relaxed spirometry. Another important parameter, which will also be relevant going forward, is FEV1, or forced expiratory volume in 1 second. And this is volume of air exchanged in the first second of a forced exhalation.
And now let's look at the flow-volume curve. As I mentioned earlier, I will show you the curve and what it looks like. When looking at this curve, some people may feel confused. Where is the time axis? We are used to graphs where time is on the x-axis, but here there is no time parameter at all, and that is actually intentional. On the x-axis, we have volume, the amount of air that the person inhales or in this case exhales. And on the y-axis, we see the flow rate measured in liters per second. If the value is zero, it means there is no air flow, no inhalation and no exhalation. Above zero, we record expiratory flow, so exhalation. This curve is essentially a map of breathing showing how much air is moved and how fast, but not when it happens. So, time remains behind the scenes.
So, how is this curve obtained? First, the patient performs a maximal inhalation filling the lungs as much as possible, every last alveolus. This represents the starting point in the curve. Then comes the forced exhalation. The patient exhales all the air from the lungs as quickly and as forcefully as possible. At the beginning, the air flow rate increases rapidly. The curve rises upward and reaches a peak. Then, as the lungs empty and less air remains, the flow rate decreases and the curve gradually descends back towards zero until all the air has been expelled from the lungs and the maneuver is complete. So, this curve is very useful for assessing respiratory function and lung health. It also demonstrates that in some graphs, time is not the main variable.
So, which parameters we discussed earlier can we identify here? First, peak expiratory flow. This is the highest point in the curve where air flow reaches its maximum. And secondly, vital capacity or other forced vital capacity, this represents the total volume of air exhaled after maximal inhalation. And as mentioned before, this forced vital capacity may be slightly lower than the vital capacity measured during normal spirometry.
Before we move on to discussing where these measurements and parameters are applied in practice, let's first talk about resistances in the respiratory system. There are two main types of resistance in the respiratory system, and the first will be elastic resistance. This is closely related to the ability of the lungs to expand and recoil, since the lungs are elastic structures. If the lungs behave like a well-oiled accordion, flexible and stretchable, then elastic resistance is considered normal. But if they resemble an old rubber balloon that doesn't want to stretch, then the resistance is increased. And a small note on terminology, we usually don't say resistance is low, we say it's either normal or increased. So, don't use the wording low resistance. Elastic resistance is influenced by lung compliance. The better the lungs expand and recoil, the more likely the resistance is normal. A similar concept also applies, by the way, to blood vessels, where wall elasticity affects resistance. We can assess elastic resistance indirectly using vital capacity. The greater the vital capacity, the better the lungs can expand and contract. If elastic resistance increases, vital capacity decreases. Simply put, the stiffer the lungs, the less air can they take in and expel. A normal value is when vital capacity reaches at least 80% of the predicted value. Values above 100% are possible, by the way, and indicate excellent function. So, those values that even exceed 100% are extremely good, and you will see them especially in individuals with well-trained respiratory systems, such as athletes or singers.
The second type is non-elastic resistance, and this we can compare to peripheral resistance in blood circulation, by the way. But, in the respiratory system, it is mainly determined by the state of the airways, especially the bronchi. If the bronchi are wide and open, air flow is easy, and resistance is normal. But, if the bronchi are narrow, for example, during an asthma attack, air flow encounters obstacles, and resistance becomes increased. This type of resistance is evaluated by using the Tiffneau index. The formula uses previously discussed parameters, which are the volume exhaled in the first second, and the forced vital capacity. So, and here you see the formula, and I also wanted you to pay attention to the word Tiffneau itself here. So, my first Tiffneau here is the correct way how to spell it. But, sometimes in some materials, you may see the kind of trivial name of it, which is a common colloquial or phonetic misspelling of the name, but it is still widely used. So, this is kind of wrong, but it is not forbidden to use. So, just FYI, this is the correct way how to spell Tiffneau, but if you spell it like this, it's not the worst mistake in the world. So, and regarding this index, this tells us whether airway resistance is normal. So, a normal value is above 70% here. So, to fully calculate it, of course, to get the percentage, you need to multiply this obtained number by 100 here.
Now, and since we are talking about resistances, we can also start to discuss the types of ventilation disorders associated with it. There are two main types, and when combined, they form a third type as well. First, we have restrictive ventilation disorders. These are characterized by reduced vital capacity. As we discussed, vital capacity is related to elastic resistance. Therefore, if vital capacity is below 80% of the predicted value, we can say that the patient has restrictive ventilation impairment. In this case, lungs are unable to fully expand.
On the other hand, if the calculated Tiffeneau index is below 70%, we are dealing with obstructive ventilation disorders. These involve limitations in airflow, especially during exhalation. If both parameters are reduced, meaning the patient has both low vital capacity and low Tiffeneau index, then this is referred to as mixed ventilation disorder. And this, of course, represents a very serious condition for the patient.
Now, let's look at some few examples of restrictive ventilation disorders first. These can occur temporarily or long-term, and in some cases may even become permanent after serious lower respiratory diseases. For example, they may develop during or after tuberculosis, during or after pneumonia, and also after severe COVID-19 infections, particularly when it has caused pneumonia. These conditions are often associated with lung fibrosis, especially when the disease has been very severe. Pulmonary fibrosis is a condition where normal alveoli, which are normally lined with a simple single-layered epithelium, are replaced by fibrous connective tissue. So, this is an example of metaplasia, as you understand. This happens because the epithelium is damaged by disease and is unable to regenerate in time. As a result, fibroblasts step in and deposit connective tissue. In a way, this acts as a repair mechanism to prevent structural collapse of the alveoli, but the downside is that this fibrous tissue is much less elastic than normal epithelium, and it also impairs gas exchange. Consequently, vital capacity decreases.
Another very important risk factor is inhalation of dust particles. Dust is extremely harmful to the lungs. For example, in certain industries like the denim or jeans industry, workers may be exposed to silica particles used to create a worn or faded effect, and standard masks, as you see here in the picture, of course, do not provide sufficient protection. And as a result, workers may develop restrictive lung disease at a young age, sometimes with severe consequences, and by these severe consequences, I mean premature death. Smoking is another key factor, clearly with tobacco, but newer research also suggests that electronic cigarettes can over time contribute to restrictive changes, especially with prolonged use, of course. In patients with more advanced restrictive disorders, symptoms begin to appear. The most characteristic then are shortness of breath and shallow breathing.
Obstructive ventilation disorders occur when airways become narrowed, inflamed, or blocked by mucus. So, what can actually narrow the airways? Essentially, there are three main mechanisms. Firstly, smooth muscle contractions in the bronchi, which causes them to narrow. Swelling in the airway walls, often due to inflammatory mediators like histamine released from basophils, which increases vascular permeability. Or excess mucus or mucin production by the respiratory epithelium, which obstructs normal air flow. Well, one major condition in this category is chronic obstructive pulmonary disease, or COPD. It is a common and treatable disease characterized by respiratory symptoms and persistent airflow limitation, usually caused by exposure to harmful substances. Again, tobacco smoking is a major cause, but electronic cigarettes, especially those with flavored additives, can also irritate the respiratory epithelium and promote excess mucus production. Over time, this mucus is not effectively cleared and symptoms gradually worsen with age and exposure, of course. Now, other important examples include asthma, where constriction of bronchi plays a key role, allergic reactions involving inflammatory mediators like histamine, bronchitis, where airway inflammation leads to narrowing and so on. When obstructive disorders become clinically apparent, the typical symptoms include wheezing, cough, and difficulty during exhalation.
And now let's focus on how we can use these parameters to determine where the patient stands in relation to these two types of resistance. As mentioned earlier, if the vital capacity is above 80% and the Tiffeneau index is above 70%, then on this diagram here, this would correspond to the zone where both values are within normal limits. So here. In such case, we say that the patient is with an essentially healthy respiratory system and there are no significant ventilation impairments. For example, if you measure both vital capacity and the Tiffeneau index in a patient and plotted the point somewhere around, let's say, here on the graph, you could confidently say that this person is within normal limits with no ventilation disorder. However, realistically, if the values are already close to the threshold as here, it would still be reasonable to start being a little cautious. Ideally, of course, you would want to be further away from these boundary values, especially so that the results are clearly better and more reassuring. As mentioned earlier, in individuals with very well-trained lungs, these values can be even above 100% and they will be located far from the border point, particularly with respect to the vital capacity.
Now, let's look at the more concerning cases. If after measuring both parameters, the point falls somewhere here where vital capacity is normal, but the Tiffeneau index is below 70%, then we are dealing with obstructive ventilation disorders. That is because the Tiffeneau index is impaired, while vital capacity is still preserved. On the other hand, if the situation is reversed, the Tiffeneau index is above 70%, but the vital capacity is below 80, then we are dealing with restrictive ventilation disorders. And in the most unfavorable case, if both the Tiffeneau index and vital capacity are below normal, oh well, then this represents mixed ventilation disorders. Of course, this is the worst-case scenario. Now, I encourage everyone to try spirometry and aim to stay within the normal range, because naturally no one wants to fall into any of the other zones on this graph. And we'll continue with more ventilation disorders.