Transcription
Today we will begin to systemically discuss the pathology of the respiratory system and its effects on the body. Breathing is often taken for granted, but damage to the respiratory system can very quickly lead to severe life-threatening conditions. We should remember that the respiratory system is not only the lungs and the respiratory system plays a key role in gas exchange, regulation of pH, and is closely connected to hemodynamics.
Before we start discussing specific diseases such as bronchitis, asthma, or pneumonia, we first need to understand the general mechanisms by which respiratory disorders develop. And the main mechanisms that cause functional disorders of respiratory system are, first of all, ventilation disturbances. I'll remind you that ventilation is the movement of air from external environment to the alveoli and back. So, what we usually refer to as breathing is essentially ventilation. Ventilation depends on several factors: the patency of the airways, whether they are narrowed or obstructed, the movement of chest, and the function of respiratory muscles. In pathological conditions, air either does not reach the alveoli sufficiently or it is not effectively removed.
Without going to specific diseases yet, some general examples. If the airways are narrowed, it becomes more difficult to exhale. If there's mucus, edema, or spasm in the airways, airway resistance increases, making breathing more difficult. In most cases, ventilation disturbances are particularly associated with problems in the elimination of carbon dioxide.
Another mechanism is diffusion impairment. In the context of this lecture, diffusion refers to the exchange of oxygen and carbon dioxide between the alveoli and the capillaries occurring by diffusion. Of course, diffusion processes also occur elsewhere in the body, but here we are focusing specifically on this one. Such problems can arise if the alveolar wall becomes thicker, meaning it is no longer a thin single-layered epithelium. Hyperplasia in the lungs, of course, is not something desirable. Another example is when the alveoli become filled with fluid or cellular material. In patients with diffusion impairment, oxygen support during cardiopulmonary bypass helps only partially because although the patient can be ventilated, the problem is that gas exchange between the alveoli and the blood cannot occur effectively. And that is why a precise ventilation strategy is required here.
Next, we have perfusion disorders. In this context, perfusion refers specifically to the blood flow through the pulmonary capillaries, and not general circulation. It is important to understand that if an alveolus is ventilated but not perfused, gas exchange will still not occur. On the other hand, if alveoli are perfused but not ventilated, then again, no effective gas exchange will take place in the blood. Perfusion problems can arise, for example, when blood flow is diverted away from the well-ventilated areas, such as in case of an embolus. So, it is important to remember that breathing is not just about air. It is always the result of the combined work of ventilation and circulation.
And the final mechanism of functional disorder is ventilation-perfusion mismatch. I will explain this a bit more in detail. We have alveolar ventilation, which is denoted by the large V. This represents the amount of air reaching the alveoli, and it is measured in liters per minute. On the other hand, we have perfusion denoted by Q, referring to the pulmonary blood flow, more specifically the volume of blood reaching the pulmonary capillaries surrounding the alveoli. This is also measured in liters per minute. When the lungs are in an upright position and at rest, ventilation is approximately 4 liters per minute, while perfusion is about 5 liters per minute. And this gives us a VQ ratio of approximately 0.8, which represents the average balance between ventilation and perfusion in a healthy individual.
But if we take this a bit further, we can divide the lungs into three different zones. The first zone corresponds to the upper part of the lungs, also called the apex. The second zone is the middle part of the lungs, and third zone is the lower part or the base of the lungs. When the body is in an upright position, just like with blood circulation, gravity plays an important role. It significantly affects both ventilation and perfusion in all three zones. Overall, the VQ ratio gradually decreases from the first zone, so from the apex to the third zone, so the base of the lungs.
Now, let's also look at how this appears in numbers. So, in the first zone, both air flow and blood flow are the lowest. Ventilation is only about 0.25 liters per minute, while perfusion is even lower, approximately 0.07 L/min. And this results in a VQ ratio of about 3.6, which is significantly higher than the average value of 0.8. In the second zone, ventilation is approximately equal to perfusion, resulting in a VQ ratio of about 1. And in the third zone, both airflow and blood flow are the highest. So, because of gravity, of course. Ventilation is around 0.8 L/min while perfusion is approximately 1.3 L/min. This gives a VQ ratio of about 0.6. So, the VQH ratio varies depending on which part of the lung we are looking at. However, if we take the overall average across all three zones, it comes to approximately 0.8, as mentioned earlier.
So, in healthy lungs with a VQ ratio of about 0.8, the alveolar partial pressure of oxygen is approximately 100 mmHg. The alveolar partial pressure of carbon dioxide is about 40 mmHg. If we look at arterial blood, the partial pressure of oxygen is around 95 mmHg. Sometimes you may also see 100 mmHg mentioned somewhere else in other sources, but 95 is more accurate. So, it is slightly lower than in the alveoli. The arterial partial pressure of carbon dioxide is about 40 mmHg, which is essentially the same as in alveoli. Remember, these are arterial values, meaning that gas exchange has already taken place. Before gas exchange, these values are different. Carbon dioxide pressure is higher and oxygen pressure is of course lower. But here we are specifically looking at arterial blood after exchange.
So any change in alveolar ventilation or perfusion in any of these zones will alter the VQ ratio. And this is called then VQ mismatch. When this happens, either ventilation or perfusion becomes the limiting factor for oxygen and carbon dioxide to exchange. This affects the availability of these gases for diffusion, leading to changes in their general partial pressures and making gas exchange less efficient.
Now, let's look at two examples. Let's take the first example, pulmonary embolism. We have here a detached thrombus, now an embolus, and this blood clot becomes lodged and blocks blood flow to a certain area of the lungs. to a specific alveolus. In this situation, blood flow to the alveoli is reduced, but the alveolus can still receive normal ventilation because there is no obstruction to air flow. So ventilation V is normal, but perfusion Q is low. This means that the VQ ratio is high, and in extreme cases, if there's no blood flow at all through the artery, the VQ ratio can even approach infinity. In such a situation, as you already know, the non-perfused tissues can become ischemic. Alveoli that are ventilated but not perfused are referred to as dead space. I will explain dead space in more detail in another part of the lecture, but for now it is important to understand that this is where no gas exchange occurs, thus dead space. In this situation, we do not get meaningful partial pressure values for oxygen or carbon dioxide. So, nothing here because in tissues without blood flow, there is no blood present, of course. Without blood, gas exchange cannot occur. The partial pressure of carbon dioxide in the alveolus becomes close to zero because no new carbon dioxide is delivered from the blood due to the blockage. Meanwhile, the partial pressure of oxygen rises to about 150 mm mercury, which is approximately the same as in inhaled air. This happens because ventilation is still present. Air enters the alveoli, but the oxygen does not diffuse into the blood. So, it essentially remains trapped in the alveolus.
Now, the opposite case. If there's an airway obstruction, as shown in the secondary picture here, which can occur in an obstructive lung disease. What happens here? Ventilation to the alveoli is reduced, while the alveolus still receives normal blood flow. So, perfusion Q is normal, but ventilation V is low. And this means that the VQ ratio is low. This, in turn, means that less carbon dioxide is transferred from the blood into the alveoli. So, less carbon dioxide is removed, and its partial pressure in the blood increases. At the same time, if ventilation is impaired or blocked, less oxygen can enter the alveoli, or maybe none at all, and therefore it cannot diffuse into the blood. As a result, its level decreases. In extreme cases, if the alveoli are not ventilated at all, and are completely closed, VQ ratio can approach zero. In such a situation, blood may be redirected away from non-ventilated alveoli toward better ventilated areas where gas exchange can still occur. In these non-ventilated alveoli, there are essentially no meaningful partial pressures of oxygen or carbon dioxide because no air is entering them. Clearly, without ventilation, gas exchange is not possible. As a consequence, the partial pressures in arterial blood begin to resemble venous values. For example, the partial pressure of oxygen may decrease around 40 mm mercury. Probably write it down. While the partial pressure of carbon dioxide increases about 46 mm mercury.
And now, once we understand this mechanism, we can move on to discuss a few more technical aspects and then begin looking at specific pathologies. >> [groaning]