Mammalian lungs have developed to allow efficient gas exchange in air. In this article, I’m going to look in detail at the human respiratory system. The figure below shows its overall structure. The complex anatomy of the lungs very much lengthens the surface area obtainable for gas exchange.
THE MECHANISM OF BREATHING
Lungs have no muscle, so how do we breathe in and out? Lungs simply expand and contract because they are lengthened and contracted by the actions of rib cage and diaphragm in motion. This is easily made achievable because two pleural membranes connect the lungs to the rib cage and diaphragm. The outer membrane lines the thoracic cavity; the inner membrane encloses the lungs. In between the two is a narrow space, the pleural cavity, occupied by pleural fluid. What this does is to allow the pleural membranes to glide unhindered over one another during breathing and at the same time prevents them from separating.
The figure below shows how we breathe in and out.
The mechanism of breathing:
(a) Inspiration (breathing in) takes place when the outer intercostal muscles shrink and draw the rib cage up towards the outside, far from the spinal column. Concurrently, the diaphragm constricts and compresses, pressing down on the abdominal organs. These movements increase the volume and therefore lower the pressure in the thorax. As the pressure in the thorax falls below that of the atmosphere, air is forced into the lungs to equalize the pressure.
(b) Expiration (breathing out) is normally a passive process: it uses no energy. When inspiration is over, the muscles inside the thorax becomes less tense and breathing out comes next and with the help of gravity, the stretchy tissues of the lung and the pressure applied by some of the organs in the stomach. An example of such organ is the liver. Of course, we can consciously speed up expiration by forcing air out of our lungs using our internal intercostal muscles. This happens, for instance, when we blow up a balloon or play a wind instrument.
Cruithne9 - Own work, CC BY-SA 4.0
To understand why two pleural membranes continue to stick together during breathing, imagine two wet pieces of glass pressed together. They can easily slide over each other, but it is virtually impossible to pull them apart without introducing air into the middle. If air is introduced into the pleural cavity, after a stab wound for example, the lung collapses. The lung itself, being elastic, shrinks to its smallest size while air fills the space between the lung and ribcage; a situation known as a pneumothorax. In this situation, the ribs and diaphragm can still move (though it’s painful) but they don’t inflate the lungs.
USING A SPIROMETER TO DETERMINE LUNG VOLUME
The figure below shows a spirometer. The trace that this apparatus produces tells us a lot about the lungs. First of all, it shows that the lungs have a total lung capacity i.e the greatest amount of air that the lungs can support during the deepest possible breath. We can never totally empty the lungs, however, because even when you have exhaled as much as possible, there is still some air in the alveoli and in the bronchi and tracheae (these are held open permanently by rings of cartilage). The volume of air that remains in the lungs after breathing out is called the residual volume. The maximum usable volume (the total lung capacity minus the residual volume) is called the vital capacity. The average vital capacity for men is 4.5 to 5 litres, for women, 3.5 to 4 litres.
Secondly, during normal breathing, the volume of air that moves in and out of the lungs in each breath is called the tidal volume. In a normal adult at rest, this is about 0.5 litres.
Thirdly, the trace shows that, after breathing in at rest, the subiect could inhale an extra 1.5 litres, the inspiratory reserve volume (IRV). He or she could also breathe out another litre: the expiratory reserve volume (ERV). These values represent the extra volumes of air that we can breathe in and out during excrcise.
Device for spirometry. The patient places his or her lips around the blue mouthpiece.
Finally, we can work out the ventilation rate: the volume of air taken into the lungs in one minute. We can do this by multiplying the number of breaths taken in a minute by the tidal volume.
Using a spirometer to determine oxygen consumption
We can use a spirometer to estimate a person’s rate of oxygen consumption. If the person rebreathes the air in the closed system of the spirometer, the composition of that air will change: oxygen levels decrease and carbon dioxide levels increase. If we include a cylinder of soda lime in the apparatus, this absorbs the carbon dioxide and so the volume of air in the spirometer decreases in volume as the oxygen is used up.
To calculate the amount of Oxygen used, we simply measure the volume decrease in a given time. If, for instance, the trace shows that in 1 minute the air volumne fell from the 1 500 cm3 mark to the 1 200 cm3 mark. So, this person used up 300 cm3 of oxygen in 1 minute,
WARNING! Re-breathing your own air can be dangerous. You should never do investigations like this without close supervision.
GAS EXCHANGE AT THE ALVEOLI
Gas exchange between air and blood occurs at the alveoli. These tiny air-sacs create a huge surface area: 1 cm3 of frog lung tissue has a surface area of about 20 cm2, but the corresponding figure for a mouse lung is over 80 cm2. Other mammals have a similar value. The total surface area of one human lung is about 100 m2.
As we breathe in, fresh air enters the lungs and passes into individual alveoli. Oxygen diffuses rapidly from the inhaled air through the walls of the alveoli and into the blood. Here, most of it combines with haemoglobin in the red blood cells. At the same time, carbon dioxide diffuses out of the blood and into the alveoli. It is breathed out during the next few expirations.
In the composition of atmospheric, alveolar and exhaled air, each of the values for exhaled air is an average of the values for inhaled and alveolar air. This is because exhaled air is a mixture of the two.
Alveoli don’t collapse when we breathe out because their surface is covered by an anti-sticking chemical called surfactant.
The composition of exhaled air varies during the course of a single expiration. The first air to emerge has a very similar composition to atmospheric air because it has been nowhere near the alveoli – it has simply filled the dead space in the trachea and bronchi. As the exhalation continues, air that has been deep inside the alveoli is breathed out. The composition of this air has been altered by gas exchange and it contains more carbon dioxide and less oxygen than atmospheric air.
THE LUNGS OF PREMATURE BABIES
Alveoli are minute bubble-like air-sacs lined with moisture, and are liable to collapse because of surface tension: if their sldes touch, they could stick together. To prevent this, the alveolar epithelium secretes a surfactant, a mixture of phospholipids, which greatly reduces the surface tension and keeps the alveoli open.
Without surfactant, the lungs cannot function effectively and severe breathing problems can develop. An unborn baby does not start to secrete surfactant until about the 22nd week of pregnancy and the lungs have not accumulated enough surfactant to cope with breathing until about the 34th week.
Any babies born before this have immature lungs and suffer from a condition called respiratory distress syndrome. The effort needed to inhale and inflate the collapsed alveoli becomes too great and, without medical help, the baby can die from exhaustion and suffocation. Surfactant can now be made artificially. It is introduced into the lungs of premature babies to help them to continue breathing. This is a major breakthrough which means that babies as young as 23 weeks (17 weeks premature) now have more of a chance of survival.
CLIMBING MOUNT EVEREST – AN EXPLANATION OF PARTIAL PRESSURES
As you study the workings of the lungs and blood in more detail, you will come across the term partial pressure. To explain this, it helps to think about someone climbing Mount Everest (height 8,848 metres).
At sea level, there is a lot of air pushing down on us, and this atmospheric pressure has a value of about 100,000 pascals (Pa) or 100 kPa. We can therefore say that the barometric pressure is 100 kPa. Dry air is 20.9 per cent oxygen at sea level, so the partial pressure of oxygen (Po2) is 20.9 per cent of 100, which is about 20.9 kPa.
As the mountaineer progresses up the mountain, the atmospheric pressure becomes less because there is less air pushing down on him. The partial pressure of oxygen decreases accordingly.
Oxygen passes into the lung tissues because of the different concentration in the alveolar air and the blood, and at higher altitudes the difference is smaller, making it difficult to take in enough oxygen to meet demands. At 5,300 metres, the Po2 is only half of that at sea level. And by the time the summit is reached it is only about 8 kPa – just over one-third that at sea level. This is why most mountaineers who attempt Everest do so with pressurised oxygen containers, and to conquer the mountain without the help of additional oxygen – as has been done – is a remarkable feat.
THE CONTROL OF BREATHING
Control of breathing is involuntary: We don’t have to think continually about breathing in and out, and our breathing rate is automatically matched to our needs. The rate changes as the brain detects the physical and chemical variations that occur in the body as we carry out different activities.
Setting a regular pattern
Breathing is controlled by a bundle of nerves called the respiratory centre. This is located in the brain in an area called the medulla oblongata. Regular nerve impulses travel down efferent nerves that pass from the respiratory centre out to both the external intercostal muscles and the diaphragm. These muscles then contract, starting off inhalation. As air enters the lungs, stretch receptors in the airways start firing and feed information to the brain about how the inflation of the lungs is progressing. The more the lungs inflate, the faster the stretch receptors feed back impulses. When the lungs are inflated sufficiently, signals from the respiratory centre stop for a short time and exhalation follows automatically.
Changing the breathing rate to meet demand
Ensuring the body has a constant supply of oxygen is obviously an important aspect of homeostasis, but, surprisingly, the body is relatively insensitive to falling oxygen levels. It is much more sensitive to an increase in carbon dioxide and so this is the indicator of the need for oxygen. The levels of oxygen in the arterial blood vary very little, even during exercise, but the carbon dioxide levels vary in direct proportion to the level of exertion. The heavier the exercise, the greater the carbon dioxide concentration. Lactic acid levels also increase during exercise. Any increase in carbon dioxide or lactic acid concentration in the blood lowers its pH. Chemoreceptors, which are extremely sensitive to the composition of the blood that flows past them, can detect very small changes in pH.
There are three types of chemoreceptor:
- Central receptors in the medulla oblongata. These are sensitive to the carbon dioxide concentration in the blood that flows through this region of the brain.
- The carotid bodies in the wall of the carotid arteries.
- The aortic bodies on the aortic arch, just above the heart.
Together, the carotid and aortic bodies are described as the peripheral chemoreceptors. These cells sense changes in carbon dioxide and pH levels and, to a lesser extent, they are also sensitive to changes in oxygen levels.
When chemoreceptors register a change in carbon dioxide levels or pH, they send nerve impulses to the respiratory centre in the brain. This responds by sending more frequent impulses to the external intercostal muscles and diaphragm. When this happens, our ventilation rate increases: we breathe harder and faster. Heart rate also increases and so the body automatically increases oxygen delivery at the same time as removing the extra carbon dioxide.
The control of breathing rate is very similar to the control of heart rate, with one important difference: we can control our breathing rate by thinking about it. This suggests that the higher, ‘conscious’ centres of the brain are more closely linked to the respiratory centre than they are to the cardiovascular centre. Also, research shows that pulse and ventilation rates change dramatically during exercise, even before the concentration of blood gases has a chance to change. It is as if the body predicts what is about to happen. How this works is not understood and is an active area of research.
The effects of oxygen deprivation
In some situations, at high altitudes for example, oxygen levels can fall without carbon dioxide levels increasing. In a rarefied or artificial atmosphere, normal breathing flushes carbon dioxide out of the blood via the lungs but there may not be enough oxygen to replace it. When this happens, the chemoreceptors often fail to register that anything is wrong, and the brain can become starved of oxygen.
The first symptoms of oxygen starvation are feeling ridiculously happy, having impaired senses and lacking judgement. When mountaineers, fighter pilots or deep-sea divers start giggling and making stupid mistakes, it is a sure sign that they are not getting enough oxygen. It is also a signal for their colleagues to act fast, if possible, and provide emergency oxygen. If they don’t get help quickly, they soon lapse into unconsciousness, and brain damage and death follow.
Athletes and Vo2(max)
Many physical activities – such as jogging, swimming, team sports – rely on energy released by the aerobic pathway of cell respiration. The level of performance an athlete can achieve is largely governed by how fast oxygen gets to the muscles.
The rate at which a person uses oxygen is called the Vo2 and is measured in terms of the volume of oxygen consumed (cm3), per kg of body mass, per minute. Vo2(max) is the maximum rate at which oxygen is consumed and is the amount of oxygen that can be delivered to the tissues when the lungs and heart are working as hard as possible. Athletes use a knowledge of Vo2(max) in their training, as a measure of how hard they are working. A training schedule, for example, may require the athlete to work at 55 per cent of their Vo2(max) for a set length of time.
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REFERENCES
https://study.com/academy/lesson/gas-exchange-in-the-human-respiratory-system.html
https://en.wikibooks.org/wiki/Human_Physiology/The_respiratory_system
https://opentextbc.ca/biology/chapter/11-3-circulatory-and-respiratory-systems/
https://www.webmd.com/lung/how-we-breathe
https://www.livescience.com/26825-human-body-system-respiration-infographic.html
https://www.healthline.com/human-body-maps/lung
https://en.wikipedia.org/wiki/Lung
https://www.visiblebody.com/learn/respiratory/5-functions-of-respiratory-system