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The body changes the pressure in the alveoli by changing the volume of the lungs. to stay at the dimensions of the lungs because of the relationship of the lungs to . ATP, produced by cellular respiration, provides the energy for the body to. A discussion of the energy cost of breathing thus is, in es- sence, a bringing . against the volume change during a single breath, a loop is described, as in Figure 1. In this pressure-volume plot of elastic and resistive forcing pressure versus. The relationship between gas pressure and volume helps to explain the detailed mechanics of breathing, it is important to keep this inverse relationship in mind. . Flying consumes a large amount of energy; therefore, birds require a lot of.
So, in summary, if you are going into respiratory acidosis the above equation will move to the right. In contrast, if you are going into respiratory alkalosis the equation will move to the left. So the body will try to breathe less to release HCO3. You can think of it like a leak in a pipe: Problems Associated With the Respiratory Tract and Breathing[ edit ] The environment of the lung is very moist, which makes it a hospitable environment for bacteria.
Many respiratory illnesses are the result of bacterial or viral infection of the lungs. Because we are constantly being exposed to harmful bacteria and viruses in our environment, our respiratory health can be adversely affected. There are a number of illnesses and diseases that can cause problems with breathing. Some are simple infections, and others are disorders that can be quite serious.
Carbon monoxide binds much tighter, without releasing, causing the hemoglobin to become unavailable to oxygen. The result can be fatal in a very short amount of time. By far the most common form of pulmonary embolism is a thromboembolism, which occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.
Symptoms may include difficulty breathing, pain during breathing, and more rarely circulatory instability and death. Treatment, usually, is with anticoagulant medication. Upper Respiratory Tract Infections[ edit ] The upper respiratory tract consists of our nasal cavities, pharynx, and larynx. Upper respiratory infections URI can spread from our nasal cavities to our sinuses, ears, and larynx.
Sometimes a viral infection can lead to what is called a secondary bacterial infection. Antibiotics aren't used to treat viral infections, but are successful in treating most bacterial infections, including strep throat.
The symptoms of strep throat can be a high fever, severe sore throat, white patches on a dark red throat, and stomach ache. Sinusitis An infection of the cranial sinuses is called sinusitis.
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This "sinus infection" develops when nasal congestion blocks off the tiny openings that lead to the sinuses. Successful treatment depends on restoring the proper drainage of the sinuses. Taking a hot shower or sleeping upright can be very helpful.
Otherwise, using a spray decongestant or sometimes a prescribed antibiotic will be necessary. Otitis Media Otitis media in an infection of the middle ear. Even though the middle ear is not part of the respiratory tract, it is discussed here because it is often a complication seen in children who has a nasal infection.
The infection can be spread by way of the 'auditory Eustachian tube that leads form the nasopharynx to the middle ear. The main symptom is usually pain.
Sometimes though, vertigo, hearing loss, and dizziness may be present. Antibiotics can be prescribed and tubes are placed in the eardrum to prevent the buildup of pressure in the middle ear and the possibility of hearing loss. Tonsillitis Tonsillitis occurs when the tonsils become swollen and inflamed. The tonsils located in the posterior wall of the nasopharynx are often referred to as adenoids.
If you suffer from tonsillitis frequently and breathing becomes difficult, they can be removed surgically in a procedure called a tonsillectomy. Laryngitis An infection of the larynx is called laryngitis. It is accompanied by hoarseness and being unable to speak in an audible voice.
Usually, laryngitis disappears with treatment of the URI. Persistent hoarseness without a URI is a warning sign of cancer, and should be checked into by your physician. Lower Respiratory Tract Disorders[ edit ] Lower respiratory tract disorders include infections, restrictive pulmonary disorders, obstructive pulmonary disorders, and lung cancer.
Lower Respiratory Infections[ edit ] Acute bronchitis An infection that is located in the primary and secondary bronchi is called bronchitis. Most of the time, it is preceded by a viral URI that led to a secondary bacterial infection. Usually, a nonproductive cough turns into a deep cough that will expectorate mucus and sometimes pus.
Pneumonia A bacterial or viral infection in the lungs where the bronchi and the alveoli fill with a thick fluid. Usually it is preceded by influenza. Pneumonia can be located in several lobules of the lung and obviously, the more lobules involved, the more serious the infection. It can be caused by a bacteria that is usually held in check, but due to stress or reduced immunity has gained the upper hand.
Restrictive Pulmonary Disorders[ edit ] Pulmonary Fibrosis Vital capacity is reduced in these types of disorders because the lungs have lost their elasticity. Inhaling particles such as sand, asbestos, coal dust, or fiberglass can lead to pulmonary fibrosis, a condition where fibrous tissue builds up in the lungs. This makes it so our lungs cannot inflate properly and are always tending toward deflation. Diagram of the lungs during an asthma attack.
Asthma Asthma is a respiratory disease of the bronchi and bronchioles. The symptoms include wheezing, shortness of breath, and sometimes a cough that will expel mucus.
The airways are very sensitive to irritants which can include pollen, dust, animal dander, and tobacco. Even being out in cold air can be an irritant. When exposed to an irritant, the smooth muscle in the bronchioles undergoes spasms. Most asthma patients have at least some degree of bronchial inflammation that reduces the diameter of the airways and contributes to the seriousness of the attack.
Emphysema Emphysema is a type of chronic obstructive pulmonary disease. Typically characterized by a loss of elasticity and surfactant in the alveoli, a loss of surface area decreases the gas exchange in the lungs. These patients have difficulty with too little expiratory pressure, not retaining inspired air long enough for sufficient gas exchange to happen. Chronic Bronchitis Another type of chronic obstructive pulmonary disease, Chronic Bronchitis is caused by overproduction of mucus in the airways, causing an inadequate expiration of inspired air.
Retention of air in the lungs reduces gas exchange at the alveoli, and can lead to a hypoxic drive. These patients are known as "blue bloaters", vulnerable to cyanosis and often have increased thoracic diameters. Respiratory Distress Syndrome[ edit ] Pathophysiology At birth the pressure needed to expand the lungs requires high inspiratory pressure.
In the case of deficiency of surfactant the lungs will collapse between breaths, this makes the infant work hard and each breath is as hard as the first breath.
If this goes on further the pulmonary capillary membranes become more permeable, letting in fibrin rich fluids between the alveolar spaces and in turn forms a hyaline membrane.
The hyaline membrane is a barrier to gas exchange, this hyaline membrane then causes hypoxemia and carbon dioxide retention that in turn will further impair surfactant production. Etiology Type two alveolar cells produce surfactant and do not develop until the 25th to the 28th week of gestation, in this, respiratory distress syndrome is one of the most common respiratory disease in premature infants. Furthermore, surfactant deficiency and pulmonary immaturity together leads to alveolar collapse.
Ventilation and dynamics of breathing. Since, in mammals, pulmonary VE represents the only means for the gas exchange of the venous blood, it is not surprising to find a close relationship between VE and VO2 [ Fig. Oxygen consumption VO2 - ventilation VE relationships during resting conditions. In both adults continuous line and newborn mammals dashed linethe mass-related changes in VO2 are accompanied by proportional changes in VE. For example, a rat, relative to its weight, ventilates times more than an elephant.
Why differences in metabolic requirements, and in VE, are met entirely by differences in frequency rather than tidal volume is not immediately obvious, except for the consideration that lung mass is directly proportional to the animal's weight, and it is probably a good design to have the stroke of a pump proportional to its size. It is interesting that these dynamic requirements are accommodated by some structural and functional properties of the respiratory pump.
This is numerically the same exponent, opposite in sign, of that relating breathing rate to BW frequency a BW Second, although the mass of the respiratory muscles is directly proportional to the animal's mass, the diaphragm of smaller animals has a greater proportion of fast twitch fibers, higher activity of enzymes involved in muscle contraction, and faster rate of pressure development than in larger species. The distribution of tidal volume in the lung is not uniform, since it is subjected to the direction of the gravitational vector with respect to the thorax.
In a standing subject breathing quietly from functional residual capacity most of the inspired air, per unit of lung tissue, is directed into the middle-lower lobes, and relatively less air reaches the top portions of the lungs.
In supine position, the areas less ventilated would become those located more ventrally, while those relatively more ventilated are the gravity dependent regions of the back.
The factors responsible for these major differences in inspired air distribution are essentially two, the curvilinearity of the lung pressure-volume relationship, and the gravity-related variation in pleural pressure. In fact, in a standing subject, pleural pressure is more negative i. Because, due to the shape of the pressure-volume curve, lung compliance decreases with increased distention, the overdistended top lung regions are less ventilated than the less inflated regions of the lower lobes.
The magnitude of the unevenness in VE distribution depends therefore on the curvilinearity of the pressure-volume curve and on the pleural pressure inequalities along the pleural space.
The shape of the pressure-volume curve is relatively similar among mammals see Fig. On the other hand, thoracic dimensions clearly differ, and if the pleural pressure value at the lung surface was strictly determined by the gravitational field, one should expect the presence of huge top-to-bottom pleural pressure differences in the largest mammals and almost no inequalities among regional pleural pressure values in tiny animals of the size of the shrew or the mouse.
This is not the case; large mammals do not have a distribution of the inspired air much worse than small mammals do because the pleural pressure gradient which is the change in pleural pressure per unitary change in lung height is smaller the bigger the animal. The precise reasons for why this is so are not clear, since it is not clear how gravity determines the regional differences in pleural pressure, but the end result is interesting: In the elephant, and possibly in some other large mammals with very heavy lungs, some direct attachments between the two pleuras thoracic and visceral have been described.
This limits the lung configurational freedom within the chest, but represents an additional mechanism for adequate ventilation of all lung regions. Although gases dissolve in blood, neither O2 nor CO2 are primarily transported in the dissolved form.
O2 is almost entirely carried by the hemoglobin, and CO2 is carried predominantly in the form of bicarbonate ions HCO Since the solubility of CO2 in the blood by far exceeds that of O2, the transport of O2 from the lungs to the peripheral tissues is more critical than the elimination of CO2 from the tissues. Because red blood cells are very similar among mammals with respect to size and hemoglobin content, the amount of O2 which can be loaded in the blood essentially depends upon two parameters, a the total mass of circulating blood, and b the blood concentration of hemoglobin.
In addition, because the amount of O2 that binds to, and is released from, hemoglobin depends on the affinity of this molecule for the gas, it is important to consider also c the O2-hemoglobin affinity curve. The total mass of circulating blood per unit of animal's weight and the hemoglobin concentration are almost constant in all mammals. The approximately constant values in hemoglobin concentration and hematocrit probably reflect the optimal compromise between the advantages of an high O2 concentration in the blood and the energetic disadvantages of an increased work load on the heart.
In fact, a higher hematocrit would raise blood viscosity, thus the increase in O2 delivery would be accompanied by an increase in cardiac work.
Human Physiology/The respiratory system
Only in circumstances of long-lasting low O2 availability e. Differences in metabolic rates appear to be matched mostly by the way O2 is unloaded at the tissue level.
It is important for small species, because of their high metabolic requirements, to have an hemoglobin with low O2 affinity i. If one wants to avoid this latter factor, it is possible to construct the iso-volume pressure-flow relationships. To this end, P- V data points are patiently collected during a number of inspiratory and expiratory forced manoeuvres, and the values measured at the same lung volume are joined together in a plot [ Fig.
Numbers refer to lung volume liters. As lung volume increases, the curves become steeper, indicating a decrease in both inspiratory and expiratory resistance. Note that the plateau during the forced expiratory manoeuvres airflow limitation is reached at lower pressures when lung volume is low. At low lung volumes the support applied to the airways by the attached alveolar walls approaches zero and the airways close trapping gas behind them.
If this did not occur the alveoli would collapse and large pressures would be required to reinflate them. Thus airway closure at low lung volumes can be regarded as a protective mechanism. However, as a result of disease processes airway closure can occur at lung volumes higher than normal. This is frequently an early manifestation of disease and the measurement of lung volume at which airways close closing volume is often used to detect pulmonary abnormalities.
Appendix 2 describes it only in first approximation. Rather, the value of resistance depends on the flow rate, and the flow rate at which R is measured needs to be specified. In turbulent flow regime normally, in the larger airways gas density affects the value of R. Gas density is increased in hyperbaria, and divers breathing from pressurised tanks have higher airways resistance.
The opposite can occur at high altitude, because the hypobaria decreases gas density. During forced expiration pleural pressure becomes considerably greater than atmospheric, depending upon the intensity of the expiratory effort.
Because the lungs have elastic recoil throughout the whole vital capacity range, alveolar pressure is always greater than pleural pressure. Hence, the alveoli have a positive transmural pressure.
However, this positive pressure within the airways decreases from the alveoli toward the mouth where it is atmospheric ; in the trachea the inside pressure is close to atmospheric pressure. Thus at the alveolar end the pressure inside the airways is greater than pleural pressure by a magnitude equal to the lung recoil pressure, whereas at the tracheal end the pressure inside the airway is less than pleural pressure.
It follows that at some point along the airways the pressure inside must be exactly equal to pleural pressure equal pressure point, EPP [ Fig. The equal-pressure-point EPP model. At top, pleural Pplalveolar Palv and intra-airways pressures at end-inspiration.
At bottom, corresponding values during a forced expiration, in which the expiratory muscles generated an expiratory pressure of 20 cm H2O. Numerical examples of an active, yet not maximal, expiration from the same lung volume, in a subject with normal lung recoil of 3 cm H2O topand in a patient with emphysema, with lung recoil of only 1 cm H2O bottom. In this latter case, EPP is very close to the most peripheral airways.
From the EPP downstream i. Of course, this increases the resistance during the forced expiration. Furthermore, the greater the degree of expiratory effort i. Thus, with the increase in effort, the driving pressure i. The result is that eventually the expiratory flow cannot increase any further, and becomes independent of the effort. This is shown by the plateau in the P- V relationship [ Fig. Hence, expiratory flow limitation is more easily present during forced expiration at low than at large lung volumes cf.
In patients with decreased lung recoil e. In fact, in some cases, even during resting breathing the expiratory airflow can be dynamically limited. In these severe cases, the only way to improve the expiratory flow is by breathing at high lung volume hyperinflationwhich increases lung recoil.
Approximately half of the resistance to flow in the airways is contributed by the upper airways larynx to mouthand most of the rest is in large central airways. Switching from nose to mouth breathing reduces upper airways resistance, and is therefore adopted when high flows are needed, as during exercise-hyperpnea. This nose-to-mouth breathing switch, albeit triggered by pressure receptors in the upper passages, seems to be a behavioural response which needs to be learned; infants are thought to be less capable of mouth-breathing than adults, and many mammalian species do not seem able or perhaps never learn?
This has profound implications with regard to disease, since even large changes in the resistance of the peripheral airways may have minimal impact on R. If one half of all the peripheral airways became occluded, peripheral resistance would double to 2.
Total resistance would only increase to 1. Thus, in the particular circumstances of obstruction in small airways, measurements of RL are an insensitive means of detection, and other methods must be devised. Tests which detect the lung volume at which airways close closing volume is one such method.
The influence on RL during breathing helium, instead of air, is another test. Helium has a density lower than air but its viscosity is almost the same. Thus, if breathing helium causes a reduction in RL, most of the resistance during air-breathing must be in larger airways where the pressure-flow regime is density dependent cf.
If breathing helium causes little reduction in the high value of RLmost of the high resistance must originate in smaller airways where the flow is laminar. When these variables are X-Y plotted, a loop is obtained [ Fig.
The mechanical work necessary to inflate the lungs from functional residual capacity FRC to VT is the whole are at the left of the inflation P-V curve. Part represents the extra work required to overcome the frictional resistance white area. Of course, for the same VT, this latter work depends not only on resistance but also on the inspiratory time, i. Changes in pleural pressure during inspiration from functional residual capacity FRC to VT, and the following expiration continuous line, 'inspiration' and 'expiration'.
The dashed lines indicate the static P-V curves of lungs and chest wall. The total inspiratory work is represented by the whole area at the left of the inspiration P-V curve. A portion of it grey-dotted area with hatching is contributed by the expanding action of the chest wall. During expiration, the work to overcome expiratory resistance is the represented by the area between the expiration P-V curve and the elastic static P-V curve of the lung.
When this area is less than the elastic energy stored at end inspiration, expiration can be an entirely passive process, not requiring expiratory muscle work.
In this case, any remaining energy stored in inspiration and not needed to generate expiratory flow would be dissipated as heat. For the same ventilation, a rapid and shallow breathing pattern reduces the elastic work of breathing, but disproportionately increases the non-elastic component. Conversely, a deep and slow pattern reduces the frictional work, but increases disproportionately the elastic work.
In order to perform the mechanical work necessary for breathing, the respiratory muscles require oxygen. During voluntary hyperventilation, the difference between total VO2 and resting VO2 should represent the oxygen consumption of breathing. This seemingly straight-forward approach to compute the cost of breathing is, in reality, complicated by a number of assumptions.
At any rate, the oxygen cost of breathing has been calculated to range between 0. The answer is that neither during inspiration nor during expiration does the system behave exactly as expected on the basis of passive measurements. During inspiration, the main reason for the difference has to do with the uneven distribution of pressure on the chest wall during muscle contraction, leading to distortion. This has several functional implications, including its effect on the energetics of breathing see next section.
The frequency dependence of Cdyn, mentioned earlier, and the decrease in lung Cdyn as the result of chest wall distortion are additional factors contributing to the difference between active and passive mechanics. During expiration, neural mechanisms aimed to control the expiratory flow and mean lung volume, including post-inspiratory muscle activity and laryngeal braking, effectively increase the expiratory resistance prolonging the expiratory time constant above its passive value.
During passive inflation of the respiratory system e. In fact, if we assume no passive tension of the diaphragm i. Schema of the pressures applied to the chest wall and its components rib cage rc and abdomen ab during passive inflation left and spontaneous breathing right.
Arrows from the chest indicate the expected direction of motion in absence of extra-diaphragmatic muscle activity. At extreme right, summary of pressures and forces determining motion of the upper portion of the rc, lower rc, and ab during spontaneous inspiration. The motion of rc is more complex than in passive conditions, because it depends on the interplay of several factors [ Fig.
First, Ppl during spontaneous inspiration becomes progressively more subatmospheric, which tends to collapse the rib cage, both in its upper and lower regions. Pab acts on the lowermost part of the rib cage the apposition area, which faces the cranial part of the abdomen with an inflatory action. In addition, the lower rib cage can be expanded by the direct outward-pulling action of the diaphragmatic fibers.
Hence, differently from the inflation of the respiratory system in passive mode, the magnitude of rib cage expansion during diaphragmatic contraction can be quite variable. For the lower portions of the rib cage, the degree of its expansion will depend on the net effect of multiple forces.
As far as the upper rib cage, the expected tendency to collapse during diaphragmatic contractions because of the negative Ppl can be partly diminished by the mechanical interdependence with the lower rib cage, and even offset or reversed into outward motion by the compensatory contraction of the intercostal muscles. It is important to realize that the mechanical arrangement of the mammalian respiratory system is such that diaphragmatic contraction alone results in a tendency for the upper rib cage to collapse inward.
This is particularly the case in infancy, when the mechanical coupling between upper and lower rib cage is not very effective because of high chest wall compliance, and the neural proprioceptive control of the intercostal muscles does not operate as in adults. A clear example of the action of the diaphragm on the chest wall is provided by adult humans with no intercostal muscle activity tetraplegic patientsin whom the upper rib cage paradoxically moves inward during inspiration [see chapter 1, Fig.
In normal subjects, therefore, absence of inward motion of the rib cage during inspiration implies that the compensatory action of the extra-diaphragmatic muscles namely, intercostal muscles is taking place. In other words, motion of the whole chest wall during active breathing as in passive conditions should not be interpreted as absence of distortion, but, rather, as full compensation of distortion.
The two concepts are quite different when examined in light of the energetics of breathing. To the extent that chest wall distortion is defined as the difference in configuration between the active and passive modes, it could be quantitatively evaluated as the difference in linear dimensions of any chest wall region between its active and passive conditions.
Of course, the functional interpretation of these differences depends on which region of the chest wall has been sampled; for example, the factors contributing to the rib cage motion at the level of the apposition area may be very difficult to sort out.