Basic lung volume, tidal volume (VT). The amount of air inhaled or exhaled each time when breathing calmly. Supplementary inspiratory volume (IRV). The maximum amount of air that can be inhaled after calm inhalation. Expiratory volume (ERV). The maximum amount of air that can continue to exhale after a calm exhalation. Residual volume (RV) supplements the residual volume that the lungs cannot exhale after exhalation.
Four lung volumes: deep inspiratory capacity (IC). The maximum amount of air that can be inhaled after a calm exhalation. It consists of tidal volume and supplementary inspiratory volume. Vital capacity The maximum amount of air that can be exhaled after inhalation. It consists of deep inhalation volume and exhalation volume. Functional remaining capacity. The amount of air contained in the lungs after a calm exhalation. It consists of expiratory volume and residual volume. Total lung capacity (TLC). The total amount of air contained in the lungs after deep breathing. It consists of vital capacity and residual capacity. Tidal volume, deep inspiratory volume, expiratory volume and vital capacity can be measured directly by spirometer, while functional residual volume and residual volume can not be measured directly by spirometer, but only indirectly. The determination of total vital capacity can be obtained by adding vital capacity and residual capacity.
Decreased vital capacity, limited lung expansion, lung tissue damage and airway obstruction can be seen in the chest cavity. The change of functional residual volume often exists at the same time as the change of residual volume, and obstructive pulmonary diseases such as bronchial asthma and emphysema have increased residual volume. Restrictive lung diseases such as diffuse pulmonary interstitial fibrosis, lung space-occupying diseases, lung tissue compression after pneumonectomy and other residual air volume decreased. Clinically, residual gas/%of total lung volume is used as the evaluation index. The measurement of pulmonary ventilation function is the amount of air inhaled or exhaled by the lungs per unit time.
Resting ventilation per minute is the product of tidal volume and respiratory rate. Normal adults breathe about 15 times per minute, the tidal volume is 500ml, and the ventilation volume is 7.5L/min. There is 140ml gas in the airway without gas exchange, which is called anatomical dead space, so the alveolar ventilation is only 5.5L/min.
If breathing is shallow and fast, the ventilation of anatomical dead space will increase relatively, which will affect alveolar ventilation. Due to insufficient local blood flow, the amount of gas entering alveoli cannot be exchanged with blood. This part of gas is called alveolar dead space. The amount of alveolar dead space plus anatomical dead space is called physiological dead space.
Alveolar ventilation = (tidal volume-physiological dead space volume) × respiratory frequency
Alveolar hypoventilation is common in emphysema; Increased alveolar ventilation is common in hyperventilation syndrome.
Maximum ventilation volume (MVV) The ventilation volume obtained by breathing as fast and as deep as possible per unit time. Patients are generally instructed to take a deep breath quickly 12 seconds, and the maximum ventilation per minute is multiplied by 5. This is a simple load test to measure airway patency, lung and chest elasticity and respiratory muscle strength. It is usually used as an indicator of whether thoracic surgery can be performed.
Forced vital capacity (FVC) expiratory vital capacity at the fastest speed. The expiratory volume of 1 s and the ratio of expiratory volume of 1 s to forced vital capacity can be calculated. Forced vital capacity is the best measurement item at present, which can reflect the expiratory resistance of the larger airway. It can be used as an auxiliary diagnosis method for chronic bronchitis, bronchial asthma and emphysema, and can also be used to evaluate the curative effect of bronchodilators.
When the maximum expiratory flow (PEFR) reaches the level of total lung capacity, blow air into the maximum expiratory flow meter and observe the maximum expiratory flow. The determination method is simple and feasible. It is widely used in epidemiological investigation of respiratory diseases, especially in judging the condition and curative effect of bronchial asthma. In the 24-hour dynamic observation of asthma patients, it is found that the lowest peak expiratory flow often appears at 0 ~ 5 am.
After reaching the alveoli, the inhaled air at the ratio of pulmonary ventilation blood flow exchanges oxygen and carbon dioxide with the blood in alveolar capillaries. The lung tissue and blood flow are affected by gravity, which makes the ventilation and blood flow of the upper and lower parts of the lung not completely consistent. If the average pulmonary ventilation and blood flow per minute can maintain a certain ratio (4 ∶ 5), gas exchange can be carried out normally.
The lung function measurements reflecting the uneven gas distribution are nitrogen clearance rate and phase ⅲ slope. The alveolar nitrogen concentration of normal people was lower than 2.5% after 7 minutes of pure oxygen washing. The slope of the third stage means that the average nitrogen concentration increased by the gas is less than 1.5% when the residual gas inhales pure oxygen and exhales 750ml and 1.250ml. Small airway dysfunction, long-term smokers or emphysema patients can cause uneven gas distribution.
If the lung ventilation is normal, the blood flow of pulmonary capillaries decreases or is blocked, the alveolar dead space increases and the ventilation/blood flow ratio increases; If the pulmonary bronchioles are blocked, the local blood flow is not fully oxygenated, forming physiological shunt, and the ventilation/blood flow ratio is reduced. Pulmonary function tests reflecting ventilation/blood flow ratio include physiological dead space measurement, alveolar arterial oxygen partial pressure difference measurement and physiological shunt measurement. The increase of physiological dead space can be seen in diseases such as red asthmatic emphysema or pulmonary embolism. The increase of physiological shunt is seen in cyanotic edema emphysema or adult respiratory distress syndrome.
Small airway ventilation function The bronchioles with an inner diameter of ≥ 2 mm in inspiratory state are called small airways, and the resistance of small airways only accounts for 20% of the total resistance of airways. It is difficult to detect by routine pulmonary function measurement reflecting airway resistance. Small airway resistance can be measured at low lung capacity; Small airway lesions are reversible in the early stage. There are two common methods to check the function of small airways:
The maximum expiratory flow-volume curve (MEFR) is to observe the expiratory flow at every moment from the total expiratory volume to the residual gas volume. When the small airway function is impaired, the flow rate of expiratory vital capacity is affected by more than 50%, especially when the expiratory vital capacity is 75%.
Closed volume (CV) is used to measure the volume that can continue to exhale when the total lung volume reaches the residual gas level and the small airway at the bottom of the lung begins to close. The increase of closed volume/vital capacity% indicates that the small airway at the bottom of the lung closes early. It can be caused by small airway disease or decreased lung elastic retraction force.
Small airway dysfunction is common in patients with air pollution, long-term heavy smoking, long-term exposure to volatile chemicals, early pneumoconiosis, bronchiolitis virus infection, asthma remission, early emphysema, pulmonary interstitial fibrosis and so on. Analysis of respiratory movement from mechanical point of view.
The change of unit capacity caused by the change of unit pressure of flexibility is the same property of all elastic objects. Respiratory system compliance can be divided into total compliance, chest wall compliance and lung compliance according to its components. Total compliance is the change of vital capacity caused by the pressure difference between alveoli and atmosphere; Chest wall compliance is the change of vital capacity caused by the difference between thoracic and atmospheric pressure; Lung compliance is the change of vital capacity caused by the pressure difference between alveoli and thoracic cavity. Lung compliance can be divided into static compliance and dynamic compliance. In the respiratory cycle, the lung compliance measured when the airflow is temporarily blocked is static lung compliance, and in the respiratory cycle, the lung compliance measured when the airflow is not blocked is dynamic lung compliance. The former reflects the elasticity of lung tissue, while the latter is also affected by airway resistance. The decrease of lung compliance is mainly seen in pulmonary diseases such as pulmonary fibrosis, pulmonary edema, atelectasis and pneumonia, which limits the expansion of the lung. In emphysema, due to the loss of elastic fibers in alveolar wall, lung elasticity decreases, so the pressure change required for lung volume expansion to a certain extent is lower than that of normal lung, so lung compliance increases.
Another clinical application of lung compliance measurement is to measure the dynamic lung compliance when the respiratory frequency increases (generally 30 beats/min and 60 beats/min or faster), which can be used as an index of small airway dysfunction. Due to the obstruction of the small airway, when the respiratory rate increases, the lung compliance decreases. This change of compliance is affected by respiratory frequency, which is called frequency-dependent compliance.
Airway resistance is the pressure difference required per unit flow. Generally, it is expressed by the pressure difference (in centimeters) when the ventilation volume is 1 liter/second. The increase of airway resistance can be seen in chronic bronchitis, acute attack of bronchial asthma, cancer, scar tissue or other obstructive ventilation disorders. In emphysema, the circumferential traction of the bronchi is weakened due to the elasticity of the lungs, and the bronchi are easily trapped when exhaling, which leads to an increase in airway resistance.
The energy consumed to overcome the resistance of lung, chest wall and abdominal organs when air enters and exits the respiratory tract. The resistance of lung and chest wall includes elastic resistance and inelastic resistance. When breathing quietly, the work done by the contraction of respiratory muscles is basically used when inhaling, while the elastic retraction force of lungs is enough to overcome the inelastic resistance of air and tissues when exhaling. When breathing quietly, the total oxygen consumption of normal people is 200 ~ 300 ml/min, and the oxygen consumption of respiratory organs accounts for less than 5% of the total oxygen consumption. When the ventilation rate per minute increases, the percentage of oxygen consumption of respiratory organs to total oxygen consumption also increases.
The main function of diffuse function lung is gas exchange, that is, the exchange of oxygen and carbon dioxide. The exchange of gas in lung is located in alveoli, which follows the diffusion principle, that is, gas molecules diffuse from high partial pressure through alveolar capillary membrane (blood gas barrier) to low partial pressure until the gas pressure on both sides of the membrane is balanced. Partial pressure refers to the percentage of gas pressure in mixed gas to total gas pressure. The partial pressure of oxygen in alveolar gas is higher than that in capillary of alveolar membrane, so oxygen diffuses from alveoli to capillary through alveolar membrane and combines with hemoglobin in red blood cells. The partial pressure of carbon dioxide in blood is higher than that in alveoli, so carbon dioxide diffuses from blood to alveoli. Because the diffusion capacity of carbon dioxide is 20 times greater than that of oxygen, once there is a diffusion obstacle, it is mainly an oxygen diffusion obstacle, and in severe cases, hypoxia can occur. The decrease of diffusion function is mainly seen in pulmonary interstitial diseases, such as diffuse pulmonary interstitial fibrosis. In other cases, such as emphysema, due to the destruction of alveolar wall, the decrease of diffusion area or the decrease of hemoglobin in anemia, the pulmonary diffusion ability can be reduced. Including the transport of oxygen and carbon dioxide.
Transport of oxygen There are two forms of transport of oxygen in blood, namely, physical dissolution and combination with hemoglobin, and the combination of oxygen and hemoglobin forms oxygenated hemoglobin, which is the main form of existence and transport of oxygen in blood. The percentage of oxygenated hemoglobin in hemoglobin is called oxygen saturation. Physical dissolved oxygen only accounts for 1.5% of arterial oxygen content, but oxygen saturation mainly depends on the change of physical dissolved oxygen partial pressure in blood, which is not a straight line, but an S-shaped curve called oxyhemoglobin dissociation curve. It can be seen from this curve that when the partial pressure is 90 ~ 100 mmHg, the arterial oxygen saturation can reach 95%; When the oxygen partial pressure drops to 60mHg, the oxygen saturation can still reach 90%; If the oxygen partial pressure drops below 60mmHg, the oxygen saturation drops sharply. The oxygen supply of body tissues mainly depends on oxygen saturation.
Transport of carbon dioxide There are three main forms of transport of carbon dioxide in blood: physically dissolved carbon dioxide only accounts for about 5% of the total carbon dioxide in whole blood, but it plays an important role in respiratory regulation and acid-base balance in the body. Bicarbonate accounts for about 88 ~ 90% of the total carbon dioxide in arterial blood, of which about 25% exists in red blood cells and 75% exists in plasma, which is the most important form of carbon dioxide transport in blood. Hemoglobin carbamate, a small part of carbon dioxide entering red blood cells can combine with α amino group of hemoglobin to form hemoglobin carbamate, accounting for 5 ~ 7% of the total carbon dioxide in blood, and its effect is slower than that of bicarbonate.
The control and adjustment of respiratory movement are carried out in the following three ways.
Central control and regulation of respiration. People's breathing is arbitrary and involuntary (that is, autonomous). Spontaneous breathing is mainly controlled by the cerebral cortex, while spontaneous rhythmic breathing comes from some nerve structures in the medulla oblongata.
The nerve reflex of respiration regulates the central nervous system to receive impulses from various receptors and realize its regulation of respiration, among which mechanical stimulation (changes in lung volume) and chemical stimulation are the most important. The reflex change of breathing caused by lung expansion or contraction is called stretch reflex, also called Herring-Braeuer reflex. This reflex is to suppress inhalation, so that it will not be too deep for too long.
Chemical regulation of respiration The chemoreceptors related to respiration can be divided into central type and peripheral type according to their positions. The central chemoreceptor is located on the surface of medulla oblongata which is sensitive to carbon dioxide. When the concentration of carbon dioxide in blood increases, it stimulates chemoreceptors, making breathing deepen and accelerate, thus discharging more carbon dioxide. However, when the concentration of carbon dioxide in blood is too high, it will inhibit the central chemical receptor. Peripheral chemoreceptors located in carotid body and aortic body are mainly sensitive to hypoxia.
When respiratory control and regulation are disturbed, it can cause abnormal respiratory rhythm. Observe the changes of cardiopulmonary function indexes through a certain exercise load.
The human body has a large reserve of respiratory and circulatory organs, so the cardiopulmonary function may be damaged before the symptoms appear. Exercise test can show the early changes of lung function more sensitively.
Shortness of breath is a common symptom, and exercise test can distinguish whether shortness of breath is caused by cardiopulmonary disease or mental factors. The former can cause changes in cardiopulmonary function through exercise test, while the latter has no obvious changes.
In addition to medical history, signs and chest X-rays, labor force identification of occupational diseases such as silicosis, lung function examination or exercise test at the initial stage of onset are also important objective indicators.
Exercise test can cause cardiopulmonary dysfunction or symptoms in some patients, which is called provocation test. Some asthma patients can cause the decline of pulmonary ventilation function and even asthma attack through exercise provocation test. Patients with early coronary heart disease can induce ECG changes or angina pectoris attacks through exercise provocation test.