Respiration is a process of gas exchange, and its function is to ensure that the body continuously obtains oxygen and discharges carbon dioxide, and to ensure normal metabolic activities. The complete respiration process includes external respiration of the respiratory system and internal respiration of full tissue. Respiratory insufficiency or respiratory failure refers to breathing disorders.
External respiratory dysfunction caused by any reason, unable to maintain the gas exchange required by the normal body, and showing a series of clinical symptoms and signs is called respiratory insufficiency. Respiratory failure refers to the development of respiratory insufficiency to a severe stage, so that the partial pressure of oxygen in arterial blood (Pa02) is lower than 60 mmHg (8.00kPa) at rest, or the partial pressure of carbon dioxide (PaC02) is higher than 50 mm Mercury (6.67kPa).
According to whether PaC02 is elevated, respiratory failure is usually divided into hypoxemia (type I) and hypoxemia with hypercapnia (type Ⅱ); respiratory failure is divided into ventilatory and exchangeable according to the main pathogenesis Qi: Respiratory failure can be divided into acute and chronic according to the course of the disease.
External breathing includes two basic links: lung ventilation and lung ventilation. Various causes are nothing more than mechanisms such as alveolar hypoventilation, dispersal disorder, alveolar ventilation, and blood flow imbalance, which obstruct the ventilation and/or exchange process, leading to respiratory insufficiency and eventually failure. Common reasons are:
(1) Insufficiency of alveolar ventilation. Normal people’s lung ventilation is about 6 to 8 liters per minute at rest. Some of them are due to the structure of the airway and the lack of blood flow through the alveoli. Dead space ventilation for blood body exchange. The total ventilation volume minus the invalid dead space ventilation volume is the alveolar ventilation volume that actually participates in the gas exchange. The calculation formula is: (tidal volume-dead space volume) × respiratory rate = effective ventilation volume: when a normal adult is resting Alveolar ventilation is about 4 liters/min. Therefore, in addition to the increase in dead space ventilation can directly reduce alveolar ventilation, all other reasons that can reduce respiratory activity, increase the elastic resistance of the chest wall and lungs, and obstruct airway ventilation can cause alveolar insufficiency. For example, when the respiratory center is inhibited by infection, trauma, anesthesia or sedatives, neuromuscular disorders (spinal cord injury) myasthenia gravis (organophosphorus poisoning) involving respiratory muscles, thoracic deformities or pleural diseases (pleural adhesions, hemothorax, pneumothorax) or Diaphragm activity limitation, central airway obstruction (inflammation of the larynx and trachea), edema, foreign body and tumor compression), and peripheral airway or small airway obstruction (chronic bronchitis) bronchial asthma, chronic obstructive pulmonary emphysema) And so on, can cause alveolar hypoventilation.
(2) Diffusion disorder refers to the obstacle of the process of oxygen and carbon dioxide exchange through the alveolar membrane. It may be due to the fact that the oxygen in the alveoli cannot normally pass through the membrane between the alveoli and the capillaries, or enter the capillaries with the blood. The blood protein is not in contact for enough time. The common reasons are: ① Lobectomy, pulmonary consolidation, atelectasis, or emphysema destroys a large number of alveoli and reduces the area of oxygen-diffused alveolar-capillary membrane. The area of acute respiratory membrane is reduced by half, which can lead to gas exchange disorder. ②The thickness of the respiratory membrane, namely the alveolar-capillary blood membrane, is about 1-4 microns. In the case of pulmonary edema, viral or simple pneumonia, and pulmonary fibrosis, it can thicken the respiratory membrane and increase the diffusion distance, which affects gas exchange. ③When entering the resting state normally, the blood flowing through the capillaries of the alveolar wall contacts the alveoli for 0.75 seconds, and the time required to complete the gas exchange is 0.25 to 0.30 seconds for oxygen, and only 0.13 seconds for carbon dioxide. Even during vigorous exercise, the blood flow rate increases, and the time for blood to contact the alveoli is shortened to 0.34 seconds, which is enough to meet the time required for gas exchange. However, under pathological conditions, such as extensive fibrosis or edema of the alveolar membranes and excessive thickening, the contact time between the relative blood and the alveoli is too short. If the blood flow speed increases (emotional agitation, activity, etc.), it can cause oxygen and hemoglobin The binding rate is reduced, causing hypoxia.
(3) The ratio of alveolar ventilation to blood flow (VA/Q) is unbalanced. When normal people breathe calmly, the average alveolar ventilation (VA) is 4 liters/min, and the average pulmonary blood flow (Q) is 5 liters/min, VA/ Q is 0.8.
Due to gravity, the distribution of gas and blood flow in the lungs is not uniform. In the upright position, the lungs can be divided into upper, middle and lower segments. Pulmonary ventilation and pulmonary blood flow increase from top to bottom, but the increase in blood flow is more obvious. The 36VA/Q ratio is 1.7 in the upper lung, 0.9 in the middle lung, and 0.6 in the lower lung. The normal VA/Q ratio changes to a certain extent, and the range of changes in the ratio will expand with age.
In lung disease, the total lung ventilation and total blood flow can sometimes be normal, but the uneven distribution and imbalance of local ventilation and blood flow can cause ventilation disorders and develop into respiratory insufficiency. If alveolar hypoventilation and blood flow reduction occur in the same location (such as lobectomy, lobar pneumonia gray liver degeneration), the remaining healthy lungs can be compensated by strengthening ventilation and blood flow, which will not affect the ventilation function. However, in most lung diseases, the changes in alveolar ventilation and blood flow are often not parallel to the mouth. This uneven distribution of ventilation and blood flow will cause a serious imbalance of the ventilation/blood flow ratio, resulting in barriers to gas exchange in the lungs, and even lead to Respiratory failure. There are two basic forms of imbalance of alveolar ventilation blood flow:
① Uneven distribution of ventilation means that the VA/Q ratio of some alveoli is increased. Insufficient ventilation distribution can cause death cavity-like ventilation (ventilation that does not participate in blood gas exchange is called dead cavity-like ventilation). The ratio of dead space volume to tidal volume in normal people (VD/VT, less than 30%, can increase as high as 60-70% in severe lung disease. Dead space volume includes dead space (referring to trachea and bronchus that do not participate in gas exchange) The volume of the lumen of the normal person is about 150m1) and the alveolar dead space (referring to the ventilated alveolar volume without blood perfusion), in addition to the so-called relative dead space increase, such as shallow breathing, at this time, although every lung The minute ventilation can be normal, but the frequency is fast, the tidal volume is small, the effective ventilation volume is small, and the ratio of dead space volume to tidal volume increases. Therefore, dead space ventilation refers to the relative reduction of ventilated alveoli and blood supply. Insufficient gas exchange. This situation is seen in pulmonary artery branch embolism, pulmonary artery low pressure and pulmonary capillary bed reduction. At this time, the blood flowing here can be fully oxygenated, but the blood flow is low, resulting in other parts of the alveoli Increased blood flow and relatively insufficient ventilation.
② Uneven blood flow distribution means that the VA/Q ratio of some alveoli is reduced. Irradiation of blood flow can cause venous blood adulteration. That is, part of the unoxygenated venous blood is mixed into the arterial blood, so it is also called blood shunt, that is, the pulmonary artery blood flows into the pulmonary vein. Blood shunts include anatomical shunts and functional shunts (ie, shunt-like perfusion). Under normal circumstances, a small part of static urine flows into the pulmonary vein and the left ventricle through the bronchial vein and the smallest vein of the left ventricle, respectively. The blood shunt of this anatomical shunt accounts for about 2 to 3% of the cardiac output. The anatomical fluid distribution can be greatly increased in the case of diseases, such as bronchiectasis with dilation of bronchial blood vessels, congenital pulmonary arterial fistula, pulmonary hypertension, and pulmonary microcirculation obstacles when pulmonary arteriovenous communication branches are open (arteriovenous short-circuit opening), etc. The direct flow of unoxygenated venous blood into the pulmonary veins increases. Functional shunting is particularly common in cases of lung diseases, such as atelectasis, lung consolidation, thickened respiratory membranes, stenosis or blockage of the trachea, when blood flows through unventilated or hyperventilated alveoli, and venous blood is not fully oxygenated. After reflux, venous blood is adulterated. The functional shunt formed by the uneven distribution of pulmonary ventilation in normal people only accounts for about 3% of the pulmonary blood flow. However, when chronic obstructive pulmonary disease develops to a severe stage, the functional shunt increases significantly, reaching 30 to 30% of the pulmonary blood flow. 50%, severely affect the ventilation function, leading to respiratory failure.
In clinical practice, simple ventilation disorder, diffusion disorder, or imbalance between ventilation and blood flow are rare, and they are often caused by multiple factors. For example, when there is insufficient ventilation, the pathological changes are not uniform and symmetrical. Alveolar ventilation is insufficient, and it is often accompanied by an imbalance between ventilation and blood flow. As the disease progresses, other factors are often involved. For example, obstructive emphysema and obstructive ventilation disorder are the main ones, but obstructive emphysema has pulmonary fibrosis and reduced lung compliance, so it also has limitations. Ventilation disorders; in emphysema, due to alveolar fusion1, the alveolar capillary network is destroyed, and there is a diffusion disorder caused by a reduction in the respiratory area; even small airway obstruction or partial alveolar ventilation caused by venous blood adulteration, or part of the pulmonary blood vessels Dead space-like ventilation caused by occlusion; if it is combined with inflammation and infection, the above-mentioned various pathogenesis can participate in it.
In this type of hypoxia, the characteristics of changes in blood oxygen parameters are the same as those caused by the decrease of oxygen in the ambient atmosphere.
When the respiratory insufficiency happens, our oxygen concentrator will be very useful.