1.Progress on the definition and diagnostic criteria of acute respiratory distress syndrome (ARDS) The naming of adult respiratory distress syndrome (Adult respirator distress syndrome (ARDS)) began in 1971 and was used for 20 years. 1992, the American Thoracic Society (ATS) and the European Society of Critical Illnesses (ESICM) held a joint In 1992, the American Thoracic Society (ATS) and the European Society of Critical Care Medicine (ESICM) jointly convened a symposium and suggested that the A in ARDS should be changed to Acute and that the syndrome should be divided into two parts, namely, ACUTE lung injury (ALI), which reflects the pathophysiological process of the syndrome, and ARDS, which is the most severe stage of the syndrome. The diagnostic criteria recommended by the Joint European and American Conference in 1992 are as follows: ALI: (1) acute onset; (2) hypoxemia, PAO2/FiO2 ≤300 mm Hg; (3) chest radiographs showing infiltrating shadows in both lungs; (4) pulmonary artery pressure (PAWP) ≤18 mm Hg, or clinical exclusion of cardiogenic factors; ARDS: (1) hypoxemia, PAO2/FiO2 ≤200 mm Hg, or clinical exclusion of cardiogenic factors; and (2) pulmonary arterial pressure ≤18 mm Hg. ARDS: (1) hypoxemia, PAO2/ FiO2≤200 mm Hg; (2) other criteria are the same as ALI; in 1999, the National Conference on Respiratory Failure held by the Respiratory Society of the Chinese Medical Association in Kunming, China, unanimously agreed on the above diagnostic criteria, but added the item of “there should be a high-risk factor for the onset of the disease” (see etiological classification). “The Fourth National Conference on Critical Care Medicine (ICU 2000) held by the Critical Care Medicine Committee of the Chinese Society of Pathophysiology in 2000 also recommended the application of the above European and American consensus criteria. 2, ALI/ARDS etiology classification and prognosis In recent years, it is recognized that the prognosis of ALI/ARDS caused by different etiologies is different, and most of them are divided into two major categories of direct lung injury and indirect lung injury: (1) direct lung injury factors: common for pneumonia, gastric aspiration; rare for pulmonary contusion, fat embolism, drowning pulmonary embolism resection or lung transplantation after reperfusion pulmonary edema. (2) Indirect lung injury factors: commonly sepsis, severe trauma with shock and massive blood transfusion; rarely cardiopulmonary diversion, acute pancreatitis, transfusion of blood preparations. Among them, sepsis has the highest chance of causing ALI and ARDS, about 40%, and the chance of ALI and ARDS in patients with other diseases also increases. For example, alcoholism, chronic lung disease and lower blood pH. (1) Fluid restriction: Animal experiments have confirmed that lowering left atrial pressure can reduce the degree of pulmonary edema. Some clinical studies also support this argument. The goal of fluid restriction should be the lowest level of intravascular volume that can provide adequate systemic perfusion and maintain acid-base balance and renal function. If systemic perfusion cannot be maintained with intravascular volume restriction, then fluids should be given. The National Institutes of Health (NIH) Acute Respiratory Distress Syndrome Network has now begun a large common study of fluid restriction versus hemodynamics and effects on the pathogenesis of ARDS. (2) Application of pulmonary surfactants: Lung surfactant replacement therapy has been successfully used in children with neonatal respiratory distress syndrome. However, the application of synthetic surfactants in adult patients has not achieved the expected results. Clinical studies on new preparations containing recombinant surfactant proteins and improved inhalation methods including endotracheal drip and bronchoalveolar lavage are underway. (3) Inhalation of nitric oxide and other vasodilators: Since the report of the effectiveness of nitric oxide inhalation in 1993, the results of application in many countries have shown doubtful efficacy, and it was found that inhalation of NO treatment could not reduce the mortality rate and reduce the duration of mechanical ventilation. Studies have shown that the improvement in oxygenation is minimal and variable, and pulmonary artery pressure is only slightly reduced on the first day of treatment, so the use of this agent is no longer recommended internationally for the treatment of ALI/ARDS, and it is now thought that it may play a role in emergency treatment of refractory hypoxemia. Other vasodilators, including sodium nitroprusside, hydralazine, prostaglandin E1, and prostacyclin, have also been shown to be ineffective. (4) Glucocorticoids and other anti-inflammatory drugs: Clinical applications have shown that these drugs are ineffective when used before the onset of ALI/ARDS or early in the course of the disease. Recently, encouraging results have been obtained in two groups of patients with ARDS who had not responded to other treatments: 16 patients treated with methylprednisone showed not only an improvement in the ALI/ARDS observations but also an improvement in sepsis compared with 8 control subjects. Compared with the control group, the methylprednisone-treated group had improved lung injury scores, PAO2/FiO2, and reduced MOF scores. The NIH-ARDS Network is currently in the midst of a study on the application of steroid therapy in patients with advanced ARDS. (5) Lidocaine on the prevention and treatment of ALI: In recent years, especially in 2000, it was found that lidocaine has the ability to significantly inhibit neutrophils involved in a number of inflammatory responses (such as chemotaxis, adhesion and respiratory bursts of oxygen free radicals, etc.), to reduce systemic inflammatory response, to reduce pancreatic enzyme-induced lung injury, as well as to inhibit and reduce the body’s response to endotoxin, etc. However, due to the vasodilator effect of lidocaine, the body’s response to endotoxin has been improved. However, due to the vasodilating effect of lidocaine, the blood concentration should not exceed 5mg / L. There are prospects for further research. 4, mechanical ventilation progress Mechanical ventilation is the most important symptomatic treatment to rescue ALI / ARDS, due to different periods of people’s understanding of the syndrome in different depths, so the mechanical ventilation and the mechanical ventilation caused by the “medical harm” is also different. Over the past half century, the ventilation mode has gone through the process of pressure-conversion mode – volume-conversion mode – new pressure-conversion mode. This process reflects the deepening understanding of ALI/ARDS, and also greatly changes the prognosis of ALI/ARDS. (1) Ventilator-induced lung injury (VILI) and protective lung ventilation: In the study of CT scanning of ARDS lungs, it was found that the distribution of lung lesions in ALI/ARDS was uneven, with alveolar atrophy in some areas and normal ventilation in others, but the ventilated lungs only accounted for 1/2 to 1/3, or even 1/4 of the total number of lungs, leading to the new concept of “infant lung”. The new concept of “infant lung” has been proposed. The above findings have led to a reflection on the reasons for the exacerbation of certain conditions with the application of mechanical ventilation, and the realization that if the tidal volume of mechanical ventilation (10-12 ml/kg of body weight) at the time of alveolar normalization is applied to patients with ALI/ARDS whose ventilatory capacity is already markedly reduced, it is bound to result in the overexpansion of the ventilated alveoli. It has been demonstrated that this portion of the alveoli may take up to a tidal volume equivalent to 40 to 48 ml/kg body weight. This type of lung injury produced by mechanical ventilation is difficult to distinguish from ALI/ARDS both in terms of lung tissue changes and function, and is referred to as ventilator-induced lung injury (VILI).The mechanism of VILI is primarily the overexpansion of the ventilated alveoli caused by relatively or absolutely large tidal volumes of ventilation. That is, lung volume injury (Volutrauma). Experimentally, it was found that when the alveolar epithelial cells were overly stretched, on the one hand, inflammatory cells and related mediators in the lungs could be significantly up-regulated, and on the other hand, atrophied or non-expanded alveoli, whose functional residual air volume had been extremely reduced, were bound to repeatedly undergo the process of opening and atrophy under large positive-pressure ventilation. The greater the tidal volume applied to the atrophied alveoli, the greater the difference in volume (i.e., shear force) between inspiratory and expiratory alveoli, which is another important physical cause of further alveolar damage. In addition, capillary stress failure caused by mechanical ventilation can also increase capillary permeability and exacerbate pulmonary edema. The above understanding has led to the improvement of mechanical ventilation and the proposal of “protective lung ventilation strategy”. (2) Protective ventilation consists of the following key points: (1) low tidal volume, i.e., the tidal volume is set between the upper and lower inflection points (UIP, LIP) of the static pressure-volume curve (PV curve), and the NIH suggests that 6 ml/kg body weight is the ideal tidal volume for mechanical ventilation. (2) The ideal method for high PEEP is to set PEEP above the lower inflection point of the PV curve. However, under the condition of unconditional recording of the PV curve, PEEP can be set at 20 cmH2o first, and then gradually drop 2 to 3 cmH2o at a time, and the PEEP value with a drop of 2 to 3 cmH2o in PEEP and no decrease in PaO2 is considered as the most desirable PEEP value. The combined effect of low tidal volume and high PEEP can, on the one hand, keep the reopened alveoli open, and on the other hand, reopen the alveoli in the non-ventilated area, which is called “lung opening”. (3) Limiting inspiratory pressure. Peak inspiratory pressure is equal to PEEP plus the inspiratory-expiratory pressure difference. The inspiratory-expiratory pressure difference is usually 10-15 cmH2o, which is the pressure that provides the tidal volume. If the peak inspiratory pressure is >35 cm, there is a risk that the tidal volume will exceed the upper inflection point, which may cause alveolar injury; therefore, the upper limit of inspiratory pressure is usually limited to less than 30 to 35 cmH2o. (4) Permissive hypercapnia: application of small VT and pressure limitation may reduce minute alveolar ventilation and cause a subsequent rise in PaCO2. As long as the rate of increase in PaCO2 is not too rapid, the kidneys have time to compensate and maintain pH >7.20-7.25, the body can tolerate it and it is called permissive hypercapnia. If PaCO2 rises too rapidly, the following methods can be used to increase CO2 excretion, including appropriately increasing the frequency of ventilation and adding endotracheal blowing (TGI) to reduce dead space. (3) Modern pressure preset ventilation: (1) Pressure support ventilation (PSV) is also known as inspiratory pressure support. The basic working principle is that when the patient inhales, the ventilator provides a constant airway pressure to help overcome inspiratory resistance and expand the lungs. This mode of ventilation is well synchronized. It has lower peak and mean airway pressures compared to controlled ventilation. When applying PSV, two parameters should be adjusted, one is the trigger sensitivity and the other is the pressure support (PS) level. Trigger sensitivity is usually set at -0.2 kPa, or PEEP (PEEPi) – (O2 level if PEEP is applied or if endogenous PEEP (PEEPi) is present in the patient. Commonly used PSV levels are 0.5 to 3.0 kPa. implementation of PSV requires the patient to be breathing spontaneously, so it should not be used for those with depressed or unstable central drive. (2) Pressure-controlled ventilation (PCV): controlled ventilation means that the patient’s breathing is completely controlled by the ventilator, and the constant pressure in the airway during PCV is conducive to the distribution of gases. PCV is generally used to complete certain special ventilation, such as inverse ratio ventilation, in addition to respiratory center inhibition, respiratory muscle paralysis, and cardiorespiratory function reserve depletion. When applying PCV, it is often necessary to apply tranquilizers and/or inotropic agents to prevent the incongruity between autonomous breathing and the ventilator. (3) Pressure-controlled-inverse ratio ventilation (PC-IRV). The inspiratory time (Ti)/expiratory time (Te) of normal breathing and conventional ventilation is mostly 1:1.5 to 2.5. If Ti/Te ≥ 1, it is inverse ratio ventilation (IRV). Theoretically, IRV has the following advantages: 1) Ti lengthens the inspiratory peak pressure, 2) increases the functional residual air volume of the lungs, and 3) Te shortens the airway to produce PEEP, which is favorable for atrophic alveolar reexpansion and improves oxygenation. However, the clinical application is not ideal and has many adverse effects. Including the reduction of venous return blood volume, cardiac output and so on. It is generally believed that inverse ratio ventilation I/E should not be greater than 1.5:1.(4) Proportional assisted ventilation (PAV). It can provide synchronized pressure assistance in proportion to the patient’s instantaneous inspiratory effort.PAV is characterized by the ventilator adapting to the patient, and the pressure delivered is augmented in proportion to the patient’s exertion. For example, PAV is 3:1, i.e., 1/4 of the inspiratory airway pressure is generated by respiratory muscle movement and 3/4 is provided by the ventilator. This way of human-machine coordination is the most ideal. (5) Airway Pressure Release Ventilation (APRV): APRV involves the addition of two valves on the expiratory circuit, the pressure release valve of which is connected to a timer. During APRV, this valve opens and gas escapes, resulting in a decrease in airway pressure, an increase in expiration, a decrease in functional residual gas volume, and an increase in carbon dioxide exhalation. These new modes of ventilation require more clinical observation. 5, other therapies related to ventilator ventilation (1) prone position: under mechanical ventilation, this position can increase the patient’s dorsal alveolar expansion, thus improving oxygenation, clinical observation shows that the effect on early ALI/ARDS patients is better, and those with late onset of the disease have poor or ineffective results. The timing and duration of the prone position varies widely among reports. It is generally believed that if PAO2/FiO2＜60 mmHg, prone position treatment should be started immediately for more than 8h. (2) Package therapy: In recent years, some authors have suggested that the therapeutic effect of ALI/ARDS can be improved if LPVS is supplemented with several other effective methods, which is called “package therapy”. This treatment includes LPVS (VT5~7ml/kg, PIP>35cm; PEEP12~15cmH2o, prone position (2h each time), dehydration (diuretics or continuous veno-venous hemofiltration), and NO inhalation (5~20PPm). (3) Continuous dilatation (SI) method: a new method proposed after 1999, the principle is to first use 30-50 cmH2o continuous dilatation for 10 seconds to 1-2min, and then use high PEEP (about 20 cmH2o), low tidal volume (6 mg/kg) ventilation. The preliminary results were very good.