ARDS
acute respiratory distress syndrome (acute respiratory distresssyndrome, ARDS) is a serious infection, trauma, shock and other lung diseases after the attack outside the alveolar capillary damage occurs as the main performance of the clinical syndrome, are acute lung injury ( acute lung injury, ALI) or type the serious stage. The clinical features include rapid breathing and distress frequency, progressive hypoxemia, X ray showed diffuse alveolar infiltrates.
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About the cause migration of inflammatory cells in the pathogenesis of inflammatory mediator release and accumulation of alveolar capillary damage and increased permeability of pathological changes in exudative proliferative fibrosis of clinical laboratory examinations of lung function Determination of pulmonary vascular permeability and hemodynamics treatment of respiratory support treatment measures blood volume to maintain the appropriate application of adrenal cortex hormones to correct acid-base and electrolyte disorders to explore other treatment complications of nutritional support Introduction to the intrinsic and infant respiratory distress syndrome rather similar, but different etiology and pathogenesis, as show the difference, the 1972 proposed adult respiratory distress syndrome Ashbaugh (adult respiratory distress syndrome) in the name. Now note that the intrinsic also occur in children, so the European and American scholars to discuss collaborative consensus to acute (acute) instead of adults (adult), called acute respiratory distress syndrome, abbreviated still ARDS. Because of modern recovery technology, and critical illness raise the level of the early rescue of patients from early death, the occurrence and who died of ARDS increased. Back in the early 80s the United States estimated 15 million patients each year as many as ARDS. ARDS research for 20 years although putting in a lot of manpower, material resources, in the pathogenesis, pathophysiology and treatment of respiratory support have significant progress, but mortality remains as high as 50% to 70%. In addition to the primary disease with the appropriate signs, but when the lung damage just a few hours, the patient can no respiratory symptoms. Then accelerated respiratory rate, shortness of breath gradually increased, no abnormal signs were found in the lungs, or breathing can be heard when the small wet rales. X-ray showed clear lung fields, increased lung markings or only vague, suggesting that fluid accumulation around the vessels. Arterial blood gas analysis showed PaO2 and PaCO2 low. With the progress of the disease, patients with respiratory distress, feeling his tight chest, difficulty breathing, cyanosis, often accompanied by irritability, anxiety, lungs extensive stromal invasion, may be associated with odd vein dilation, or a small amount of pleural effusion reaction. For obvious hypoxemia caused by hyperventilation, PaCO2 decreased respiratory alkalosis. Respiratory distress with normal oxygen therapy can not make improvements. If the condition continues to deteriorate, respiratory distress and cyanosis continues to grow, chest X-ray showed pulmonary infiltration shadow of a large fusion, and even develop into a Lead to respiratory muscle fatigue, lack of ventilation, carbon dioxide retention, resulting in mixed acidosis. Cardiac arrest. Some patients had multiple organ failure. The cause of many causes of ARDS, there are several of each type of disease or risk factors. Septic shock, hemorrhagic, cardiogenic, anaphylactic trauma burns, fat embolism, pulmonary contusion, non-thoracic trauma (especially head trauma) Gram-negative bacteria infection drowning sepsis, viral pneumonia, bacterial pneumonia, fungal pneumonia, Pneumocystis carinii carinii pneumonia, miliary tuberculosis, aspiration of gastric contents (especially pH 0.6, prompt mechanical ventilation. 2. Lung compliance measurement: usually measured at the bedside chest of total compliance,
chi pink dazzle, application of PEEP in patients, according to the following formula to calculate dynamic compliance (Cdyn) compliance testing not only for diagnosis, to determine efficacy, but also to monitor whether the pneumothorax or atelectasis and other complications have practical value. Cdyn = maximum airway pressure tidal volume - expiratory pressure of 3. PaO2 decreased arterial blood gas analysis is commonly used in ARDS diagnosis and monitoring indicators. Arterial blood gas analysis can be calculated according to the alveolar arterial oxygen difference (PA-aO2), static arterial shunt (Qs / Qt), respiratory index (PA-aO2/PaO2), oxygenation index (PaO2/FiO2) and other derived indicators, the diagnosis and evaluation of severity is very helpful. If Qs / Qt was advocated for disease classification increased to above 15%, 25% and 35% were classified as mild, moderate and varying degrees of severity. Respiratory index reference range of 0.1 to 0.37,> 1 indicates that the oxygenation was significantly decreased. > 2 often need mechanical ventilation. Oxygenation index reference range 53.2 ~ 66.7kPa (400 ~ 500mmHg), ARDS is reduced to 26.7kPa (200mmHg). Pulmonary vascular permeability and hemodynamics 1. ARDS pulmonary edema fluid protein measurement, the pulmonary capillary permeability, moisture and protein molecules into the interstitial or alveolar, the protein content of edema fluid and plasma protein ratio increase, if the ratio> 0.7, consider the ARDS, 2.67kPa, pulmonary artery pressure and pulmonary capillary wedge pressure (PAP-PCWP) increased (> 0.67kPa), PCWP General 1.57kPa (16cmH2O), then acute left heart failure, can be excluded ARDS. 4. Extravascular lung water content with the current double-tracer dilution method dye by central venous or right heart catheter tube 5cm indocyanine green dye into the glucose solution 10ml, and then in the femoral artery through a catheter connected with the thermistor record heat dilution curves, and detection using dye dilution curve density meter, and then calculated by computer processing of lung water, can be used to determine the extent of pulmonary edema, fate and efficacy, but need equipment conditions. ARDS therapy treatment is the key to the primary disease and its causes, such as handle the trauma, sooner or later find the foci, for applications sensitive to bacteria disease, antibiotics, suppression of inflammation and further damage to the lungs for; more urgent patients to promptly correct severe hypoxia, treatment of underlying disease to win the valuable time. In the treatment of respiratory support, to be crushed to prevent respiratory tract infections and oxygen toxicity and other secondary complications. According to the pathogenesis of lung injury, and explore new pharmacological treatment is also an important research direction. Treatment of a respiratory support. Oxygen therapy without delay to correct hypoxia, can be via face mask continuous positive airway pressure (CPAP) oxygen, but most need the help of mechanical ventilation, oxygen intake. Generally believed that the FiO2> 0.6, PaO2 remained 0.98kPa, alveolar diameter increasingly small, PEEP> 1.47kPa (15cmH2O), alveolar little capacity increase, the pleural pressure with alveolar pressure increases, affecting venous return, especially in hypovolemia, vasoconstriction, poor regulatory function of the circumstances, will reduce the cardiac output, although it can be too high PEEP improve the PaO2 and SaO2, often due to reduced cardiac output, but affect the tissue oxygen supply. High PEEP will increase the swelling chest and the incidence of mediastinal oxygen. Best PEEP should be more than 90% SaO2, and PEEP FiO2 down to the level of safety limits 〔generally 1.47kPa (15cmH2O)〕. Patients in maintaining an effective blood volume, to ensure tissue perfusion conditions, PEEP pleasant low 0.29 ~ 0.49kPa (3 ~ 5cmH2O) began to gradually increase to the optimal PEEP, such as PEEP> 1.47kPa (15cmH2O), SaO2 2.45kPa (25cmH2O), complicated by the occurrence of pneumothorax and pneumomediastinum rate of 14% and the mortality is almost 100%. Now, some scholars advocate low tidal volume, low ventilation, or even to allow a certain hypoventilation and mild carbon dioxide retention, the peak inspiratory pressure (PIP) <3.92kPa (40cmH2O) <1.47kPa (15cmH2O), if necessary, adjust with the pressure volume control (PRVCV) or pressure control inverse ratio ventilation pressure regulator volume control 〔PIP, <2.94 ~ 3.43kPa (30 ~ 35cmH2O)〕. Outside there is also a result of inhaled nitric oxide (NO), R oxygenation membrane oxygenation or high-frequency ventilation, can reduce or prevent barotrauma of mechanical ventilation. 3. Membrane oxygenator ARDS by artificial airway mechanical ventilation, oxygen therapy is poor, respiratory function and can not be corrected in the near future occasions, it was applied extracorporeal membrane oxygenation patterns, the root of bilateral saphenous vein with the expansion tube ah expansion of deduction were deep into the inferior vena cava catheter. Is the development of the intravascular oxygenator / exclude CO2 device (IVOX), oxygenation and CO2 in order to eliminate function with the hollow fiber membrane from the femoral vein catheter inserted into the inferior vena cava, the nitrogen with a vacuum suction through IVOX, can improve gas exchange. With mechanical ventilation can reduce the mechanical ventilation of a parameter to reduce the complications of mechanical ventilation. Maintain proper blood volume trauma excessive bleeding, requiring blood transfusion. Avoid excessive blood transfusion, drip rate should not be too fast, the best enter the new blood. Stock more than 1 week of blood micro-particles, can cause micro-embolism,
Chi dazzle flat iron, damage to pulmonary capillary endothelial cells, must be added with a micro-filter. In ensuring the blood volume, blood pressure, under the premise requires a negative balance and out of mild liquid (-500 ~-1000ml / d). To promote regression of edema fluid can be used Furosemide (furosemide), daily 40 ~ 60mg. Increase in endothelial cell permeability,
CHI Turbo Ceramic Flat Iron, permeable to interstitial colloid, the increased pulmonary edema, it is not appropriate in the early ARDS to the colloid. If low serum protein concentration is a different matter. Application of adrenal cortex hormones protect the capillary endothelial cells that prevent white blood cells, platelet aggregation and adhesion formation of microthrombi wall; stability of lysosomal membranes, decreased complement activity, inhibition of membrane phospholipid metabolism, reduce the synthesis of arachidonic acid prevent prostaglandin and thromboxane A2 of life; protection of alveolar type Ⅱ cells secrete surfactant; with anti-inflammatory and promote interstitial lung fluid absorption; relieve bronchial spasm; inhibition of late pulmonary fibrosis. Currently considered to irritant gas inhalation, fractures caused by traumatic fat embolism caused by non-infectious ARDS, early hormone can be applied. Dexamethasone 60 ~ 80mg / d, or hydrocortisone 1000 ~ 2000mg / d, every 6h1, once every 2 days, effective to continue using the 1 to 2 days withdrawal, with no response sooner or later disabled. ARDS associated with sepsis or severe lower respiratory tract infection hanged hormones. Correct the acid-base and electrolyte imbalance and respiratory failure the same general principles. Focusing on prevention. Nutritional support in patients with ARDS in a high metabolic state, should be completed in time to add heat and high-protein, high fat nutrients. As soon as possible to give a strong nutritional support, nasogastric or intravenous supplies, to keep the total calorie intake 83.7 ~ 167.4kJ (20 ~ 40kCal/kg). Explore other treatment 1. Pulmonary surfactant replacement therapy at home and abroad there is a natural extract and artificial surfactant preparations, treatment of infant respiratory distress syndrome has a good effect of exogenous surfactant in ARDS PaO2 increased only temporarily . 2. Suction NO NO the vascular endothelial cell-derived relaxing factor, has a wide range of physiological activity in the pathogenesis of many diseases. The physiological role in ARDS and possible clinical application has been studied extensively. NO is generally believed that access to better lung ventilation, pulmonary vascular expansion in the area, so that the proportion of low ventilation and blood flow in blood vessels to expand and improve the ratio of ventilation and blood flow, reducing pulmonary shunt to reduce the oxygen concentration. In addition NO can reduce pulmonary artery pressure and pulmonary vascular resistance without affecting systemic vascular expansion and cardiac output. Some scholars reported that the inhaled NO and intravenous Ami de Forest formyl acid (almitrine bismyslate) in combination, to improve gas exchange and reduce mean pulmonary arterial hypertension have synergistic effect. Poor pulmonary ventilation which allows the vessels contract, blood flow to better ventilated lung areas; and can stimulate the surrounding chemical receptors, increased respiratory drive and increase ventilation; its possible pulmonary hypertension can be offset by NO. NO is currently used in clinical studies yet to be thorough, and there are many specific operational issues to be resolved. 3. Oxygen free radical scavengers, antioxidants and immune therapy based on the pathogenesis of ARDS, the incidence for the major component of the drug given to the appropriate intervention to reduce lung and other organ damage, is one of the focus. Peroxide dismutase (SOD), catalase (CAT), to prevent oxidation by O2 and H2O2 induced acute lung injury; uric acid can inhibit the O2, OH generation and PMNs respiratory burst; vitamin E have some anti- oxidant effectiveness, but increases the risk of nosocomial infection. Lipoxygenase and cyclooxygenase pathway inhibitors such as ibuprofen, which will enable thromboxane A2 and prostaglandin reduction, combined inhibition of complement and PMNs, PMNs in the lungs to prevent aggregation. Immunotherapy in and through the causative agent of inflammatory mediators and inhibition effects against the cells to treat ARDS. There are currently studied in anti-endotoxin antibodies, anti-TNF, IL-1, IL-6, IL-8, and antibodies against cell adhesion molecules or drugs. Complications in patients with acute respiratory distress syndrome shortly after, a few days or weeks after the disease without remission, may be due to lack of oxygen supply caused by complications of other organs occurs. Oxygen for too long can cause serious complications such as renal failure, such as has not been timely treatment may be due to severe hypoxia and death. Due to acute respiratory distress syndrome, lung infection in patients with low capacity defense in the course of their illness often occurs with bacterial pneumonia. More Atlas Atlas entry Open Category: Medicine I to perfect
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