Adult respiratory distress syndrome

Introduction to adult respiratory distress syndrome Adult respiratory distress syndrome (ARDS) is a normal cardiopulmonary function in patients with acute osmotic pulmonary edema and progressive hypoxic respiratory failure due to severe disease outside the lungs or within the lungs. Although the causes are different, the pathological and functional changes of lung tissue damage are roughly the same. The clinical manifestations are acute respiratory distress, refractory hypoxemia, because of their clinical similar respiratory distress syndrome, and their etiology and pathogenesis. Not the same, so the crown is "adult" to show the difference, the disease is onset, rapid development, if not early diagnosis and treatment, the mortality rate is as high as 50% or more (25%-90%), often died of more dirty The function is depleted. basic knowledge The proportion of illness: 3% Susceptible people: more common in young and middle-aged Mode of infection: non-infectious Complications: bacterial pneumonia

Causes of adult respiratory distress syndrome

Traumatic traumatic infection (20%):

Suppurative infections can cause bacterial toxins or cell rupture products to enter the pulmonary circulation. Under the action of endotoxin, vasoactive substances are released in the body, which can increase capillary permeability. Infection can also be transferred to the lungs, which can lead to pulmonary failure.

Excessive blood loss (15%):

The low blood volume caused by a large amount of blood loss in shock and trauma can cause a decrease in cardiac output and also a decrease in pulmonary blood flow. Due to the reduction in pulmonary blood volume and the continuous receipt of microemboli from the systemic circulation, the pulmonary vascular bed can be blocked, hindering the progress of gas exchange.

Traumatic brain injury (10%):

This is because brain trauma can stimulate strong sympathetic impulses, leading to significant peripheral vasoconstriction, followed by acute heart failure and pulmonary edema.

ARDS is an acute alveolar-capillary membrane injury caused by many reasons. Some reasons can directly damage the lungs: such as 1 inhalation of smoke, poisonous gas, stomach contents and drowning; 2 taking excessive heroin or salicylate; 3 bacteria, viruses and Pulmonary infection caused by fungi, etc.; 4 fat, amniotic fluid and thrombosis cause pulmonary embolism; and 5 lung contusion, radiation damage and oxygen poisoning, etc. Some systemic pathological processes can cause lung injury, such as sepsis, shock, diffuse intravascular Coagulation, allergic reactions, trauma and burns, burn area of more than 40% may lead to a significant reduction in Pao2, and some treatments may also cause ARDS, such as hemodialysis, extracorporeal circulation, use of nylon silk to remove white blood cells.

According to the different causes and characteristics of the lesions, ARDS has more than 20 names, such as post-traumatic wet lung, sepsis lung, shock lung, post-transfusion lung, microvascular leakage syndrome, congestive atelectasis, hyaline disease, emerging lung Syndrome, zombie syndrome, progressive lung consolidation, etc.

Pathological changes in adult respiratory distress syndrome

The pathological changes of acute alveolar-capillary membrane damage caused by various causes are similar, and can be divided into acute stage and chronic stage lesions:

(1) Acute stage lesions

Mainly for pulmonary edema caused by extensive alveolar vascular endothelium and alveolar epithelial damage, first of all, interstitial edema, alveolar edema, lung weight up to three times normal, high liquid protein content in alveolar cavity, even bloody liquid, There are blood cells, macrophages, cell debris, amorphous substances, fibrin strips and residues of surface active substances. Occasionally, substances such as cell debris and proteins form transparent membranes in fibrin mesh.

(two) chronic stage lesions

After a few days of onset, the disease enters the chronic phase. The lesions are mainly cell proliferation. Fibrosis can occur after two weeks. Type II epithelial cell hyperplasia replaces degenerative necrotic type I alveolar epithelial cells, and the infiltration of various cells increases the alveolar septal increase. Thick, alveolar cavity and protein-rich liquid in the alveolar duct are mechanized to form fibrosis.

Pathogenesis of adult respiratory distress syndrome

The pathology of ARDS is mainly caused by pulmonary edema and pulmonary cell edema and subsequent cell proliferation and fibrosis. The mechanism of cell proliferation and fibrosis is the same as that of inflammatory repair. Therefore, the mechanism of acute lung injury is emphasized here.

Patients with ARDS have pulmonary hypertension, so some people emphasize that pulmonary microvascular hypertension is the cause of pulmonary edema, but the patient's pulmonary wedge pressure is often not high, indicating that capillary pressure is not necessarily high, edema fluid protein content is abundant, animal experiments also prove that In the animal model similar to ARDS, the lung lymph fluid flow rate increases, and the ratio of protein concentration in plasma lymph fluid to plasma protein concentration is greater than 0.7; at this time, intravenously injected polymer dextran (molecular weight 500,000) can penetrate into alveolar fluid, indicating Pulmonary edema in ARDS is mainly osmotic pulmonary edema, which is caused by increased permeability due to alveolar-capillary membrane damage.

The mechanism of increased alveolar capillary membrane permeability in ARDS has not been fully elucidated. Some primitive causes can directly damage the alveolar capillary membrane to increase its permeability, such as inhalation of gastric acid, poisonous gas, smoke, radiation damage and cytotoxic effects. A large number of experiments have shown that the more important is secondary damage, that is, the alveolar-vascular membrane damage caused by the accumulation of white blood cells and platelets in the lungs increases the permeability.

(1) The role of neutrophils in the pathogenesis of ARDS

The number of neutrophils in the peripheral blood of patients with ARDS is reduced. The lung biopsy shows neutrophil accumulation and infiltration in the lung. The neutrophils in the bronchoalveolar lavage can be increased by 20 to 100 times. Nowadays, neutrophils are generally considered. Aggregation, activation, release of oxygen free radicals, proteases and lipid metabolites in the lungs, leading to damage to the pulmonary microvascular membrane and alveolar epithelium, is the main pathogenesis of ARDS pulmonary edema.

1. Neutrophils accumulate in the pulmonary vasculature. Normally, about 10-20% of neutrophils accumulate in the pulmonary capillary bed in the straight steric position. This is a physical detainment, because an alveoli has nearly a thousand Segment capillary, each capillary is 1 ~ 30m (average 8m), diameter 1 ~ 15m (average 5m), a blood cell from the pulmonary artery into the pulmonary vein to pass more than 100 capillary nodes, neutrophil diameter It is larger than the diameter of the capillary, and its shape is closer to the spherical shape than the red blood cells, so the deformability is poor and the deformation speed is slow. Therefore, the neutrophils are easily detained in the pulmonary capillary bed. Due to the large capacity of the pulmonary capillary bed, Leukocyte retention has little effect on pulmonary vascular resistance and pulmonary artery pressure. Physically detained neutrophils generally do not enter the alveolar space, so 90 to 95% of cells in normal human bronchoalveolar eluate are macrophages.

The accumulation of neutrophils in the pulmonary vasculature during ARDS is a chemical adhesion, which is the result of the action of chemokines. Experiments have shown that neutrophils are activated by chemokines and between vascular endothelial cells. The affinity is significantly enhanced, the total area of alveolar capillaries is 60m2, and a large number of neutrophils can be adhered to reduce the number of white blood cells in the peripheral blood.

There are many types of chemokines, mainly complement activation products C5a, fibrin degradation products (FDP), arachidonic acid metabolites such as leukotriene B4 (LTB4), hydroxyrachhipenoic acid (HETE) and thromboxane A2 (AXA2). ), platelet activating factor (PAF), and other chemotactic proteins, peptides and lipids, among which the more studied is the role of complement, plasma C5a is often elevated 8 hours before clinical diagnosis of ARDS, activated complement It does not directly damage pulmonary vascular endothelial cells. It activates neutrophils to cause damage, and the complement of sheep perfusion can cause pulmonary edema, such as the complement of granulocytes reduced by re-perfusion with nitrogen mustard. The occurrence of pulmonary edema is obvious. Activated neutrophils can infiltrate into the interstitial lung and enter the alveolar space. In the bronchoalveolar lavage of ARDS patients, there are complement fragments and a large number of neutrophils. In recent years, neutral granules have been found. There is a group of glycoproteins on the surface of the cells, which are related to the adhesion and phagocytosis of granulocytes. They are macrophage-1 (Mac-1) lymphocyte function-associated antigen-1 (lymphocyte function). Associated antegen-1, LFA-1), in which Mac-1 is most closely related to adhesion function, only a small amount of Mac-1 is expressed on the surface of normal neutrophils. In pathological conditions, the action of chemokines makes neutral particles Increased expression of Mac-1 on the cell surface promotes adhesion between neutrophils and vascular endothelial cells.

2, neutrophil damage to alveolar-capillary membrane in animal experiments intravenous injection of endotoxin, air and other models that can replicate acute pulmonary microvascular injury, activated with phorbol myristate acetate (PMA) Perfusion of neutrophils into isolated lungs can also increase pulmonary capillary permeability. For example, hydroxyurea, nitrogen mustard, etc. reduce the number of neutrophils in animals, and endotoxin, air emboli, etc. damage the pulmonary microvessels. Significantly alleviated, cell culture found that neutrophils secreted tightly to endothelial cells in order to increase the permeability of the monolayer of pulmonary artery endothelium, the above description is reduced, cell culture must be found that neutrophils must be closely adhered to Endothelial cells can increase the permeability of monolayer pulmonary artery endothelium. The above indicates that adhesion and activation of neutrophils play an important role in the pathogenesis of ARDS. It is likely to be the release of oxygen free radicals and proteases during neutrophil activation. , lipid metabolites and peptides cause damage to the alveolar-capillary membrane.

(1) Effect of oxygen free radicals: When neutrophils are activated, the oxygen consumption increases sharply, increasing several times to several tens of times than when resting. At this time, NADPH oxidase on the cell membrane is activated. Converting reduced coenzyme II (NADPH) to oxidized form (NADP), oxygen molecules obtain electrons to form superoxide anion O2-, and O2- can also generate H2O2 and OH·, normal neutrophils and their activator PMA Perfusion of isolated lungs can cause pulmonary edema, and edema fluid has high protein content; if neutrophils and PMA infusion in patients with hereditary chronic granulomatosis do not cause pulmonary edema, because of neutrophils in patients with chronic granulomatosis Lack of NADPH oxidase, less generation of oxygen free radicals, in addition, intravenous injection of oxygen free radical scavengers, such as superoxide dismutase (SOD), catalase, peroxidase, dimethyl thiourea, etc. It can alleviate the acute lung injury of experimental animals. It can be seen that neutrophils activate lung injury by releasing oxygen free radicals.

Oxygen free radical damage to lung microvascular endothelium and alveolar epithelial cells may have the following aspects: 1 acting on the cell membrane and organelle membrane, causing lipid peroxidation, thereby impairing the structure and function of cell membrane and cell membrane; 2 acting on enzyme, Inactivated; 3 acts on 1-protease inhibitor, inactivates it, thereby enhancing the destruction of tissue by lysosome-releasing protease; 4 acting on plasma components can form a strong chemoattractant, causing More neutrophils accumulate and activate in the lungs, producing more oxygen free radicals, which form positive feedback and aggravate lung damage.

(2) The role of protease: lysosomes in neutrophils contain a variety of neutral proteases and acid proteases. When neutrophils are activated or destroyed, these enzymes can cause decomposition and tissue structure of surrounding proteins. Destruction, the permeability of alveolar-capillary membrane is increased, among which neutrophil elastase is more studied. For example, it is found that the activity of elastase in bronchoalveolar eluate of ARDS patients is very high, and the animals are injected. When the toxin or oleic acid replicates the ARDS model, the elastase content in the plasma and alveolar eluate also increases; the injection of neutrophil elastase into the animal can increase the permeability of the pulmonary vascular endothelium and alveolar epithelium; Elastase leads to endothelial cell dispersion, etc., indicating that neutrophil elastase is associated with lung injury in ARDS, elastase can degrade elastin, collagen, fibronectin (FN), etc., fibronectin in endothelial cells Inter- and endothelial cells and the basement membrane play an "anchor" role, fibronectin is impaired, then vascular permeability Increase.

Liver and alveolar macrophages can synthesize 1-protease inhibitor (1-PI), which inhibits elastase, although plasma 1-PI in ARDS patients can be normal, 1-PI in bronchoalveolar eluate The activity is reduced, which may be caused by the oxidative inactivation of free radicals produced by neutrophils. The imbalance between protease and protease inhibitors further damages the tissue damage of the protease and increases the permeability of the alveolar-capillary membrane.

3, the role of lipid metabolites endotoxin and many other pathogenic factors activate neutrophils, macrophages, mast cells, endothelial cells and other cell membrane phospholipase A2, membrane phospholipids are cleaved into arachidonic acid, the latter Prostaglandins are produced by cyclooxygenase, and leukotrienes are produced by the lipoxygenase pathway. It is generally believed that leukotrienes, TXA2, and PGF2 can both contract pulmonary arterioles to cause pulmonary hypertension and increase pulmonary microvascular permeability. PGI2 and PGE1 have the effect of dilating blood vessels, lowering blood pressure, and reducing vascular permeability. In animals and patients with acute lung injury, alveolar eluates and blood TXA2, PGF2 and LTs are increased, and experiments have shown that PGI2 and PGE1 has a certain therapeutic effect on acute lung injury. Activation of leukocytes, macrophages, mast cells and endothelial cells can also release platelet activating factor (PAF). PAF can promote platelet aggregation and TXA2 synthesis, leading to microvascular permeability. Increase.

4, the role of protein substances after the activation of macrophages and other protein substances can be released, the most important of which are tumor necrosis factor (TNF) and interleukin IIL-1), human and animal plasma during endotoxemia Increased TNF and IL-1, TNF can increase pulmonary vascular permeability and promote neutrophil accumulation in the lung; IL-1 stimulates T lymphocytes to produce interleukin-2 (IL-2), the latter It also increases pulmonary vascular permeability.

In conclusion, it is now generally believed that neutrophil macrophages accumulate in the lungs, activate the release of a large number of oxygen free radicals and proteases and lipid metabolites and proteins, causing damage and permeability of the alveolar-capillary membrane. Lead to pulmonary edema, which is the main pathogenesis of ARDS. Although patients with leukopenia have sepsis can also develop acute lung injury, the use of drugs to make animal neutropenia has no significant effect on lung injury caused by oleic acid, but These facts are not sufficient to deny the pathogenic role of neutrophils, because the number of neutrophils in the peripheral blood does not necessarily reflect the number of granulocytes in the pulmonary circulation, and how much neutrophil activation is needed to cause acute lungs. The damage is not known, and only a part of the neutrophils that normally accumulate in the pulmonary blood vessels are activated enough to damage the lungs and cause ARDS.

(B) the role of coagulation system in the pathogenesis of ARDS

Lung biopsy and postmortem anesthesia in ARDS patients found that pulmonary arterial thrombosis can occur before pulmonary congestion, edema, hemorrhage and hyaline membrane formation, ARDS patients with diffuse intravascular coagulation, hypoxemia and lung compliance Sexual downsizing is much heavier than those without DIC. Proliferating substances released by neutrophil activation and lung tissue damage, pulmonary vascular endothelial injury and blood stasis can lead to platelet aggregation and intravascular coagulation to form microthrombus, in the lungs. Extensive microthrombus formation may cause: 1 increased pulmonary circulation resistance increases pulmonary arterial pressure, unblocked pulmonary vessels increase blood volume and capillary pressure, leading to pressure pulmonary edema; 2 vascular activity of blood vessel wall and platelet release from thrombus injury The substance is degraded by fibrin, which can increase vascular permeability and cause osmotic pulmonary edema; 3 platelet consumption, anticoagulant effect of fibrin degradation products, and damage of blood vessel wall can cause intrapulmonary hemorrhage; 4 platelet release 5- Media such as HT contract the bronchi and affect lung ventilation. In recent years, the most striking effect of fibrin degradation products (FDP) has been found to be serious. In patients with burned or infected wounds, the level of FDP in the blood of patients with combined ARDS is much higher than that of patients without ARDS, and there is a certain parallel relationship between the disease of ARDS and the concentration of FDP. Injecting fibrin fragments D (FD) into the blood vessels of rabbits can cause Progressive peripheral blood thrombocytopenia, leukocyte infiltration in the interstitial lung, increased pulmonary vascular permeability and pulmonary insufficiency; such as injection of plasma albumin, fibrin and fibrin fragments E, the above lesions do not appear, it is likely to be on the small plate There are FD-specific membrane receptors, which bind to FD to activate platelets, causing platelet aggregation and release reactions. In addition, FD is also a chemotactic compound that promotes aggregation, adhesion and activation of neutrophils in the lungs, thereby aggravating Lung damage.

The permeability of normal pulmonary capillary endothelium is 10 times higher than that of alveolar epithelium. The change of pulmonary capillary permeability in ARDS is earlier than that of alveolar epithelium. Therefore, pulmonary interstitial edema occurs first, then alveolar edema occurs, and alveolar epithelial damage causes II. The reduction of surfactants produced by epithelial cells can lead to atelectasis and a functional shunt.

In systemic pathological processes such as sepsis, shock, etc., neutrophils adhere to the vascular endothelium and tissue damage caused by intravascular coagulation, not only in the lungs, but also in the liver, kidney, intestine, heart, endocrine organs, etc. Because of this, ARDS can not be regarded as only the lung damage, but the blood flow of the lung is the largest, and the area of the capillary bed is also the largest, so the lung is the most affected, so that the patient mainly presents with acute respiratory failure.

Changes in pulmonary respiratory function in adult respiratory distress syndrome

The external respiratory dysfunction caused by ARDS is mainly caused by alveolar ventilation-blood flow imbalance, plus diffuse dysfunction, which is characterized by hypoxemia respiratory failure. In extremely severe cases, hypercapnia may occur when total alveolar ventilation is reduced. Syndrome respiratory failure.

(a) alveolar ventilation - imbalance of blood flow ratio

As the type II alveolar epithelial cells are damaged, the production of surfactants is reduced, alveolar edema causes the surfactant to be diluted and destroyed, and the surfactants consumed by alveolar hyperventilation consume, resulting in increased alveolar surface tension and decreased lung compliance. Lead to atelectasis, resulting in functional shunt and true shunt, neutrophils and other media released by leukotrienes and other bronchoconstriction, and edema fluid block small airways, gas can cause pulmonary ventilation disorders and form a functional shunt , ARDS patients with a flow rate up to 30% of the pulmonary blood flow, pulmonary thrombosis, pulmonary vasoconstriction caused by vasoactive substances, and pulmonary vascular edema compression of the blood vessels, not only increase pulmonary vascular resistance to the pulmonary artery Increased pressure can increase dead space ventilation. Therefore, alveolar ventilation-blood flow imbalance is the most important cause of respiratory failure in patients.

(two) diffuse dysfunction

Pulmonary interstitial and alveolar edema, the formation of transparent membranes and hyperplasia of cells in the chronic phase and pulmonary fibrosis can increase the thickness of the diffuse membrane, leading to diffuse dysfunction.

(3) Reduction of alveolar ventilation

The distribution of pulmonary lesions in ARDS is uneven, restrictive ventilation caused by decreased lung compliance and obstructive ventilation caused by small airway obstruction, resulting in partial alveolar ventilation reduction, unaffected or lighter alveolar Compensatory ventilation is enhanced, and excessive carbon dioxide is discharged, so the patient's Paco2 is reduced. When the alveolar-capillary membrane damage is more extensive and severe, the total alveolar ventilation of the whole lung will be reduced, and CO2 will be retained and hypercapnia will occur. At this point Pao2 will drop further.

Pulmonary ventilation disorder, Pao2 reduces the stimulation of vascular chemoreceptors, pulmonary congestion and pulmonary edema stimulate the J sensor, causing respiratory distress in patients, [juxtapulmonary capillary receptor is located next to the alveolar capillaries, can feel the capillaries Stress is irritated, pulmonary congestion, and pulmonary edema are caused by stimuli and reflexes.

Adult respiratory distress syndrome prevention

The prognosis of ARDS is related to the correctness of the primary disease and the response to treatment. If the sepsis caused by severe infection is not controlled, the prognosis is very poor. The mortality of bone marrow transplantation is almost the same. 100%, if complicated with multiple organ failure, the prognosis is very poor, and is related to the number and speed of affected organs, such as 3 organ failure, lasting more than 1 week, the mortality rate can be as high as 98. After active treatment, if the continuous pulmonary vascular resistance increases, the ARDS caused by poor prognosis of fat embolism, after active treatment, mechanical ventilation can achieve 90% survival, acute pulmonary edema and ARDS caused by irritating gas, generally detached On-site, timely treatment, can also achieve better results, and other patients with ARDS after PEEP0.98 (10cmh20) treatment, PaO2 significantly increased the prognosis. Most of the patients with rapid ARDS relief can return to normal. Among the 40% of ARDS recoverers with abnormal lung function, 20% showed obstructive ventilation damage, 30% decreased diffuse, and PaO2 decreased during 20% exercise.

Complications of adult respiratory distress syndrome Complications bacterial pneumonia

Shortly after the illness in patients with acute respiratory distress syndrome, if the condition does not resolve after several days or weeks, complications of other organs may occur due to insufficient oxygen supply. Excessive hypoxia may cause serious complications such as renal failure. If not treated promptly, it can die due to severe hypoxia. Because of the low ability of patients with acute respiratory distress syndrome to prevent lung infection, bacterial pneumonia often occurs during the course of their illness.

Symptoms of adult respiratory distress syndrome Common symptoms Shortness of breath Cardiogenic respiratory distress, difficulty breathing, purpura

In addition to the primary symptoms such as trauma, infection, poisoning and other symptoms and signs, mainly manifested as sudden, progressive respiratory distress, shortness of breath, cyanosis, often accompanied by irritability, anxiety, sweating, etc., respiratory distress Features can not be improved with the usual treatment, nor can it be explained by other primary cardiopulmonary diseases (such as pneumothorax, emphysema, atelectasis, pneumonia, heart failure).

Adult respiratory distress syndrome

Early signs can be normal, or only the dry lungs, wheezing, late audible blisters, or tubular breath sounds.

X-ray chest radiographs can be abnormal in the early stage, or mildly interstitial changes, showing increased edge texture of the lungs, followed by patchy, and even into a large infiltrating shadow, bronchial inflated signs in large shadows .

Diagnosis and diagnosis of adult respiratory distress syndrome

Up to now, due to the lack of specific detection indicators, it has brought difficulties to early and early stages. Any basic diseases or incentives that may cause ARDS, once respiratory changes or blood gas abnormalities occur, should be alert to the possibility of intrinsic occurrence, establish a comprehensive clinical diagnosis. , laboratory and auxiliary examinations, necessary dynamic follow-up observations, and exclusion of other diseases of similar performance, for disease statistics and scientific research needs, must be based on established diagnostic criteria, various diagnostic criteria have been proposed over the years, very different European and American scholars discussed in 1992 at academic conferences in the United States and Europe, respectively, in 1992, and published in various magazines in 1994 on the definition and diagnostic criteria for ALI and ARDS.

ARDS diagnostic criteria

Except for the specified PaO/FiO 26.7 kPa (200 mmHg), the other indicators are the same as ALI.

In 1995, the National Conference on Critical and Critical Emergency Education (Lushan) proposed the diagnostic criteria for ARDS staging in China according to the above criteria:

1. There are primary causes of ARDS.

2. The diagnosis of a priori ARDS should have three of the following five items:

(1) Respiratory frequency 20 to 25 beats / min.

(2) (FiO20.21) PaO2 9.31 kPa ( 70 mmHg), > 7.8 kPa (60 mmHg).

(3) PaO2/FiO2 39.9 kPa ( 300 mmHg).

(4) PA-aO2 (FiO20.21) 3.32 to 6.65 kPa (25 to 50 mmHg).

(5) The chest radiograph is normal.

3. The diagnosis of early ARDS should have 3 of 6 items.

(1) Respiratory rate > 28 beats / min.

(2) (FiO20.21) PaO2 7.90 kPa (60 mmHg) > 6.60 kPa (50 mmHg).

(3) PaCO2 < 4.65 kPa (35 mmHg).

(4) PaO2/FiO2 39.90 kPa ( 300 mmHg) > 26.60 kPa (> 200 mmHg).

(5) (FiO21.0) PA-aO2>13.30 kPa (>100 mmHg) <26.60 kPa (<200 mmHg).

(6) Chest radiograph shows no alveolar consolidation or consolidation 1/2 lung field.

4. The diagnosis of advanced ARDS should have 3 of the following 6 items:

(1) Respiratory distress, frequency > 28 beats / min.

(2) (FiO20.21) PaO2 6.60 kPa ( 50 mmHg).

(3) PaCO2>5.98 kPa (>45 mmHg).

(4) PaO2/FiO2 26.6 kPa ( 200 mmHg).

(5) (FiO21.0) PA-aO2>26.6 kPa (>200 mmHg).

(6) Chest radiograph shows alveolar consolidation 1/2 lung field.

The disease must be differentiated from large inseparable atelectasis, spontaneous pneumothorax, upper respiratory airway obstruction, acute pulmonary embolism and cardiogenic pulmonary edema. The medical history and physical examination and chest x-ray examination can be used to identify the heart and lungs. Patients with edema have increased difficulty in breathing when lying in bed, coughing pink foamy sputum, wet sputum at the bottom of both lungs, and better treatment for cardiotonic and diuretic; if there is difficulty, it can be determined by measuring PAwP and super-productive check Identification.

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