Increased lung water content

Introduction Pulmonary edema and pathological state of increased lung water content caused by fluid exchange dysfunction between blood vessels and tissues in the lung, regardless of the cause of pulmonary edema, the respiratory pathophysiology is substantially the same, that is, the liquid is stored in the lung and Gas exchange disorders, lung compliance decreased, ventilation / blood flow imbalance, leading to hypoxemia. The clinical manifestations were sudden onset, difficulty in breathing, hair set, frequent cough, a lot of foamy sputum, diffuse wet warm sounds in both lungs, and X-ray showed a butterfly-shaped blushing shadow on both lungs. Pulmonary edema can seriously affect respiratory function, which is a common respiratory emergency. The target of treatment is aimed at pathophysiology and basic diseases. Early diagnosis and treatment play a decisive role in the prognosis and outcome of pulmonary edema.

Cause

The causes of pulmonary edema are divided into the following six categories according to the pathogenesis:

(1) Increased pulmonary capillary pressure

Seen in various causes of left heart failure (mitral stenosis, hypertensive heart disease, coronary heart disease cardiomyopathy, etc.), excessive infusion, pulmonary venous occlusive disease (pulmonary venous fibrosis, congenital pulmonary vein stenosis, mediastinal tumor, mediastinum) Granuloma, fibrous mediastinal inflammation, etc. can cause pressure in the pulmonary capillaries, causing extravasation of the blood vessels to produce pulmonary edema.

(B) increased pulmonary capillary permeability

Biological and physicochemical substances can directly and indirectly damage permeable membrane cells, leading to pulmonary edema. Common clinical reasons are: bacterial or viral pneumonia, radiation pneumonitis, allergic alveolitis, inhaling harmful gases such as phosgene and ozone. , chlorine, nitrogen oxides, uremia, oxygen poisoning, DIC, severe burns, drowning, etc.

(three) plasma colloid osmotic pressure reduction

Such as liver disease, kidney disease, protein-losing enteropathy, dystrophic hypoproteinemia, etc., when the plasma protein drops to 5 g / L or albumin drops below 2g / L, can lead to pulmonary edema.

(four) lymphatic dysfunction

When some lesions such as silicosis cause poor drainage of the lymphatics in the lungs, the interstitial lung may have stagnation of water and pulmonary edema.

(5) Increased negative pressure in the tissue gap

Sudden occlusion of the atmosphere, or removal of a large number of pneumothorax and pleural effusion in a short period of time can cause the lung pressure to drop suddenly, forming a negative pressure on the lung tissue and attracting capillaries, thus causing pulmonary edema.

(6) Comprehensive factors or unexplained acute respiratory distress syndrome, high altitude pulmonary edema, neurogenic pulmonary edema, overdose of anesthesia, pulmonary embolism, sub-pain, electric shock cardioversion.

mechanism

There are four cavities in the anatomy of the lungs, namely the pulmonary vascular lumen, the pulmonary interstitial, the lymphatic vessels and the alveoli, with liquid movement exchange between them and maintaining a dynamic balance. The movement of this liquid depends on the physico-mechanical effects of the four cavities and the permeability of the alveolar-capillary membrane. Under normal circumstances, the fluid is continuously filtered out of the pulmonary capillaries into the interstitial lung, while the lymphatic system continuously draws fluid out of the interstitial, and through the rhythmic contraction of the lymphatic vessels, the fluid is returned to the vein through the right thoracic duct. In some pathological conditions, such as left heart failure, excessive infusion, increased pulmonary capillary pressure, or hypoproteinemia of various causes, the plasma colloid osmotic pressure is reduced, so that the liquid movement balance in the lung is abnormal, filtered out More fluid than recovery, the formation of pulmonary edema, this mechanism is called "high pressure pulmonary edema."

Hypoxia, inflammation, toxic irritation, radiation damage, and vasoactive substances can cause damage or reaction of pulmonary capillary endothelial cells, increase the permeability of capillary wall, and produce pulmonary edema, called "osmotic pulmonary edema". . When the lymphatic vessel function is normal, its compensatory ability is very large, but when it exceeds its saturation amount, or due to pathological state, it causes lymphatic dysfunction, reduces drainage, or can not fully exert its compensatory ability, it will form pulmonary edema. The intrapulmonary edema fluid initially accumulates in the interstitial space between the alveolar capillaries. This stage is "interstitial pulmonary edema"; or the interstitial fluid is too much, and the tension is increased, the capillary endothelium and alveolar epithelium can be removed from the base. The membrane peels off, causing more fluid to ooze out and allowing the fluid to enter the alveoli, forming "alveolar pulmonary edema."

an examination

Related inspection

Pulmonary diffusion function measurement (DL) intrapulmonary shunt (Qsp, Qs/Qt) serous effusion serous effusion cell count blood pH (pH)

First, medical history

There are symptoms depending on the primary disease. Such as physical and chemical stimulation caused by acute bronchial inflammation, cough, asthma, dyspnea, etc.; pneumonia caused by cough, cough, fever and other respiratory infections; left heart failure caused by heart palpitations, shortness of breath. Precordial discomfort, nocturnal dyspnea, etc.; mediastinal tumors have signs of shortness of breath and superior vena cava obstruction; hypoproteinemia causes malnutrition, clinical symptoms of liver and kidney disease; oxygen poisoning caused by long time Inhaled a high concentration (60%) oxygen history.

Second, physical examination

The early manifestations of pulmonary edema are chest tightness, cough, difficulty in breathing, shallow breathing, irritability, light or inconspicuous hair, and generally no wet sound in the lungs; small bronchial lumen is narrowed due to compression of interstitial edema fluid. Or due to new membrane edema, the lungs can smell wheezing or dry sound absorption. Symptoms in the alveolar edema stage are aggravated; breathing difficulties are severe, forced sitting, pale and heart-sweat. Bun, cough and cough a lot of white or bloody foamy sputum, the lungs are covered with wet sound, and often have heart rate increased arrhythmia, or signs of galloping horses. The disease continues to progress, and severe hypoxia, acid-base balance disorders, shock, and mental disorders can occur.

Third, laboratory inspection

Due to different causes, the corresponding indicators change with the primary disease, such as infectious diseases, blood white blood cells, hypoproteinemia caused by decreased total protein in the blood, albumin decreased, or changes in liver and kidney function indicators. Arterial blood gas analysis changes during pulmonary edema. There is no change in blood oxygen partial pressure in the early stage of interstitial pulmonary edema. Due to alveolar hyperventilation, the partial pressure of carbon dioxide is reduced, resulting in respiratory alkalosis. When the disease progresses to alveolar edema, alveolar ventilation Functional and diffuse dysfunction, ventilatory / blood flow imbalance, it causes hypoxemia and increased blood carbon dioxide partial pressure, respiratory acidosis, metabolic acidosis can also occur.

Fourth, equipment inspection

1. X-ray examination: It is very important for clinical diagnosis and can be used to observe the distribution area of pulmonary edema. The characteristic of interstitial pulmonary edema is that the lung texture is thicker and thicker, the blur is unclear, the lung field transmittance is low and fuzzy, and the pulmonary leaflet interval is widened to form the KER-ley B line. Alveolar edema is mainly characterized by acinar-like densification shadows, which are merged into irregular flaky fuzzy shadows. The diffuse distribution of the oil lung door extends outwards and gradually becomes lighter, forming a typical butterfly-like shadow. Sometimes there are asymmetrical large shadows in the lower reaches of the two lungs, which are not easily distinguished from inflammation.

2, chest CT and chest MRI: CT can be used for quantitative diagnosis of M can determine the water content of the lung according to the strength of the signal, and the liquid flowing in the blood vessels is almost not developed, thus distinguishing between pulmonary congestion and pulmonary interstitial edema. But both are expensive and not suitable for routine applications.

3, pulmonary function test: interstitial and alveolar pulmonary edema caused by decreased lung capacity, so there is a decrease in tidal volume and vital capacity, functional residual capacity decreased, but exhaled time is slightly prolonged, diffuse disorder and other changes.

4, radionuclide examination: blood perfusion lung scan and nebulization inhalation lung scan, observe the clearance rate of the second albumin, lower than those without pulmonary edema. It is also useful for perfusion lung scan with TC-human hemagglutinin microcapsule or In-transferrin. As the pulmonary vascular permeability increases, the marker protein diffuses out of the blood vessel, is lost from the blood vessel, and accumulates in the pulmonary interstitium. By measuring the intensity of the Y-ray outside the chest wall, the vascular protein throughput can be effectively determined. This method is especially suitable for osmotic pulmonary edema.

5, cardiac catheterization: the use of floating heart catheter to measure pulmonary artery pressure, the average pressure of normal pulmonary artery is 1.33 - 2.4 kPa (10-18nnHL) pulmonary systolic blood pressure on average 2. L-4.0 kPa (16-30), pulmonary diastolic blood pressure averaged 0.67-2 kPaO (5-15) pulmonary artery wedge pressure averaged 0.67-l.6 kPa is a 12 M person in the pulmonary artery wedge pressure higher than 2.67 kPa (20 It indicates the presence of pulmonary edema. The disease is also often increased due to increased pulmonary blood flow resistance caused by pulmonary interstitial fluid and hypoxemia caused by pulmonary edema. Cardiac catheterization is helpful for cardiogenic and non-cardiac origin. Identification of pulmonary edema in patients with wide cardiac origin, pulmonary wedge pressure greater than 1.6 kPa (12 mmHg), pulmonary artery diastolic pressure and pulmonary wedge pressure difference is less than 0.67 kPa6 (5 mmHg); non-cardiac pulmonary wedge pressure is often less than 1.6 kPa (12 mmHg) ), the difference between pulmonary artery diastolic pressure and pulmonary wedge pressure is greater than 0.67 kPa (5 mmHg).

Differential diagnosis

Increased lung water content is differentiated from the following symptoms:

1, lung stagnation of blood: difficulty breathing, two lungs wet rales, cough pink foam sputum and even hemoptysis. The clinical features of left heart failure are mainly due to pulmonary blood stasis and pulmonary edema caused by left atrial and/or right ventricular failure. The clinical features of right heart failure are caused by systemic venous stasis and water and sodium retention due to right atrium and/or right ventricular failure.

2, lung suppuration: the disease is often accompanied by eye disease. The sputum suffering from the disease, eyeball congestion, edema, sag, purulent secretions, and tofu slag-like necrotic tissue covering the eyeball, resulting in blindness of both eyes. Anatomical pathology, the lungs are dark purple, with hard nodules and cystic lesions, or abscesses of varying sizes. Sickness of breathing is difficult. When breathing, the head tends to rise upwards, the mouth is large, or the head and neck are extended out of the water. The movement is sluggish and sluggish. It often inhabits the shore or the table; the appetite is obviously reduced.

3, increased pulmonary blood: common in aortic valve insufficiency, usually asymptomatic, but once the disease, the disease progresses rapidly, the left heart bulge is caused by aortic valve insufficiency, pulmonary blood is increased due to high left ventricular pressure , causing high left atrial pressure, and then causing lung stagnation.

4, pulmonary hydrops medicine is usually called "the pleural effusion", water is deposited outside the lungs, it can be caused by infection and inflammation (such as: pneumonia, tuberculosis can be combined with pleural effusion), but also some autoimmune diseases Caused (such as: lupus erythematosus), there are many lung diseases will be combined with pleural effusion. It may be just coughing, especially in the middle of the night, coughing, unable to lie flat as a characteristic, often mistaken for tracheal inflammation or cold and not paid attention. In fact, if you have difficulty breathing, shortness of breath, paroxysmal nocturnal dyspnea, sitting breathing, or even sitting and sleeping, etc., do not ignore it. These are one of the clinical symptoms of acute hydronephrosis.

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