High altitude pulmonary edema

Introduction to high altitude pulmonary edema High altitude pulmonary edema refers to the recent arrival of the plateau (generally 3,000 meters above sea level), difficulty breathing during rest, chest tightness, cough, cough, white or pink foam, and the patient feels weak or reduced mobility. basic knowledge The proportion of illness: 0.0035% Susceptible people: no special people Mode of infection: non-infectious Complications: heart failure

Causes of high altitude pulmonary edema

(1) Causes of the disease

The disease is often caused by upper respiratory tract infection, fatigue, excessive physical activity and cold. In recent years, the incidence of acute high altitude pulmonary edema has been significantly reduced in China due to improved living conditions such as transportation, housing and medical care in the plateau.

(two) pathogenesis

The pathogenesis of high altitude pulmonary edema is not clear, and it is difficult to explain its pathogenesis by a single mechanism. The following factors may be related to the pathogenesis of this disease (Figure 1).

Pulmonary hypertension

By right heart catheterization and color Doppler echocardiography, the pulmonary arterial pressure of the high altitude pulmonary edema is significantly higher than that of the normal person with the same altitude at the early stage or recovery stage, and the pulmonary circulation pressure of some susceptible people can exceed the systemic circulation pressure. Pulmonary hypertension is the basic factor in the occurrence of this disease. The pulmonary artery pressure of a patient with high altitude pulmonary edema and cerebral edema was measured at 4700m using right heart catheter. The average pulmonary artery pressure was 41.25mmHg and the recovery period was 33.7mmHg. Hultgren underwent catheterization of 5 cases of re-entry plateau pulmonary edema with an average pulmonary artery pressure of 45 mmHg, of which 1 case was as high as 66 mmHg, but pulmonary wedge pressure and left atrial pressure were basically normal. Pulmonary hypertension was caused by hypoxic pulmonary arteriole contraction. However, there are still many disputes about how it causes pulmonary edema. Hultgren suggested that hypoxic pulmonary vasoconstriction causes heterogeneous obstruction of the pulmonary vascular bed, resulting in reduced or blocked regional microcirculation blood flow. Capillaries in unobstructed areas are susceptible to pulmonary hypertension and high flow and passive expansion, increased blood volume, and accelerated blood flow Resulting in increased capillary blood volume and increased pressure, liquid leakage due to a sudden pressure increase in pulmonary microcirculation can directly damage endothelial cells (or) alveolar epithelial cells, and leading to increased vascular permeability.

2. High intrapulmonary perfusion

The typical X-ray signs of patients with high altitude pulmonary edema are scattered flaky or cloud shadows in the lungs. This may be caused by uneven occlusion of the pulmonary vascular bed and uneven distribution of blood flow in the lungs. It has been reported that the congenital side People with pulmonary artery defects are more sensitive to pulmonary edema because the total blood output from the ventricle enters one side of the lung, and the lungs are excessively perfused. In addition, after the vasodilator is used in patients with high altitude pulmonary edema, pulmonary artery pressure, especially microcirculation pressure and The blood flow is significantly reduced. These data are sufficient to show that excessive fluid in the lung is an important factor in the occurrence of high altitude pulmonary edema. The reason is:

(1) Acute hypoxia causes sympathetic excitation, peripheral vasoconstriction, redistribution of blood flow, and a significant increase in pulmonary blood flow.

(2) Hypoxia causes uneven contraction of pulmonary muscular arterioles, while non-muscular blood vessels such as Precapillary arteriole are expanded by the impact of pulmonary hypertension, thus increasing blood flow in the area and appearing in the lungs. Overperfusion.

(3) Due to the obstacles of coagulation and fibrinolysis mechanism, micro-thrombus formation in the small arterioles and capillaries of the lungs, so that the blood flow is blocked, causing the whole blood of the lungs to transfer to the unblocked area, causing blood flow of the local capillaries. Sudden increase in pressure and exudation of water to the stroma and alveoli. In the past, plateau pulmonary edema was a low-protein hydrostatic edema caused by pulmonary hypertension. Modern studies have shown that it is a high-flow. High-permeability edema caused by high flow rate and high pressure, Schoene and other bronchoscopy, the amount of protein in the alveolar lavage fluid of patients with high altitude pulmonary edema is significantly higher than that of the control group, and contains a lot of red blood cells, white blood cells and Macrophages, autopsy found that the amount of protein in the pulmonary edema fluid increased significantly, alveolar scattered bleeding, fibrin exudation and transparent membrane formation in the blood vessel wall, the mechanism of increased vascular permeability is not fully understood, West observed with electron microscopy When the rabbit capillary pressure exceeds 50 mmHg, the capillary endothelium and alveolar epithelium are severely damaged, and the vascular permeability is clear. Significantly increased, it is currently believed that microvascular stenosis and pulmonary hypertension caused by high intrapulmonary flow can cause mechanical damage to the capillary wall, and thus vascular endothelial cells, platelets, white blood cells, etc. release various kinetic factors (drived factor) Such as nitric oxide, endothelin-1, etc., these factors will lead to stress failure of the capillary membrane, telangiectasia, thinning of the wall, enlargement of endothelial cell voids, and increased vascular permeability.

3. Ventilation regulation is abnormal

Compared with the plateau testers, unaccustomed patients showed that HVR should be inactivated, and Matsuzawa et al studied the hypoxia and hypercapnia ventilatory reactions of 10 patients with susceptibility to high altitude pulmonary edema. As a result, the HVR of the patient group should be sloped (VE/ SaO2) was significantly lower than the control group (P<0.01), but there was no significant difference in high-carbonation ventilation between the two groups. Selland examined 8 patients with susceptibility to high altitude pulmonary edema, and 5 of them had a decrease in HVR. Generally speaking, the human body After entering the plateau, due to the hypoxic stimulation of the surrounding chemoreceptors, the lung ventilation increased, and the alveolar oxygen partial pressure increased. However, when the ventilation reaction was inactivated, the alveolar oxygen partial pressure decreased due to the increase of ventilation when the hypoxic environment was exposed, resulting in Severe hypoxia, especially at night, more severe hypoxemia; this is consistent with high altitude pulmonary edema at night, but some HVR-negative people do not develop pulmonary edema after reaching the plateau, therefore, HVR for high altitude pulmonary edema The occurrence may play a secondary role.

4. Genetic factors

Recently, Japanese scholar Hanaoka (1998) found that the incidence of human leukocyte antigen (HLA) is significantly higher in patients with susceptibility to high altitude pulmonary edema compared with normal people. HLA is a polymorphic membrane protease on the cell surface that controls cell surface antigens. Produced, is a very complex gene system, it has many subtypes including A, B, C, D, D subtypes including DR, DQ and DP 3 sites, while the genetic locus controlling human immune response is in the D position Point, the two subtypes of HLA-DR6 and/or HLA-DQ4 in patients with high altitude pulmonary edema were significantly higher than those in the control group (P<0.01), and the former in the DR6 and/or DQ4 positive patients were higher than the negative ones. Hypoxic pulmonary vasoconstriction (pulmonary hypertension) and lower HVR suggest that there may be some intrinsic link between HLA and pulmonary hypertension. Previously, pulmonary arteries caused by primary pulmonary hypertension, collagen disease and AIDS have been found. High blood pressure is related to HLA, especially DR6, which may be related to immune inheritance. Whether the increase of HLA in patients with high altitude pulmonary edema can also reflect the fact that this disease is related to immune inheritance and needs to be studied.

The main pathological changes of acute high altitude pulmonary edema are pulmonary edema, pulmonary embolism and pulmonary infarction. The lung tissue is highly congested and edema. The weight of the lung is 2 to 4 times larger than that of normal people. The trachea and bronchi are filled with pink foam liquid, and the alveolar cavity is filled with edema fluid. , alveolar wall thickening, pulmonary arterioles and telangiectasia, congestion and rupture, extensive microthrombus formation in the lumen, alveolar fibrin exudation and transparent membrane formation, similar to neonatal transparent membrane, left heart is normal; right The atria, the right ventricle and the main pulmonary artery dilate.

Plateau pulmonary edema prevention

Although a lot of explorations have been made on the prediction of susceptibility, but the ideal method has not been found. The author believes that hypoxic ventilation, pulmonary impedance differential waves, lung diffusion capacity, changes in oxygen saturation after maximum exercise, etc. The disease has a certain value. Before entering the mountain, it should adapt to the psychology and physical fitness. If there are conditions, it is best to carry out intermittent hypoxia stimulation and exercise in the low pressure chamber, so that the body can switch to the plateau hypoxia from the plain. The environment has a certain degree of physiological adjustment. It is currently considered that in addition to being particularly susceptible to hypoxia, stepped uphill is the safest and safest method to prevent acute altitude sickness. Experts suggest that if you enter the mountain, you need to enter more than 4000m. When the plateau is used, it should stay at 2500~3000m for 2~3 days, and then the daily rising speed should not exceed 600~900m. After reaching the plateau, avoid drinking and taking sedative hypnotics for the first two days. Do not do heavy physical activity, but light. Degree activities can promote habits, avoid cold, pay attention to heat preservation, advocate multi-use high-carbohydrate diet, use acetazolamide, dexamethasone, acanthopanax before going up the mountain Compound Codonopsis, sulpiride and other drugs may be effective for preventing and mitigating the symptoms of acute mountain sickness.

High altitude pulmonary edema complications Complications heart failure

Concurrent heart failure.

Symptoms of high altitude pulmonary edema Common symptoms: pale and tired, low fever, dry cough, sitting, breathing, pink, foam, shock, lung disease, long-term lung disease, wet, cold, snoring, coma

Symptom

The disease usually occurs within 24 to 72 hours of reaching the plateau. It is often extremely fatigued based on the symptoms of acute mountain sickness, severe headache, chest tightness, palpitations, nausea and vomiting, difficulty breathing and frequent dry cough. It is difficult to fall asleep at night, lips and nails. Bed bun, heart rate is faster, breathing is fast and shallow, respiratory rate can reach 40 times / min, some patients with cold and low heat, pale, cold skin, with the development of the disease, breathing difficulties, a small number of patients can not sit flat Breathing, coughing out of the foam, initially white or light yellow, then become pink, the amount can be from the mouth and nostrils, nervous system symptoms are blurred, hallucinations, feeling slow, severe coma.

2. Signs

The most important sign is that the lungs hear snoring and wet voices. In severe cases, the sound can be heard only by the ear sticking to the chest wall. The voice is most common on the bottom of the lungs, but it can only appear on one side. In the pulmonary valve area, the second tone is hyperthyroidism. In some patients, the anterior ventricular systolic murmur can be heard. In the right heart failure, the jugular vein is engorged, the edema, the liver is big and tender, and Hultgren counts 150 patients. Heart rate >120 beats / min was 26.7%, breathing >24 beats / min 26%, blood pressure >150/90mmHg 11%, body temperature 38 °C was 20%, fundus examination retinal varices, arterial spasm, optic disc congestion, Scattered spotted or flaming bleeding spots.

Examination of high altitude pulmonary edema

1. Analysis of acute altitude sickness and normal blood gas at an altitude of 4558m:

2. X-ray findings of the lungs appear earlier than clinical signs and have a greater diagnostic value. The lung field transmittance is weakened and there are scattered flaky or flocculent blurred shadows. The near lung door is more likely to form a butterfly wing shape; the lesion may be localized or bilateral lung field asymmetry; Wide range, blended into cotton balls.

3, laboratory tests can be based on the condition of blood, urine routine, blood electrolytes and blood gas analysis, liver and kidney function, electrocardiogram and other examinations.

Diagnosis and differentiation of high altitude pulmonary edema

diagnosis

Diagnosis of people who quickly enter the plateau above 3000m above sea level, severe headache, extreme fatigue, severe cyanosis, difficulty breathing (quiet), cough, coughing white or pink foam, hearing wet voice in both lungs, chest X-ray The smear or cloud infiltrates the shadow and the diagnosis is established. Attention should be paid to early diagnosis. On the basis of acute high altitude disease, there may be incentives such as sensation, and one of the following conditions should consider the possibility of the disease: 1 difficulty breathing, cyanosis, coughing, mucus or serous foam. 2 Night awakening due to paroxysmal dyspnea, irritability, cough and convulsions. 3 heart rate significantly increased, heart sounds strong, P2 hyperthyroidism or division, the pre-cardiac area has a systolic murmur of level II or above, and occasionally gallop. Pulmonary auscultation has scattered voices or snoring.

Differential diagnosis

Differential diagnosis of this disease is easily confused with pneumonia or lung infection. In general, pneumonia often has high fever, obvious symptoms of poisoning, increased white blood cell count, yellow or rust color sputum; and high altitude pulmonary edema, cyanosis, low body temperature or low fever, white blood cell increase is not significant, there is a typical white or pink foam , Typical lung shadows on the X-ray can be identified. It should be differentiated from edema caused by bronchial asthma and other causes. Such as a variety of organic heart disease caused by cardiogenic pulmonary edema, pulmonary edema caused by lung infections, and other physical and chemical factors caused by osmotic pulmonary edema.

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