Acute respiratory distress syndrome

Introduction Acute respiratory distress syndrome (ARDS) refers to acute progressive hypoxic respiratory failure caused by various intrapulmonary and extracranial factors other than cardiogenic, clinically manifested as acute respiratory distress, refractory hypoxemia Symptoms and pulmonary edema. ARDS is a continuous pathological process with an early stage of acute lung injury (ALI). ARDS can induce or combine MODS or MOF. ARDS is a typical manifestation of the development of acute lung injury to the later stage. The disease has a rapid onset, rapid development, poor prognosis, and a mortality rate of more than 50%.

Cause

There are many primary diseases or underlying diseases or virulence factors that induce ARDS, which are summarized as follows:

1, shock. Various types of shock, such as infectious, hemorrhagic, cardiogenic and allergic, especially septic shock caused by Gram-negative bacilli sepsis.

2, trauma. Multiple trauma, pulmonary contusion, craniocerebral trauma, burns, electric shock, fat embolism, etc.

3. Infection. Severe infection of lungs or systemic bacteria, viruses, fungi, protozoa, etc.

4. Inhale toxic gases. Such as high concentration of oxygen, ozone, ammonia. Fluorine, chlorine, nitrogen dioxide, phosgene, aldehydes, smoke, etc.

5, aspiration. Gastric juice (especially pH <2.5 water, amniotic fluid, etc.).

6, overdose. Barbiturates, salicylic acid, hydrochlorothiazide, colchicine, arabinose, heroin, methadone, magnesium sulfate, terbutaline, streptokinase, fluorescein, and the like. The ADRS caused by poisoning of poisonous drugs has been reported in China and it is worth noting.

7, metabolic disorders. Liver failure, uremia, diabetic ketoacidosis. Acute pancreatitis 2%-18% complicated by acute respiratory distress syndrome.

8, blood system diseases. A large number of people lose blood and wrong blood type blood transfusion, DIC and so on.

an examination

Related inspection

Intrapulmonary shunt (Qsp, Qs/Qt) resting ventilation per minute (VE) Respiratory muscle function measurement Impulsive pulmonary function (IOS) Alveolar ventilation per minute (VA)

Pulmonary function test

(1) The spirometer measures lung capacity and vital capacity, and residual gas and functional residual gas are reduced. Increased respiratory dead space, if the dead volume / tidal volume (VD / VT) > 0.6, suggesting that mechanical ventilation is required.

(2) Determination of lung compliance At the bedside, it is often the total compliance of the thoracic lung. Patients with end-expiratory positive pressure ventilation can calculate the dynamic compliance (Cdyn) compliance test according to the following formula. Efficacy, and has practical value for monitoring the presence or absence of complication such as pneumothorax or atelectasis.

(3) Arterial blood gas analysis PaO2 reduction is a common indicator for ARDS diagnosis and monitoring. According to the arterial blood oxygenation analysis, the alveolar arterial oxygen pressure difference (PA-aO2), the arterial blood shunt (Qs/Qt), the respiratory index (PA-aO2/PaO2), and the oxygenation index (PaO2/FiO2) can be calculated. Indicators are very helpful in diagnosing and evaluating the severity of a disease. For example, Qs/Qt increase is advocated for disease grading, with more than 15%, 25% and 35%, respectively, divided into light, medium and heavy severity. The respiratory index reference range is 0.1 to 0.37, and >1 indicates a significant decrease in oxygenation function. >2 often requires mechanical ventilation. The oxygenation index reference range is 53.2 to 66.7 kPa (400 to 500 mmHg), and the ARDS is reduced to 26.7 kPa (20 mmHg).

2. Pulmonary vascular permeability and hemodynamics

(1) Determination of pulmonary edema fluid protein ARDS, pulmonary capillary permeability increased, water and macromolecular protein into the stroma or alveolar, so that the ratio of protein content of edema fluid to plasma protein content increased, if the ratio of > 0.7, consider ARDS , <0.5 for cardiogenic pulmonary edema.

(2) Alveolar-capillary membrane permeability (ACMP) assay using dual-nuclear in vivo labeling technique, 113 indium (113In) autologous labeled transferrin to determine the amount of protein accumulation in the lung, while 99m (99mTe) Autologous labeling of red blood cells to correct the effects of blood flow distribution in the chest. The ratios of pulmonary heart radiation counts of 113 indium and 99 m were calculated, and the plasma protein accumulation index was obtained by observing the change of 2 hours. The healthy person reference value is 0.138×10-3/min.

(3) Hemodynamic monitoring By introducing a four-chamber floating catheter, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), pulmonary circulation resistance (PVR), PVO2, CVO2, Qs/Qt, and The measurement of cardiac output (CO) by hot dip method is not only valuable for diagnosis and differential diagnosis, but also an important monitoring indicator for mechanical ventilation therapy, especially the effect of PEEP on circulation function. The mean venous arterial pressure in patients with ARDS was >2.67 kPa, pulmonary arterial pressure and pulmonary capillary wedge pressure difference (PAP-PCWP) increased (>0.67 kPa), and PCWP was 1.57 kPa (16 cmH2O), which was acute left heart failure, and ARDS was excluded. .

(4) Determination of pulmonary extravascular water content is currently measured by dye double trace dilution method, 10 ml of 5 cm guanidine green dye glucose solution is injected from the central vein or right heart catheter tube, and then recorded in the femoral artery through a catheter connected to the thermistor. The thermodilution curve is used to measure the dye dilution curve with a densitometer, and the amount of lung water can be calculated by computer processing. It can be used to determine the degree of pulmonary edema, outcome and efficacy, but certain equipment conditions are required.

Differential diagnosis

Diagnostic points

Any of the following five items can be diagnosed as ALI or ARDS.

1. High risk factors for morbidity, such as severe infection, trauma, shock and aspiration.

2. Acute onset, respiratory rate and/or respiratory distress.

3. X-ray chest radiograph shows that the lungs have infiltration shadows.

4. Pulmonary capillary wedge pressure 18mmHg or clinically excluded cardiogenic pulmonary edema.

Differential diagnosis

It needs to be distinguished from the following symptoms: shortness of breath: shortness of breath (shortness of breath), a clinically common respiratory symptom, often caused by respiratory diseases or early symptoms of respiratory insufficiency caused by organs or tissue lesions that affect breathing. The condition is further aggravated by respiratory distress or difficulty breathing, and even respiratory failure and life-threatening. Because of the anatomical and physiological characteristics of the respiratory system, infants are more prone to shortness of breath and respiratory distress once the disease affects breathing.

Acute Respiratory Distress Syndrome: Acute Respiratory Distress Syndrome (ARDS) is a type of acute respiratory failure. Due to various reasons (except left heart failure), dysfunction of fluid exchange in the vascular tissue of the lungs leads to an increase in lung water content and lung compliance. Sexual reduction, alveolar collapse, ventilation, imbalance of blood flow, with severe hypoxemia and extreme difficulty in breathing are typical symptoms.

Cardiogenic respiratory distress: refers to cardiogenic dyspnea caused by factors such as increased hydrostatic pressure, common in cardiac edema caused by left ventricular dysfunction, and thus caused by respiratory failure. Cardiac dyspnea is mainly caused by left heart and/or right heart failure. The mechanism of the two is different. The dyspnea caused by left heart failure is more serious. Breathing increases, difficulty, respiratory sputum often occurs immediately after birth or within a few hours, the upper and lower sternum inspiratory depression, the nose flaps. The extent of atelectasis and the severity of respiratory failure are exacerbated. In severe respiratory distress syndrome, fatigue of the diaphragm and intercostal muscles leads to carbon dioxide retention and respiratory acidosis. Because blood can't be exchanged for oxygen through the atelectasis (such as right to left shunt in the lung), infants develop hypoxemia, leading to metabolic acidosis.

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