Pulmonary embolism

Introduction Pulmonary embolism refers to the pulmonary artery and its branches are blocked by emboli, which causes the blood flow of the corresponding donor lung tissue to be interrupted, and the pathological changes of lung tissue necrosis are called pulmonary infarction. Embolons are often derived from the systemic venous system or the thrombus produced by the heart. Elderly people stay in bed for a long time, bed after surgery, postpartum and traumatic venous thrombosis and embolism leading to pulmonary infarction. The disease is a serious risk, often sudden death, the disease is not uncommon, clinical error, missed diagnosis, often confirmed from autopsy.

Cause

(a) thrombosis Pulmonary embolism is often a complication of venous thrombosis. The embolus is usually derived from the deep veins of the lower extremities and pelvis and causes embolism by circulation to the pulmonary artery. But rarely from the upper limbs, head and neck veins. Stasis of blood flow, increased blood coagulation and venous endothelial injury are contributing factors to thrombosis. Therefore, trauma, long-term bed rest, varicose veins, venous cannula, pelvic and hip surgery, obesity, diabetes, contraceptives or other causes of hypercoagulability, etc., are prone to induce venous thrombosis. Early thrombosis and the role of the fibrinolytic system, the highest risk of pulmonary embolism in the first few days of thrombosis.

(B) heart disease is the most common cause of pulmonary embolism in China, accounting for 40%. Several times, all kinds of heart disease, combined with atrial fibrillation, heart failure and subacute bacterial endocarditis have a higher incidence. Right heart chamber thrombosis is most common, and a few are also derived from the venous system. In addition to subacute bacterial endocarditis, bacterial emboli can also be caused by pacemaker infection. The former infectious emboli is mainly from the tricuspid valve. Occasionally, the mitral palsy of the congenital heart can be diverted from the left heart to the right heart and reach the pulmonary artery.

(C) pregnancy and childbirth pulmonary embolism in pregnant women several times the age of non-pregnant women, the highest incidence of postpartum and caesarean section. Increased intra-abdominal pressure during pregnancy and hormonal relaxation of vascular smooth muscle and pelvic vein pressure can cause slow venous blood flow, alter blood rheology and aggravate venous thrombosis. In addition, with the increase of blood coagulation factors and platelets, the plasma pro-plasmin-plasmin proteolytic system activity is decreased. However, these changes were not significantly different from those without thromboembolism. Amniotic fluid embolism is also a serious complication during childbirth.

(5) Other rare causes are fat embolism caused by long bone fractures, air embolism caused by accidents and decompression sickness, parasites and foreign body embolism. In the absence of significant triggering factors, a reduction in hereditary anticoagulant factors or an increase in plasminogen activator inhibitors should also be considered.

an examination

Related inspection

Chest CT examination

Blood gas analysis

At the time of embolization, due to V/Q ratio imbalance and hyperventilation, hypoxemia and hypocapnia are often associated, but in the case of small pulmonary embolism or chronic pulmonary embolism, normal arterial oxygen partial pressure and Arterial carbon dioxide partial pressure, at this time can not rule out further pulmonary embolism examination. When hypoxemia is present, arterial oxygen partial pressure is proportional to the extent of embolism and pulmonary hypertension.

2. Determination of plasma D-dimer

D-dimer is a cross-linked fibrin degradation product that occurs only when fibrinogen formation and decomposition are in a stable state. If the plasma D-dimer concentration>500g/L is used as the positive threshold for diagnosing vascular embolization, it has good sensitivity for judging pulmonary embolism, and maintains high sensitivity after 3 and 7 days, but its specificity. Sexually low, because many diseases can be related to the formation and degradation of fibrin, such as myocardial infarction, tumors, infections or inflammatory diseases. Its specificity for diagnosing pulmonary embolism is also affected by age.

3. ECG

Electrocardiographic abnormalities of pulmonary embolism are more common, but lack specificity. ECG abnormalities can be found in 97% of large pulmonary embolisms and 77% of sub-large pulmonary embolisms, which occur several hours after onset and often disappear within a few weeks. Therefore, dynamic electrocardiogram observation is needed for pulmonary embolism. The most common change is the T wave inversion and ST segment depression of the V1 to V2 leads. A more significant change is the deepening of the S-wave of the I lead, the deep Q wave and the inverted T wave of the III lead, the so-called SIQIIITIII type similar to the old myocardial infarction. Other changes include right-axis deviation, clockwise transposition, complete and incomplete right bundle branch block, right ventricular hypertrophy, pulmonary P-wave and low voltage, and arrhythmias can also occur.

Differential diagnosis

Cardiopulmonary embolism can cause changes in cardiopulmonary function, the extent of the change depends on the extent of pulmonary occlusion, speed, and original cardiopulmonary function. Light heart and lung function can be no significant changes, severe cases can lead to hypoxemia, hypocapnia, alkaliemia, increased pulmonary circulation resistance, pulmonary hypertension, acute right ventricular dysfunction. X-ray examination can show typical signs such as patchy infiltration, atelectasis, and diaphragmatic elevation. Generally speaking, when pulmonary vascular bed obstruction is >30%, the mean pulmonary artery pressure starts to rise, and when the right atrial pressure is increased by >35%, the pulmonary vascular bed loss is >50%, which can cause a significant increase in pulmonary artery pressure and pulmonary vascular resistance. Reduced and acute pulmonary heart disease. Repeated pulmonary embolism produces persistent pulmonary hypertension and chronic pulmonary heart disease. In patients with impaired cardiopulmonary function, the hemodynamic effects of pulmonary embolism are far more prominent than the usual patients.

Body Pulmonary Embolism: The body or pulmonary artery is blocked by emboli from blood flow. Mainly thromboembolism. It can also be caused by air, fat, or septic emboli. Clinical symptoms include sudden shortness of breath, chest pain, hemoptysis, and even shock and loss of consciousness. Signs of cyanosis, rapid heart rate or arrhythmia, the second heart sounds in the pulmonary valve area. X-ray chest can have wedge-shaped, flaky shadows, which can be accompanied by pleural effusion. Electrocardiogram showed pulmonary P wave and right ventricular strain.

Air embolism: This is a disease caused by a gas embolus originating from the lung that blocks the blood vessels of the brain. It is usually caused by excessive inflation of the lungs due to the expansion of the lungs when the surrounding pressure is reduced (such as when rising from deep water diving). Common features are pain and/or neurological symptoms. Typical symptoms are early loss of consciousness, with or without convulsions or other central nervous system symptoms. Mild signs and symptoms can sometimes occur from behavioral changes to hemiparesis.

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