pulmonary embolism
Introduction
Introduction to pulmonary embolism Pulmonary embolism refers to the pathological and clinical state caused by the insertion of the embedding material into the pulmonary artery and its branches, blocking the blood supply of the tissue. Common emboli are thrombus, and the rest are rare new biological cells, fat droplets, bubbles, veins. The input drug particles even block the pulmonary vasculature caused by the tip of the catheter. Since lung tissue is subjected to dual blood supply to the bronchial artery and pulmonary artery, and gas exchange can also be performed directly between the lung tissue and the alveoli, most pulmonary embolism does not necessarily cause pulmonary infarction. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: cardiogenic shock
Cause
Cause of pulmonary embolism
Thrombosis (20%):
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.
Heart disease (20%):
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.
Tumor (15%):
Tumors are the second cause in China, accounting for 35%, which is much higher than 6% abroad. Lung cancer, digestive system tumors, choriocarcinoma, leukemia, etc. are more common. Only about one-third of malignant tumors complicated with pulmonary embolism are tumor thrombi, and the rest are thrombosis. It is speculated that tumor patients may have thromboplastin (thromoboplastin) and other substances that can activate the coagulation system such as histone, cathepsin and proteolytic enzymes. Therefore, the incidence of pulmonary embolism in tumor patients is high, and may even be its first symptoms.
Childbirth (10%):
Pregnancy and childbirth pulmonary embolism in pregnant women several times the age of paired 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.
Other (10%):
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.
Pathological changes
Most acute pulmonary embolism can involve multiple pulmonary arteries. The embolization site is more right lung than left lung, lower lobe is more than upper lobe, but rare embolism is in the right or left pulmonary artery trunk or riding across the pulmonary bifurcation. When the thromboembolism is poor, the surface of the cardiac pathway is gradually covered with endothelial-like cells. After 2 to 3 weeks, it is firmly attached to the artery wall and the blood vessels are reconstructed. Early emboli retraction, recanalization of blood flow, cellulose, platelet aggregates and thrombolytic processes covering the surface of the embolus can produce new emboli to further embolize small blood vessel branches. Whether the embolus causes pulmonary infarction is determined by the size of the affected vessel, the extent of obstruction, the ability of the bronchial artery to supply blood flow, and the appropriate ventilation of the obstructed area. The histological features of pulmonary infarction are intra-alveolar hemorrhage and alveolar wall necrosis, but inflammation is rarely found. When there is no pulmonary infection or the embolus is non-infectious, there is very little void. Loss of pulmonary surfactant in the infarct area can lead to atelectasis, common oozing on the surface of the pleura, and 1/3 of blood. If it survives, the infarct will eventually form a scar.
After pulmonary embolism, the physiological dead space is increased, and the ventilation efficiency is reduced. However, since acute pulmonary embolism can stimulate ventilation, increase respiratory rate and minute ventilation, it usually offsets the increase of physiological dead space and maintains PaCO2: no increase or even decrease. Alveolar hyperventilation is not associated with hypoxemia and cannot even be eliminated by oxygen inhalation. The mechanism is still unclear and is presumed to be related to the reflex of lung parenchyma in the vascular embolization area. Although PaCO2 is usually reduced, CO2 retention may occur when neuromuscular disorders, severe pleural pain, and severe pulmonary embolism do not correspondingly increase the physiological dead space of increased ventilation compensation. PaO2 is common in acute pulmonary embolism, and the ventilatory/blood flow ratio imbalance may be the main mechanism. Local bronchoconstriction, atelectasis and pulmonary edema are the anatomical basis. If the cardiac output cannot be consistent with the metabolic needs, the mixed venous oxygen partial pressure will decrease, which may further aggravate the ventilatory/blood flow ratio imbalance and hypoxemia.
Prevention
Pulmonary embolism prevention
Although the embolism of pulmonary embolism can be derived from any systemic and right atrium of the body, but most of it is from the deep veins of the lower extremities. Therefore, the most important prevention of pulmonary embolism is to treat thrombosis and thrombosis of the lower extremities, and actively treat the feet. Department of infection (including ankles) and prevention of varicose veins, in the case of acute thrombophlebitis, should rest in bed, lower extremity reduction activities, the use of antibiotics and anticoagulants, surgery and trauma should reduce bedtime, encourage early get out of bed If you need to stay in bed for a long time, you should regularly do active and passive activities of the lower limbs to reduce blood stagnation. In addition to active treatment of cardiopulmonary diseases, patients with chronic cardiopulmonary diseases should also reduce bed rest. Prophylactic anticoagulant therapy is available when there is evidence of thrombosis or embolism. Long-distance ride, the rider should move the lower limbs in time to prevent thrombosis, suspected venous thrombosis or thrombophlebitis can do lower limb impedance volume map, vascular ultrasound Doppler, radionuclide or conventional venography, etc. For timely diagnosis, early treatment, for "primary" (hereditary) hypercoagulable state or with deep veins Patients with a family history of thrombosis-pulmonary embolism should be examined early and found to have defects in the coagulation mechanism, such as ATIII, C protein, S protein and plasminogen deficiency. After the onset, anticoagulation should be performed for a lifetime, and the inferior vena cava filter should be actively installed.
The key to preventing pulmonary embolism is to prevent the primary disease.
Complication
Pulmonary embolism complications Complications cardiogenic shock
Causes acute pulmonary hypertension and right heart failure, followed by lung ischemia, hypoxia and left cardiac output, circulatory failure, may also be combined with hemoptysis, pulmonary infarction, massive pulmonary embolism leading to myocardial ischemia and cardiogenic shock.
Symptom
Pulmonary embolism symptoms common symptoms right heart failure chest pain cardiopulmonary embolism large hemoptysis arrhythmia hemoptysis dyspnea hairy hypoglycemia hypothermia malignant pleural effusion
Symptoms : The clinical manifestations of pulmonary embolism can range from asymptomatic to sudden death. Common symptoms are dyspnea and chest pain, with an incidence of more than 80%. Pleural pain is caused by inflammation of the adjacent pleural cellulose, and sudden onset often indicates pulmonary infarction. The pleural involvement can be radiated to the shoulder or abdomen. If there is pain in the back of the chest, it is similar to a myocardial infarction. Chronic pulmonary infarction may have hemoptysis. Other symptoms are anxiety, which may be caused by pain or hypoxemia. Syncope is often a sign of pulmonary infarction.
Signs: Common signs are increased breathing, purpura, wet rales or wheezing in the lungs, pulmonary vascular murmurs, pleural friction or pleural effusion. Signs of the circulatory system have tachycardia, P2 hyperactivity and shock or acute and chronic pulmonary heart disease. About 40% of patients have low to moderate fever, and a few have high fever in the early stages.
Examine
Pulmonary embolism examination
1, routine laboratory tests such as chest X-ray ECG blood gas analysis blood biochemical tests can be carried out if necessary, fiberoptic bronchoscopy, bacterial culture.
2. Lung perfusion imaging.
3. Pulmonary angiography and nuclear magnetic resonance imaging.
Diagnosis
Diagnosis and diagnosis of pulmonary embolism
diagnosis
Clinical symptoms and signs are often non-specific, and the changes are quite large. It is difficult to distinguish from other cardiovascular diseases. Although the severity of symptoms is related to the size of the embolus and the extent of embolization, it is not necessarily proportional to the original heart and lung disease. Repayment ability is closely related.
1, acute large-area pulmonary embolism: manifested as sudden onset of severe dyspnea, myocardial infarction - like sternal pain, syncope, cyanosis, right heart failure, shock, sweating, cold limbs and convulsions, and even cardiac arrest or Ventricular fibrillation and rapid death.
2, moderate-sized pulmonary embolism: often have post-sternal pain and hemoptysis, when the patient's original heart, lung disease compensation function is very poor, can produce syncope and high blood pressure.
3, micro-embolism of the lung: can produce adult respiratory distress syndrome.
4, pulmonary infarction: often have fever, mild jaundice.
About 20% to 30% of patients have not died or failed to be diagnosed and treated. If they can be diagnosed and given anticoagulant therapy in time, the mortality rate is expected to drop to 8%. Therefore, early diagnosis is very important. The medical history should be carefully collected. LDH increased, arterial blood PO2 decreased, PA ~ aO2 widened, ECG had T wave and ST segment changes (similar to myocardial infarction pattern), P wave and QRS waveform changes (similar to acute pulmonary heart disease pattern), X-ray showed patchy Infiltration, atelectasis, diaphragmatic elevation, pleural effusion, especially the circular dense shadow (Hamptom hump) with the pleural basal convex surface facing the hilum and the dilated pulmonary artery with distal lung pattern sparse (Westermark sign) The diagnosis of embolization is of great value. Radionuclide ventilation/perfusion scan is the most sensitive non-invasive method for diagnosing pulmonary embolism. Although the specificity is low, there are typical multiple, segmental or wedge-shaped perfusion defects and ventilation is normal or increased. In combination with clinical, diagnosis can be established. Pulmonary angiography is the most specific method for diagnosing pulmonary embolism. It is suitable for clinical and radionuclide scans and cases requiring surgical treatment. Or "pruning" sign, the contrast can not be displayed 2mm small diameter blood vessels, and therefore multiple small embolization often easily missed, MRI is a useful noninvasive technique pulmonary embolism, pulmonary filled seen clearly larger Defect embolism.
Differential diagnosis
Pulmonary embolism is easily confused with pneumonia, pleurisy, pneumothorax, chronic obstructive pulmonary disease, lung tumor, coronary heart disease, acute myocardial infarction, congestive heart failure, cholecystitis, pancreatitis and other diseases.
1, acute myocardial infarction acute pulmonary embolism can appear severe chest pain with ECG like a myocardial infarction pattern, need to be differentiated from acute myocardial infarction.
2, coronary artery insufficiency in the elderly patients with acute pulmonary embolism or recurrent pulmonary embolism ECG can appear II, III, aVF lead ST segment, T wave changes, and even V1-4 lead shows "coronal T", while Chest pain, shortness of breath, easy to diagnose coronary insufficiency or subendocardial myocardial infarction, usually ECG in addition to ST, T changes in the electrocardiogram, the right axis of the ECG axis is obvious or SIQIIITIII type and "pulmonary P" wave ECG changes often improve or disappear within 1 to 2 weeks. Unlike patients with coronary heart disease, patients with pulmonary embolism have labor dyspnea, while coronary heart disease is labor angina and radionuclide myocardial imaging is completely different. Embolism lacks typical myocardial perfusion defects or "reperfusion" performance.
3, pneumonia fever, chest pain, cough, leukocytosis, X-ray chest showed infiltration of shadows and other easy to be confused with pulmonary embolism, is one of the most misdiagnosed diseases of pulmonary embolism, such as can pay attention to more obvious breathing difficulties, jugular vein filling Lower extremity phlebitis, X-ray chest radiograph showed repeated infiltration shadows and regional pulmonary vascular texture reduction and blood gas abnormalities, etc., should be suspected of pulmonary embolism, and further CT and MRI examinations, more can be identified.
4, pleural effusion about 1/3 of patients with pulmonary embolism can occur pleural effusion, easily misdiagnosed as viral or tuberculous pleurisy, the latter given long-term anti-tuberculosis treatment, and pulmonary embolism of patients with pleural effusion lack of tuberculosis systemic symptoms, chest The liquid is mostly bloody, the amount is small, the absorption is fast (natural absorption within 1 to 2 weeks), the arterial blood gas and the lower extremity vein are normal, and the chest X-ray can simultaneously find that the absorption of lung infiltration or infarction is different from tuberculous pleurisy. .
5, atelectasis after pulmonary atelectasis may be confused with pulmonary embolism, arterial blood gas is usually not normal, the surrounding veins are normal to help distinguish, if necessary, can do CT, MRI or pulmonary angiography to identify.
6, bronchial asthma secondary to pulmonary embolism bronchospasm sometimes need to be distinguished from wheezing wheezing, pulmonary embolism patients wheezing can occur, but rare, when it appears is only a new episode, lack of asthma History; bronchial asthma patients with arterial blood gas can also be abnormal, but enhanced CT is more normal, such as clinically suspected pulmonary embolism can be further pulmonary angiography.
7, primary pulmonary hypertension and pulmonary embolism similar, symptoms are fatigue, labor dyspnea, chest pain, syncope and hemoptysis, etc., clinical right heart failure, hemodynamics have increased right ventricular pressure, and Pulmonary hair pressure is normal, the difference is that the patients with primary pulmonary hypertension are younger (20-40 years old than 50 years old), more women, progressive deterioration, non-stop stable period, lung perfusion scan without lung segment Sexual defect, pulmonary systolic pressure is more than 60mmHg, pulmonary angiography without "pruning" and other changes are different from pulmonary embolism.
8. Patients with acute pulmonary embolism in the aortic dissection have severe chest pain, widening of the superior mediastinum (caused by expansion of the superior vena cava), pleural effusion, and shock with the aortic dissection. The latter has a history of hypertension and pain. Widely, regardless of breathing, cyanosis is not obvious, and echocardiography is helpful for identification.
9, hyperventilation syndrome (anxiety disorders) mostly episodes of dyspnea, chest tightness, dying, arterial blood gas hypocapnia and respiratory alkalosis, ECG can be associated with T wave low and inverted, etc., need to be acute Different from pulmonary embolism, hyperventilation syndrome generally has no structural cardiopulmonary disease changes, often with mental and psychological disorders, and the symptoms can be relieved and disappeared.
The thinking of differential diagnosis is as follows: 1 characteristics of symptoms and signs; 2 accompanying symptoms and signs; 3 tips for related medical history; 4 results of laboratory tests, taking dyspnea as an example, dyspnea of pulmonary embolism is sudden, Often accompanied by chest pain, hemoptysis, shock or syncope, if the medical history suggests some risk factors such as fractures or long-term brakes, laboratory tests revealed lower extremity venous thrombosis, imaging showed pulmonary hypertension or right ventricular enlargement or even pulmonary obstruction, ie It is not difficult to identify with other diseases.
