Introduction to pulmonary embolism

Introduction Pulmonary embolism refers to the pathological and clinical state of the embedding material entering the pulmonary artery and its branches, blocking the blood supply to the tissue. Causes (1) 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. (3) Tumors are the second cause in China, accounting for 35%, which is much higher than 6% in foreign countries. 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. (D) 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. Symptoms 1. Clinical manifestations of pulmonary embolism have a variety of clinical manifestations, which is actually a broader clinical spectrum. What you see is mainly determined by the number of vascular occlusions, the speed of occurrence and the basic state of the heart and lungs, 2 to 3 lung segments, without any symptoms; severe 15 to 16 lung segments, can occur shock or sudden death. But there are basically four clinical syndromes: 1 acute pulmonary heart disease: sudden dyspnea, sudden death, cyanosis, right heart failure, hypotension, wet limbs, seen in patients with sudden embolization above the two lungs; 2 pulmonary infarction: sudden breathing Difficulties, chest pain, hemoptysis and pleural friction or pleural effusion; 3 "unexplained dyspnea": relatively small embolization area, is the only symptom suggesting an increase in invalid cavity; 4 chronic recurrent pulmonary thromboembolism: slow onset, found Later, mainly manifested as severe pulmonary hypertension and right heart dysfunction, is a type of clinical progression. In addition, there are rare contraceptive embolisms and non-thrombotic pulmonary embolisms. The former has multiple strokes with pulmonary embolism. It is opened by the pulmonary foramen ovale and the venous embolus reaches the systemic circulation. The latter may be caused by long bone fracture. Fat embolism syndrome or air embolism associated with a central venous catheter. 1. Common symptoms of pulmonary embolism, whether symptoms or signs are non-specific and insensitive to the diagnosis of acute or chronic pulmonary thromboembolism. (1) Dyspnea: It is the most common symptom of pulmonary embolism, accounting for 84% to 90%, especially after activity. It is often seen after going to the stairs, and it is relieved when resting. Sometimes the patient's self-reported activity is “depressed” and needs to be distinguished from the labor “angina pectoris”. This is often the starting point for correct diagnosis or misdiagnosis, and should be especially seriously asked. Dyspnea may be related to respiratory and circulatory dysfunction. Difficulty breathing (shortness of breath) sometimes disappears quickly, and can occur repeatedly after several days or months. It is caused by recurrence of pulmonary embolism and should be taken seriously. Difficulty breathing can be light and heavy, especially those with mild breathing difficulties. (2) Chest pain: about 70%, sudden occurrence, more related to breathing, increased cough, about 66% of patients with pleural pain, usually a small embolism located in the periphery, involving the pleura. The cause of pleural chest pain is still controversial, but it is still believed that the onset of chest pain of this nature, whether or not combined with hemoptysis, suggests that there may be pulmonary infarction. Larger emboli can cause severe crushing pain. It is located behind the sternum and is difficult to tolerate. It radiates to the shoulders and chest, which is similar to the onset of angina pectoris, accounting for about 4%, which may be related to coronary artery spasm and myocardial ischemia. In addition to the identification of coronary heart disease and angina pectoris, chest pain should also be differentiated from dissecting aneurysms. (3) hemoptysis: It is a symptom of pulmonary infarction, which occurs within 24 hours after infarction. The amount is not much, bright red, and it can become dark red after a few days, the incidence rate is about 30%. The hemoptysis of chronic embolic pulmonary hypertension is mostly from the compensatory dilatation and rupture of the bronchial artery system in the bronchial submucosa. (4) Panic: The incidence rate is about 55%. The cause is unclear and may be related to chest pain or hypoxemia. Do not easily diagnose snoring or hyperventilation syndrome with anxiety and difficulty breathing. (5) Cough: about 37%, mostly dry cough, or a small amount of white sputum, can also be accompanied by wheezing, the incidence rate is about 9%. (6) syncope: about 13%, although small pulmonary embolism can also cause dizziness due to temporary cerebral circulatory disorders, but the main cause of syncope is caused by massive pulmonary embolism (blocking blood vessels above 50%) Cerebral insufficiency. This may also be the only or earliest symptom of chronic embolic pulmonary hypertension, which should be taken seriously, most with hypotension, right heart failure and hypoxemia. (7) Abdominal pain: Pulmonary embolism sometimes has abdominal pain, which may be related to stimulation of the diaphragm or intestinal ischemia. Although more than 90% of patients with pulmonary embolism may have difficulty breathing, typical pulmonary infarction with pleural pain, dyspnea and hemoptysis account for only 28%. 2. Physical examination (1) General examination: There is often low fever, accounting for 43% of pulmonary embolism. It can last for about one week, and high fever can reach more than 38.5 °C. Fever can be caused by pulmonary infarction or pulmonary hemorrhage, atelectasis or additional infection, and may also be caused by thrombophlebitis. Therefore, even if the clinician finds that the lung infiltration shadow is not necessarily lung inflammation, it is necessary to think about the possibility of pulmonary embolism. 70% of patients with pulmonary embolism have a faster respiratory rate, ≥20 times/min, which is diagnostic, up to 40-50 times/min. 44% have sinus tachycardia. 19% of cyanosis occurs, which may be caused by intrapulmonary shunting or by the opening of the foramen ovale. Excessive sweating 11%, although low blood pressure is not very common, but usually prompted for massive pulmonary embolism. (2) Cardiac vascular system signs: mainly the performance of acute and chronic pulmonary hypertension and right heart dysfunction. In addition to increased heart rate, arrhythmia can also occur, such as pre-systolic contraction, supraventricular tachycardia, atrial flutter and atrial fibrillation. There may be systolic pulsation between the second and third intercostals of the left sternal border, which may cause closed vibration of the pulmonary valve, 53% of the second sound of the pulmonary artery, 23% of the jet sound or systolic jet noise. When there is tricuspid regurgitation, the tricuspid systolic murmur may occur between the fourth and fifth ribs of the left sternal border. As the inspiratory increases, when the right ventricle is enlarged and occupyes the apical region, the murmur can be transmitted to the apical region. Even the midline of the sputum is easily confused with mitral regurgitation in rheumatic heart disease. Right atrial atrial gallbladder (24%) and ventricular galloping (3%) can also be heard, reflecting a decline in right heart compliance (such as right ventricular hypertrophy, dilatation) and right ventricular dysfunction. Jugular vein filling and pulsation enhancement are important signs of pulmonary embolism and an important window for right heart function changes. The second heart sound split disappeared or was fixedly split. Signs of right heart failure such as enlarged liver, hepatic jugular vein reflux and lower extremity edema. Acute to pulmonary embolism or severe pulmonary hypertension may have a small to moderate amount of pericardial effusion. Pericardial effusion and pericardial friction sounds can also occur in "post-myocardial infarction syndrome" after pulmonary embolism. (3) signs of respiratory system: when one side of the lung lobe or whole lung embolism can occur, the trachea can be moved to the affected side, and the diaphragm is lifted. The lesions were percussed with dullness, and the lungs were audible and wheezing and dry and wet voices (15%). Pulmonary vascular murmurs can also be heard, the intensity is not large, which is characterized by increased murmur during inhalation, some patients have pleural friction sounds, and corresponding signs of pleural effusion. In addition to the cardiopulmonary signs caused by pulmonary embolism itself, the signs of other underlying diseases that induce pulmonary embolism should also be carefully examined. Some literatures suggest that up to 90% of embolisms of pulmonary embolism originate from deep vein thrombosis, and deep vein thrombosis is considered to be a marker of pulmonary embolism. Therefore, examination of venous thrombosis is very important. Unfortunately, about half of the physical examinations of patients with deep venous thrombosis of the lower extremities are normal. Common abnormalities are seen in the swelling of the affected limb or the asymmetrical swelling of the lower limbs. The difference in the circumference of the limbs between the two limbs is diagnostic. Usually the swelling of the lower leg reflects the blockage of the iliac vein. The swelling of the lower extremity suggests that the external iliac vein or the femoral condyle is blocked. The simple femoral vein thrombosis usually does not show swelling. Accompanying swelling can be conscious of limb pain, tenderness, positive Homan sign, increased stiffness, superficial vein dilatation, acute skin flushing, fever, and hyperpigmentation in chronic cases. Simple venous insufficiency without occlusion only varicose veins, otherwise it is often accompanied by swelling. Limb swelling caused by local venous occlusion does not reflect right heart dysfunction, but sometimes it can be both, and should be carefully identified. 2. Diagnosis of clinical signs and symptoms is often non-specific, and the changes are quite large, 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, and is often closely related to the compensatory ability of the original heart and lung diseases. (A) acute large-area pulmonary embolism: manifested as sudden onset of severe dyspnea, myocardial infarction-like post-sternal pain, syncope, cyanosis, right heart failure, shock, sweating, cold limbs and convulsions. Even cardiac arrest or ventricular fibrillation and rapid death. (B) medium-sized pulmonary embolism: often have post-sternal pain and hemoptysis. When the patient's original heart and lung disease compensation function is very poor, it can produce syncope and high blood pressure. (C) microembolism of the lung: can produce adult respiratory distress syndrome. (D) pulmonary infarction: often have fever, mild jaundice. About 20% to 30% of patients die without timely or failure 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%, so early diagnosis is very important. Care should be taken to collect medical history. Serum LDH increased, arterial blood PO2 decreased, and PA ~ aO2 broadened. Electrocardiograms have T-wave and ST-segment changes (similar to myocardial infarction patterns), P-wave and QRS waveform changes (similar to acute pulmonary heart disease patterns). X-ray shows patchy infiltration, atelectasis, diaphragmatic elevation, pleural effusion, especially the round dense shadow of the pleural basal convex surface toward the hilum (Hamptom hump) and the dilated pulmonary artery with distal lung pattern sparse ( Westermark et al. are of great value in the diagnosis of pulmonary embolism. 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 the ventilation is normal or increased. Combined with clinical diagnosis, the diagnosis can be established. . Pulmonary angiography is the most specific method for diagnosing pulmonary embolism and is suitable for clinical and nuclear scans where suspicious and surgical treatment is required. It is characterized by vascular lumen filling defect, arterial truncation or "pruning sign". Contrast can not show small blood vessels ≤ 2mm in diameter, so multiple small embolizations are often missed. The clinical types of pulmonary embolism are different and need to be different from the disease they identify. Pulmonary manifestations are often misdiagnosed as other chest and lung diseases. Patients with pulmonary hypertension and heart disease are easily misdiagnosed as other heart diseases. The most important clinically misdiagnosed diseases are myocardial infarction, coronary insufficiency, pneumonia, congestive heart failure (left heart), cardiomyopathy, primary pulmonary hypertension, pleurisy, bronchial asthma, pericarditis, dissection aneurysm and rib fracture Wait. 1. Acute pulmonary embolism in acute myocardial infarction may have severe chest pain with electrocardiogram resembling myocardial infarction pattern, which needs 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 ST, T wave changes in II, III, aVF lead, and even V1-4 lead shows "coronal T", Chest pain and shortness of breath are easy to diagnose as coronary insufficiency or subendocardial myocardial infarction. In addition to ST, T changes in the electrocardiogram of pulmonary embolism, the right axis of the ECG axis is obvious or SIQIIITIII type and "Pulmonary P" wave appear. The ECG changes often improve or disappear within 1~2 weeks, which is different from those of coronary heart disease. Patients with pulmonary embolism have labor dyspnea, and coronary heart disease is labor angina. Radionuclide myocardial imaging is completely different. Pulmonary 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 easily confused with pulmonary embolism, is one of the most misdiagnosed diseases of pulmonary embolism. If you can pay attention to obvious breathing difficulties, jugular vein filling, lower extremity phlebitis, X-ray chest radiograph showing repeated infiltration shadows and regional pulmonary vascular texture reduction and blood gas abnormalities, etc., should be suspected of pulmonary embolism, and then further CT and MRI, etc. Check, more can be identified. 4. About 1/3 of patients with pleural effusion can develop pleural effusion, which is easily misdiagnosed as viral or tuberculous pleurisy, and the latter is given long-term anti-tuberculosis treatment. Patients with pulmonary embolism complicated by pleural effusion lack the symptoms of systemic poisoning of tuberculosis. The pleural fluid is mostly bloody, with less amount and absorption faster (natural absorption within 1 to 2 weeks). Arterial blood gas and lower extremity veins are normal. X-ray chest radiographs can also find that the absorption of lung infiltration or infarction is different from tuberculous pleurisy. 5. Atelectasis after atelectasis may be confused with pulmonary embolism, arterial blood gas is usually not normal. Peripheral veins are normal for differentiation, and CT, MRI, or pulmonary angiography can be used for identification when needed. 6. Bronchial bronchospasm secondary to pulmonary embolism sometimes needs to be distinguished from wheezing wheezing. Although the wheezing of patients with pulmonary embolism can occur, but it is rare, when it appears, it is only a new episode, lacking the history of asthma; arterial blood gas in patients with bronchial asthma can also be abnormal, but the CT is more normal, such as clinically suspected pulmonary embolism Pulmonary angiography can be performed further. Read more...