Health Worlds

Condition analysis:
The clinical manifestations of pulmonary embolism from asymptomatic to sudden death. Common symptoms are dyspnea and chest pain, the occurrence rate of 80% or more. Pleural pain is caused by inflammation of the adjacent pleural cellulose, often prompted by a sudden pulmonary embolism. Phrenic pleural involvement may be directed to the shoulder or abdominal radiation. If chest pain, just like a heart attack. Chronic pulmonary embolism may have hemoptysis. Other symptoms of anxiety, pain or hypoxemia may be caused. Syncope is often a sign of pulmonary embolism. Common signs of respiratory faster, cyanosis, pulmonary rales or wet wheeze, pulmonary vascular murmur, pleural friction rub, or signs of pleural effusion. Signs are tachycardia, circulatory system, P2 hyperthyroidism and shock, or acute and chronic pulmonary heart disease corresponding performance. About 40% of the patients had low to moderate degree of fever, a few patients have high fever early.
Suggestion:
Pulmonary embolism is the wedge material into the pulmonary artery and its branches, blocking the blood supply caused by tissue pathology and clinical status. Thrombotic embolus is common, the rest is a rare new biological cells, lipid droplets, bubbles, particles or drug infusion catheter tip caused by pulmonary vascular occlusion.

Overof foreign high incidence of pulmonary embolism, the incidence of the U.S. each year about 60 million, one third of the deaths, representing


the third cause of death. There are also reports in recent years with the increase in adults receiving anticoagulant therapy, the incidence rate showed a decreasing trend. There is no precise epidemiological data in China, but the Fu Wai Hospital, more than 900 reported cases of autopsy data cardiopulmonary disease, lung blood clots blocking a large section of more than 100 persons (11%), rheumatic heart disease accounted for 29% of the autopsy, myocardial disease 26%, 19% of pulmonary heart disease, cardio vascular disease that often complicated by pulmonary embolism.
The formation of pulmonary embolism pulmonary embolism symptoms and signs of clinical manifestations from asymptomatic to sudden death. Common symptoms are dyspnea and chest pain, the occurrence rate of 80% or more. Pleural pain is caused by inflammation of the adjacent pleural cellulose, often prompted by a sudden pulmonary embolism. Phrenic pleural involvement may be directed to the shoulder or abdominal radiation. If chest pain, just like a heart attack. Chronic pulmonary embolism may have hemoptysis. Other symptoms of anxiety, pain or hypoxemia may be caused. Syncope is often a sign of pulmonary embolism. Common signs of respiratory faster, cyanosis, pulmonary rales or wet wheeze, pulmonary vascular murmur, pleural friction rub, or signs of pleural effusion. Signs are tachycardia, circulatory system, P2 hyperthyroidism and shock, or acute and chronic pulmonary heart disease corresponding performance. About 40% of the patients had low to moderate degree of fever, a small number of patients
Early pulmonary embolism and pulmonary infarction had high fever. ECG electrocardiogram of pulmonary embolism pulmonary embolism diameter as the size and scope of involvement varies. Light had no abnormalities, most patients mainly as sinus tachycardia, pulmonary P waves, severe pulmonary heart disease S Q T . Some patients may appear incomplete right bundle branch block. Routine chest X ray chest often can not determine the diagnosis of PE, about 10% of patients with pulmonary embolism have positive performance, but the lack of specificity. Mainly fine grain for regional pulmonary blood vessels, heart enlargement, pulmonary hypertension, pleural effusion, interstitial edema, atelectasis, pulmonary infiltrative changes, hemi-diaphragm increased. Transesophageal echocardiography echocardiography in cases of massive PE, 92% sensitivity and specificity close to 100%, but a third of patients with pulmonary embolism in general the performance was normal. Differences usually manifested right ventricular enlargement, pulmonary hypertension, under the port vein dilation, ventricular septal shift to the left ventricle. However, echocardiography in the diagnosis of deep venous thrombosis has great value. Pulmonary ventilation / perfusion (V / Q) imaging of lung ventilation / perfusion scan showed no perfusion defect, pulmonary embolism can be discharged. Normal ventilation, or a more or larger section of lung perfusion defects, or ventilation, in the true long sub-segments of two or more perfusion defects, the presence of highly suggestive of pulmonary embolism.
Pulmonary embolism pulmonary embolism pulmonary angiography is diagnostic "gold standard", which is an invasive examination. However, the probability of death Check close to 1% of the elderly, critically ill patients in particular have a certain risk, generally do not advocate the examination. Thrombosis causes vein thrombosis pulmonary embolism are often complications. Emboli from the lower limbs and pelvis are usually deep-vein thrombosis caused by circulation to the pulmonary artery. But rarely from the upper limbs, head and neck veins. Blood stasis, blood coagulation and vascular endothelial injury is the increased thrombosis contributing factor. Therefore, trauma, prolonged bed rest, varicose veins, venous cannulation, pelvic and hip surgery, obesity, diabetes, birth control pills, or other causes such as hyperthyroidism clotting mechanism, are likely to cause venous thrombosis. Crisp early thrombosis, coupled with the role of fibrinolytic system, so in the first few days of thrombosis highest risk for pulmonary embolism.
Heart disease, heart disease, pulmonary embolism check for the most common cause of pulmonary embolism was 40%. Several times and all kinds of heart disease, atrial fibrillation, heart failure and subacute bacterial endocarditis who have a higher prevalence. The right heart chamber thrombus up to see, a few also from the venous system. In addition to bacterial emboli seen in subacute bacterial endocarditis, but also the pacemaker infection. The former mainly from the tricuspid valve infective emboli, and occasionally in patients with congenital heart mitral valve vegetation can be diverted from the defect into the left heart through the right heart to reach the pulmonary artery. Cancer tumors causes in our country for the second, accounting for 35%, 6% higher than abroad. To lung cancer, digestive system tumor, choriocarcinoma, leukemia and other more common. Malignant pulmonary embolism is only about 1 / 3 of tumor thrombus, the rest are blood clots. It is speculated that cancer patients may have blood clotting kinase (thromoboplastin) can activate the coagulation system, and other substances, such as histones, and proteolytic enzymes cathepsin, it is the high incidence of cancer in patients with pulmonary embolism, and even now its first symptoms. Pulmonary embolism in pregnancy and childbirth, pregnancy and delivery in pregnant women, many times greater than the age matched non-pregnant women, postpartum, and the highest incidence after cesarean delivery. Intra-abdominal pressure increases during pregnancy and hormonal relaxation of vascular smooth muscle and pots vein compression can cause venous flow is slow, change the rheology properties, increased venous thrombosis. Also with increased clotting factor and platelet and plasma plasminogen - Plasma fibroin dissolved system activity was reduced. However, these changes in pregnant women with and without thrombosis compared to no absolute differences. Amniotic fluid embolism is a serious complication of childbirth. Other rare the cause of the other long bone fractures caused by a fat embolism, decompression sickness Zaocheng accidents and air embolism, parasites and foreign body embolism. No obvious precipitating factors, anticoagulation should also take into account the genetic factors that reduce or plasminogen activation inhibitor increased. Pathology of acute pulmonary embolism can affect more than the majority of branch pulmonary artery, the site of the right lung embolism than the left lung, lower lobe than on the leaves, but rarely in the right or left pulmonary embolism, or riding across the pulmonary trunk bifurcation. Thromboembolus machine of the bad, the easy way through the heart of the formation of debris embolization in small vessels.
Radiographic examination and diagnosis of pulmonary embolism if the fibrinolytic mechanism can not dissolve clots, emboli 24 hours after the surface of endothelial cells that gradually covered, 2 to 3 weeks after the firm posted on the arterial wall, vascular reconstruction. Emboli early withdrawal, the scouring action of reperfusion blood flow to cover the surface of the cellulose in embolus, the process of platelet aggregation and thrombolytic properties, can generate a new embolic occlusion of small blood vessels branch further. Pulmonary embolism is emboli caused by the size of involved vessels, blocking range, the ability of bronchial artery blood supply and adequate ventilation or obstructed area of the decision. The histological features of pulmonary embolism as alveolar hemorrhage and alveolar wall necrosis, but rarely found in inflammation, infection or pulmonary embolism had no non-infectious, the rarely produced empty. Infarcted loss of pulmonary surfactant can lead to atelectasis, pleural effusion common surface, 1 / 3 to bloody. If alive, the final infarct region scarring. Physiological dead space after pulmonary embolism caused by increased ventilation efficiency decreased, but due to acute pulmonary embolism can stimulate ventilation, increased respiratory rate and minute ventilation, usually offset by the increase in physiological dead space to maintain PaCO2: do not increase or even decrease. Independent of alveolar hyperventilation and hypoxia, or even eliminate the oxygen. The mechanism is not clear, suggesting that regional parenchymal and vascular thrombosis reflection related. Although PaCO2 usually lower, but neuromuscular disorders, severe pleural and pulmonary embolism in patients with severe pain can not be a corresponding increase in ventilation compensatory increase in physiological dead space, may appear CO2 retention. Also common in acute pulmonary embolism PaO2 decreased ventilation / perfusion ratio imbalance may be the main mechanism, local bronchoconstriction, atelectasis and pulmonary edema Weiqi anatomy. If cardiac output can not be consistent with the metabolic needs, mixed venous oxygen partial pressure will decrease, further increasing ventilation / perfusion ratio imbalance and hypoxemia. Direct effect of mechanical pulmonary embolism after embolization and the chemical mechanisms and reflex hemodynamic responses caused is more complex. And the small number of small emboli pulmonary embolism does not cause hemodynamic changes. Generally, pulmonary vascular bed obstruc 30%, the mean pulmonary artery pressure began to increase,> 35%, right atrial pressure and pulmonary vascular bed loss 50%, can cause pulmonary artery pressure, pulmonary vascular resistance increased significantly, cardiac index reduction, and acute pulmonary heart disease. Recurrent pulmonary embolism, pulmonary hypertension lasting and chronic pulmonary heart disease. In the original patients with impaired cardiopulmonary function, hemodynamics of pulmonary embolism in patients with far more prominent than usual. Clinical diagnosis about 20% to 30% of patients were not timely diagnosis and treatment or fails to death, if timely diagnosis and given anticoagulant therapy, the mortality dropped to 8% is expected, so early diagnosis is very important. History should be carefully collected. Elevated serum LDH, arterial PO2 fell, PA ~ aO2 widened. ECG T wave and ST segment changes (similar to myocardial infarction graphics), P wave and QRS wave changes (similar to acute pulmonary heart disease graphics). X ray showed patchy infiltrates, atelectasis, diaphragmatic elevation and pleural effusion, especially in the basement of pleural circular convex compact towards the hilar shadow (Hamptom hump) and the expansion of the pulmonary artery with distal lung pattern sparse ( Westermark sign) and so the diagnosis of pulmonary embolism are of great value. Pass radionuclide lung
Acute pulmonary embolism gas / perfusion scan diagnosis of pulmonary embolism is the most sensitive noninvasive method, specificity was low, but there are typically multiple, segmental or wedge-shaped perfusion defects and normal or increased ventilation, combined with clinical, diagnosis can be established . Diagnosis of pulmonary embolism, pulmonary angiography is the most specific method for clinical and radionuclide scanning and the need for surgical treatment of suspicious cases. Showed filling defects in the vessel lumen, arterial truncated or "pruning sign." 2mm diameter imaging can not show the small blood vessels, so often multiple small embolic easily missed. MRI useful for the diagnosis of pulmonary embolism noninvasive technology, large pulmonary embolism can be seen clearly when the filled defect. Check the overof routine laboratory tests, such as chest X-ray ECG, blood gas analysis, blood tests, if necessary, to fiberoptic bronchoscopy, sputum bacterial culture and so on. Pulmonary perfusion imaging, pulmonary angiography and electron beam CT (EBCT) can display the lung blood vessels, is noninvasive, very high detection rate of pulmonary embolism (sensitivity 95%, specificity 97%, positive predictive value 93% negative predictive value 95%), can replace conventional pulmonary angiography. Chest spiral CT scan and pulmonary angiography for pulmonary embolism pulmonary segments over the role of similar, but can not detect the following sub-paragraph embolism (6% -16% positive rate).
Suspected acute pulmonary embolism diagnosis flow chart D-dimer D-dimer exchange-linked fibrin degradation products of good markers to plasma 1 - dimer is greater than 500 g / L as a positive diagnostic value, the judge lung embolism with a sensitivity of 95% -98%, D-dimer positive as the discharge diagnosis of pulmonary embolism has great value. D-dimer in older people may be physiological higher than 500 g / L, it is more than 70 years of age, the diagnostic specificity was only 14.3%. Transthoracic echocardiography and transesophageal echocardiography can be direct or indirect signs suggest the existence of pulmonary embolism is a valuable screening method. indirect signs: right ventricular expansion of 71% to 100%, right pulmonary artery diameter increased 72%, 38% smaller left ventricular diameter, left ventricular septal and contradictions, and pulmonary hypertension 42% and other, indirect signs of the restriction is small previous pulmonary embolism and right heart disease are easy to negative findings. direct signs: right heart thrombi can have two types: active, a snake-like movement of the organization and not active, no pedicle and dense tissue. The former 98% of pulmonary embolism; which 40% occurred, mortality, the former was 44%, which is 9%. Mixed emboli pulmonary embolism was 62%, mortality was 29%. Transthoracic echocardiography in the detection of right heart thrombosis was 5.6%, transesophageal echocardiography picture shows the 14%. Pulmonary embolism can be found in about 11% to 14%. Transesophageal echocardiography, the positive rate found in pulmonary arteries than transthoracic echocardiography, the diagnosis of pulmonary embolism with a sensitivity of 97%, a specificity of 88%, positive predictive accuracy was 91%, negative predictive accuracy of 96% . When the concurrent pulmonary hypertension and pulmonary heart disease, the signs of a corresponding ultrasound, such as pulmonary artery and right ventricular outflow tract flow acceleration, tricuspid transvalvular pressure gradient increased, the pulmonary valve echo curve " " lighter, shrink interim shut down and increase the right atrium and other rooms. It has been reported in recent years with the diagnosis of peripheral intravascular ultrasound efficacy evaluation of pulmonary embolism and do. Check deep vein thrombosis pulmonary embolism from deep vein majority, so the discovery of venous thrombosis diagnosis of pulmonary embolism, although not directly, but it can give great tips. Venous thrombosis in nearly half of the normal physical examination, it often requires the use of other tests to confirm the number of commonly used methods are the following species. (1) to determine a standard method of deep vein thrombosis: venous congestion can display the location, scope, extent and condition of collateral circulation. Angiography showed that venous thrombosis can occur in unilateral or bilateral lower extremities, can also be limited to the calf veins, but also direct access to the inferior vena cava. Although venography clearly showed lesions, but can cause local pain, allergic reaction and phlebitis increased, even can make emboli shedding, the risk of pulmonary embolism occurs again, therefore, has little application. The main indication is the of emboli to be clearly inferior vena cava filter implantation in enucleation and pulmonary emboli in patients. (2) intravenous radionuclide imaging: The commonly used method is to 99Tc venography, venous contours were clear, safe, painless, especially for allergy to contrast agents or in combination in patients with lung perfusion scan done. Imaging findings are: obstruction of blood flow (complete and incomplete); collateral circulation; venous valvular incompetence, blood reflux into the superficial vein, superficial vein compensatory enlargement, and twisted. Venography in line with about 90%. (3) intravascular ultrasound: According to the spectrum is proportional to blood flow velocity deviation and the principle obstacles in check blood flow, suggesting the formation of venous thrombosis. The probe used parts of a femoral vein, popliteal vein and posterior tibial vein, the accuracy of the method was 93%. The advantage is to repeat the check on the peroneal sensitive detection of venous thrombosis. (4) impulse oscillation lung function: from Hull and other reports. The specific method is used to tie in the thigh with a central blood pressure, inflation pressure of 50 ~ 60mmHg, venous occlusion, one minute after the sudden deflation, deflation record volume chart before and after the change in impedance. Under normal circumstances, the end of electrical impedance to increase inflation, deflation after the electrical resistance decreased 3s. When deep venous thrombosis, the resistance rate of rise or fall significantly slower; compliance with venography was 77% to 95%, a sensitivity of 65% to 86%, specificity 95% to 97%. On cardiac dysfunction and peroneal vein thrombosis diagnosis is not sensitive enough; development of good collateral circulation were also false negative results. Pulmonary embolism in the West is a very common disease is not uncommon in China, because the lack of inspection means and sufficient vigilance, resulting in misdiagnosis lot, giving the illusion of a rare disease. Foreign autopsy, the clinical misdiagnosis of pulmonary embolism was 67%, false-positive diagnosis rate of 63%, only 1 / 3 of the patients receive the correct diagnosis. Relevant data show that domestic misdiagnosis rate of 79%, due to lack of timely and correct diagnosis, treatment and prognosis of patients, therefore, an early correct diagnosis of pulmonary embolism is important. Chest CT examination in recent years developed spiral CT, electron beam CT in particular can show pulmonary artery, which is the scanning speed, no movement artifacts, the image clearer, more conducive to reconstruction, direct indication of pulmonary vascular segments. Enhanced CT can clearly show thrombus site, shape, and the relationship and the cavity wall damage conditions. Direct signs include: half-moon or circular filling defects, complete obstruction, orbital signs, etc.; indirect signs are: expansion of the main pulmonary artery and left pulmonary artery, a small blood vessel cross-section, lack of support, mosaic symptoms, pulmonary infarction, pleural and changes. Compared with conventional pulmonary angiography, enhanced CT diagnosis of pulmonary embolism, the average sensitivity was 90%, the average specificity of 92%. The biggest advantage is non-invasive, particularly valuable for emergency patients, to guide treatment and evaluate the efficacy is reliable. Spiral CT examination of the most effective parts of emboli is the first 2 to 4 vessels, on the small, there are difficulties surrounding the diagnosis of pulmonary embolism. Pulmonary embolism by magnetic resonance (MRI) examination, the image is similar to catheter angiography, sensitivity and specificity is high. Also used for the inspection of deep vein thrombosis. Arterial blood gas analysis mainly as PaO2 <80mmHg, PA- 20mmHg, hypocapnia <36mmHg in fact, physiological changes in the aging process, PaO2 slowly reduced, while the PA-aDO2 is increased with increasing age. Diagnosis of pulmonary embolism is difficult, about 20% -30% of patients with pulmonary embolism due not timely diagnosis and aggressive treatment died. Timely diagnosis and anticoagulant, thrombolytic therapy can make the mortality rate to 80%. Differential diagnosis of pulmonary embolism is easy with pneumonia, pleurisy, pneumothorax, chronic obstructive pulmonary disease, lung cancer, coronary heart disease, acute myocardial infarction, congestive heart failure, cholecystitis, pancreatitis and other diseases, confused, need to be carefully identified. Complications of acute pulmonary hypertension and right heart failure, followed by lung ischemia, hypoxia and left cardiac output, circulatory failure. Can also be combined hemoptysis, pulmonary infarction, myocardial ischemia caused massive pulmonary embolism and cardiogenic shock. 1 OverIn addition to oxygen therapy, pain, shock and heart failure, and correct other symptomatic treatment of bronchial dilation, the specific methods include anticoagulation, thrombolysis and surgery. Medical treatment (a) General treatment: The need for first aid disease patients with absolute bed rest should be kept oxygen (b) of heparin anticoagulation therapy 1 2 vitamin K antagonist (c) fibrinolytic agents: the Thrombolysis fibrin solvent can promote the dissolution of venous thrombosis and pulmonary emboli blocking blood circulation restoration is a safe method of treatment. Surgical treatment (a) pulmonary embolectomy (b) of the vena cava surgery: primary prevention of recurrent thrombosis and even pulmonary vascular compromise, in addition to correct shock and heart failure oxygen pain and other symptomatic treatment of bronchial relaxation measures, including specific methods anticoagulant thrombolytic and surgical treatment of the process of anticoagulant therapy and thrombolytic therapy methods see "myocardial infarction." Inferior vena cava surgery for anticoagulant therapy and repeated risk of fatal bleeding embolization, ligation, or can be set to a special clip or filtration devices and other methods. Pulmonary resection mortality rate is high, only thrombolysis or aggressive treatment of vasopressin in patients with continued shock. Overof pulmonary disease, senile old common symptoms of pulmonary embolism shortness of breath, chest pain, tachycardia and tachypnea. All patients had at least chest pain, breathing difficulties or a symptom of tachycardia, 35% of the patients of the three symptoms simultaneously. ECG examination revealed sinus tachycardia, ST segment and T wave abnormality, incomplete right bundle branch block, appear in the DIII lead T-wave inversion. Echocardiography examination, can be expressed as normal, may have expanded the performance of right ventricle, the vena cava can be a mild expansion of the left ventricular septum can be offset. In the elderly, pulmonary embolism is often missed. Only the alert to this disease in order to improve the number of diagnosis and shorten the time needed for diagnosis and improve prognosis. Symptoms and signs of PE, no specific clinical features, in elderly patients, rapid breathing (respiratory 16min), pleurisy, chest pain, tachycardia is the most common signs and symptoms in all patients are alone or present. The number of pulmonary artery involvement, embolic level of necrosis of lung tissue caused by the decision whether the patient's symptoms. Only 20% of the elderly for tracking the performance of dyspnea, chest pain, chest slightly. If there is no breathing difficulties, pulmonary embolism is difficult to set up. If the patient showed extreme difficulty breathing and fainting or shock there, and more prompt massive PE without the presence of pulmonary infarction. About 33% of elderly patients with pleural effusion, usually unilateral. About 67% of the effusion is bloody (red blood cell c 100000 / ml) to distinguish cancer and trauma. However, many elderly patients with clinical manifestations of pulmonary embolism in a non-specific symptoms, including persistent fever, mental status changes shape, no respiratory symptoms or similar symptoms of respiratory tract infections reflect the performance of older people often slow and may be a misunderstanding of symptoms in the elderly one reason for the high rate of PE misdiagnosed. Closely related to DVT and PE, about 50% of patients with proximal DVT may be suffering from PE but no clinical symptoms, about 80% of the symptoms and not for lack of timely diagnosis. Therefore, leg swelling, leg pain should attach great importance and should be related to examination, diagnosis of DVT and PE is an important clue. Diagnostic prognosis: 65 years of age hospitalized patients with pulmonary smooth plug mortality was 21%. 65 years of age and older with chronic heart failure, chronic obstructive pulmonary disease (COPD), cancer, myocardial infarction, stroke, pulmonary embolism elderly hip fracture, the mortality rate increased significantly. Although heparin to prevent further embolization, but pulmonary embolism in patients older than 65 years recurrence rate for the first year of 8%, the mortality rate was 39% (21% in the first year of hospital mortality and 18% other). The main treatment of pulmonary embolism was symptomatic treatment and thrombolytic treatment, anticoagulant treatment. Symptomatic treatment is to maintain hemodynamic stability, control shock and heart failure, severe chest pain may be given analgesics. Anticoagulant treatment should be implemented as soon as possible, even though it's not directly dissolve clots, but can prevent further development of thrombosis, or recurrence. Commonly used drugs are heparin and warfarin. Recommended heparin treatment for at least 5-7 / d, the same time give oral anticoagulant warfarin ,3-5d was later changed to oral warfarin alone. Old dose of anticoagulant medication increased with age and time should be reduced. Mainly based on clotting time and prothrombin time to adjust. Clotting time 1.5-2 times control in normal, prothrombin time 1.5-2.5 times normal, heparin-related bleeding in patients with acute venous thromboembolism incidence of disease on average approximately 3%. Low molecular weight heparin may be safer than unfractionated heparin and effective. Speed with low molecular weight rare to find a bleeding liver, the total mortality rate lower than unfractionated heparin. Thrombolytic therapy of pulmonary embolism is still controversial, but the incidence within the 5d bulk of pulmonary embolism or pulmonary embolism with significant hypoxemia in the absence of contraindications, there are still many advocates thrombolytic thrombolytic therapy. The drug is commonly used urokinase and recombinant tissue-type plasminogen activator. Surgical treatment: In order to prevent further loss of deep venous thrombosis caused by pulmonary smooth filtering plug prevents the umbrella, or titanium metal Greenfild filtration device. Filtration device, whether placed on long-term anticoagulant therapy should be considered, because the filtration device placed embolism after filtration devices up to 16%, for chronic thromboembolic pulmonary hypertension and pulmonary thromboendarterectomy with possible surgery, but the surgery difficult, can be stripped to the sub-intimal pulmonary artery segment level. Prevention of pulmonary embolism drug safety, above all, to prevent emboli formation. Deep vein thrombosis from the main (long-term bed venous stasis), right heart (rheumatic heart disease, etc.), and may bolt from fat (trauma, fracture), tumor thrombus (cell rupture), bacteria bolt (infection), blood viscosity is too high. The elderly and those who have these risk factors, once dizziness, breath, chest tightness, chest pain, in addition to concern about cardiovascular disease, but also consider possible pulmonary embolism. The basic rule, especially coronary heart disease ECG immediately after the respiratory treatment, timely diagnosis and treatment. Although the treatment of pulmonary embolism thrombosis, some or all are free to dissolve and disappear, but after treatment of acute pulmonary embolism mortality than non-treatment of low 5 to 6 times, so, once the diagnosis, which should be actively treated, unfortunately, the patients can get proper treatment only 30%. The treatment of pulmonary embolism in patients through the critical objective is to make the period of remission embolism caused by cardiopulmonary disorders and the prevention of recurrence; as much as possible to restore and maintain adequate circulating blood volume and tissue oxygen supply. Of large pulmonary embolism or the treatment of patients with acute pulmonary heart disease, including timely oxygen, relieve pulmonary vascular spasm, anti-shock, anti-arrhythmia, thrombolysis, anticoagulation, and surgical and other treatment. Chronic thromboembolic pulmonary hypertension and chronic pulmonary heart disease, treatment includes blocking emboli s, to prevent further embolism, pulmonary artery thrombosis endarterectomy, lower pulmonary artery pressure and improve heart function and so on. 1, the treatment of acute pulmonary embolism (1) first aid measures: the most dangerous acute pulmonary embolism during the first two days, the patient should be income ICU ward, continuous monitoring of blood pressure, heart rate, respiration, electrocardiogram, central venous pressure and blood gas. General treatment: the patient quiet, warm, oxygen; as sedation, analgesia, if necessary, morphine, pethidine, codeine; for the prevention of lung infection and antibiotic treatment of phlebitis. ease caused by high vagal tone of the pulmonary vascular spasm and coronary artery spasm, intravenous atropine 0.5 ~ 1.0mg, if not relief can be repeated every 1 to 4 hours 1, can also papaverine 30mg subcutaneous, intramuscular or intravenous injection, 1 / / h, the drug also has sedative and reduce platelet aggregation. anti-shock: septic shock were given dopamine 5 ~ 10 g / (kg? Min), dobutamine 3.5 ~ 10 g / (kg? Min) or norepinephrine 0.2 ~ 2.0 g (kg? Min), rapid correction hypotension caused by cardiac arrhythmia, such as atrial flutter, atrial fibrillation and so on. Maintain the mean arterial blood pres 80mmHg, cardiac i 2.5L / (min? M2) and urine ou 50ml / h. At the same time actively thrombolysis, anticoagulant therapy, to fight the disease quickly ease. Be noted that 80% of those who died of acute pulmonary embolism died within 2h after the onset, therefore, be stepped up rescue treatment. improve breathing: such as bronchial spasm can be applied to aminophylline, two hydroxypropyl theophylline (asthma may be) such as bronchodilators and mucus solvent. Phentolamine can also be dissolved in 10 ~ 20mg of 5% to 10% glucose intravenous infusion in 100 ~ 200ml, can relieve bronchial spasm, but also expansion of the lung blood vessels. Respiratory failure in patients with severe hypoxemia may be short-term mechanical ventilation therapy. (2) thrombolytic therapy: Thrombolysis in acute pulmonary embolism 30 years ago was introduced to the medical profession when as a complex, heroic, desperate last treatment, requires a huge human, material and financial support. Although in 1977 and 1978 the U.S. Food and Drug Administration has approved streptokinase and urokinase for the treatment of pulmonary embolism, but until the 20th century, actually mid-80s rarely used. Thrombolytic therapy for acute myocardial infarction in the success of thrombolytic therapy to pulmonary embolism re-examination and the subsequent series of clinical trials has led to pulmonary embolism, thrombolytic therapy has become more modern safe, rapid, simple and more effective. Thrombolytic therapy is the drug directly or indirectly, the plasma protein plasminogen into plasmin, the rapid lysis of fibrin, clot dissolution; both removal and inactivation by coagulation factor , V and , interfere with blood clotting, and strengthen the fiber protein and fibrinogen degradation, inhibition of transformation of fibrinogen to fibrin and interfere with fibrin polymerization, to play anticoagulant effect. Commonly used thrombolytic drugs are: streptokinase (streptokinase, SK): is from Group C -hemolytic streptococcus bacteria in purified protein, and plasminogen to form activated complex, so that changes in the other plasminogen into plasmin. Streptokinase with antigen, at least 6 months can not be applied, as inactivation of drugs and circulating antibodies can cause severe allergic reactions. urokinase (urokinase, VK): is the culture from human urine or isolated from human embryonic kidney cells, without antigen, directly to plasminogen into plasmin play thrombolysis. alteplase (recombinant tissue plasminogen activator, rt-PA): is a new thrombolytic agent, a variety of cell lines using recombinant DNA technology to produce, alteplase (rt-PA) no antigen, directly plasminogen into plasmin, the fibrin SK or UK is more than the specific (less systemic plasminogen activation). Indications for thrombolytic therapy in acute pulmonary embolism are: massive pulmonary embolism (blood vessels more than two lobes); vascular anatomy of pulmonary embolism regardless of the size of those associated with hemodynamic changes; concurrent shock and low perfusion or arterial hypotension, lactic acidosis, and (or) decrease cardiac output; the original sub-massive pulmonary embolism, heart and lung disease caused by circulatory failure; symptomatic pulmonary embolism. Contraindications to thrombolytic therapy in pulmonary embolism: an absolute contraindication are: the recent activity of gastrointestinal bleeding; cerebrovascular accident within two months, intracranial or spinal trauma or surgery; active intracranial disease (arterial tumors, vascular malformations, tumors). Relative contraindications are: uncontrolled hypertension (systolic blood pressure 180mmHg, diastolic blood pressure 110mmHg); hemorrhagic diabetes, including those with severe renal and liver disease; recent (10 days) surgery major surgery, can not be squeezed puncture of blood vessels to stop bleeding, organ biopsy, or childbirth; size of the recent trauma including cardiopulmonary resuscitation; infective endocarditis; pregnancy; hemorrhagic retinopathy; pericarditis; aneurysm; left atrial thrombus; potential bleeding disorders. The most important complication of thrombolytic therapy is bleeding, individual statistics vary, an average of 5% to 7%, fatal bleeding was about l%. 3 The incidence of major bleeding thrombolytic drugs similar to alteplase (rt-PA), UK and SK were 13.7%, 10.2% and 8.8%. The most serious is intracerebral hemorrhage was 1.2%, about half of the deaths, diastolic blood pressure is another risk factor for intracranial hemorrhage. Small retroperitoneal bleeding, more hidden, more performance for the shock of unknown cause, should be observed. Another more important is pulmonary angiography in the femoral vein bleeding puncture site, hematoma formation and more. "Acute pulmonary embolism thrombolysis, anticoagulation bolt complex multi-center clinical trial Yan," 101 patients without intravenous thrombolytic hemorrhage occurred in 1 case, 5 cases of puncture site bleeding. Usually a small amount of bleeding can not be processed immediately stopping severe bleeding, cryoprecipitate lost and (or) of fresh frozen plasma and amino benzyl amine or aminocaproic acid. Intracranial hemorrhage Please neurosurgeons emergency consultation. Other side effects of thrombolytic drugs may also have fever, allergic reactions, hypotension, nausea, vomiting, myalgia and headache. Allergic reactions common in patients with streptokinase. Contemporary pulmonary embolism, thrombolytic therapy has been great progress, safe, effective, simple and standardized treatment regimens tend to not necessarily have to do pulmonary angiography, the treatment time window extended to 14 days, or according to the weight of fixed dose administration, peripheral venous 2h infusion, not to indicators for monitoring blood clotting, can be implemented in the general wards. Therefore, thrombolytic therapy should actively promote universal. (3) anticoagulant treatment: pulmonary embolism, anticoagulant therapy is effective and important. According to a group of statistics of 516 cases of pulmonary embolism, anticoagulation treatment group survival rate was 92% and the recurrence rate was 16% instead of the anticoagulant therapy group were 42% and 55%, the difference is very significant. 1 to 4 weeks of anticoagulant therapy, pulmonary blood clots were completely dissolved at 25%, 4 months to 50%. Commonly used anticoagulant drugs heparin and warfarin. Pulmonary embolism heparin: standard heparin is a mucopolysaccharide sulfur esters from pig intestines mucosa or partially purified from bovine liver, and its molecular weight from 3 ~ 30kDa, an average of 15kDa. Low molecular weight heparin (LMWHs) are fragments of unfractionated heparin, and plasma proteins than unfractionated heparin and endothelial cells with less. Therefore, low molecular weight heparin has greater bioavailability, better predictability of dose response and longer half-life. Heparin mainly through antithrombin (AT ) work, which is a enzyme, inhibiting thrombin (factor a), Xa, a, a and a, and then make AT conformational change and improve its activity about 100 times to 1000. Prevention of additional thrombus formation, the mechanism of endogenous fibrinolysis dissolves the clot has formed, but heparin can not directly dissolve thrombus that aly exists. 35 cases of pulmonary embolism were randomized to compare the effect of heparin and placebo, the results of 16 cases of heparin-treated patients without recurrence in 1 case, while 19 patients were treated with placebo in 10 patients with recurrent pulmonary embolism, 5 patients died, indicating that the lung embolism heparin is effective. However, the role of heparin is limited, because the combination of thrombin clots can not heparin - antithrombin suppression, so as unfractionated heparin and plasma protein binding of heparin resistance may occur. Heparin is the basis for the treatment of acute pulmonary embolism, hemorrhage before treatment should be considered risk factors, such as previous history of application of anticoagulant bleeding, thrombocytopenia, vitamin K deficiency, old age, underlying diseases and combined drug therapy. Check the most frequently overlooked is the fecal occult blood positive rectal examination. Reported in the literature, Raschke dosage regimen of up to fast, effective and safe heparin, the first few days of heparin to achieve adequate anticoagulation effect of heparin infusion often need 1500 ~ 2000U / h. Table 3 is based on weight "Raschke" heparin computation. Commonly used in a hospital administration is intravenous infusion of heparin, the load capacity of 2000 ~ 3000U / h, followed by 700 ~ 1000U / h or 15 ~ 20U / (kg? H) to maintain. Heparin in patients with pulmonary embolism has been reported shorter half-life of about 50% of normal, therapeutic dose should be increased. Need to monitor treatment with unfractionated heparin, activated partial thromboplastin time (APTT) at least 1.5 times greater than the control value (usually 1.5 to 2.0 times), given within the effective range of the minimum heparin anticoagulation therapy dose. Plasma heparin levels between about 0.2 ~ 0.5U/ml. Determination of plasma heparin levels is particularly useful in two situations: monitoring the lupus anticoagulant or anti-lipid antibodies baseline APTT increased heart patients; Monitoring of deep vein thrombosis and pulmonary embolism require large daily doses of heparin patients. Time course of medication to calm the acute clinical situation improved significantly dissolves blood clots, usually 7 to 10 days. Heparin in the treatment process can occur a small number of patients with thrombocytopenia, therefore, required every 3 to 4 days 1 replatelet count, platelet count (70 ~ 100) 109 / L can still be applied when the heparin, less than 50 109 / L when should stop the medication. The most important side effect of heparin is bleeding, the risk of bleeding than the basis of platelet count, and age, underlying diseases, and liver dysfunction and also associated with drugs. Most moderate bleeding stop heparin therapy is sufficient for Heparin half-life of only 60 ~ 90min, APTT usually recovered within 6h.



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