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1、Guidelines on the diagnosis and management of acute pulmonary embolism,2008ESC,Classes of recommendations,Levels of evidence,Predisposing factors,Predisposing factors for venous thromboembolism: Table 3,Natural history,The risk of VTE after surgery is highest during the first 2 weeks after surgery b

2、ut remains elevated for 2 3 months. Antithrombotic prophylaxis significantly reduces the risk of perioperative VTE.The longer the duration of antithrombotic prophylaxis, the lower the incidence of VTE.,Most patients with symptomatic DVT have proximal clots, and in 40 50% of cases this condition is c

3、omplicated by PE, often without clinical manifestations. Asymptomatic PE is common in the postoperative phase, particularly in patients with asymptomatic DVT who are not given any thromboprophylaxis PE occurs 3 7 days after the onset of DVT,shock or hypotension in 510% of cases, and in up to 50% of

4、cases without shock but with laboratory signs of right ventricular dysfunction (RVD) and/or injury ,which indicates a poorer prognosis. complete resolution; two-thirds of all patients without anticoagulation, about 50% , within 3 months anticoagulation treatment at least 3-12 months of anticoagulati

5、on treatment,Pathophysiology,The consequences of acute PE are primarily haemodynamic and become apparent when 3050% of the pulmonary arterial bed is occluded by thromboemboli. Large and/or multiple emboli might abruptly increase pulmonary vascular resistance to a level of afterload which cannot be m

6、atched by the right ventricle (RV). Sudden death:Electormechanical dissociation syncope and/or systemic hypotension,Pathophysiology,Patients surviving: activate the sympathetic system resting pulmonary flow, left ventricular filling and output, Together with systemic vasoconstriction, RV coronary pe

7、rfusion and the function of the RV Secondary haemodynamic destabilization may occur, usually within rst 2448 h, recurrent emboli or deterioration of RV function increased RV myocardial oxygen demand and decreased RV coronary perfusion Respiratory insufciency in PE is predominantly a consequence of h

8、aemodynamic disturbances.,Severity of pulmonary embolism,Principal markers useful for risk stratification in acute pulmonary embolism Table 4 Risk stratication according to expected pulmonary embolism-related early mortality rate Table 5,Diagnosis,Diagnosis :probability X-ray and blood gas analysis:

9、 plate-like atelectasis; pleural effusion; elevation of a hemidiaphragm. PE is generally associated with hypoxaemia, but up to 20% of patients with PE have a normal (PaO2) and D(A-a)O2 ECG :inversion of T waves in leads V1V4,QR pattern in lead V1,classic S1O3T3, right bundle-branch block. such chang

10、es are generally associated with the more severe forms of PE and may be found in right ventricular strain of any cause. In summary :clinical signs, symptoms and routine laboratory tests do not allow the exclusion or conrmation of acute PE but increase the index of its suspicion.,Assessment of clinic

11、al probability,Clinical prediction rulers for PE: the Wells score and the revised Geneva score,Auxiliary examination,D-dimer ultrasonography Ventilation perfusion scintigraphy Computed tomography Pulmonary angiography Echocardiography,Diagnostic strategies,suspected high-risk PE: suspected non-high-

12、risk PE:,Diagnostic strategies,Validated diagnostic criteria for diagnosing PE in patients without shock and hypotension (non-high-risk PE) according to clinical probability,Recommendations: diagnosis,Recommendations: diagnosis,Recommendations: diagnosis,Prognostic assessment,Clinical assessment of

13、haemodynamic status Markers of right ventricular dysfunction Markers of myocardial injury Additional risk markers (Table12),Treatment,Haemodynamic and respiratory support Thrombolysis Surgical pulmonary embolectomy Percutaneous catheter embolectomy and fragmentation,Initial anticoagulation,Objective

14、: prevent death and recurrent events UFH LMWH fondaparinux anticoagulant treatment should be considered in patients with suspected PE while awaiting denitive diagnostic conrmation. an initial course of heparin in addition to VKAs UFH is given 80 U/kg as a bolus injection followed by infusion at the

15、rate of 18 U/kg/h should be preferred to xed dosages of heparin. Subsequent adjusted using (aPTT)-based (table15),Initial anticoagulation,The aPTT should be measured 46h after the bolus injection and then 3 h after each dose adjustment, or once daily when the target therapeutic dose has been reached

16、. aPTT is not a perfect marker of the intensity of the anticoagulant effect of heparin. Therefore, it is not necessary to increase the infusion rate above 1667 U/h provided the anti-factor Xa heparin level is at least 0.35 IU/mL, even if the aPTT ratio is below the therapeutic range.,Initial anticoagulation,anticoagulation with unfractionated heparin, LMWH or fondaparinux should be initiated without delay in patients with confirmed PE and those with a high or intermediate clinical probability o

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