1.Symptoms: The symptoms of pulmonary thromboembolism lack specificity and depend mainly on the size and number of emboli, the site of embolism and the presence of underlying diseases of the heart, lungs and other organs of the patient. Smaller emboli may not have any clinical symptoms. Larger emboli may cause dyspnea, cyanosis, syncope, and sudden death. Sometimes syncope may be the only or the first symptom of APTE. When pulmonary embolism causes pulmonary infarction, “pulmonary infarction triad” may appear clinically, which manifests as: ① chest pain, such as pleuritic chest pain or angina-like pain; ② hemoptysis; ③ dyspnea. In case of co-infection, it is accompanied by cough, sputum and high fever. Due to hypoxemia and right heart insufficiency, hypoxic manifestations such as irritability, dizziness, chest tightness, palpitations, etc. may occur. Because of the lack of clinical specificity of the above symptoms, it brings some difficulties to the diagnosis, and should be differentiated from angina pectoris, stroke and pneumonia. 2. Signs: mainly respiratory and circulatory signs, especially increased respiratory rate (more than 20 times/min), accelerated heart rate (more than 90 times/min), and decreased blood pressure.
Jugular venous filling or abnormal pulsation suggests increased right heart load; lower limb venous examination reveals that the circumference of one thigh or calf increases more than 1 cm compared with the opposite side.
Pulmonary thromboembolism should be highly suspected. Other respiratory signs include hyperacusis or splitting of heart sounds and systolic murmurs in the tricuspid region. 3, clinical syndromes of pulmonary embolism Acute pulmonary embolism can be divided into three types of syndromes, which help to estimate the prognosis and guide the development of treatment plan (see Table 3). Among them, massive pulmonary embolism predisposes to cardiogenic shock and multi-organ failure. Renal insufficiency, hepatic insufficiency and mental stress are common clinical manifestations and are emergencies requiring urgent management. Laboratory tests 1. Arterial blood gas analysis: It is a screening index for the diagnosis of APTE. It should be based on the measurement value of the first arterial blood gas analysis when the patient is in the prone position at the time of consultation, not on oxygen, and characterized by hypoxemia, hypocarbia, increased alveolar arterial partial pressure of oxygen difference [P(A-a)O2] and respiratory alkalosis. Because arterial partial pressure of oxygen decreases with age, the normal predicted value of partial pressure of oxygen should follow the formula PaO2(mm
Hg)=106 C 0,14 ×
age (years) for calculation. It is worth noting that the detection index of blood gas analysis is not specific, and according to statistics, about 20% of patients diagnosed with APTE have normal blood gas analysis results. 2. Plasma D-dimer: It is a soluble degradation product produced by cross-linked fibrin under the action of fibrinolytic system. In thromboembolism, its blood concentration increases due to thrombofibrinolysis. The sensitivity of plasma D-dimer for the diagnosis of APTE is 92%-100%, but its specificity is low, only 40%-43%, and D-dimer can be increased during surgery, trauma and acute myocardial infarction. The main value of plasma D-dimer determination is to exclude APTE.9 Patients with low-suspicion APTE are preferred to have their plasma D-dimer quantified by ELISA, and APTE can be excluded if it is less than 500 μg/L; patients with high-suspicion APTE are not recommended to have this test, because for these patients, APTE cannot be excluded regardless of the plasma D-dimer test results, and they all need to undergo pulmonary arteriography and other means. Pulmonary arteriography and other means are needed for evaluation. 3.Electrocardiogram: It is not specific for the diagnosis of APTE. Early ECG often shows ST-segment depression and T-wave inversion in chest leads V1-V4 and limb leads II, III and aVF, and in some cases SⅠQⅢTⅢ (i.e. deepening of S-wave in lead I, Q/q wave and T-wave inversion in lead III), which is caused by acute pulmonary artery blockage, pulmonary hypertension, increased right heart load and right heart dilatation. Attention should be paid to differentiate it from non-ST-segment elevation acute coronary syndrome and observe the dynamic changes of ECG. 4. Echocardiography: It has important value in suggesting the diagnosis, prognosis assessment and excluding other cardiovascular disorders.10 Echocardiography can provide direct and indirect signs of APTE. The direct sign can visualize proximal pulmonary artery or right heart cavity thrombus, but the positive rate is low, and the diagnosis can be made definitively if the patient’s clinical presentation is also consistent with PTE. Indirect signs are mostly manifestations of right heart overload, such as decreased local motion of the right ventricular wall, enlargement of the right ventricle and/or right atrium, increased velocity of tricuspid regurgitation and abnormal leftward motion of the ventricular septum, and widening of the pulmonary artery trunk. 5.Pulmonary artery embolism: If pulmonary artery embolism causes pulmonary hypertension or pulmonary infarction, pulmonary ischemic signs such as sparse and slender pulmonary texture, prominent or aneurysmal dilatation of pulmonary artery segment, widening or truncation of right lower pulmonary artery trunk, and enlarged right ventricle may appear on X-ray. Localized infiltrative shadows in the lung field; wedge-shaped shadows with the tip pointing to the hilum; disciform atelectasis; elevated diaphragm on the affected side; small amount of pleural effusion; thickened pleural adhesions, etc. may also appear. 6.CT pulmonary arteriogram: CT has the characteristics of non-invasive, fast scanning speed, clear image, and more economical, which can visually determine the site and scope of pulmonary artery embolism, the degree and shape of pulmonary artery embolism; the direct signs of PTE are low-density filling defect in the pulmonary artery, partially or completely enclosed within the opaque blood flow (orbital sign), or a complete filling defect with no distal vessels; indirect Indirect signs include wedge-shaped strips of high density in the lung field or disciform atelectasis, dilated central pulmonary artery and reduced or absent distal vascular distribution.11 CT pulmonary angiography is an important noninvasive technique for the diagnosis of PTE, with a sensitivity of 90% and specificity of 78% to 100%. Its limitation lies mainly in the poor sensitivity to subsegmental and distal intra-pulmonary artery thrombi. In clinical applications, CT pulmonary angiography should be judged in conjunction with the patient’s clinical likelihood score. In low-risk patients, a normal CT result can exclude PTE; in patients with a high-risk clinical score, a negative CT pulmonary angiogram does not exclude a single subsegmental pulmonary embolism. If CT shows segmental or above segmental thrombus, it can confirm the diagnosis of PTE, but for suspected subsegmental or more distant thrombus, further combination with lower extremity venous ultrasound, pulmonary ventilation and perfusion scan or pulmonary angiography is required to clarify the diagnosis.