PTE is fromveinPulmonary circulation and respiratory dysfunction are the main clinical and pathophysiological characteristics of diseases caused by pulmonary artery or its branches blocked by thrombus in the system or right heart.
differential diagnosis
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Due to the lack of specificity in the clinical manifestations of PTE, it is easy to be confused with other diseases, so that the rate of missed diagnosis and misdiagnosis is extremely high in clinical practice.The differential diagnosis of PTE is important to detect and diagnose PTE in time.
Due to hemodynamic changes, some PTE patients may have insufficient coronary artery blood supply, myocardial hypoxia, chest tightness, angina pectoris like chest pain, and myocardial ischemia like changes in electrocardiogram, which are easily misdiagnosed as angina pectoris or myocardial infarction caused by coronary heart disease.Coronary heart disease has its own characteristics,Coronary angiographysoatherosclerosisEvidence of lumen obstruction, ECG andMyocardial enzymeThe level has corresponding characteristic dynamic changes.It should be noted that PTE and coronary heart disease can sometimes coexist.
When PTE hascoughHemoptysis, dyspnea, pleurisy like chest pain, atelectasis and shadow of the lungs, especially when accompanied by fever, are easily misdiagnosed as pneumonia.Pneumonia has corresponding lungs andSystemic infectionThe symptoms such as purulent sputumshiver、High feverThe white blood cells in peripheral blood and the proportion of neutrophils increased significantly. Antibacterial treatment can achieve curative effect.
CTEPH usually has high pulmonary artery pressure, right heart hypertrophy and right heart failure, which should be differentiated from idiopathic pulmonary hypertension.CTPA and other examinations showed that CTEPH had evidence of pulmonary artery obstruction. Radionuclide pulmonary perfusion scan showed pulmonary perfusion defects with segmental distribution, while idiopathic pulmonary hypertension had no pulmonary artery space occupying sign. Radionuclide pulmonary perfusion scan was normal or generally radioactive sparse.CTEPH should also be differentiated from other types of pulmonary hypertension.
(4) Aortic dissection
PTE can show chest pain, and some patients may have shock, which needs to be differentiated from aortic dissection. Most of the latter have high blood pressure and severe pain. Chest films often show widened mediastinum, and cardiovascular ultrasound and chest CT angiography can show signs of aortic dissection.
(5) Pleural effusion caused by other reasons
PTE patients may have pleurisy like chest pain and pleural effusion, which should be differentiated from pleural effusion caused by tuberculosis, pneumonia, tumor, heart failure and other reasons.Other diseases have their own clinical characteristics,Examination of pleural effusionIt is often helpful for identification.
(6) Syncope caused by other reasons
When PTE has syncope, it should be differentiated from syncope caused by vagal reflex, cerebrovascular syncope, arrhythmia and other reasons.
(7) Shock caused by other reasons
The shock caused by PTE belongs to extracardiac obstructive shock, which is characterized by low arterial blood pressure and high venous pressure. It should be differentiated from cardiogenic, hypovolemic, and blood volume redistribution shock.
Pathophysiology
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1. Thrombosis causing PTE can come from the inferior vena cava, superior vena cava or right heart cavity, most of which come from the deep veins of the lower limbs, especially from the upper end of the popliteal vein to the proximal end of the lower limbs of the iliac vein segmentDeep vein(about 50%~90%).Pelvic venous plexus is also an important source of thrombosis.Inner neck andSubclavian veinThe number of thrombus originating from the superior vena cava pathway increased more than before due to the insertion, indwelling of catheter and intravenous chemotherapy.Thrombosis from the right cardiac cavity accounted for a small proportion.
2,pulmonary arteryThromboembolism can be either single site or multi site.Pathological examinationIt is more common to find multiple or bilateral thromboembolism.It is generally believed that embolism is more likely to occur in the right and lower lobes.It may be secondary in the embolic area after embolismThrombosis, participate in the pathogenesis.After the embolus blocks the pulmonary artery and its branches to a certain extent, the contraction of the pulmonary artery caused by mechanical obstruction, neurohumoral factors and hypoxia will lead toPulmonary circulationIncreased resistancePulmonary hypertension;The right ventricular afterload increases and the right ventricular wall tension increases to a certain extentAcute pulmonary heart disease, right ventricle enlargement, right ventricle may appearCardiac insufficiencyThe amount of blood returning to the heart is reduced, and the venous system is congested;The enlargement of the right heart causes the ventricular septum to move to the left, which damages the function of the left ventricle, leading toCardiac outputDecline, which may causeSystemic circulationhypotensionOr shock;Intraaortic hypotension and elevated right atrial pressure reduce coronary artery perfusion pressure and myocardial blood flow, especially the subendocardial myocardium is in a low perfusion state. In addition, myocardial oxygen consumption increases during PTE, which can cause myocardial ischemia and induce angina pectoris.
3. The pulmonary blood flow at the embolic site decreases,AlveoliThe volume of ineffective cavity increases;Redistribution of pulmonary blood flow and imbalance of ventilation/blood flow ratio;The increase of right atrial pressure can lead to the opening of the functionally closed foramen ovale, resulting in intracardiac right to left shunt;Neurohumoral factors can cause bronchospasm;Capillary permeability increased, interstitial and alveolar fluid increased or bleeding;Embolization sitePulmonary surfactantDecreased secretion, collapsed alveoli and decreased respiratory area;Lung compliance decreases, lung volume shrinks and atelectasis may occur;If involvedpleura, can appearpleuralFluid accumulation.The above factors lead tobreathingIncomplete function, appearingHypoxemia, compensatoryHyperventilation(hypocapnia) or relatively low alveolar ventilation.
4. Because lung tissue receives pulmonary arteryBronchial arteryAnd gas diffusion in the alveoli, so PTE rarely occursPulmonary infarction。If there is a basic heart and lung disease or the condition is serious, which affects the multiple oxygen supply of the lung tissue, it may lead to pulmonary infarction.
5. The severity of the disease caused by PTE depends on the combined effect of the above mechanisms.The size and number of emboli, the interval between successive emboli of multiple emboli, whether there are other cardio pulmonary diseases at the same time, individual differences in response, and the speed of thrombolysis have an important impact on the pathogenesis and prognosis.
If the thrombus in the pulmonary artery is not completely dissolved after acute PTE, or PTE occurs repeatedly, chronic thromboembolic pulmonary hypertension (CTEPH) may occur, and thenChronic pulmonary heart disease, right heart compensatory hypertrophy and right heart failure.
Treatment measures
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1、 First aid measures
l. General treatment: intensive care should be carried out, and patients with severe chest pain should be given analgesics and sedatives.
2. Correct acute right heart failure (dopamine, etc.)
4. Improve oxygenation and ventilation function Oxygen inhalation or noninvasive face mask ventilation, and conduct artificial ventilation through tracheal intubation when necessary.
2、 Thrombolytic therapy
1. Thrombolysis indication: The thrombolysis time window is generally specified to be within 14 days, but in view of the possible dynamic formation process of thrombus, this time window is not absolute.At present, the accepted indication for thrombolytic therapy is massive pulmonary thromboembolism, which is characterized by right ventricular dysfunction, hypotension or cardiogenic shock.If there is no contraindication to treatment for such patients, thrombolytic treatment should be given actively and rapidly.
2. Absolute contraindication: active internal hemorrhage, recent spontaneous intracranial hemorrhage.
3. Relative contraindication: major surgery, delivery, organ biopsy or blood vessel puncture that cannot compress the hemostasis site within 2 weeks;Ischemic stroke within 2 months;Gastrointestinal bleeding within 10 days;Severe trauma within 15 days;Neurosurgery or ophthalmic surgery within 1 month;Uncontrollable severe hypertension (systolic pressure>180mmHg, diastolic pressure>110mmHg);Cardiopulmonary resuscitation was performed recently;Platelet count<100 × 109/L;Pregnancy;Bacterial endocarditis;Severe liver and kidney dysfunction;Diabetic hemorrhagic retinopathy, etc.
Clinical classification
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(1) Acute pulmonary thromboembolism
1. Massive PTE is clinically characterized by shock and hypotension, that is, systemic arterial systolic pressure<90mmHg, or a decrease of ≥ 40mmHg from the base value, lasting for more than 15 minutes.New occurrence must be excludedArrhythmia, hypovolemia or infection poisoning and other causes of blood pressure decline.
2. Non massive PTE does not meet the above criteria for large-area PTE, and there is no PTE with shock and hypotension.Some cases of non large-area PTE are clinically rightCardiac insufficiency, orEchocardiographyIt shows that the motor function of the right ventricle is weakened (front wall of the right ventricleRange of motion<5mm), which belongs to sub massive PTE subtype.
Most of them can be traced back to the relevant clinical manifestations of pulmonary hypertension with chronic and progressive development, and right heart failure occurs later;The imaging examination confirmed pulmonary artery obstruction, which was often multiple and extensive, and chronic embolism signs such as pulmonary artery sticking to the vascular wall, surrounding or eccentric distribution, and lumps with calcification tendency could be seen;DVT can often be found;Right heart catheterization showed that the mean pulmonary artery pressure at rest was>25 mmHg, and the mean pulmonary artery pressure after exercise was>3 OmmHg;Echocardiography showed right ventricular wall thickening (right ventricular free wall thickness>5mm), which met the diagnostic criteria of chronic pulmonary heart disease.
Clinical symptoms
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Symptoms are diverse and nonspecific.Common symptoms include:
Sometimes the so-called "triple syndrome" occurs clinically, that is, dyspnea, chest pain and hemoptysis occur at the same time
Common signs
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1、 Respiratory system: fast breathing rate, cyanosis.Wheezing sounds and moist rales can be heard in both lungs, occasionallyPleural fricative soundOr corresponding signs of pleural effusion;
2、 Cardiac signs: fast heart rate, P2 hyperactivity and systolic murmur;Tricuspid regurgitant murmur;Pericardial friction sound or pleural pericardial friction sound;There may be signs of right heart failure, such as distension of the jugular vein, hepatomegaly, and tenderness;Liver neck reflux sign (+), etc.
3、 Signs of phlebitis or embolism of lower limbs: swelling of one limb (the control side>1cm, 15cm above the patella, 10cm below the patella), local tenderness and skin temperature rise
Supplementary Examination
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1、 Blood gas analysis showed that D-dimer was strongly positive (>500mg/l);PaO2 decreased.
2、 X-ray chest film: the typical changes are triangular shadows distributed in lobes, and also can be manifested as patchy shadows, discoid atelectasis, reduction of local pulmonary markings at the distal end of obstruction, etc. X-ray films of small infarcts are completely normal.It can be associated with pleural effusion and pulmonary hypertension, resulting in corresponding imaging changes (seePulmonary heart disease)。
3、 ECG examination: the typical EKG changes of acute pulmonary embolism are right deviation of QRS axis, pulmonary P wave, SI, QIIIT III (that is, deepening of s wave in lead I, inversion of small Q wave and T wave in lead III).However, the positive rate of typical changes was low.Only seen in massive or extensive embolism.More than 5 to 24 hours after onset, several days to 3Weeks laterRestore.Dynamic observation is helpful to the diagnosis of this disease.
IVultrasonicCardiogram: ventricular enlargement can be seen to know whether the main pulmonary artery and its left and right branches are blocked;
5、 Fast spiral CT or ultrahigh speed CT enhanced scanning: it can display the situation of large vessel embolism above the segment;
VInuclear magnetic resonance(MRl): It can display the pulmonary artery or the left and right branches of vascular embolism.
7、 Radionuclide lung ventilation/perfusion (V/Q) scan: the first choice for non-invasive diagnosis of PE.The typical change is that the lung ventilation scanning is normal, while the perfusion is typical defect (V/Q mismatch distributed by leaf segment).The positive rate of lesions above sub segment was more than 95%.The performance of V/Q imaging can be divided into
(2) Suspicious pulmonary embolism: both ventilation and perfusion are defective, which may be pulmonary parenchymal disease or pulmonary embolism, with little diagnostic significance.
(3) Pulmonary embolism was basically excluded: perfusion imaging was normal.
8、 Pulmonary angiography (CPA): CPA is the most reliable method for diagnosing PE at present, which can determine the location and extent of obstruction.
It is somewhat traumatic.
1. The clinical symptoms of PE were highly suspicious, pulmonary ventilation and perfusion scanning could not be confirmed.PE cannot be excluded;
2. Those who are ready for pulmonary embolectomy or inferior vena cava surgery.
9、 Examination of deep veins of lower limbs:
1. Ultrasound Doppler examination of blood vessels
2. Radionuclide venography can detect lower limb thrombosis.