What Are the Symptoms of Blood Clots in the Lungs?

Pulmonary embolism (PE) is a general term for a group of diseases or clinical syndromes caused by various emboli obstructing the pulmonary artery system, including pulmonary thromboembolism (PTE), fat embolism syndrome, amniotic fluid embolism, air embolism, etc.

Pulmonary thromboembolism

Definition of pulmonary thromboembolism

PTE is a disease caused by a thrombus from the venous system or the right heart that obstructs the pulmonary artery or its branches, with pulmonary circulation and respiratory dysfunction as its main clinical and pathophysiological characteristics.

Pathophysiology of pulmonary thromboembolism

1. The thrombus that causes PTE can originate from the inferior vena cava approach, superior vena cava approach, or right ventricle, most of which originate from the deep veins of the lower limbs, especially the deep veins from the upper end of the sacroiliac vein to the proximal vein of the lower limb (about Accounting for 50% to 90%). The pelvic venous plexus is also an important source of thrombosis. Insertion, indwelling catheters, and intravenous chemotherapy in the jugular and subclavian veins have increased the number of thrombus originating from the superior vena cava approach. The proportion of thrombus from right ventricle is small.

2. The thromboembolism of the pulmonary artery can be either single-site or multi-site. Pathological examination is more common for multi-site or bilateral thromboembolism. It is believed that embolism is more likely to occur in the right and lower lobe. After the occurrence of embolism, there may be secondary thrombosis in the local area of the embolism and participate in the pathogenesis. After the emboli obstructs the pulmonary artery and its branches to a certain extent, the mechanical blockage, coupled with the contraction of the pulmonary artery caused by neurohumoral factors and hypoxia, results in increased pulmonary circulation resistance and pulmonary hypertension; increased post-load load in the right ventricle and increased tension in the right ventricle wall, To a certain extent, it causes acute pulmonary heart disease. The right ventricle is enlarged, and right ventricular dysfunction may occur. The amount of blood returned to the heart is reduced, and the venous system is congested. Decreasing the amount can cause systemic hypotension or shock; intraaortic hypotension and right atrial pressure increase, reducing coronary perfusion pressure and reducing myocardial blood flow, especially the hypoventricular myocardium in a hypoperfusion state, plus PTE When myocardial oxygen consumption increases, it can cause myocardial ischemia and induce angina.

3. Pulmonary blood flow at the site of embolism decreases, and the volume of ineffective alveolar space increases; redistribution of blood flow in the lungs, imbalance of ventilation / blood flow ratio; elevated right atrial pressure can cause the functionally closed oval foramen to open and produce intracardiac Right-to-left shunting; neurohumoral factors can cause bronchospasm; increased capillary permeability, increased interstitial and alveolar fluid or bleeding; reduced alveolar surfactant secretion at the site of embolism, alveolar collapse, and reduced breathing area; lung compliance Sexual decline, reduced lung volume and atelectasis; if the pleura is involved, pleural effusion may occur. The above factors lead to respiratory insufficiency, hypoxemia, compensatory hyperventilation (hypocapnia) or relative hypoalveolar ventilation.

4. Because the lung tissue receives multiple oxygen supplies such as pulmonary arteries, bronchial arteries, and alveolar gas diffusion, pulmonary infarction rarely occurs during PTE. If there is a basic cardiopulmonary disease or a serious condition that affects the multiple oxygen supply to the lung tissue, it may cause 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, the presence of other cardiopulmonary diseases at the same time, the differences in individual responses, and the speed of thrombolysis have important effects on the pathogenesis and prognosis.

If the pulmonary artery thrombosis is not completely dissolved after acute PTE, or if PTE occurs repeatedly, chronic thromboembolic pulmonary hypertension (CTEPH) may be formed, followed by chronic pulmonary heart disease, right heart compensatory hypertrophy, and right heart failure.

Differential diagnosis of pulmonary thromboembolism

Due to the lack of specificity in the clinical manifestations of PTE, it is easy to be confused with other diseases, and the clinical missed and misdiagnosed rate is extremely high. Doing a good job in the differential diagnosis of PTE is of great significance for timely detection and diagnosis of PTE.

(A) coronary atherosclerotic heart disease (coronary heart disease)

Due to hemodynamic changes, some patients with PTE may suffer from insufficient coronary blood supply, myocardial hypoxia, and chest tightness, angina pectoris-like chest pain, electrocardiogram ischemia-like changes, and are easily misdiagnosed as angina pectoris or myocardial infarction caused by coronary heart disease. Coronary heart disease has its own pathological characteristics. Coronary angiography can show evidence of coronary atherosclerosis and lumen obstruction. The electrocardiogram and myocardial enzyme levels have corresponding characteristic dynamic changes during myocardial infarction. Note that PTE and coronary heart disease can sometimes coexist.

(B) Pneumonia

When PTE has cough, hemoptysis, dyspnea, pleuritic chest pain, atelectasis, and lung shadows, especially when accompanied by fever, it is easy to be misdiagnosed as pneumonia. Pneumonia has manifestations of corresponding lung and systemic infections, such as purulent sputum, chills, high fever, a significant increase in peripheral blood leukocytes, and an increase in the proportion of neutrophils. Antibacterial treatment can be effective.

(3) Non-thromboembolic pulmonary hypertension such as idiopathic pulmonary hypertension

CTEPH usually has high pulmonary arterial pressure, right heart hypertrophy and right heart failure, and it needs to be distinguished from idiopathic pulmonary hypertension. CTPA and other examinations showed evidence of intrapulmonary obstruction in CTEPH. Radionuclide lung perfusion scans showed pulmonary perfusion defects distributed in the lung segment, while idiopathic pulmonary hypertension did not have intrapulmonary space occupying signs. Radionuclide lung perfusion scans Normal or radioactive sparse. CTEPH also needs to be distinguished from other types of pulmonary hypertension.

(D) aortic dissection

PTE can show chest pain, and some patients may have shock, which needs to be distinguished from aortic dissection. The latter has high blood pressure and severe pain. Chest radiographs often show widening of the mediastinum. Cardiovascular ultrasound and chest CT angiography can show aortic dissection. Sign.

(V) Pleural effusion caused by other reasons

PTE patients may develop pleurisy-like chest pain and pleural effusion, which needs to be distinguished from pleural effusion caused by tuberculosis, pneumonia, tumors, heart failure and other reasons. Other diseases have their own clinical characteristics, and pleural effusion tests often help to identify them.

(VI) Syncope due to other reasons

When PTE has syncope, it needs to be distinguished from syncope caused by other causes such as vagal reflex, cerebrovascular syncope, and arrhythmia.

(7) Shock due to other reasons

PTE-induced shock is an extracardiac obstructive shock, which is characterized by low arterial blood pressure and elevated venous pressure, and needs to be distinguished from cardiogenic, hypovolemic, and redistributive shock.

Treatment of pulmonary thromboembolism

First aid measures

l. General treatment: intensive care should be carried out, and bedridden for 1-2 weeks. Those with severe chest pain should be given analgesics and sedatives.

2. Correction of acute right heart failure (dopamine, etc.)

3. Prevention and treatment of shock.

4. Improve oxygenation and ventilation function. Inhale oxygen or non-invasive mask ventilation, if necessary, intubate artificial ventilation.

Second, thrombolytic therapy

1. Indications for thrombolysis: The time window for thrombolysis is generally specified within 14 days, but in view of the possible dynamic formation of thrombus, the time window is not absolute. The currently accepted indication for thrombolytic therapy is massive pulmonary thromboembolism, which is characterized by right ventricular dysfunction with hypotension or cardiogenic shock. If there is no contraindication to treatment for such patients, thrombolytic therapy should be given actively and promptly.

2. Absolute contraindications: active internal bleeding, recent spontaneous intracranial hemorrhage.

3. Relative contraindications: major surgery, childbirth, organ biopsy or vascular puncture at the hemostatic site that cannot be compressed 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; difficult to control severe hypertension (systolic blood pressure> 180mmHg, diastolic blood pressure> 110mmHg); recent cardiopulmonary resuscitation; platelet count <100 × 109 / L; pregnancy; bacterial intracardiac Meningitis; severe liver and kidney dysfunction; diabetic hemorrhagic retinopathy.

Clinical classification of pulmonary thromboembolism

(A) acute pulmonary thromboembolism

1. Large-area PTE (massive PTE) is clinically characterized by shock and hypotension, that is, systemic arterial systolic blood pressure <90mmHg, or a decrease of 40mmHg from the basic value, which lasts for more than 15 minutes. The blood pressure drop due to other causes, such as new arrhythmia, hypovolemia, or infection, must be excluded.

2. Non-massive PTE (non-massive PTE) does not meet the above criteria for large-area PTE, and there is no PTE of shock and hypotension. In some cases of non-large-area PTE, right ventricular dysfunction appears clinically, or existing right ventricular motor function is weakened on the echocardiogram (the right ventricular anterior wall motion amplitude is <5mm), which is a sub-massive PTE (sub-massive PTE) type.

(B) chronic thromboembolic pulmonary hypertension (CTEPH)

It can be traced back to the clinical manifestations of chronic and progressive pulmonary hypertension, with right heart failure in the later stage; imaging examinations confirmed pulmonary artery occlusion, which often showed multiple sites and extensive obstructions. Chronic embolism signs such as eccentric distribution, calcified mass, etc .; DVT can often be found; right heart catheterization examination shows average pulmonary arterial pressure> 25mmHg, mean pulmonary artery pressure> 30mmHg after activity; echocardiogram examination shows right ventricle Wall thickening (right ventricular free wall thickness> 5mm), in line with the diagnostic criteria for chronic pulmonary heart disease.

Clinical symptoms of pulmonary thromboembolism

Symptoms are diverse and non-specific. Common symptoms are:

1. Dyspnea; 2. Chest pain; 3. Fainting; 4. Irritability 5. Hemoptysis; 6. Cough; Palpitations

Sometimes the so-called "triple sign" occurs, that is, dyspnea, chest pain, and hemoptysis occur at the same time

Common signs of pulmonary thromboembolism

First, the respiratory system: fast breathing frequency, cyanosis. Both lungs can hear wheezing, wet rales, and occasionally corresponding signs of pleural friction or pleural effusion;

Heart signs: fast heart rate, P2 hyperactivity and systolic murmurs; tricuspid regurgitation murmurs; pericardial friction sounds or pleural pericardial friction sounds; signs of right heart failure such as jugular vein irritation, liver tenderness, and liver-neck reflux Sign (+) and so on.

Signs of phlebitis or embolism in the lower extremities: swelling of one limb (> 1cm above the contralateral side, 15cm above the sacrum, and 10cm below)

Auxiliary examination of pulmonary thromboembolism

I. Blood gas analysis, D-dimer was strongly positive (> 500 mg / l); PaO2 decreased.

2. X-ray chest radiograph: Typical changes are triangular shadows with leaf segment distribution, which can also be expressed as patchy shadows, disc atelectasis, and localized pulmonary texture reduction at the distal end of obstruction. Small infarct x-rays were completely normal. Pleural effusion and pulmonary hypertension can be combined with corresponding imaging changes (see Pulmonary Heart Disease).

3. ECG examination: The typical EKG change of acute pulmonary embolism is the right deviation of QRS axis. Pulmonary type P wave, SI, QIIIT type III (ie, the I wave in lead I deepens, and the small Q wave and T wave inversion in lead III). However, the positive rate of typical changes is low. Only seen in large or extensive embolism. It appears more than 5-24 hours after the onset, and recovers within a few days to 3 weeks. Dynamic observation is helpful for the diagnosis of this disease.

4. Echocardiography: You can see that the ventricles are enlarged, and understand whether the main pulmonary artery and its left and right branches are blocked;

Five, rapid spiral CT or ultra-high-speed CT enhanced scan: can show the situation of large vessel embolism above the segment;

Sixth, magnetic resonance (MRl): can show pulmonary artery or left and right branches of blood vessel embolism.

Seven, radionuclide lung ventilation / perfusion (V / Q) scan: currently the preferred method for non-invasive diagnosis of PE. Typical changes are normal lung ventilation scans and typical perfusion defects (V / Q mismatch in leaf segment distribution). The positive rate for lesions above the sub-segment was> 95%. The performance of V / Q imaging can be divided into

(1) Highly suspected pulmonary embolism: lung ventilation scans are normal. The perfusion was typical defects (V / Q mismatch);

(2) Suspicious pulmonary embolism: Ventilation and perfusion defects, which may be parenchymal pulmonary disease or pulmonary embolism, have little diagnostic significance.

(3) Pulmonary embolism is basically excluded: perfusion imaging is normal.

Pulmonary angiography (CPA): CPA is currently the most reliable method for diagnosing PE, and can determine the location and extent of the obstruction.

Somewhat traumatic.

1. The clinical symptoms are highly suspicious. PE, pulmonary ventilation, and perfusion scan cannot confirm the diagnosis. Cannot exclude PE;

2. Those who are preparing for pulmonary embolism or inferior vena cava surgery.

Nine, deep vein examination of the lower limbs:

1. Doppler examination of blood vessels

2. Radionuclide venography can detect lower extremity thrombosis.