What Are the Different Signs of a Pulmonary Embolism?

Pulmonary embolism is a pathological process in which a thrombus or other substance occludes the pulmonary artery or its branch. It is often a comorbidity. Necrosis of the lung tissue after vascular obstruction is called pulmonary infarction. Clinical symptoms include dyspnea, severe chest pain, hemoptysis, and fever. May have dry chest, wet rales, pleural friction sounds, pleural effusion signs and shock, cyanosis and other manifestations.

Overview of acute pulmonary embolism

Acute pulmonary embolism is a clinical and pathophysiological syndrome of pulmonary circulation disorder caused by endogenous or exogenous emboli blocking the trunk or branch of the pulmonary artery.

Human lungs The morbidity is second only to coronary heart disease and hypertension, and the mortality rate ranks third, second only to tumors and myocardial infarction. However, due to the lack of attention to the prevention and treatment of this disease, it has been missed and misdiagnosed frequently in primary hospitals. The combined effects of blood flow stasis and venous injury and blood hypercoagulable state are prone to cause thrombosis. Shedding of the thromboembolism can lead to the fall of pulmonary embolism. Embolism is often associated with sudden changes in blood flow, such as sudden movement of bedridden patients after prolonged illness or forced defecation of pulmonary embolism. Most of the emboli come from the deep veins of the lower limbs and can also come from the pelvic vein or the right heart.

Causes of acute pulmonary embolism

Most patients with APE have a cause of disease, such as lower limb or pelvic vein thrombosis, prolonged bed rest or inactivity, slow

Acute pulmonary embolism Cardiopulmonary diseases, surgery, trauma, malignant tumors, pregnancy and oral contraceptives, etc., should pay special attention when asking medical history. Symptoms and signs: dyspnea, severe chest pain, hemoptysis, and fever. Physical examination: Pay attention to the performance of chest dryness, wet rales, pleural friction sounds, pleural effusion signs, shock, and cyanosis. Causes of the disease Pay attention to long-term bed rest, atrial fibrillation, long-term heart failure, bacterial endocarditis, major thoracotomy, peri-inflation angiography, artificial pneumoperitoneum, fractures of tibia, femur, and pelvis, cancer, and polycythemia vera , Thrombocytosis, oral contraceptives, diabetes, Behcet's disease and other causes and causes. The combined effects of blood flow stasis and venous injury and blood hypercoagulable state are prone to cause thrombosis. Shedding of the thromboembolism can lead to the fall of pulmonary embolism. Embolism is often associated with sudden changes in blood flow, such as sudden movement of bedridden patients after prolonged illness or forced defecation of pulmonary embolism. Most of the emboli come from the deep veins of the lower limbs and can also come from the pelvic vein or the right heart.

Classification of acute pulmonary embolism and pulmonary embolism

The pulmonary vascular bed has a large reserve capacity, and one of the functions of the pulmonary function is to filter the blood, preventing small thrombus from flowing into the systemic circulation.

Acute pulmonary embolism Lung tissue has a strong autolytic effect on thrombi and a small thrombus. Therefore, in some patients, when small blood clots block the pulmonary vascular bed, the clinical symptoms do not continue to occur due to the autolysis of the lung tissue, which is also called clinical non-dominant pulmonary embolism, so it is difficult to make a clinical diagnosis.

Acute pulmonary embolism is classified by clinically diagnosable range of pulmonary embolism

(1) Clinical occult pulmonary embolism: clinically undiagnosable.

(2) Pulmonary embolism accompanied by transient clinical symptoms: clinically difficult to diagnose.

(3) Clinically dominant pulmonary embolism: clinically diagnosed, including:

Acute extensive pulmonary embolism: Refers to a thrombus that has blocked more than two pulmonary lobe arteries or the same range of pulmonary vascular beds.

Acute sub-extensive pulmonary embolism: refers to a thrombus that has blocked more than one lung segment or two or less pulmonary lobe arteries or the same range of pulmonary vascular beds.

Chronic pulmonary embolism with pulmonary hypertension.

Classification of acute pulmonary embolism by thrombus size

1) Pulmonary embolism caused by massive thrombus: Thrombus occludes arteries above regional pulmonary artery branches.

(2) Pulmonary embolism caused by microthrombus: refers to a disease in which a muscular artery (small arteries with an outside diameter of 100 m to 1000 m) is diffusely embolized.

Acute pulmonary embolism is classified by time of onset

1) Acute pulmonary embolism: refers to those with short onset time, usually within 14 days, and those with fresh blood clots blocking the pulmonary artery. If the onset time exceeds 14 days, within 3 months, it is subacute pulmonary embolism.

(2) Chronic pulmonary embolism: the onset time is more than 3 months, and the pulmonary artery thrombosis has been mechanized.

Acute pulmonary embolism pulmonary infarction

(1) Pulmonary infarction type: Acute pulmonary embolism with necrosis of lung tissue is called pulmonary infarction, and pathology is called hemorrhagic necrosis. When thrombus occludes the end of pulmonary artery, it can easily cause pulmonary infarction.

(2) Non-infarction type: Pulmonary infarction is not easy to occur after the pulmonary artery trunk with large diameter is blocked.

The severity of acute pulmonary infarction depends on the scope of the pulmonary artery obstruction. The larger the scope of the obstructed vascular bed, the more severe the condition. The incidence of pulmonary infarction is low. Some people think that pulmonary embolism patients with pulmonary infarction account for about 10% to 15% of the total number of patients with pulmonary embolism.

Acute pulmonary embolism

That is, pulmonary embolism is combined in the critical stage of multiple diseases, and the clinical symptoms and degrees of different diseases are different. This may be related to the susceptibility of pulmonary embolism in the end stage of some diseases. possibility.

Diagnosis of acute pulmonary embolism

The clinical application according to the diagnostic criteria proposed by Japanese scholars is relatively extensive. Judging by the score is easier to grasp.

Acute pulmonary embolism Pulmonary embolism assessment score scale

Project by project

WBC>80001 Primary diseases and factors of acute pulmonary embolismWBC > 80001

Malignant tumor 1 Platelet 1

Thrombophlebitis1 Bilirubin> 1.2mg / dl1

Heart disease 1GOT> 40u1

Surgery 1 GPT> 35u1

Pregnancy, obstetrics and gynecology diseases 1Lactate dehydrogenase> 450u1

Quiet bed 1CO diffusion <80% 1

<85mmHg1 Acute pulmonary embolism

Dyspnea 2 Fibrinogen <150mg / dl2

Chest pain 2 Fibrinogen> 350mg / dl2

Blood sputum 211 fibrin degradation products> 5ng / ml3

Cough 212 antithrombin II <28mg / dl1

Fever 2 (5) ECG

Heart palpitations 1 Right ventricular hypertrophy 3

Swollen edema 1 P wave of lung type 3

sweating 1 right axis of the electric axis 3

Loss of consciousness 1 SIQIIITIII2

1 Signs of acute pulmonary embolism Incomplete right bundle branch block 1

Body temperature> 37.8 1 (6) Chest X-ray

Breathing> 16 times 2 Infiltrated shadow 2

Pulse rate> 100 times 2Pleural effusion 1

Blood pressure <100mmHg1 Granular, reticulated shadow 3

Pulmonary sounds in the lungs 2 Pulmonary arterial hypertrophy in the hilum 2

Hepatomegaly 2 Diaphragm elevation 2

(4) Inspection results

(7) Lung ventilation-perfusion scan imaging

Pulmonary perfusion scan showed regional blood flow defect;

Lung ventilation scan was normal;

Check the above two items.

Hepatomegaly 2 Diaphragm elevation 2

(4) Inspection results

(7) Lung ventilation-perfusion scan imaging

Pulmonary perfusion scan showed regional blood flow defect;

Lung ventilation scan was normal;

Check the above two items.

(8) Pulmonary angiography

vascular occlusion sign;

Vascular filling defect.

Judge

A diagnosis above 22 points can be confirmed;

A score of 20 or more is extremely suspicious;

suspicious 17 to 19 points;

15 to 16 minutes must check (7), (8).

Acute pulmonary embolism laboratory test

Although some laboratory tests are non-specific, if they can be used reasonably, they have important value. The first is the ECG changes, APE's

Observe under a microscope The pathophysiological basis of ECG changes is acute right ventricular dilatation.The ECG changes are often transient and changeable and require dynamic observation. The common ECG change is the right deviation of the QRS axis, "SQT" (Lead I S The wave becomes deeper,> 115mm, Q wave and T wave inversion in lead III), right wave anterior T wave inversion, clockwise transposition, complete or incomplete right bundle branch block, chest X-ray Patients with plain film pulmonary embolism may be normal, which can be manifested by regional reduced pulmonary blood flow or uneven distribution of pulmonary blood, elevation of the diaphragm on the affected side, peripheral wedge-shaped dense shadow (hump sign) above the diaphragm, shadow of the lungs, or pleural effusion Fluid, widening of the right lower pulmonary artery, and arterial blood gas analysis: if PaCO2 decreases, pH increases, with or without PaO2 decreases, all are conducive to the possibility of APE. 1. Examine blood, blood lactate dehydrogenase, blood gas analysis, blood coagulation function test.

2. ECG has arrhythmia, such as atrial fibrillation, right bundle branch block, etc .; ECG can see the right axis of the electrical axis is shifted clockwise; SQT wave is inverted, pulmonary P wave.

3. Chest radiographs may have multiple infiltrations, pleural effusions, and elevated diaphragms.

4. Pulmonary ventilation-perfusion scan The radioactive element 133Xe inhalation scan and lung perfusion scan were performed at the same time. The former was normal, while the latter showed defects, and most were pulmonary embolism.

5. Pulmonary angiography can confirm the diagnosis. Selective pulmonary angiography has the best effect. For example, the magnification technique (geometric magnification and oblique technique) can distinguish the obstruction of small arteries with a diameter of 0.5mm. Those who have the conditions can use digital subtraction angiography, the image is clearer. Pulmonary arterial pressure> 10.6kPa (80mmHg) is contraindicated.

Clinical types of acute pulmonary embolism

Sudden death type;

acute pulmonary heart disease type;

Unexplained dyspnea type;

pulmonary infarction type;

chronic embolic pulmonary hypertension type.

Clinical experience shows that the symptoms of the original cardiopulmonary disease suddenly aggravated or sudden breathing difficulties, but after the corresponding strengthening of the heart, diuretic, vasodilator and other treatments are not effective, especially those who have been in bed for a long time with atrial fibrillation Or severe heart dysfunction, the use of a large number of diuretics, obvious signs of dehydration or lower limb edema, the possibility of pulmonary embolism should be considered.

Differential diagnosis of acute pulmonary embolism

Differentiation of acute pulmonary embolism from coronary heart disease and acute myocardial infarction

Extensive pulmonary embolism is a clinical acute, severe, and critical disease. Because it is different from the treatment of coronary heart disease and acute myocardial infarction, early identification is needed

Acute pulmonary embolism diagnosis. Chest pain caused by pulmonary embolism is related to invasion and pleura. Compared with coronary heart disease and myocardial infarction, chest pain is dull and accompanied by dyspnea. If chest pain occurs, an electrocardiogram should be performed first, which is one of the indicators of early differential diagnosis. After the onset of myocardial infarction, the ST segment of II, III, and aVF increased, and the ST segment of V1 to V5 decreased, showing a pattern of inferior myocardial infarction. The ST segment elevation was more obvious after 3 hours, and pathological Q of II, III, and aVF appeared after 24 hours P wave of pulmonary embolism II, III, aVF increased (pulmonary P wave), ST segment of I, II, aVF, V1-V5 decreased, and then gradually recovered. Right ventricular hypertrophy, pulmonary P wave, and right bundle branch block are more common in chronic pulmonary embolism with persistent pulmonary hypertension, but less common in acute pulmonary embolism.

Acute pulmonary embolism pneumonia, pleurisy, pneumothorax

Each disease has chest pain, but clinically, pneumonia can be seen with fever, cough, rust-colored sputum, marked increase in white blood cells, and chest X-rays showing inflammatory infiltrates of the lungs. Pleurisitis clinically has night sweats, low fever, pleural effusion, pleural adhesion, and positive tuberculin test. X-rays of the pneumothorax show special signs of the chest such as compressed lung shadows and weakened breathing sounds on the affected side.

Acute pulmonary embolism aortic dissection aneurysm

Thoracic aortic dissection aneurysms can have chest pain or they can occur suddenly, but patients often have a history of hypertension. X-ray can be seen in the upper mediastinum shadow widened, aorta widened and prolonged, often due to hypertension and ECG manifestations of left ventricular surface high voltage and left ventricular strain, and occasional secondary ST-T changes can be identified.

Treatment of acute pulmonary embolism

The treatment of acute pulmonary embolism is to save lives and stabilize the disease, reopen the pulmonary blood flow, and prevent the progress of chronic pulmonary embolism. In the acute phase, anticoagulant therapy and thrombolytic therapy were used to correct right heart dysfunction and hypotension as the main body, while simultaneously correcting hypoxemia, analgesia and antiarrhythmia. When medical treatment is not effective, choose interventional or surgical treatment.

Acute pulmonary embolism treatment plan

Acute pulmonary embolism (1) Emergency treatment

General treatment

Pulmonary embolism is most dangerous within 1 to 3 days. Patients should be admitted to the ward and continuously monitor blood pressure, heart rate, breathing, electrocardiogram, and arterial blood gas.

Symptomatic treatment

(1) Sedation pain: keep patients quiet, warm, and inhale oxygen, and give morphine, dulidine, codeine, etc. when necessary to stop pain.

(2) Treatment of acute right ventricular dysfunction: Digitalis has a poor curative effect and is susceptible to poisoning. If necessary, rapid digitalis preparations (such as cedilan) can be used with caution. Dobutamine or dopamine is generally used at 20-40 mg. Dissolve 250ml in 5% glucose slowly intravenously to increase the stroke volume.

(3) Anti-shock treatment: First, add fluid, but pay attention to avoid pulmonary edema; if the fluid does not work, intravenous dopamine, alamin, etc. Maintain systemic systolic pressure above 90mmHg.

(4) Improving breathing: if combined with bronchospasm, bronchodilators and mucolytic agents such as aminophylline and asthma can be applied.

(Two) anticoagulant therapy

The purpose is to: (1) prevent the occurrence of thrombus extension around the pulmonary artery thrombus. (2) Inhibit the secretion of nerve and humoral factors caused by thrombus. (3) Prevent the progression of venous thrombosis.

Heparin was used initially in anticoagulant therapy and later maintained with Warhdn. Heparin has a rapid effect and has the above three effects, while warfarin has a relatively long onset of effect and lacks an inhibitory effect on the secretion of neurohumoral factors. Heparin has an important role in the treatment of pulmonary embolism. The survival rate of the heparin group is 92%, and the survival rate of the non-heparin group is 42%. The contrast between the two groups is significantly different. The rate of pulmonary embolism also depends on whether heparin is used. Heparin The group was 16% and the non-heparin group was 55%. The results show the application value of heparin, but the use of heparin is limited in some diseases.

Absolute contraindications: acute phase of cerebral hemorrhage, digestive system bleeding, malignant tumors, arteriovenous malformations.

Relative contraindications: previous bleeding disorders, untreated severe hypertension, major surgery and biopsy within 2 weeks after delivery. Heparin is excreted in the liver and excreted in the urine, and should be reduced in patients with severe liver and kidney disease.

In the suspected acute pulmonary embolism phase, 5000 units of heparin were first injected intravenously. After the diagnosis was confirmed, the heparin continued to stand still for 500 to 1000 units per hour, which increased the APTT by 1.5 to 2.0 times compared with the control value. To prevent new thrombosis and thrombus extension, heparin is used for 7 to 10 days. The biggest side effect of heparin is bleeding. The incidence of intermittent intravenous bleeding is 10% to 12%. The incidence of continuous intravenous drip bleeding is 1% to 5%. The chance of bleeding is caused by long-term drinking, women, and combination with antiplatelet drugs. Thrombocytopenia, etc., the cumulative effect often appears on the 3rd day after medication.

Compared with unfractionated heparin, low-molecular-weight heparin has a longer half-life and lower bleeding tendency, and is widely used in clinical practice. Low-molecular-weight heparin has the same side effects as ordinary heparin except that it has fewer thrombocytopenia than ordinary heparin. The dosage is generally in the range of 4000 8000 units / 12h.

Acute pulmonary embolism Shoot.

The purpose of adding warfarin after heparin treatment is to prevent recurrent pulmonary embolism and prevent the extension of venous thrombosis. The recurrence rate of venous thrombosis in the warfarin group was 2%, and the recurrence rate in the non-use group was 17%. One year later, the recurrence rate in the warfarin group was 4%, and that in the non-warfarin group was 32%, showing a significant difference. Warfarin's onset time is 2 to 3 days, so the drug is started 3 to 4 days before heparin is discontinued. The dose of warfarin will extend the PT value by 1.5 to 2.5 times the control value, and the international standardization ratio will be 2.0 to 2.5. between. Warfarin's side effects are also bleeding, with bleeding rates up to 2.4% to 10%. Factors that increase the risk of bleeding include: over 60 years of age, diastolic hypertension, peptic ulcers, liver and kidney disease, affecting warfarin metabolism and increasing efficacy. Drug combination. Warfarin affects the development of the fetus in the first trimester through the placenta, so it is best to use heparin instead of warfarin during pregnancy.

(Three) thrombolytic therapy

The ultimate goal of the treatment of acute pulmonary embolism is to remove thrombus, and the thrombolytic therapy adopted in recent years is safe and effective. From 1967 to 1973, 16 hospitals in the United States carried out research on thrombolytic therapy. Pulmonary angiography, hemodynamics, and pulmonary perfusion imaging were used to evaluate the thrombolytic effects of urokinase and streptokinase. Pulmonary angiography results in an improved blood flow defect rate of 53% in the urokinase group and only 9% in the heparin group alone, showing an exact thrombolytic effect. Thrombolytic therapy can improve the function of deep vein valves, improve the ability of pulmonary capillaries to diffuse, and increase the volume of pulmonary capillaries, thus establishing a treatment method for acute pulmonary embolism.

Thrombolytic drugs and protocols approved by the U.S. Drug and Food Administration (FDA):

(1) Streptokinase: 250,000 units of load, intravenous injection for 30 min, then 100,000 units / h, intravenous administration for 24 consecutive hours, approved in 1977.

(2) Urokinase: the load is 4400 units / kg, intravenously for 10 minutes, and then 4400 units / kg / h, intravenously for 12 to 24 hours, approved in 1978.

(3) t-PA: 100mg, continuous intravenous injection within 2 hours, approved in 1990.

Domestic thrombolytic programs:

(1) UK: 20,000 IU / kg, 2 hours intravenous drip;

(2) rt-PA: 50-100mg, intravenous drip for 2 hours;

(3) SK: The load is 500,000 IU, and the continuous infusion is 10,000 IU / h.

The results show that the three thrombolytic agents have the same effectiveness and safety. The rt-PA 2-hour infusion can dissolve blood clots more quickly than UK and SK 12-24 hours infusion, and can improve the hemodynamic instability more quickly.

UPET (urokinasePulmonaryembolismtrial) is used by first intravenously injecting UK4400 units / kg within 10 minutes, and then continuously injecting the same dose every hour for 12 hours. In 1997, the national clinical observation study of acute pulmonary embolism hosted by the Fuwai Cardiovascular Hospital of China recommended the use of 1 to 1.5 million units (20,000 units / kg), 2 hours of intravenous infusion, and then low molecular weight heparin anticoagulation continued for one week.

Indications for thrombolytic therapy:

(1) Extensive acute pulmonary embolism.

(2) Non-extensive acute pulmonary embolism with severe cardiopulmonary disease, anticoagulant therapy is not effective.

(3) Deep vein thrombosis.

Acute pulmonary embolism contraindications

(1) Peptic ulcer with bleeding.

(2) Recent cerebrovascular disease or cerebrospinal spinal surgery.

(3) Intracranial tumors.

The main complication of thrombolytic therapy is bleeding, and the incidence of bleeding in the United States is reported to be 5% to 7%. In order to reduce bleeding, a small dose (250,000 to 500,000 units) of urokinase can be directly injected into the pulmonary artery thrombus through a catheter, and the thrombolytic effect is better. In patients with repeated episodes of acute pulmonary embolism, a large dose (1.5 million units) of urokinase can be applied once (within 2 hours), and then small and medium doses (250,000 to 500,000 units) can be administered intravenously daily (for 3 days ), At the same time heparin anticoagulation, the total amount of urokinase reached 2.5 to 4 million units, can also receive the expected therapeutic effect. In the treatment of thrombolysis, the individualization of treatment should be emphasized according to the degree of the disease and the clinical type of pulmonary embolism.

Prevention of acute pulmonary embolism

Taking appropriate precautions can reduce the incidence and mortality of pulmonary embolism.

(1) Drug method: The purpose should be to prevent deep vein thrombosis.

(B) surgical methods: the method of inferior vena cava occlusion is mainly used to prevent the occurrence of fatal massive pulmonary embolism or repeated non-fatal pulmonary embolism. It is mainly applicable to the following situations: anticoagulation contraindications: such as large deep venous thrombosis that occurs quickly after major surgery and severe trauma, heparin allergy or bleeding quality. Recurrent pulmonary embolism occurred during anticoagulation therapy. Deep venous thrombosis and pulmonary embolism occur repeatedly due to abnormal congenital coagulation mechanism. Pulmonary embolism occurred repeatedly in patients with severe heart and lung disease. Major surgery is needed, but the patient has acute iliac and femoral vein thrombosis.

Inferior vena cava ligation

The disadvantages of this method are greater, such as greater risk of surgery, reduced venous return after vena cava blockage, affecting cardiac output, and prone to postoperative complications such as lower limb swelling, congestion, and skin ulcers. Therefore, this method is rarely used at present.

2. Inferior vena cava mesh placement or special umbrella filter

Is the widely used method. The indications are as follows: Proximal vein thrombosis of the lower extremity, anticoagulation therapy is contraindicated or has complications. Pulmonary embolism after repeated anticoagulation. Large area pulmonary embolism with hemodynamic changes. The advantages of venous filter placement are that it can prevent fatal pulmonary embolism caused by large emboli shedding, without significantly affecting venous return, and has fewer complications. Inferior vena cava mesh placement must be performed under anesthesia, which is more dangerous. It is relatively easy to place the umbrella filter in the inferior vena cava through a catheter. If properly placed, more than 98% of patients can maintain blood flow to the inferior vena cava for a long time, and the incidence of recurrent pulmonary embolism is also low. Disadvantages are the appearance of venous stasis in the lower extremities and the risk of filter detachment, migration and venous perforation.