Home Orthopedics Tella disease treatment. Thromboembolism of the branches of the pulmonary artery: pathophysiology, clinical picture, diagnosis, treatment

Tella disease treatment. Thromboembolism of the branches of the pulmonary artery: pathophysiology, clinical picture, diagnosis, treatment

Blockage by blood clot pulmonary artery- a condition that threatens the patient’s life. Thromboembolism is a complication of injuries, surgical interventions and pathologies associated with thrombus formation. The lack of specific symptoms and the difficulty of timely diagnosis make pulmonary embolism (PE) the third leading cause of death.

The term “embolism” means blocking the lumen of a vessel. PE - blockage of the main trunk of the pulmonary artery or its branches by blood clots brought by the bloodstream. In the International Classification of Diseases (ICD-10), pulmonary embolism is listed under code I26.

The pulmonary artery is a blood vessel of the pulmonary circulation. Through it, venous blood enters the lungs, where, saturated with oxygen, it turns into arterial blood. From the lungs it returns to the left ventricle of the heart, from where it begins its journey through the systemic circulation to deliver nutrition to every cell of the body. If the lumen of the pulmonary artery is blocked, local and systemic blood flow is disrupted, and tissues and organs are deprived of oxygen.

As a result of vascular obstruction, pulmonary vascular resistance increases. The respiratory surface area decreases, causing gas exchange to deteriorate. Hemorrhage occurs in the lung tissue, and it becomes less elastic. Impaired blood supply to the lungs causes general oxygen starvation, which reflexively increases the depth and frequency of breathing and narrows the lumen of the bronchi.

With massive embolism of the main pulmonary trunk, acute failure right ventricle (acute cor pulmonale), which leads to the death of the patient. Blockage of artery branches causes less fatal consequences, and timely diagnosis and correct treatment save the patient's life.

Reasons for the development of pathology

The causes of pulmonary embolism lie in vascular pathologies that occur with the formation of blood clots, or diseases associated with impaired hemostatic function. In 90% of cases, the pulmonary vessels are blocked by an embolus, the source of which is:

  • pool of the inferior vena cava;
  • iliofemoral veins;
  • veins of the pelvis, including the prostate gland;
  • deep and superficial veins shins.

Blood clots also form in the cavity of the heart during arrhythmia - their appearance is caused by the vortex movement of blood. Medicine identifies several main causes of pulmonary embolism.

Blood flow disturbance

Venous stagnation- one of the main causes of embolism. Impaired blood flow is provoked by:

  • varicose veins and heart failure;
  • obesity, which is an additional burden on the heart and the entire circulatory system and disrupts cholesterol metabolism;
  • prolonged bed rest or immobility as a result of injury;
  • increased blood pressure.

Damage to the vascular wall

Damage to the vascular wall triggers the formation of a blood clot as a protective reaction to “repair” it. Damaging factors can be viral and microbial infections, oxygen deprivation, intravascular operations, stenting, and vein replacement. The loss of elasticity of the vessels leads to the fact that the brittle wall is unable to hold the blood clot. Floating blood clots attached to it with only a small base are the easiest to come off.

Increased blood clotting and viscosity

The parietal thrombus experiences constant resistance to blood flow. The thicker it is, the more pressure the clot is subjected to. Therefore, increased blood clotting plays an important role in pulmonary embolism. It is caused by taking certain hormonal drugs, malignant tumors, and pregnancy.

Increased blood viscosity (imbalance between the liquid part and shaped elements) is another reason for the formation of blood clots and their separation from the vascular wall. Blood thickens with dehydration, erythrocytosis and polycythemia, and uncontrolled use of diuretics.

Other factors that increase the risk of pulmonary embolism

Factors that increase the risk of embolism are extensive surgical operations, childbirth, injuries with fractures of large bones. Diseases that provoke thromboembolism include:

  • diabetes;
  • coronary heart disease;
  • stenosis mitral valve;
  • active phase of rheumatism;
  • thrombophlebitis;
  • antiphospholipid syndrome (autoimmune disease).

The danger also increases during chemotherapy sessions, in old age and in the postpartum period. PE occurs more often in smokers than in non-smoking patients.

Classification of pulmonary embolism

Pulmonary thromboembolism is classified according to the location of the thrombus, the degree of vascular occlusion and the clinical course of the pathology. With a massive embolism, the thrombus is located in the main trunk or in its large branches. Emboli can be localized in the vessels of segments and lobes of the lungs on the right or left side. Small artery blockages are usually bilateral. Forms of pulmonary embolism according to severity (volume of cut-off blood flow):

Clinical course of pulmonary embolism

Lightning-fast progression occurs with complete occlusion of the lumen of the main artery and its branches. The patient quickly dies from cardiac and respiratory failure.

In the acute course, there is an increasing obstruction of the branches of the pulmonary artery and partially the vessels of the segments and lobes of the lungs. Over the course of several days, cardiac and respiratory failure progresses, and blood supply to the brain is disrupted. Embolism is complicated by pneumoinfarction.

With a prolonged course of pulmonary embolism (up to 3 weeks), the middle and small branches of the pulmonary artery are switched off from the bloodstream. Right ventricular failure progresses, multiple pulmonary infarctions occur, and repeated embolisms are possible with increased symptoms and death.

The chronic course is a recurrent blockage of the segmental and lobar branches of the pulmonary artery. Most often occurs in patients who have undergone surgery, with cancer, heart and vascular diseases.

Symptoms of thromboembolism

Symptoms of pulmonary embolism are not specific; they mask a dangerous complication under other diseases. The clinic depends on how quickly the process develops and its severity. It can manifest itself as cardiovascular and pulmonary-pleural syndromes. There are common signs for all types of pulmonary embolism:

  • sudden, unexplained shortness of breath;
  • heartbeat over 100 beats;
  • pain arising in different parts of the chest;
  • intestinal paresis;
  • peritoneal irritation, liver enlargement, sharp pain in the right hypochondrium, hiccups;
  • drop in blood pressure;
  • increased blood flow to the veins of the neck and solar plexus.

Some patients develop extrasystole, atrial fibrillation, cerebral circulatory insufficiency with focal lesions, hemorrhages and cerebral edema. Neurological symptoms: fainting, dizziness, convulsions, motor and psycho-emotional agitation. Due to respiratory failure, the skin becomes bluish, the breathing rate increases, and it becomes wheezing due to bronchospasm. The patient coughs up sputum with blood, and the temperature rises. Within 1–3 days, infarction pneumonia develops.

The chronic course of pulmonary embolism occurs when thrombosis of small branches of the pulmonary artery occurs. Episodes can be repeated from 2 to 20 times during life. The more often they occur, the higher the likelihood of developing a massive embolism. The clinical signs of this form are blurred and difficult to diagnose. The most pronounced manifestations:

  • frequently recurring pneumonia of unknown etiology;
  • pleurisy with a short course (several days);
  • tachycardia;
  • attacks of suffocation and constant difficulty breathing;
  • heart failure in the absence of cardiac pathology.

Possible fainting states and an increase in temperature that is not controlled by antibiotics.

Diagnosis of the disease

Diagnosis of pulmonary embolism is carried out to determine the location of the thrombus, assess the volume of the lesion, and search for the source of the embolus. During the initial examination, the patient's medical history is collected and risk factors are assessed. Laboratory tests include biochemistry, gas composition, blood clotting, and urine testing. The blood is also tested for D-dimer. This is a substance whose levels increase if blood clots are forming in the body. If this indicator is normal, there is no pulmonary embolism.

Using an ECG, PE is differentiated from myocardial infarction, pericarditis and heart failure. A cardiogram, compared with the medical history, makes it possible to make the correct diagnosis with high accuracy. X-ray of the lungs excludes pneumothorax, pneumonia, rib fracture, tumor, pleurisy. EchoCG shows pressure in the pulmonary artery, the condition of the right ventricle, and the presence of blood clots in the cavities of the heart.

Perfusion scintigraphy (an X-ray of the lungs with a contrast agent injected) shows the amount of blood entering the lung tissue, which allows us to evaluate the decrease in blood flow. Pulmonary angiography indicates the exact location of the clot and its size. Search for the source of the embolus is performed using Doppler ultrasound leg vessels.

Treatment of pulmonary embolism

A patient with pulmonary embolism is placed in the intensive care unit, where he receives emergency help- installation of an intravenous catheter to monitor venous pressure and intravenous administration of heparin, dopamine, rheopolyglucin (for detoxification and plasma replacement) and antibiotics, if necessary. Oxygen therapy is carried out. Resuscitation measures are designed to prevent the development of chronic hypertension in the pulmonary artery and sepsis, as well as restore blood supply to the lungs.

Drug treatment

At an early stage, thrombolytics are used to treat PE. Low molecular weight heparins (Nadroparin calcium, Enoxaparin sodium) are administered for 7–10 days; Warfarin and Cardiomagnyl are prescribed before their discontinuation.



Fibrinolytic enzymes (Streptokinase and Urokinase) are administered by drip. During their administration, heparin therapy is stopped. If a pulmonary infarction develops, antibiotics are prescribed.

Surgery

Surgical treatment is performed if blood clots cannot be dissolved with medication or more than half of the lungs are affected. The thrombus is removed from the vessel or a targeted injection of thrombolytic into the artery is performed. But such operations are performed only for embolism of the main trunk and large branches of blood vessels.

Installation of a vena cava filter

A vena cava filter is a high-tech device that prevents a blood clot from entering the pulmonary circulation. It is given to patients with high risk TELA or its episodes in the past. Place of installation - inferior vena cava. A vena cava filter is a mesh that allows particles no larger than 4 mm to pass through. Blood cells pass through it freely, but blood clots get stuck. The filter's own anticoagulant system and anticoagulants dissolve blood clots directly on the filter.

This is what vava filters look like

When to be afraid of an embolism

The main “supplier” of embolus into the vessels of the lungs is the veins of the lower extremities. Venous congestion, inflammation of the vascular walls, thick blood - this is the prospect of a serious, life-threatening complication. The patient and his or her physician should always be wary of the development of pulmonary embolism. The risk increases if there is a family history of this pathology.

Varicose veins and subsequent thrombus formation also have external causes - a sedentary lifestyle, professional activity, bad habits. The older a person gets, the greater the risk of thromboembolism increases due to age-related changes circulatory system. Injuries over the age of 60 are also fraught with this severe complication. Femoral neck fractures in old people often result in massive pulmonary embolism.

Preventive measures

Prevention of pulmonary thromboembolism consists of timely treatment of varicose veins and maintaining other provoking diseases in a compensated state. Long-term immobilized patients should use compression stockings and “walk around” as soon as possible after illness.

Patients with at least one risk factor, as well as people over 40 years of age who have undergone surgery, should undergo courses of physiotherapy (pneumomassage) for prevention, always wear compression stockings and undergo regular examinations. The doctor should give more specific recommendations depending on the patient’s condition. At the same time, a healthy lifestyle always remains relevant - quitting smoking, moderate physical activity, maintaining a normal weight and a balanced diet.

Pulmonary embolism (PE) is a sudden blockage of the branches or trunk of the pulmonary artery by a thrombus (embolus) formed in the right ventricle or atrium of the heart, venous bed great circle blood circulation and carried with the blood stream. As a result of pulmonary embolism, the blood supply is cut off lung tissue. The development of pulmonary embolism often occurs rapidly and can lead to the death of the patient.

0.1% of the world's population dies from pulmonary embolism every year. About 90% of patients who died from pulmonary embolism were not diagnosed correctly and the necessary treatment was not carried out.

Among the causes of death of the population from cardiovascular diseases, pulmonary embolism ranks third after coronary artery disease and stroke. PE can be fatal in non-cardiological pathologies, occurring after operations, injuries, or childbirth. With timely optimal treatment of pulmonary embolism, there is a high mortality rate reduction of up to 2–8%.

Reasons for the development of pulmonary embolism

The most common causes of pulmonary embolism are:

— deep vein thrombosis (DVT) of the leg (in 70–90% of cases), often accompanied by thrombophlebitis. Thrombosis of deep and superficial veins of the leg may occur simultaneously

- thrombosis of the inferior vena cava and its tributaries

- cardiovascular diseases predisposing to the appearance of blood clots and embolisms in the pulmonary artery (coronary heart disease, the active phase of rheumatism with the presence of mitral stenosis and atrial fibrillation, hypertonic disease, infective endocarditis, cardiomyopathies, non-rheumatic myocarditis)

- septic generalized process

- oncological diseases (usually cancer of the pancreas, stomach, lungs)

— thrombophilia (increased intravascular thrombus formation due to disruption of the hemostatic regulation system)

- antiphospholipid syndrome - the formation of antibodies to phospholipids of platelets, endothelial cells and nervous tissue (autoimmune reactions); manifests itself as an increased tendency to thrombosis of various localizations.

Risk factors for vein thrombosis and pulmonary embolism are:

- long-term state of immobility (bed rest, frequent and long flights, trips, paresis of limbs), chronic cardiovascular and respiratory failure, accompanied by a slowdown in blood flow and venous stagnation.

- taking large amounts of diuretics (massive loss of water leads to dehydration, increased hematocrit and blood viscosity);

malignant neoplasms- some types of hemoblastoses, polycythemia vera (a high content of red blood cells and platelets in the blood leads to their hyperaggregation and the formation of blood clots);

- long-term use of some medicines(oral contraceptives, replacement hormone therapy) increases blood clotting;

- varicose veins (with varicose veins of the lower extremities, conditions are created for stagnation of venous blood and the formation of blood clots);

- metabolic disorders, hemostasis (hyperlipid proteinemia, obesity, diabetes mellitus, thrombophilia);

- surgical operations and intravascular invasive procedures(For example, central catheter V large vein);

- arterial hypertension, congestive heart failure, strokes, heart attacks;

— spinal cord injuries, fractures of large bones;

- chemotherapy;

- pregnancy, childbirth, postpartum period;

- smoking, old age, etc.

Classification of pulmonary embolism

Depending on the location of the thromboembolic process, the following types of pulmonary embolism are distinguished:

Massive (thrombus is localized in the main trunk or main branches of the pulmonary artery)

- embolism of segmental or lobar branches of the pulmonary artery

- embolism of small branches of the pulmonary artery (usually bilateral)

Depending on the volume of disconnected arterial blood flow during PE, the following forms are distinguished:

- small (less than 25% of the pulmonary vessels are affected) - accompanied by shortness of breath, the right ventricle functions normally

- submassive (submaximal - the volume of affected pulmonary vessels is from 30 to 50%), in which the patient experiences shortness of breath, normal blood pressure, right ventricular failure is mild

- massive (volume of disconnected pulmonary blood flow is more than 50%) - loss of consciousness, hypotension, tachycardia, cardiogenic shock is observed, pulmonary hypertension, acute right ventricular failure

- fatal (the volume of cut-off blood flow in the lungs is more than 75%).

PE can occur in severe, moderate or mild form.

The clinical course of pulmonary embolism can be:

- acute (fulminant), when there is an immediate and complete blockage of the main trunk or both main branches of the pulmonary artery by a thrombus. Acute respiratory failure, respiratory arrest, collapse, and ventricular fibrillation develop. Death occurs within a few minutes; pulmonary infarction does not have time to develop.

- acute, in which there is a rapidly increasing obturation of the main branches of the pulmonary artery and parts of the lobar or segmental ones. It begins suddenly, progresses rapidly, and symptoms of respiratory, cardiac and cerebral failure develop. It lasts for a maximum of 3–5 days and is complicated by the development of pulmonary infarction.

- subacute (protracted) with thrombosis of large and medium branches of the pulmonary artery and the development of multiple pulmonary infarctions. Lasts several weeks, slowly progresses, accompanied by an increase in respiratory and right ventricular failure. Repeated thromboembolism may occur with exacerbation of symptoms, which often results in death.

- chronic (recurrent), accompanied by recurrent thrombosis of the lobar and segmental branches of the pulmonary artery. It manifests itself as repeated pulmonary infarctions or repeated pleurisy (usually bilateral), as well as gradually increasing hypertension of the pulmonary circulation and the development of right ventricular failure. It often develops in the postoperative period, against the background of existing oncological diseases and cardiovascular pathologies.

Symptoms of pulmonary embolism

The symptoms of pulmonary embolism depend on the number and size of thrombosed pulmonary arteries, the rate of development of thromboembolism, the degree of disturbances in the blood supply to the lung tissue, and the initial condition of the patient. With PE there is a wide range of clinical conditions: from practically asymptomatic to sudden death.

The clinical manifestations of pulmonary embolism are nonspecific; they can be observed in other pulmonary and cardiovascular diseases, their main difference is a sharp, sudden onset in the absence of other visible reasons this state(cardiovascular failure, myocardial infarction, pneumonia, etc.). The classic version of PE is characterized by a number of syndromes:

  1. Cardiovascular:

- spicy vascular insufficiency. There is a drop in blood pressure (collapse, circulatory shock), tachycardia. Heart rate can reach more than 100 beats. in a minute.

- acute coronary insufficiency (in 15-25% of patients). It manifests itself as sudden severe chest pain of various types, lasting from several minutes to several hours, atrial fibrillation, and extrasystole.

- acute cor pulmonale. Caused by massive or submassive pulmonary embolism; manifested by tachycardia, swelling (pulsation) of the neck veins, positive venous pulse. Edema does not develop in acute cor pulmonale.

- acute cerebrovascular insufficiency. General cerebral or focal disorders, cerebral hypoxia occur, and in severe cases - cerebral edema, cerebral hemorrhages. Manifested by dizziness, tinnitus, deep fainting with convulsions, vomiting, bradycardia or coma. Psychomotor agitation, hemiparesis, polyneuritis, and meningeal symptoms may be observed.

  1. Pulmonary-pleural:

- acute respiratory failure is manifested by shortness of breath (from a feeling of lack of air to very pronounced manifestations). The number of respirations is more than 30-40 per minute, cyanosis is noted, the skin is ashy-gray and pale.

- moderate bronchospastic syndrome is accompanied by dry wheezing.

pulmonary infarction, infarction pneumonia develops 1–3 days after pulmonary embolism. There are complaints of shortness of breath, cough, pain in chest on the side of the lesion, aggravated by breathing; hemoptysis, increased body temperature. Fine bubble moist rales and pleural friction noise become audible. Patients with severe heart failure have significant pleural effusions.

  1. Feverish syndrome - subfebrile, febrile body temperature. Associated with inflammatory processes in the lungs and pleura. The duration of fever ranges from 2 to 12 days.
  2. Abdominal syndrome is caused by acute, painful swelling of the liver (in combination with intestinal paresis, irritation of the peritoneum, hiccups). Manifested by acute pain in the right hypochondrium, belching, vomiting.
  3. Immunological syndrome (pulmonitis, recurrent pleurisy, urticaria-like skin rash, eosinophilia, the appearance of circulating immune complexes in the blood) develops at 2-3 weeks of the disease.

Complications of pulmonary embolism

Acute pulmonary embolism can cause cardiac arrest and sudden death. When compensatory mechanisms are triggered, the patient does not die immediately, but in the absence of treatment, secondary hemodynamic disorders progress very quickly. The patient's existing cardiovascular diseases significantly reduce compensatory possibilities cardiovascular system and worsen the prognosis.

Diagnosis of pulmonary embolism

In the diagnosis of pulmonary embolism, the main task is to establish the location of blood clots in the pulmonary vessels, assess the degree of damage and the severity of hemodynamic disorders, and identify the source of thromboembolism to prevent relapses.

The complexity of diagnosing pulmonary embolism dictates the need to locate such patients in specially equipped vascular departments that have the widest possible capabilities for conducting special studies and treatment. All patients with suspected pulmonary embolism undergo the following examinations:

— thorough medical history, assessment of risk factors for DVT/PE and clinical symptoms

general and biochemical blood and urine tests, blood gas analysis, coagulogram and D-dimer study in blood plasma (method for diagnosing venous thrombi)

— ECG in dynamics (to exclude myocardial infarction, pericarditis, heart failure)

chest x-ray (to exclude pneumothorax, primary pneumonia, tumors, rib fractures, pleurisy)

- echocardiography (to detect increased pressure in the pulmonary artery, overload of the right heart, blood clots in the cavities of the heart)

— lung scintigraphy (impaired blood perfusion through the lung tissue indicates a decrease or absence of blood flow due to pulmonary embolism)

- angiopulmonography (for precise definition location and size of the thrombus)

— Doppler ultrasound of peripheral veins, contrast venography (to identify the source of thromboembolism)

Treatment of pulmonary embolism

Patients with pulmonary embolism are admitted to the intensive care unit.

IN emergency The patient is given full resuscitation measures.

Further treatment of pulmonary embolism is aimed at normalizing pulmonary circulation and preventing chronic pulmonary hypertension.

In order to prevent recurrence of pulmonary embolism, strict bed rest is necessary. To maintain oxygenation, constant oxygen inhalation is carried out.

A massive infusion therapy to reduce blood viscosity and maintain blood pressure.

In the early period, the administration of thrombolytic therapy is indicated in order to dissolve the blood clot as quickly as possible and restore blood flow in the pulmonary artery. In the future, heparin therapy is performed to prevent recurrence of pulmonary embolism.

In case of infarction-pneumonia, antibacterial therapy is prescribed.

In cases of massive pulmonary embolism and the ineffectiveness of thrombolysis, surgical thromboembolectomy (removal of a blood clot) is performed. As an alternative to embolectomy, catheter thromboembolic fragmentation is used. For recurrent pulmonary embolism

Prognosis and prevention of pulmonary embolism involves placing a special filter in the branch of the pulmonary artery, the inferior vena cava.

With early provision of the full amount of care to patients, the prognosis for life is favorable. In case of severe cardiovascular and respiratory disorders against the background of extensive pulmonary embolism, the mortality rate exceeds 30%.

Half of recurrent pulmonary embolisms occur in patients who did not receive anticoagulants. Timely, correctly administered anticoagulant therapy halves the risk of recurrent pulmonary embolism.

To prevent thromboembolism, early diagnosis and treatment of thrombophlebitis and the administration of indirect anticoagulants to patients at risk are necessary.

The heart is an important organ in the human body. The cessation of his work symbolizes death. There are a large number of diseases that negatively affect the functioning of the entire cardiovascular system. One of these is pulmonary embolism, a clinical pathology whose symptoms and therapy will be discussed further.

What is the disease

PE, or pulmonary embolism, is a common pathology that develops when the pulmonary artery or its branches are blocked by blood clots. They most often form in the veins of the lower extremities or pelvis.

Thromboembolism is in third place among the causes of mortality, second only to ischemia and myocardial infarction.

Most often, the disease is diagnosed in old age. Men are three times more likely than women to suffer from this disease. If therapy for pulmonary embolism (ICD-10 code - I26) is started in a timely manner, it is possible to reduce mortality by 8-10%.

Reasons for the development of the disease

During the development of pathology, clots form and block blood vessels. Among the causes of pulmonary embolism are the following:

  • Impaired blood flow. This can be observed against the background of the development of: varicose veins, compression of blood vessels by tumors, previous phlebothrombosis with destruction of vein valves. Blood circulation is disrupted when a person is forced to remain immobile.
  • Wall damage blood vessel, as a result of which the blood clotting process starts.
  • Vein prosthetics.
  • Installation of catheters.
  • Vein surgery.
  • Infectious diseases viral or bacterial nature, causing endothelial damage.
  • Disruption of the natural process of fibrinolysis (dissolution of blood clots) and hypercoagulation.

The combination of several causes increases the risk of developing pulmonary embolism; clinical pathology requires long-term treatment.

Risk factors

The likelihood of the formation of pathological processes is significantly increased by the following risk factors for pulmonary embolism:

  1. Long travel or forced bed rest.
  2. Cardiac or
  3. Long-term treatment with diuretics, which leads to loss of large amounts of water and increased blood viscosity.
  4. Neoplasms, for example, the formation of hemablastosis.
  5. Increased levels of platelets and red blood cells in the blood, which increases the risk of blood clots.
  6. Long-term use of hormonal contraceptives, hormone replacement therapy - this increases blood clotting.
  7. Disturbance of metabolic processes, which is often observed in diabetes mellitus and obesity.
  8. Vascular operations.
  9. Previous strokes and heart attacks.
  10. High blood pressure.
  11. Chemotherapy.
  12. Spinal cord injuries.
  13. The period of bearing a baby.
  14. Smoking abuse.
  15. Elderly age.
  16. Phlebeurysm. Creates favorable conditions for blood stagnation and blood clot formation.

From the listed risk factors, we can come to the conclusion that no one is immune from the development of pulmonary embolism. ICD-10 code of this disease- I26. It is important to suspect a problem early and take action.

Types of disease

The clinic for pulmonary embolism will depend on the type of pathology, and there are several of them:

  1. Massive pulmonary embolism. As a result of its development, most of the lung vessels are affected. The consequences may be shock or the development of hypotension.
  2. Submassive. A third of all blood vessels in the lungs are affected, resulting in right ventricular failure.
  3. Non-massive form. It is characterized by damage to a small number of vessels, so symptoms of pulmonary embolism may be absent.
  4. Fatal when more than 70% of the vessels are affected.

Clinical course of the pathology

The pulmonary embolism clinic may be:

  1. Lightning fast. Blockage of the main pulmonary artery or main branches. Respiratory failure develops and respiratory arrest may occur. Death is possible within a few minutes.
  2. Spicy. The development of pathology occurs quickly. The onset is sudden, followed by rapid progression. Cardiac symptoms are observed, developing within 3-5 days
  3. Protracted. Thrombosis of large and medium arteries and the development of several pulmonary infarctions continue for several weeks. The pathology slowly progresses with increasing symptoms of respiratory and heart failure.
  4. Chronic. Recurrent thrombosis of the branches of the pulmonary artery is constantly observed. Repeated pulmonary infarctions or bilateral pleurisy are diagnosed. Hypertension gradually increases. This form most often develops after surgical interventions, against the background of oncology and existing cardiovascular diseases.

Development of the disease

Pulmonary embolism develops gradually, passing through the following stages:

  1. Airway obstruction.
  2. Increased pressure in the pulmonary artery.
  3. As a result of obstruction and blockage, gas exchange is disrupted.
  4. The occurrence of oxygen deficiency.
  5. The formation of additional pathways for the transport of poorly oxygenated blood.
  6. Increased load on the left ventricle and the development of its ischemia.
  7. Decrease in cardiac index and drop in blood pressure.
  8. Pulmonary arterial pressure increases.
  9. Deterioration of coronary circulation in the heart.
  10. Pulmonary edema.

Many patients suffer pulmonary infarction after PE.

Signs of the disease

Symptoms of pulmonary embolism depend on many factors:

  • General condition of the patient's body.
  • Number of damaged arteries.
  • The size of the particles that clog the blood vessels.
  • Rate of disease progression.
  • Degree of disturbances in lung tissue.

Treatment of pulmonary embolism will depend on the clinical condition of the patient. For some, the disease occurs without causing any symptoms and can lead to sudden death. The difficulty of diagnosis also lies in the fact that the pathology’s symptoms resemble many cardiovascular diseases, but the main difference is the suddenness of the development of pulmonary embolism.

The pathology is characterized by several syndromes:

1. From the cardiovascular system:

  • Development of heart failure.
  • Reduced blood pressure.
  • Heart rhythm disturbance.
  • Increased heart rate.
  • The development of coronary insufficiency, which manifests itself as sudden intense pain in the chest, lasting from 3-5 minutes to several hours.

  • Pulmonary heart syndrome is manifested by swelling of the veins in the neck, tachycardia.
  • General cerebral disorders with hypoxia, cerebral hemorrhages and in severe cases with cerebral edema. The patient complains of tinnitus, dizziness, vomiting, convulsions and fainting. In severe situations, there is a high probability of developing coma.

2. Pulmonary-pleural syndrome manifests itself:

  • The appearance of shortness of breath and the development of respiratory failure. The skin becomes gray and cyanosis develops.
  • Whistling sounds appear.
  • Pulmonary infarction most often develops 1-3 days after pulmonary embolism, a cough appears with the discharge of sputum mixed with blood, the body temperature rises, and when listening, moist fine bubbling rales are clearly audible.

3. Feverish syndrome with the appearance febrile temperature bodies. It is associated with inflammatory processes in the lung tissue.

4. Enlarged liver, irritation of the peritoneum, and intestinal paresis cause abdominal syndrome. The patient complains of pain in the right side, belching and vomiting.

5. Immunological syndrome is manifested by pulmonitis, pleurisy, skin rashes, and the appearance of immune complexes in a blood test. This syndrome usually develops 2-3 weeks after the diagnosis of PE.

Diagnostic measures

In diagnosing this disease, it is important to establish the location of blood clot formation in the pulmonary arteries, as well as to assess the degree of damage and the severity of the disorders. The doctor is faced with the task of determining the source of thromboembolism in order to prevent relapse.

Given the difficulty of making a diagnosis, patients are sent to special vascular departments, which are equipped with technology and have the ability to conduct comprehensive research and therapy.

If PE is suspected, the patient undergoes the following examinations:

  • Taking anamnesis and assessing all risk factors.
  • General blood and urine analysis.
  • Blood test for gas composition, determination of D-dimer in plasma.
  • Dynamic ECG to rule out heart attack or heart failure.
  • X-ray of the lungs to exclude pneumonia, pneumothorax, malignant tumors, pleurisy.

  • For detection high pressure Echocardiography is performed in the pulmonary artery.
  • Lung scintography will show decreased or absent blood flow as a result of the development of pulmonary embolism.
  • To detect the exact location of the thrombus, angiopulmonography is prescribed.
  • Contrast venography to detect the source of pulmonary embolism.

After production accurate diagnosis and identifying the cause of the disease, therapy is prescribed.

First aid for pulmonary embolism

If an attack of the disease develops while a person is at home or at work, then it is important to provide timely assistance to him in order to reduce the likelihood of developing irreversible changes. The algorithm is as follows:

  1. Place the person on a flat surface; if he has fallen or is sitting at his workplace, do not disturb him or shift him.
  2. Unbutton the top button of the shirt, remove the tie to ensure the flow fresh air.
  3. If breathing stops, perform resuscitation actions: artificial respiration and, if necessary, indirect cardiac massage.
  4. Call an ambulance.

Proper assistance with pulmonary embolism will save a person’s life.

Treatment of the disease

Therapy for pulmonary embolism is expected only in a hospital. The patient is hospitalized and prescribed complete bed rest until the threat of vascular blockage passes. Treatment of pulmonary embolism can be divided into several stages:

  1. Urgent resuscitation measures to eliminate the risk of sudden death.
  2. Restoring the lumen of the blood vessel as much as possible.

Long-term therapy for pulmonary embolism involves the following measures:

  • Removing a blood clot from the vessels of the lungs.
  • Organizing events for
  • Increase in the diameter of the pulmonary artery.
  • Expansion of the smallest capillaries.
  • Carrying out preventive measures to prevent the development of diseases of the circulatory and respiratory systems.

Treatment of pathology involves the use of medications. Doctors prescribe to their patients:

1. Drugs from the group of fibrinolytics or thrombolytics. They are inserted directly into the pulmonary artery through a catheter. These medicines dissolve blood clots, within a few hours after the administration of the medicine the person’s condition improves, and after several days there is no trace of the blood clots.

2. At the next stage, the patient is recommended to take Heparin. At first, the drug is administered in a minimal dosage, and after 12 hours it is increased several times. The drug is an anticoagulant and, together with Warfarin or Phenilin, prevents the formation of blood clots in the pathological area of ​​the lung tissue.

3. If there is no severe pulmonary embolism, then clinical guidelines imply the use of Warfarin for at least 3 months. The drug is prescribed in a small maintenance dosage, and then it can be adjusted based on the results of examinations.

All patients undergo therapy aimed at restoring not only the pulmonary arteries, but the entire body. It means:

  • Cardiac treatment with Panangin and Obzidan.
  • Taking antispasmodics: “Papaverine”, “No-shpa”.
  • Taking medications to correct metabolic processes: medications containing vitamin B.
  • Antishock therapy with Hydrocortisone.
  • Anti-inflammatory treatment with antibacterial agents.
  • Taking antiallergic medications: Suprastin, Zodak.

When prescribing drugs, the doctor must take into account that, for example, Warfarin penetrates the placenta, so use is prohibited during pregnancy, and Andipal has many contraindications; it should be prescribed with caution to patients at risk.

Most drugs are introduced into the body by drip infusion into a vein, intramuscular injections painful and provoke the formation of large hematomas.

Surgery

Surgical treatment of pathology is rarely carried out, since such an intervention has a high mortality rate for patients. If surgery cannot be avoided, intravascular embolectomy is used. The bottom line is that a catheter with a nozzle is used to remove a blood clot through the chambers of the heart.

The method is considered risky and is resorted to in cases of emergency.

For pulmonary embolism, it is also recommended to install filters, for example, the Greenfield umbrella. It is inserted into the vena cava, and its hooks open there to fix it to the walls of the vessel. The resulting mesh allows blood to pass freely, but clots are retained and removed.

Treatment of grade 1 and 2 pulmonary embolism has a favorable prognosis. The number of deaths is minimal, the likelihood of recovery is high.

Complications of pulmonary embolism

Among the main and most dangerous complications diseases can be called:

  • Sudden death due to cardiac arrest.
  • Progression of secondary hemodynamic disorders.
  • Repeated pulmonary infarction.
  • Development of chronic pulmonary heart disease.

Disease prevention

In the presence of serious cardiovascular pathologies or a history of surgical interventions, it is important to prevent pulmonary embolism. The recommendations are as follows:

  • Avoid excessive physical activity.
  • Spend a lot of time walking.

  • Follow a daily routine.
  • Ensure adequate sleep.
  • Eliminate bad habits.
  • Review your diet and remove harmful foods from it.
  • Regularly visit a therapist for preventive examinations and a phlebologist.

These simple preventive measures will help you avoid serious complications of the disease.

But to prevent pulmonary embolism, it is important to know what conditions and diseases may predispose to the development of venous thrombosis. Special attention You should pay attention to your health:

  • People diagnosed with heart failure.
  • Bedridden patients.
  • Patients undergoing long courses of diuretic therapy.
  • Hosts hormonal drugs.
  • Sufferers diabetes mellitus.
  • Having suffered a stroke.

Patients at risk should undergo periodic therapy with heparin drugs.

PE is a serious pathology, and at the first symptoms it is important to provide timely assistance to the person and send him to the hospital or call an ambulance. This is the only way to prevent the development of serious consequences and save a person’s life.

) – acute occlusion by a thrombus or embolus of the trunk, one or more branches of the pulmonary artery.

TELA – component syndrome of thrombosis of the system of the superior and inferior vena cava (usually thrombosis of the pelvic veins and deep veins of the lower extremities), therefore in foreign practice these two diseases are combined under common name – « venous thromboembolism».

PE occurs with an incidence of 1 case per 100,000 population per year. It ranks third among the causes of mortality after ischemic heart disease and acute cerebrovascular accidents.

Objective reasons for late diagnosis of pulmonary embolism:
clinical symptoms of pulmonary embolism in many cases are similar to diseases of the lungs and cardiovascular system
the clinical picture is associated with exacerbation of the underlying disease (ischemic pulmonary disease, chronic heart failure, chronic diseases lungs) or is one of the complications of oncological diseases, injuries, extensive surgical interventions
symptoms of pulmonary embolism are nonspecific
There is often a discrepancy between the size of the embolus (and, accordingly, the diameter of the blocked vessel) and clinical manifestations - slight shortness of breath with a significant size of the embolus and severe pain in the chest with small blood clots
instrumental methods for examining patients with pulmonary embolism, which have high diagnostic specificity, are available to a narrow range of medical institutions
specific diagnostic methods, such as angiopulmonography, scintigraphy, perfusion-ventilation studies with isotopes, spiral computed tomography and magnetic resonance imaging, used to diagnose pulmonary embolism and its possible causes, are feasible in a few scientific and medical centers

!!! During life, the diagnosis of pulmonary embolism is established in less than 70% of cases. In almost 50% of cases, episodes of pulmonary embolism go undetected.

!!! In most cases, at autopsy, only a thorough examination of the pulmonary arteries can detect blood clots or residual signs of previous pulmonary embolism.

!!! Clinical signs of deep vein thrombosis of the lower extremities are often absent, especially in bedridden patients.

!!! In 30% of patients with pulmonary embolism, venography does not reveal any pathology.

According to various authors:
V 50% embolization of the trunk and main branches of the pulmonary artery occurs
V 20% embolization of the lobar and segmental pulmonary arteries occurs
V 30% cases, embolization of small branches occurs

Simultaneous damage to the arteries of both lungs reaches 65% of all cases of pulmonary embolism, in 20% only the right lung is affected, in 10% only the left lung is affected, the lower lobes are affected 4 times more often than the upper lobes.

Based on clinical symptoms, a number of authors distinguish three variants of pulmonary embolism:
1. "Infarction pneumonia"- corresponds to thromboembolism of small branches of the pulmonary artery.
Manifests as acute shortness of breath, worsening as the patient transitions to vertical position, hemoptysis, tachycardia, peripheral pain in the chest (site of lung damage) as a result of involvement in pathological process pleura.
2. "Unmotivated shortness of breath"- corresponds to recurrent pulmonary embolism of small branches.
Episodes of sudden onset, rapidly passing shortness of breath, which after some time may manifest themselves as a clinical manifestation of chronic pulmonary heart disease. Patients with this course of the disease usually do not have a history of chronic cardiopulmonary diseases, and the development of chronic pulmonary heart disease is a consequence of the accumulation of previous episodes of pulmonary embolism.
3."Acute cor pulmonale"- corresponds to thromboembolism of large branches of the pulmonary artery.
Sudden onset of shortness of breath, cardiogenic shock or hypotension, retrosternal angina pain.

!!! The clinical picture of pulmonary embolism is determined by the volume of damage to the pulmonary arteries and the pre-embolic cardiopulmonary status of the patient.

Patient complaints(in descending order of frequency of occurrence):
dyspnea
chest pain (pleural and retrosternal, angina)
anxiety, fear of death
cough
hemoptysis
sweating
loss of consciousness

!!! Unfortunately, signs with high specificity have low sensitivity, and vice versa.

Sudden shortness of breath- the most common complaint with pulmonary embolism, which intensifies when the patient moves to a sitting or standing position, when blood flow to the right side of the heart decreases. In the presence of a block of blood flow in the lung, the filling of the left ventricle decreases, which contributes to a decrease in cardiac output and a drop in blood pressure. In heart failure, shortness of breath decreases with the patient's orthoposition, but in pneumonia or chronic nonspecific lung diseases, it does not change when the patient's position changes.
Some cases of pulmonary embolism, manifested only by shortness of breath, are often not noticed, and the correct diagnosis is made late. In elderly patients with severe cardiopulmonary pathology, decompensation can quickly develop even with thromboembolism of small branches of the pulmonary artery. Signs of pulmonary embolism are often mistaken for an exacerbation of the underlying disease, and the correct diagnosis is made late.

!!! REMEMBERWhen shortness of breath occurs in patients at risk, it is always necessary to exclude pulmonary embolism. Sudden, unexplained shortness of breath is always a very alarming symptom.

Peripheral chest pain with PE, most typical for damage to small branches of the pulmonary artery, it is caused by the inclusion of visceral layers of the pleura in the inflammatory process.

Pain in the right hypochondrium indicates acute enlargement of the liver and stretching of Glisson's capsule.

Retrosternal angina pain characteristic of embolism of large branches of the pulmonary artery, occurs as a result of acute dilatation of the right parts of the heart, leading to compression of the coronary arteries between the pericardium and the dilated right parts of the heart. Most often, chest pain occurs in patients with coronary artery disease undergoing pulmonary embolism.

Hemoptysis(noted very rarely) with infarction pneumonia as a result of pulmonary embolism in the form of blood streaks in the sputum, it differs from hemoptysis with mitral valve stenosis - bloody sputum.

Excessive sweating occurs in 34% of cases among patients predominantly with massive pulmonary embolism, and is a consequence of increased sympathetic activity, accompanied by feelings of anxiety and cardiopulmonary distress.

!!! REMEMBERClinical manifestations, even in combination, have limited value to make a correct diagnosis. However, PE is unlikely in the absence of three the following symptoms: shortness of breath, tachypnea (over 20 per minute) and pain resembling pleurisy. If additional signs (changes in chest x-rays and blood PO2) are not detected, the diagnosis of pulmonary embolism can actually be excluded.

During auscultation of the lungs pathologies are usually not detected, tachypnea is possible. Swelling of the jugular veins is associated with massive pulmonary embolism. Arterial hypotension is characteristic; The patient may faint when sitting.

!!! Worsening of the underlying cardiopulmonary disease may be the only manifestation of pulmonary embolism. In this case, the correct diagnosis is difficult to establish.

Strengthening of the second tone over the pulmonary artery And appearance of systolic gallop rhythm with PE, they indicate an increase in pressure in the pulmonary artery system and hyperfunction of the right ventricle.

Tachypnea with PE most often exceeds 20 respiratory movements per minute. and is characterized by persistence and shallow breathing.

!!! The level of tachycardia in pulmonary embolism is directly dependent on the size of vascular damage, the severity of central hemodynamic disorders, respiratory and circulatory hypoxemia.

Typically, PE manifests as one of three clinical variants::
massive PE, in which the thromboembolus is localized in the main trunk and/or main branches of the pulmonary artery
submassive pulmonary embolism- embolization of the lobar and segmental branches of the pulmonary artery (the degree of perfusion disturbance corresponds to the occlusion of one of the main pulmonary arteries)
thromboembolism of small branches pulmonary artery

With massive and submassive pulmonary embolism, the following clinical symptoms and syndromes are most often observed::
sudden shortness of breath at rest (orthopnea is not typical!)
ashy, pale cyanosis; with embolism of the trunk and main pulmonary arteries, pronounced bluishness of the skin is observed, up to a cast-iron tint
tachycardia, sometimes extrasystole, atrial fibrillation
increased body temperature (even in the presence of collapse), associated primarily with the inflammatory process in the lungs and pleura; hemoptysis (observed in 1/3 of patients) due to pulmonary infarction
pain syndrome in the following variants:
1 - angina-like with pain localized behind the sternum,
2 - pulmonary-pleural - acute pain in the chest, aggravated by breathing and coughing
3 - abdominal - acute pain in the right hypochondrium, combined with intestinal paresis, persistent hiccups (caused by inflammation of the diaphragmatic pleura, acute swelling of the liver)
When auscultating the lungs, weakened breathing and fine moist rales in a limited area (usually over the right lower lobe), pleural friction noise are heard
arterial hypotension (or collapse) in combination with increased venous pressure
acute pulmonary heart syndrome: pathological pulsation, accent of the second tone and systolic murmur in the second intercostal space to the left of the sternum, presystolic or protodiastolic (more often) “gallop” at the left edge of the sternum, swelling of the jugular veins, hepatojugular reflux (Plesch’s symptom)
cerebral disorders caused by cerebral hypoxia: drowsiness, lethargy, dizziness, short-term or long-term loss of consciousness, motor agitation or severe adynamia, cramps in the limbs, involuntary defecation and urination
acute renal failure due to impaired intrarenal hemodynamics (in case of collapse)

Even timely recognition of massive pulmonary embolism does not always provide effective therapy; therefore, diagnosis and treatment of thromboembolism of small branches of the pulmonary artery, often (in 30-40% of cases) preceding the development of massive pulmonary embolism, are of great importance.

Thromboembolism of small branches of the pulmonary artery can manifest:
repeated "pneumonia" unknown etiology, some of them occur as pleuropneumonia
quickly transient (2-3 days) dry pleurisy, exudative pleurisy, especially with hemorrhagic effusion
repeated unmotivated fainting, collapse, often combined with a feeling of lack of air and tachycardia
a sudden feeling of constriction in the chest, accompanied by difficulty breathing and a subsequent increase in body temperature
"unreasonable" fever that does not respond to antibiotic therapy
paroxysmal shortness of breath with a feeling of lack of air and tachycardia
emergence and/or progression of heart failure resistant to treatment
the appearance and/or progression of symptoms of subacute or chronic cor pulmonale in the absence of anamnestic indications of chronic diseases of the bronchopulmonary apparatus

In the objective status, it is important not only to identify the above-mentioned clinical syndromes, but also to identify signs of peripheral phlebothrombosis. Phlebothrombosis of the extremities can be localized in both superficial and deep veins. Its objective diagnosis is based on a thorough search for asymmetry in the volume of soft tissues of the lower leg, thigh, pain on palpation of muscles, and local compaction. It is important to identify asymmetry in the circumference of the lower leg (by 1 cm or more) and the thigh at a level of 15 cm above the patella (by 1.5 cm or more). The Lowenberg test can be used - the appearance of pain in the calf muscle when pressure with a sphygmomanometer cuff is in the range of 150-160 mm Hg. Art. (normally, pain occurs at pressure above 180 mm).

When analyzing the clinical picture, the doctor must receive answers to the following questions that will allow him to suspect the presence of pulmonary embolism in the patient:
1? is there shortness of breath, if so, how did it arise (acute or gradual); in what position - lying or sitting is it easier to breathe
With PE, shortness of breath occurs acutely, orthopnea is not typical.
2? Is there pain in the chest, its nature, location, duration, connection with breathing, coughing, body position, etc. characteristics
The pain may resemble angina pectoris, localized behind the sternum, and may intensify with breathing and coughing.
3? were there any unmotivated fainting spells?
PE is accompanied or manifested by syncope in 13% of cases.
4? is there any hemoptysis?
Appears with the development of pulmonary infarction 2-3 days after pulmonary embolism.
5? Is there swelling of the legs (paying attention to their asymmetry)
Deep vein thrombosis of the legs is a common source of pulmonary embolism.
6? have there been any recent surgeries, injuries, heart disease with congestive heart failure, arrhythmias, is he taking oral contraceptives, is he pregnant, is he being seen by an oncologist.

The presence of predisposing factors for pulmonary embolism (for example, paroxysmal atrial fibrillation) should be taken into account by the physician when acute cardiorespiratory disorders occur in the patient.

For a preliminary assessment of the probability of pulmonary embolism, you can use the approach proposed by Rodger M. and Wells P.S. (2001), who assessed the diagnostic significance in points clinical signs :
Clinical symptoms of deep vein thrombosis of the lower extremities (at least their swelling and pain on palpation along the deep veins) – 3 points
When making a differential diagnosis of pulmonary embolism, the most probable is 3 points
Tachycardia - 1.5 points
Immobilization or surgery during the last 3 days - 1.5 points
History of deep vein thrombosis of the lower extremities or pulmonary embolism - 1.5 points
Hemoptysis – 1 point
Oncological process currently or up to 6 months ago – 1 point

If the amount does not exceed 2 score probability of pulmonary embolism low; with the sum of points 2-6 moderate; if the amount is more than 6 points – high.

Conclusion: as a result of assessing the clinical manifestations, it can be concluded that there is a low, moderate or high probability of PE in a given patient, and to confirm or exclude this diagnosis in most cases it is necessary to perform several non-invasive tests (tests used individually do not have a sufficiently high sensitivity and specificity) or angiopulmonography.

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Treatment of pulmonary embolism is challenging. The disease occurs unexpectedly and progresses quickly, as a result of which the doctor has a minimum of time at his disposal to determine the tactics and method of treating the patient. Firstly, there cannot be standard treatment regimens for PE. The choice of method is determined by the localization of the embolus, the degree of impairment of pulmonary perfusion, the nature and severity of hemodynamic disorders in the systemic and pulmonary circulation. Secondly, treatment of pulmonary embolism cannot be limited to eliminating the embolus in the pulmonary artery. The source of embolization should not be overlooked.

Urgent Care

Events emergency care PE can be divided into three groups:

1) maintaining the patient’s life in the first minutes of pulmonary embolism;

2) elimination of fatal reflex reactions;

3) elimination of the embolus.

Life support in cases of clinical death of patients is carried out primarily by resuscitation. The priority measures include the fight against collapse with the help of pressor amines, correction of the acid-base state, and effective oxygen barotherapy. At the same time, it is necessary to begin thrombolytic therapy with native streptokinase drugs (streptodecase, streptase, avelysin, celease, etc.).

The embolus located in the artery causes reflex reactions, due to which severe hemodynamic disorders often occur with non-massive pulmonary embolism. To eliminate pain, 4-5 ml of a 50% analgin solution and 2 ml of droperidol or seduxen are injected intravenously. Drugs are used if necessary. With pronounced pain syndrome analgesia begins with the administration of drugs in combination with droperidol or seduxen. In addition to the analgesic effect, the feeling of fear of death is suppressed, catecholaminemia, myocardial oxygen demand and electrical instability of the heart are reduced, and the rheological properties of blood and microcirculation are improved. In order to reduce arteriolospasm and bronchospasm, aminophylline, papaverine, no-spa, and prednisolone are used in normal doses. Elimination of embolus (basis pathogenetic treatment) is achieved by thrombolytic therapy initiated immediately after the diagnosis of PE. Relative contraindications to thrombolytic therapy, which exist in many patients, are not an obstacle to its use. High probability fatal outcome justifies the risk of treatment.

In the absence of thrombolytic drugs, continuous intravenous administration of heparin at a dose of 1000 units per hour is indicated. The daily dose will be 24,000 units. With this method of administration, relapses of pulmonary embolism occur much less frequently, and rethrombosis is more reliably prevented.

When clarifying the diagnosis of pulmonary embolism, the degree of occlusion of the pulmonary blood flow, and the localization of the embolus, a conservative or surgical treatment method is selected.

Conservative treatment

The conservative method of treating pulmonary embolism is currently the main one and includes the following measures:

1. Providing thrombolysis and stopping further thrombus formation.

2. Reduction of pulmonary arterial hypertension.

3. Compensation for pulmonary and right heart failure.

4. Elimination of arterial hypotension and bringing the patient out of collapse.

5. Treatment of pulmonary infarction and its complications.

The scheme of conservative treatment of pulmonary embolism in the most typical form can be presented as follows:

1. Complete rest of the patient, supine position of the patient with the head end raised in the absence of collapse.

2. For chest pain and severe cough administration of analgesics and antispasmodics.

3. Oxygen inhalations.

4. In case of collapse, the entire complex is carried out therapeutic measures acute vascular insufficiency.

5. For cardiac weakness, glycosides (strophanthin, corglycon) are prescribed.

6. Antihistamines: diphenhydramine, pipolfen, suprastin, etc.

7. Thrombolytic and anticoagulant therapy. Active beginning thrombolytic drugs (streptase, avelysin, streptodecase) is a metabolic product of hemolytic streptococcus - streptokinase, which, activating plasminogen, forms a complex with it, promoting the appearance of plasmin, which dissolves fibrin directly in the blood clot. Thrombolytic drugs are usually administered into one of the peripheral veins of the upper extremities or into the subclavian vein. But for massive and submassive thromboembolism, the most optimal is to inject them directly into the area of ​​the thrombus occluding the pulmonary artery, which is achieved by probing the pulmonary artery and placing a catheter under the control of an X-ray machine to the thrombus. The introduction of thrombolytic drugs directly into the pulmonary artery quickly creates their optimal concentration in the area of ​​the thromboembolus. In addition, during probing, an attempt is simultaneously made to fragment or tunnel thromboemboli in order to speedy recovery pulmonary blood flow. Before administering streptase, the following blood parameters are determined as initial data: fibrinogen, plasminogen, prothrombin, thrombin time, blood clotting time, bleeding duration. Sequence of drug administration:

1. 5000 units of heparin and 120 mg of prednisolone are injected intravenously.

2. 250,000 units of streptase (test dose), diluted in 150 ml of saline, are administered intravenously over 30 minutes, after which the blood parameters listed above are examined again.

3. In the absence of an allergic reaction, which indicates good tolerability of the drug, and a moderate change in control parameters, a therapeutic dose of streptase begins at the rate of 75,000-100,000 U/h, heparin 1000 U/h, nitroglycerin 30 mcg/min. Approximate composition of solution for infusion:

The solution is administered intravenously at a rate of 20 ml/hour.

4. During the administration of streptase, 120 mg of prednisolone is administered intravenously every 6 hours. The duration of streptase administration (24-96 hours) is determined individually.

Monitoring of the listed blood parameters is carried out every four hours. During treatment, a decrease in fibrinogen below 0.5 g/l, a prothrombin index below 35-4-0%, changes in thrombin time greater than a sixfold increase compared to the initial data, changes in coagulation time and bleeding duration greater than a threefold increase compared to the initial data are not allowed. . A complete blood count is performed daily or as indicated, platelets are determined every 48 hours and within five days after the start of thrombolytic therapy, a general urinalysis - daily, an ECG - daily, pulmonary perfusion scintigraphy - as indicated. The therapeutic dose of streptase ranges from 125,000-3,000,000 units or more.

Treatment with streptodecase involves the simultaneous administration of a therapeutic dose of the drug, which is 300,000 units of the drug. The same parameters of the coagulation system are monitored as during treatment with streptase.

Upon completion of treatment with thrombolytics, the patient is transferred to treatment with maintenance doses of heparin of 25,000-45,000 units per day intravenously or subcutaneously for 3-5 days under the control of clotting time and bleeding duration.

On the last day of heparin administration, indirect anticoagulants (pelentan, warfarin) are prescribed. daily dose which are selected in such a way that the prothrombin index is kept within the range (40-60%), the international normalized ratio (IHO) is 2.5. Treatment with indirect anticoagulants can, if necessary, continue for a long time (up to three to six months or more).

Absolute contraindications to thrombolytic therapy:

1. Disturbed consciousness.

2. Intracranial and spinal formations, arteriovenous aneurysms.

3. Severe forms arterial hypertension with symptoms of cerebrovascular accident.

4. Bleeding of any location, excluding hemoptysis caused by pulmonary infarction.

5. Pregnancy.

6. The presence of potential sources of bleeding (stomach or intestinal ulcer, surgical interventions within 5 to 7 days, condition after aortography).

7. Recent streptococcal infections (acute rheumatism, acute glomerulonephritis, sepsis, prolonged endocarditis).

8. Recent traumatic brain injury.

9. Previous hemorrhagic stroke.

10. Known disorders of the blood coagulation system.

11. Inexplicable headache or visual impairment within the last 6 weeks.

12. Cranial or spinal surgery within the last two months.

13. Acute pancreatitis.

14. Active tuberculosis.

15. Suspicion of dissecting aortic aneurysm.

16. Acute infectious diseases at the time of admission.

Relative contraindications to thrombolytic therapy:

1. Exacerbation peptic ulcer stomach and duodenum.

2. History of ischemic or embolic strokes.

3. Taking indirect anticoagulants at the time of admission.

4. Serious injury or surgical interventions more than two weeks ago, but not more than two months;

5. Chronic uncontrolled arterial hypertension (diastolic blood pressure more than 100 mm Hg).

6. Severe renal or liver failure.

7. Catheterization of the subclavian or internal jugular vein.

8. Intracardiac thrombi or valvular vegetations.

For vital indications, one must choose between the risk of the disease and the risk of therapy.

The most common complications when using thrombolytic and anticoagulant drugs are bleeding and allergic reactions. Their prevention comes down to carefully following the rules for using these drugs. If there are signs of bleeding associated with the use of thrombolytics, the following is administered intravenously:

  • epsilon-aminocaproic acid - 150-200 ml of 50% solution;
  • fibrinogen - 1-2 g per 200 ml of physiological solution;
  • calcium chloride - 10 ml of 10% solution;
  • fresh frozen plasma. The following are administered intramuscularly:
  • hemophobin - 5-10 ml;
  • vikasol - 2-4 ml of 1% solution.

If necessary, transfusion of freshly citrated blood is indicated. In case of an allergic reaction, prednisolone, promedol, and diphenhydramine are administered. The antidote for heparin is protamine sulfate, which is administered in an amount of 5-10 ml of a 10% solution.

Among the drugs latest generation It is necessary to note a group of tissue plasminogen activators (alteplase, actilise, retavase), which are activated by binding to fibrin and promote the transition of plasminogen to plasmin. When using these drugs, fibrinolysis increases only in the thrombus. Alteplase is administered in a dose of 100 mg according to the following scheme: bolus administration of 10 mg over 1-2 minutes, then during the first hour - 50 mg, in the next two hours - the remaining 40 mg. Retavase, which is used in clinical practice since the late 1990s. The maximum lytic effect when used is achieved within the first 30 minutes after administration (10 units + 10 units intravenously). The incidence of bleeding with tissue plasminogen activators is significantly less than with thrombolytics.

Conservative treatment is possible only when the patient remains able to provide relatively stable blood circulation for several hours or days (submassive embolism or small branch embolism). For embolism of the trunk and large branches of the pulmonary artery, the effectiveness of conservative treatment is only 20-25%. In these cases, the method of choice is surgical treatment - embolothrombectomy from the pulmonary artery.

Surgery

The first successful operation for pulmonary embolism was performed by F. Trendelenburg's student M. Kirchner in 1924. Many surgeons attempted embolothrombectomy from the pulmonary artery, but the number of patients who died during the operation was significantly greater than those who underwent it. In 1959, K. Vossschulte and N. Stiller proposed performing this operation in conditions of temporary occlusion of the vena cava using transsternal access. The technique provided wide free access, rapid approach to the heart and elimination of dangerous dilatation of the right ventricle. The search for safer methods of embolectomy led to the use of general hypothermia (P. Allison et al., 1960), and then artificial circulation (E. Sharp, 1961; D. Cooley et al., 1961). General hypothermia has not become widespread due to lack of time, but the use of artificial circulation has opened new horizons in the treatment of this disease.

In our country, the technique of embolectomy in conditions of occlusion of the vena cava was developed and successfully used by B.C. Savelyev et al. (1979). The authors believe that pulmonary embolectomy is indicated for those who are at risk of death from acute cardiopulmonary failure or the development of severe post-embolic hypertension of the pulmonary circulation.

Currently, the optimal methods of embolectomy for massive pulmonary embolism are:

1 Operation in conditions of temporary occlusion of the vena cava.

2. Embolectomy through the main branch of the pulmonary artery.

3. Surgical intervention under conditions of artificial circulation.

The use of the first technique is indicated for massive embolism of the trunk or both branches of the pulmonary artery. In the case of a predominantly unilateral lesion, embolectomy through the corresponding branch of the pulmonary artery is more justified. The main indication for surgery under cardiopulmonary bypass for massive pulmonary embolism is widespread distal occlusion of the pulmonary vascular bed.

B.C. Savelyev et al. (1979 and 1990) distinguish absolute and relative readings to embolothrombectomy. These include absolute indications:

  • thromboembolism of the trunk and main branches of the pulmonary artery;
  • thromboembolism of the main branches of the pulmonary artery with persistent hypotension (with pressure in the pulmonary artery below 50 mm Hg)

Relative indications are thromboembolism of the main branches of the pulmonary artery with stable hemodynamics and severe hypertension in the pulmonary artery and right heart.

They consider the following to be contraindications to embolectomy:

  • severe concomitant diseases with a poor prognosis, such as cancer;
  • diseases of the cardiovascular system, in which the success of the operation is doubtful and the risk is not justified.

A retrospective analysis of the possibilities of embolectomy in patients who died from a massive embolism showed that success can be counted on only in 10-11% of cases, and even with a successfully performed embolectomy, the possibility of re-embolism cannot be excluded. Therefore, the main direction in solving the problem should be prevention. PE is not a fatal condition. Modern methods for diagnosing venous thrombosis make it possible to predict the risk of thromboembolism and carry out its prevention.

The method of endovascular rotary disobstruction of the pulmonary artery (ERDPA), proposed by T. Schmitz-Rode, U. Janssens, N.N., should be considered promising. Schild et al. (1998) and used in a fairly large number of patients B.Yu. Bobrov (2004). Endovascular rotary disobstruction of the main and lobar branches of the pulmonary artery is indicated for patients with massive thromboembolism, especially in its occlusive form. ERDLA is performed during angiopulmonography using a special device developed by T. Schmitz-Rode (1998). The principle of the method is the mechanical destruction of massive thromboemboli in the pulmonary arteries. He can be in an independent way treatment for contraindications or ineffectiveness of thrombolytic therapy or precede thrombolysis, which significantly increases its effectiveness, reduces its duration, reduces the dosage of thrombolytic drugs and helps reduce the number of complications. Performing ERDLA is contraindicated in the presence of a traveling embolus in the pulmonary trunk due to the risk of occlusion of the main branches of the pulmonary artery due to migration of fragments, as well as in patients with non-occlusive and peripheral forms of embolism of the branches of the pulmonary artery.

Prevention of pulmonary embolism

Prevention of pulmonary embolism should be carried out in two directions:

1) prevention of the occurrence of peripheral venous thrombosis in the postoperative period;

2) in case of already formed venous thrombosis, it is necessary to carry out treatment to prevent the separation of thrombotic masses and their throwing into the pulmonary artery.

To prevent postoperative thrombosis of the veins of the lower extremities and pelvis, two types of preventive measures are used: nonspecific and specific prevention. Nonspecific prevention includes the fight against physical inactivity in bed and improvement of venous circulation in the inferior vena cava system. Specific prevention peripheral venous thrombosis involves the use of antiplatelet agents and anticoagulants. Specific prophylaxis is indicated for thrombotic patients, nonspecific - for everyone without exception. Prevention of venous thrombosis and thromboembolic complications is described in detail in the next lecture.

For already formed venous thrombosis, use surgical methods anti-embolic prophylaxis: thrombectomy from the iliocaval segment, plication of the inferior vena cava, ligation of the main veins and implantation of a vena cava filter. The most effective preventive measure received in the last three decades wide application in clinical practice, is the implantation of a vena cava filter. The most widely used umbrella filter was proposed by K. Mobin-Uddin in 1967. Throughout the years of use of the filter, various modifications of the latter have been proposed: “ hourglass", Simon Nitinol Filter, Bird's Nest Filter, Greenfield Steel Filter. Each of the filters has its own advantages and disadvantages, but none of them fully meets all the requirements for them, which determines the need for further searches. The advantage of the hourglass filter, used in clinical practice since 1994, is its high embolic activity and low ability to perforate the inferior vena cava. Main indications for implantation of a vena cava filter:

  • embolic (floating) thrombi in the inferior vena cava, iliac and femoral veins, complicated or uncomplicated pulmonary embolism;
  • massive pulmonary embolism;
  • repeated pulmonary embolisms, the source of which is unknown.

In many cases, implantation of vena cava filters is more preferable than surgical interventions on veins:

  • in elderly and old age with severe concomitant diseases and a high risk of surgery;
  • in patients who have recently undergone surgery on the abdominal, pelvic and retroperitoneal organs;
  • with recurrent thrombosis after thrombectomy from the iliocaval and iliofemoral segments;
  • in patients with purulent processes in the abdominal cavity and in the retroperitoneal space;
  • with severe obesity;
  • during pregnancy for more than 3 months;
  • with old non-occlusive thrombosis of the iliocaval and iliofemoral segments, complicated by pulmonary embolism;
  • in the presence of complications from a previously installed vena cava filter (weak fixation, threat of migration, incorrect choice of size).

The most serious complication of the installation of vena cava filters is thrombosis of the inferior vena cava with the development of chronic venous insufficiency of the lower extremities, which is observed, according to various authors, in 10-15% of cases. However, this is a small price to pay for the risk of possible pulmonary embolism. The vena cava filter itself can cause thrombosis of the inferior vena cava (IVC) if the blood clotting properties are impaired. The occurrence of thrombosis late after filter implantation (after 3 months) may be due to both the capture of emboli and the thrombogenic effect of the filter on the vascular wall and flowing blood. Therefore, at present, in some cases, the installation of a temporary vena cava filter is provided. Implantation of a permanent vena cava filter is advisable when identifying disorders of the blood coagulation system that create a risk of recurrent pulmonary embolism during the patient’s life. In other cases, it is possible to install a temporary vena cava filter for up to 3 months.

Implantation of a vena cava filter does not completely solve the process of thrombus formation and thromboembolic complications, therefore constant drug prevention should be carried out throughout the patient’s life.

A serious consequence of pulmonary embolism, despite treatment, is chronic occlusion or stenosis of the main trunk or main branches of the pulmonary artery with the development of severe hypertension of the pulmonary circulation. This condition is called chronic post-embolic pulmonary hypertension (CPEPH). The incidence of this condition after thromboembolism of large arteries is 17%. The leading symptom of CPEPH is shortness of breath, which can be observed even at rest. Patients are often bothered by a dry cough, hemoptysis, and heart pain. As a result of hemodynamic failure of the right heart, enlarged liver, dilatation and pulsation of the jugular veins, ascites, and jaundice are observed. According to most clinicians, the prognosis for CPEPH is extremely unfavorable. The life expectancy of such patients, as a rule, does not exceed three to four years. With a pronounced clinical picture of post-embolic lesions of the pulmonary arteries, surgical intervention is indicated - intimothrombectomy. The outcome of the intervention is determined by the duration of the disease (occlusion period is no more than 3 years), the level of hypertension in the pulmonary circulation (systolic pressure up to 100 mm Hg) and the condition of the distal pulmonary arterial bed. Adequate surgical intervention it is possible to achieve regression of severe CPEPH.

Pulmonary embolism is one of the most important problems of medical science and practical healthcare. Currently, there are every opportunity to reduce the mortality rate from this disease. We cannot accept the opinion that pulmonary embolism is something fatal and unpreventable. Accumulated experience suggests the opposite. Modern diagnostic methods make it possible to predict the outcome, and timely and adequate treatment gives successful results.

It is necessary to improve methods of diagnosis and treatment of phlebothrombosis as the main source of embolism, to increase the level of active prevention and treatment of patients with chronic venous insufficiency, identify patients with risk factors and promptly treat them.

Selected lectures on angiology. E.P. Kokhan, I.K. Zavarina



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