Pulmonary embolism (TELA) - Treatment

Pulmonary embolism (PE) is the occlusion of the main trunk of the pulmonary artery or its branches of various calibers by a thrombus that initially formed in the veins of the systemic circulation or in the right cavities of the heart and carried into the vascular bed of the lungs by the blood flow.

Pre-hospital emergency care

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Anesthesia

The following are administered intravenously by jet stream in 10-15 ml of isotonic sodium chloride solution:

• 1-2 ml of 0.005% fentanyl solution (has an analgesic effect) with 2 ml of 0.25% droperidol solution (has a neuroleptic effect) - neuroleptanalgesia method; with systolic blood pressure below 100 mm Hg, 1 ml of droperidol is administered;
• 1-2 ml of 2% promedol solution or 1 ml of 1% morphine solution or 3 ml of 50% analgin solution with 1 ml of 2% promedol solution.

Before administering analgin, it is necessary to determine whether the patient has tolerated it in the past.

Anesthesia prevents the development of reflex pain shock. Morphine, along with the analgesic effect, causes an increase in the depth and decrease in the frequency of breathing; thus, dyspnea, so characteristic of pulmonary embolism, is reduced. Droperidol has a beneficial effect on microcirculation, reduces spasm of the pulmonary arteries and arterioles, and calms patients.

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Intravenous administration of heparin

10,000-15,000 IU of heparin is administered in 10 ml of isotonic sodium chloride solution.

Heparin inhibits blood coagulation factors (thrombin, factors IX, X, XI, II), potentiates the action of antithrombin III. In addition to the anticoagulant effect, heparin prevents secondary thrombosis of the pulmonary artery distal and proximal to the embolus, relieves spasm of the pulmonary arterioles and bronchioles caused by the action of platelet serotonin, histamine, reduces platelet aggregation, prevents the spread of the venous thrombotic process, which is the source of pulmonary embolism.

Heparin also prevents the formation of fibrin, which is especially important since venous thrombi largely consist of fibrin threads and the red blood cells captured by them.

Intravenous administration of euphyllin

10 ml of 2.4% solution of euphyllin in 10-20 ml of isotonic sodium chloride solution is administered intravenously, very slowly (over 5 minutes). If systolic blood pressure is below 100 mm Hg, euphyllin is not administered.

Intravenous infusion of euphyllin relieves bronchospasm, reduces pulmonary hypertension, and stops spasm of the pulmonary artery.

Stopping the collapse

400 ml of rheopolyglucin is administered intravenously at a rate of 20-25 ml per minute (the high rate of administration is due to severe hypotension).

Rheopolyglucin (rheomacrodex) is a 10% solution of low-molecular Dextran, reduces the adhesive-aggregation function of platelets, increases the volume of circulating blood, and increases arterial pressure. The administration of rheopolyglucin is contraindicated for patients with high CVP.

2 ml of a 0.2% solution of norepinephrine in 250 ml of isotonic sodium chloride solution is administered intravenously by drip at an initial rate of 40-50 drops per minute (the rate is subsequently reduced to 10-20 drops per minute) or 0.5 mg of angiotensinamide in 250 ml of 0.9% sodium chloride solution (the rate of administration is the same).

Norepinephrine and angiotensinamide increase arterial pressure by causing spasm of the arteries and arterioles (i.e. increasing peripheral resistance). Norepinephrine also increases cardiac output.

If arterial hypotension persists, 60-90 mg of prednisolone is administered intravenously.

If conditions permit, it is better to administer dopamine intravenously instead of norepinephrine, since it increases cardiac output when administered at a rate of 5-17 mcg/kg per minute and does not worsen cerebral and coronary perfusion. If collapse persists, the rate of administration is increased.

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Emergency care in the development of life-threatening syndromes

In cases of severe acute respiratory failure, endotracheal intubation and artificial ventilation are performed using any hand-operated device. If artificial ventilation is not possible, inhalation oxygen therapy is used.

In the event of clinical death, indirect cardiac massage is performed, artificial ventilation is continued; if artificial ventilation is not possible, mouth-to-mouth artificial respiration is performed.

During cardiac massage, the pressure created in the right ventricle stretches the elastic wall of the pulmonary artery and part of the blood, bypassing the centrally located embolus, enters the distal vascular bed of the lungs, which leads to a partial restoration of pulmonary blood flow,

At the same time, indirect cardiac massage may be ineffective due to the possibility of fragmentation of large thrombi and increased embolization.

In case of embolism of the main trunk or main branches of the pulmonary artery, clinical death occurs almost immediately and assistance begins immediately with resuscitation techniques - cardiac massage and mouth-to-mouth breathing. But in this situation, clinical resuscitation is usually ineffective.

When arrhythmias develop, antiarrhythmic therapy is administered depending on the type of rhythm disturbance.

In case of ventricular paroxysmal tachycardia and frequent ventricular extrasystoles, lidocaine is administered intravenously by jet stream - 80-120 mg (4-6 ml of 2% solution) in 10 ml of isotonic sodium chloride solution, after 30 minutes - another 40 mg (i.e. 2 ml of 1% solution).

In case of supraventricular tachycardia, supraventricular extrasystoles, 2-4 ml of 0.25% solution of isoptin (finoptin) in 10 ml of isotonic sodium chloride solution is administered intravenously. Isoptin is administered quickly under the control of arterial pressure.

In case of supraventricular tachycardia, supraventricular or ventricular extrasystole, as well as ventricular paroxysmal tachycardia, cordarone can be used - 6 ml of a 5% solution in 10-20 ml of isotonic sodium chloride solution intravenously slowly.

After the pain syndrome, acute respiratory failure, and collapse have been relieved, the patient is immediately hospitalized in the intensive care and resuscitation department. Transportation is carried out on a stretcher with the head end slightly raised.

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Provision of inpatient care

In the intensive care unit, catheterization of the subclavian vein is performed due to the need to infuse thrombolytic and other agents into the vein, as well as to measure central venous pressure.

In some cases, it is possible to establish intravenous administration of drugs into the cubital vein by means of a simple puncture.

Thrombolytic therapy

Thrombolytic therapy is the mainstay of treatment and should be initiated immediately.

Thrombolytic therapy is effective when used in the first 4-6 hours from the onset of the disease and is indicated primarily for massive thromboembolism, i.e. occlusion of large branches of the pulmonary artery. When thrombolytic therapy is prescribed after 4-6 hours from the onset of the disease, its effectiveness is questionable.

According to the criteria developed by V. S. Savelyev et al. (1990), thrombolytic therapy is indicated for perfusion deficit of 30-59%, angiographic index of 16-17 points according to Miller, systolic and end-diastolic pressure in the right ventricle of 40-59 and 10-15 mm Hg, respectively, and mean pressure in the pulmonary trunk of 25-34 mm Hg. With lesser degrees of perfusion deficit and lower pressure in the right ventricle and pulmonary trunk, anticoagulant therapy is sufficient. Thrombolytic therapy is of no use for perfusion deficit greater than 60%, angiographic index higher than 27 points according to Miller, systolic and end-diastolic pressure in the right ventricle higher than 60 and 15 mm Hg. accordingly, the average pressure in the pulmonary trunk exceeds 35 mm Hg.

The necessary conditions for thrombolytic therapy of pulmonary embolism are:

• reliable verification of the diagnosis (positive results of angiography or highly probable results of ventilation-perfusion lung scingiography);
• the possibility of laboratory monitoring of the adequacy of the treatment;
• a clear understanding of the nature of possible complications of thrombolytic therapy and ways to eliminate them.

Thrombolytic therapy is contraindicated in the following situations:

• early (up to 10 days) periods after injury or surgery;
• concomitant diseases that increase the risk of developing hemorrhagic complications (peptic ulcer in the acute phase, uncorrected arterial hypertension, recent stroke, etc.);
• when using streptoidase or its acylated complexes with plasminogen or streptodecase - recent (up to 6 months) streptococcal infections or treatment with drugs obtained from the waste products of beta-hemolytic streptococcus;
• active tuberculosis process;
• varicose veins of the esophagus;
• initial hypocoagulation;
• hemorrhagic diathesis of any etiology.

Plasmin, which is one of the serine proteases, plays a major role in dissolving the thrombus. Plasmin is formed from the inactive precursor of plasminogen - beta-globulin with a molecular weight of 92,000 Daltons, which is synthesized mainly in the liver.

The concentration of plasminogen in the blood (1.5-2 μmol/l) significantly exceeds the value required for physiological fibrinolysis.

The conversion of plasminogen proenzyme into active plasmin occurs under the influence of various plasminogen activators, among which, depending on their origin, the following three groups are distinguished:

• internal (humoral) plasminogen activators, which are present in the blood as precursors (coagulation factor XII, prekallikrein);
• external (tissue) plasminogen activators, which are secreted into the lumen of the vessel by endothelial cells or released from damaged tissues;
• exogenous plasminogen activators, which are introduced into the blood for therapeutic purposes (for example, streptokinase, urokinase and other drugs).

The main mechanism of plasminogen activation is the secretion of a potent tissue plasminogen activator by endothelial cells.

Specific plasminogen activator inhibitors and plasmin inhibitors are constantly present in human blood.

Thus, the fibrinolytic action of plasmin depends on its relationship with plasminogen activator inhibitors and plasmin inhibitors.

Free plasmin circulating in the blood breaks down fibrin, fibrinogen, factors V and VIII.

There are two ways to increase the fibrinolytic activity of the blood in PE:

• the introduction of plasminogen activators, which enhance the formation of plasmin from endogenous plasminogen;
• by introducing in vitro activated plasmin, thereby increasing its content in the blood.

Plasminogen activators

Streptokinase (cneptokinase, celiase, avelizin, kabikinase) is an indirect plasminogen activator obtained from a culture of beta-hemolytic streptococcus C.

Streptokinase forms a complex with plasminogen, the molecule of which undergoes informational changes that lead to the exposure of the active center. The streptokinase-plasminogen complex plays the role of an enzyme in the conversion of endogenous plasminogen into plasmin. The resulting plasmin causes enzymatic destruction of fibrin by both exothrombolysis (dissolution of the thrombus from the outside) and endothrombolysis associated with the penetration of streptokinase into the thrombus and the activation of plasminogen located on the surface of the fibrin threads.

The destruction of the fibrin network leads to the disintegration of the constituent elements of the thrombus and its disintegration into small fragments, which are either carried away by the blood flow or dissolved by plasmin.

Streptokinase and other thrombolytic drugs block platelet and erythrocyte aggregation, reduce blood viscosity, and cause bronchodilation through fibrin degradation products circulating in the blood. Thrombolytic drugs improve myocardial contractility (fibrin degradation products have a direct inotropic effect).

Streptokinase treatment method

1,000,000-1,500,000 IU of streptokinase is dissolved in 100-200 ml of isotonic sodium chloride solution and administered intravenously by drip over 1-2 hours. To prevent allergic reactions, it is recommended to administer 60-120 mg of prednisolone intravenously before or together with streptokinase.

There is a second method of streptokinase treatment, which is considered more rational. First, 250,000 IU is administered intravenously (this ensures neutralization of antistreptococcal antibodies circulating in the blood in most patients who have not had a streptococcal infection in the recent past). To prevent allergic complications, prednisolone is administered at a dose of 60-90 mg before streptokinase administration. In the absence of pronounced allergic reactions (a sharp increase in body temperature, persistent chills, urticaria, bronchospasm), streptokinase administration continues at a dose of 100,000 IU/h. The duration of streptokinase administration depends on the clinical effect and is 12-24 hours.

Before starting streptokinase treatment, it is advisable to determine the activated partial thromboplastin time (APTT), prothrombin time, thrombin time (TT), plasma fibrinogen concentration, red blood cell count, platelet count, hemoglobin content, hematocrit, and conduct a tolerance test to streptokinase, the results of which can be used to assess the hemostatic system's response to the administration of streptokinase.

A repeat laboratory test is performed 3-4 hours after the administration of streptokinase. The administration regimen can be considered optimal if the fibrinogen concentration in the blood plasma decreases to 1.5-1 g/l, and TT increases 2 times compared to the norm (30 s). With a more pronounced decrease in fibrinogen concentration and prolongation of TT, the dose of streptokinase should be reduced, in the opposite situation - increased.

Streptokinase dose adjustment also depends on the streptokinase tolerance test results. With normal tolerance to streptokinase, high plasma fibrinogen levels (over 1.5 g/L) and less than 2-fold prolongation of TT indicate an excess of streptokinase-plasminogen complexes and a deficiency of unbound plasminogen. In this case, it is necessary to reduce the streptokinase dose by 25-50%. More than 5-fold change in TT indicates a small amount of streptokinase-plasminogen complexes and an excess of unbound plasminogen, which is converted into plasmin with the development of hyperplasminemia. In this situation, it is necessary to increase the streptokinase dose by 2 times (up to 200 thousand U/h).

In case of high initial tolerance to streptokinase and insufficient prolongation of TT during thrombolytic therapy, it is necessary to increase the dose of streptokinase.

If it is impossible to perform a streptokinase tolerance test, the streptokinase dose can be adjusted based on the results of determining euglobulin lysis (a characteristic of fibrinolysis), plasminogen concentration, alpha2-antiplasmin (an indirect indicator of plasmin activity), and D-dimers (products of fibrin proteolysis by plasmin).

Less than twofold increase in euglobulin lysis, increased concentration of fibrinogen/fibrin degradation products (less than 100 μg/ml) are signs of insufficient thrombolytic effect. A marked decrease in fibrinogen concentration with a high content of its degradation products and low - D-dimers indicate the prevalence of fibrinogenolysis over fibrinolysis and a high risk of hemorrhagic complications.

Streptokinase is derived from bacteria, which is why it has antigenic properties. Human blood always contains antibodies against streptokinase due to frequent streptococcal infections. The titer of antibodies against streptokinase increases rapidly within a few days after its administration and reaches a peak after a few weeks. This peak can be 1000 times higher than the basal level; only after 6 months do the titers of antibodies to streptokinase return to the initial (pre-administration) values. Therefore, repeated administration of streptokinase within 6 months of the treatment may be dangerous.

Side effects of streptokinase: fever, chills, headaches, nausea, pain in the lumbar region.

Streptodecase is streptokinase immobilized on water-soluble dexgran. The drug has a prolonged effect. The half-life of streptodecase reaches 80 hours, which allows the drug to be administered once as a bolus. Gradual release of the enzyme from the complex with dextran provides a significant increase in the fibrinolytic activity of the blood for 3-14 days without a noticeable decrease in plasma concentrations of fibrinogen and other factors of the blood coagulation system.

Method of treatment with stretodecase

The total dose of streptodecase is 3,000,000 U. First, 1,000,000-1,500,000 U of the drug is diluted in 10 ml of isotonic sodium chloride solution and administered intravenously as a bolus of 300,000 U (3 ml of solution); if there are no adverse reactions, the remaining 2,700,000 U of the drug diluted in 20-40 ml of isotonic sodium chloride solution is administered over 5-10 minutes after 1 hour. Repeated administration of streptodecase is possible no earlier than after 3 months.

Currently, streptodecase-2 is being produced, which is more effective than streptodecase.

Urokinase is an enzyme that directly converts plasminogen into plasmin. It was first discovered in human urine and is also found in blood. It is obtained from a culture of human embryonic kidney cells.

Urokinase is administered intravenously by jet stream at a dose of 2,000,000 U over 10-15 minutes (dissolved in 20 ml of isotonic sodium chloride solution). 1,500,000 U can be administered as a bolus, then 1,000,000 U as an infusion over 1 hour.

The most popular method of administering urokinase is as follows: 4400 U/kg of the patient's body weight is administered intravenously during the first 15-30 minutes, then the administration is continued for 12-24 hours at a dose of 4400 U/kg/h with dose adjustment based on the results of control determinations of TV and fibrinogen concentration. Allergic reactions are significantly less common with urokinase than with streptokinase.

Actilyse (alteplase) is a recombinant tissue plasminogen activator, identical to human tissue plasminogen activator, has no antigenic properties and does not cause allergic reactions. The drug is available in vials containing 50 mg of plasminogen activator, in addition, a vial with solvent is included. 100 mg is administered intravenously by drip over 2 hours.

Prourokinase, a single-chain urokinase plasminogen activator obtained by a recombinant method, is administered intravenously by drip at a dose of 40-70 mg for 1-2 hours. If thrombolytic therapy is complicated by bleeding, it is necessary to stop administering the thrombolytic and transfuse fresh frozen plasma intravenously, as well as administer the fibrinolysis inhibitor trasylol intravenously by drip at a dose of 50 thousand units.

A technique for administering thrombolytics into the subclavian vein and pulmonary artery has been developed.

Administration of activated plasmin

Fibrinolysin (plasmin) is plasminogen (profibrinolysin) isolated from human plasma and activated in vitro by trypsin. Fibrinolysin solution is prepared from powder immediately before administration to avoid loss of activity during storage at room temperature.

Fibrinolysin is administered intravenously by drip - 80,000-100,000 U in 300-400 ml of isotonic sodium chloride solution, while heparin is added to the solution - 10,000 U per 20,000 U of fibrinolysin. The infusion rate is 16-20 drops per minute.

Exogenous plasmin (fibrinolysin) acts slowly and is not effective enough in dissolving arterial thrombi. In addition, it often causes pyrogenic and allergic reactions, so it is rarely used today.

During thrombolytic therapy, there is a risk of thrombolytic complications in the early stages after the end of thrombolytic administration due to the pronounced consumption of plasminogen. Heparin therapy is indicated for the prevention of thrombus formation. It is very important to determine the time of the beginning of heparin therapy after the end of thrombolytic administration.

Too early initiation of heparin therapy worsens hypocoagulation caused by fibrinogen/fibrin degradation products formed as a result of thrombolytic use. Delaying heparin therapy increases the risk of recurrent thrombosis.

Unlike myocardial infarction, in PE heparin is not administered together with thrombolytics.

Heparin therapy can be started if after completion of thrombolytic therapy the fibrinogen concentration is not lower than 1 g/l (normal 2-4 g/l) and TT is extended no more than 2 times. Usually heparin treatment is started 3-4 hours after completion of thrombolytic therapy.

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Anticoagulant therapy

Heparin treatment begins immediately after the diagnosis of PE (in the absence of contraindications), if thrombolytic therapy is not administered, or 3-4 hours after its completion. An adequate dose of heparin is selected individually. The optimal dose is considered to be the one at which the blood clotting time and APTT are extended by 2 times compared to the initial ones. The most common method of heparin therapy is the following: 10 thousand units of heparin are immediately administered intravenously by jet stream, and then a constant intravenous infusion of 1-2 thousand units of heparin per hour is started for 7-10 days. Rich (1994) recommends administering 5000-10,000 units of heparin immediately by jet stream intravenously, then a constant infusion of 100-15 units/kg/min. If APTT is more than 2-3 times higher than baseline, the heparin infusion rate is reduced by 25%.

Less commonly, treatment is carried out with heparin in the form of injections under the skin of the abdomen 5-10 thousand IU 4 times a day.

Indirect anticoagulants (antivitamin K) are prescribed 4-5 days before the expected discontinuation of heparin - phenylin up to 0.2 g/day or pelentan up to 0.9 g/day. The adequacy of the dose of indirect anticoagulants is controlled by determining the prothrombin time. S. Rich (1996) recommends using warfarin at a dose of 10 mg per day for 2 days, then the dose is adjusted depending on the prothrombin time (optimal is its reduction to 50%). For at least 5 days, warfarin should be combined with heparin, since warfarin initially reduces the level of protein C, which can cause thrombosis.

Thus, for 4-5 days, the patient with PE simultaneously receives heparin injections and takes indirect anticoagulants. The simultaneous use of heparin and indirect anticoagulants is due to the fact that the latter initially reduce the level of proteins C and S (natural coagulation inhibitors), which can contribute to thrombosis.

The minimum duration of therapy with indirect anticoagulants is 3 months, after relapse of phlebothrombosis or pulmonary thromboembolism - 12 months. After repeated relapses of thrombosis of the main veins of the lower extremities and failure to perform surgical prophylaxis of pulmonary embolism, anticoagulant therapy is prescribed for life.

Due to the need for long-term use of indirect anticoagulants, it is important to consider their interaction with other drugs.

In case of thromboembolism of segmental and small branches of the pulmonary artery, it is possible to limit oneself to anticoagulant therapy with heparin and antiplatelet agents.

Ticlid is prescribed - 0.2 g 2-3 times a day, Trental - initially 0.2 g 3 times a day (2 pills 3 times a day) after meals, when the effect is achieved (after 1-2 weeks) the dose is reduced to 0.1 g 3 times a day. When taking Trental, dizziness, nausea, and redness of the skin of the face are possible.

Acetylsalicylic acid (aspirin) is also used as an antiplatelet agent in small doses - 150 mg per day (such doses inhibit the production of prostaglandin thromboxane and reduce platelet aggregation). Treatment with antiplatelet agents continues for 3 months.

By preventing secondary prolonged thrombosis in the pulmonary artery system, such treatment promotes the restoration of pulmonary blood flow under the influence of endogenous fibrinolysis.

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Relief of pain and collapse

It is performed in the same way as at the pre-hospital stage, but in addition to the intravenous infusion of rheopolyglucin, intravenous drip infusion of dopamine is used to combat collapse.

Dopamine (dopamine) - stimulates myocardial pp-receptors, as well as vascular alpha-receptors. Depending on the infusion rate and dose, the drug has a predominantly cardiotonic or vasoconstrictive effect. With a sharp decrease in arterial pressure, dopamine is administered intravenously by drip with a gradual increase in the infusion rate from 10 to 17-20 mcg / kg per minute.

Method of dopamine administration. 4 ml (160 mg) of the drug is dissolved in 400 ml of rheopolyglucin. Thus, 1 ml of the resulting solution will contain 400 mcg of dopamine, and 1 drop - 20 mcg. If the patient's body weight is 70 kg, then the infusion rate of 10 mcg / kg per minute will correspond to 700 mcg per minute, i.e. 35 drops per minute. The infusion rate of 70 drops per minute will correspond to 20 mcg / kg per minute.

Therefore, by adjusting the number of drops per minute, it is possible to regulate the dose of dopamine entering the vein depending on the level of blood pressure.

At an infusion rate of 5-15 mcg/kg per minute, the drug has a predominantly cardiotonic effect.

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Reduction of pressure in the pulmonary circulation

To reduce pressure in the pulmonary circulation, intravenous injections of papaverine hydrochloride or no-shpa, 2 ml every 4 hours, are recommended. The drugs reduce pressure in the pulmonary artery and reduce spasm in the pulmonary arterioles and bronchi. However, pressure in the systemic circulation can also be reduced, so treatment with papaverine (no-shpa) is performed under the control of arterial pressure in the brachial artery. It should also be remembered that bladder paresis may occur when large doses of papaverine are administered.

The highest daily dose of papaverine parenterally is 600 mg, i.e. 15 ml of a 2% solution.

In addition, euphyllin is administered intravenously by drip - 10 ml of a 2.4% solution per 200 ml of isotonic sodium chloride solution. Euphyllin reduces pressure in the pulmonary artery, causing a bronchodilating effect. Euphyllin is administered under the control of arterial pressure. If the systolic arterial pressure is below 100 mm Hg, euphyllin administration should be avoided.

Long-term oxygen therapy

Inhalation of humidified oxygen through nasal catheters is the most important component of therapy at the inpatient stage.

Antibiotic therapy

Antibiotic therapy is prescribed in the development of infarction pneumonia.

Surgical treatment

Emergency embolectomy is absolutely indicated in case of thromboembolism of the pulmonary trunk or its main branches with an extremely severe degree of impaired pulmonary perfusion, accompanied by pronounced hemodynamic disorders: persistent systemic hypotension, hypertension of the pulmonary circulation (systolic pressure in the right ventricle of 60 mm Hg and higher, end diastolic - 15 mm Hg).

When conservative therapy is carried out, the probability of survival of patients is very low; 75% of such patients die in the acute stage of the disease.

The optimal method of surgical treatment is embolectomy under artificial circulation. The operation begins with auxiliary venoarterial perfusion, which is performed by catheterization of the femoral arteries.

In the absence of conditions for emergency connection of the artificial circulation apparatus, embolectomy can be performed under conditions of temporary occlusion of the vena cava or without stopping blood circulation through one of the main pulmonary arteries (with unilateral localization of thromboemboli). Catheter, endovascular embolectomy is also used.

G. P. Shorokh and A. A. Baeshko (1994) point to the need for individualization of treatment tactics for pulmonary embolism depending on perfusion scanning of the lungs. This method is based on artificial microembolization of the peripheral vascular bed of the lungs by intravenous administration of a radiopharmaceutical (albumin macroaggregate bound to 131I, 99mTc) and subsequent registration of external radiation in the chest area using a scintillation gamma camera or scanner.

Thrombolytic therapy is indicated for patients with perfusion deficit exceeding 50%. The most pronounced effect can be achieved with non-occlusive lesions of lobar and segmental arteries. Patients with the same volume of obstruction, but unstable hemodynamics and angiographically proven lesions of the main branches of the pulmonary artery should undergo embolectomy.

Patients with a perfusion deficit of less than 50% are indicated for anticoagulant therapy.