Pulmonary embolism (PE): treatment

Thromboembolism of the pulmonary artery (PE) is an occlusion of the main pulmonary artery trunk or its branches of various caliber by a thrombus, which first formed in the veins of a large circulation or in the right cavities of the heart and brought into the vascular bed of the lungs by a blood stream.

First aid at the prehospital stage

[1], [2], [3]

Anesthesia

Intravenously strontically in 10-15 ml of isotonic sodium chloride solution are administered:

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

Before the introduction of analgin, you need to find out whether it has been tolerated in the past.

Anesthesia prevents the development of reflex pain pain. Morphine, along with an analgesic effect, causes an increase in depth and a decrease in the respiratory rate; Thus, dyspnea, which is so characteristic of PE is reduced. Droperidol favorably affects microcirculation, reduces spasm of pulmonary arteries and arterioles, soothes patients.

[4], [5]

Introduction of heparin intravenously

Enter 10,000-15,000 units of heparin in 10 ml of isotonic sodium chloride solution.

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

Heparin also prevents the formation of fibrin, which is especially important, since venous thrombi largely consist of fibrin strands and the red blood cells they have captured.

Intravenous administration of euphyllin

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

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

Coping the collapse

Intravenously injected 400 ml of rheopolyglucose at a rate of 20-25 ml per minute (a high rate of administration due to pronounced hypotension).

Reopoliglyukin (reomacrodex) - 10% solution of low molecular weight Dextran, reduces the adhesion and aggregation function of platelets, increases the volume of circulating blood, raises blood pressure. In patients with high CVP, the administration of reopolyglucin is contraindicated.

Intravenous drip 2 ml 0.2% noradrenaline solution in 250 ml isotonic sodium chloride solution with an initial speed of 40-50 drops per minute (hereinafter, the speed is reduced to 10-20 drops per minute) or 0.5 mg angiotensinamide in 250 ml 0.9% sodium chloride solution (the rate of administration is the same).

Norepinephrine and angiotensinamide increase blood pressure, causing a spasm of the arteries, arterioles (ie, increasing peripheral resistance). Norepinephrine also increases cardiac output.

With persistent arterial hypotension, 60-90 mg of prednisolone is administered intravenously.

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

[6], [7]

Emergency assistance for the development of life-threatening syndromes

With severe acute respiratory failure, endotracheal intubation and mechanical ventilation are performed with any manual device. If it is not possible to carry out ventilation, inhalation oxygen therapy is used.

In case of onset of clinical death, indirect cardiac massage is performed, IVL is continued; if it is impossible to carry out ventilation, artificial respiration is made "from mouth to mouth".

With a massage of the heart, the pressure created in the right ventricle stretches the elastic wall of the pulmonary artery and part of the blood, passing the centrally placed 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 blood clots and increased embolization.

With embolism of the main trunk or main branches of the pulmonary artery, almost immediately clinical death occurs and the help begins immediately with the resuscitation techniques - heart massage and breathing "from mouth to mouth". But in this situation, clinical resuscitation is, as a rule, ineffective.

In the development of arrhythmias, antiarrhythmic therapy is performed depending on the type of rhythm disturbance.

When ventricular paroxysmal tachycardia and frequent ventricular extrasystoles are injected intravenously, lidocaine is 80-120 mg (4-6 ml of 2% solution) in 10 ml of isotonic sodium chloride solution, after 30 minutes another 40 mg (ie 2 ml of 1% solution).

With supraventricular tachycardia, supraventricular extrasystoles, 2-4 ml of 0.25% solution of isoptin (phinoptin) is injected intravenously into 10 ml of isotonic sodium chloride solution. Isoptin is administered rapidly under the control of blood pressure.

With supraventricular tachycardia, supraventricular or ventricular extrasystole, and also with ventricular paroxysmal tachycardia, it is possible to apply cordarone - 6 ml of a 5% solution in 10-20 ml of isotonic sodium chloride solution intravenously slowly.

After relief of pain syndrome, acute respiratory failure, collapse of the patient immediately hospitalized in the intensive care unit and resuscitation. Transportation is carried out on stretchers with slightly raised head end.

[8], [9], [10], [11], [12], [13], [14]

Inpatient care

In the intensive care and reanimation department, the subclavian venous catheterization is performed in connection with the need to pour thrombolytic and other agents into the vein, and also to measure the central venous pressure.

In a number of cases it is possible to establish intravenous administration of medicinal products in a qubital vein by the usual puncture.

Thrombolytic therapy

Thrombolytic therapy is the main curative measure and should be carried out immediately.

Thrombolytic therapy is effective when applied in the first 4-6 hours from the onset of the disease and is shown primarily in massive thromboembolism, i.e. Occlusion of large branches of the pulmonary artery. When the appointment of thrombolytic therapy after 4-6 hours from the onset of the disease, its effectiveness is questionable.

According to the developed VS Savelyev and soaet. (1990) criteria. Thrombolytic therapy is indicated for perfusion deficiency 30-59%, angiographic index 16-17 points for Miller, systolic and final diasgolic pressure in the right ventricle, respectively, 40-59 and 10-15 mm Hg, respectively. The average pressure in the pulmonary trunk is 25-34 mm Hg. Art. At lower degrees of perfusion deficiency and lower pressure in the right ventricle and pulmonary trunk, it is sufficient to perform anticoagulant therapy. Thrombolytic therapy is unpromising with a perfusion deficiency of more than 60%, an angiographic index above 27 points by Miller, systolic and terminal diastolic pressure in the right ventricle above 60 and 15 mm Hg. Art. Respectively, the average pressure in the pulmonary trunk exceeding 35 mm Hg. Art.

The necessary conditions for the thrombolytic therapy of pulmonary embolism are:

• reliable verification of the diagnosis (positive results of angiography or highly probable results of ventilation-perfusion lung scintigraphy);
• the possibility of laboratory control of the adequacy of 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) time after injury or surgery;
• concomitant diseases in which there is a high risk of hemorrhagic complications (peptic ulcer in the acute phase, uncorrectable arterial hypertension, recent stroke, etc.);
• when using streptoidase or its acylated complexes with plasminogen or streptodecase - recently (up to 6 months) transferred streptococcal infections or treatment with drugs obtained from the products of vital activity of beta-hemolytic streptococcus;
• active tuberculosis;
• varicose veins of the publisher;
• initial hypocoagulation;
• hemorrhagic diathesis of any etiology.

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

The concentration of plasminogen in the blood (1.5-2 μmol / l) is significantly higher than that required for physiological fibrinolysis.

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

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

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

In the human blood there are always specific inhibitors of the plasminogen activator, as well as plasmin inhibitors.

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

Circulating in the blood free plasmin cleaves fibrin, fibrinogen, factors V and VIII.

Increase fibrinolytic blood activity in PE is possible in two ways:

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

Plasminogen activators

Streptokinase (snortase, celiasis, agelizin, cabakinase) - an indirect plasminogen activator, obtained from the culture of beta-hemolytic streptococcus C.

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

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

Streptokinase and other thrombolytic drugs through fibrin degradation products circulating in the blood block the aggregation of platelets and erythrocytes, reduce the viscosity of the blood, cause bronchodilation. Thrombolytic drugs improve the contractile function of the myocardium (fibrin degradation products have a direct inotropic effect).

The treatment of streptokinase

In 100-200 ml of isotonic sodium chloride solution, 1,000,000-1,500,000 ED streptokinase is dissolved and injected intravenously for 1-2 hours. To prevent allergic reactions, it is recommended to inject 60-120 mg of prednisolone intravenously, in advance or together with streptokinase.

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

Before the start of STS treatment, it is advisable to determine the activated partial thromboplastin time (APTT), prothrombin time, thrombin time (TV), fibrinogen concentration in blood plasma, the number of erythrocytes, platelets, hemoglobin, hematocrit, test for streptokinase tolerance, evaluate the response of the hemostatic system to the administration of streptokinase.

Repeated laboratory examination is performed 3-4 h after the administration of sgregokinase. The mode of administration can be considered optimal if the concentration of fibrinogen in the blood plasma is reduced to 1.5-1 g / l, and TV increases by 2 times in comparison with the norm (30 s). With a more pronounced decrease in fibrinogen concentration and lengthening of TB, the dose of streptokinase should be reduced, in the opposite situation - increased.

Correction of the dose of streptokinase also depends on the results of the test for tolerance to streptokinase. With a normal tolerance to streptokinase, a high fibrinogen content in the plasma (> 1.5 g / L) and less than a 2-fold elongation of TB indicates an excess of streptokinase-plasminogen complexes and a deficiency of unbound plasminogen. In this case, it is necessary to reduce the dose of streptokinase by 25-50%. A more than 5-fold change in TV indicates a small number of streptokinase-plasminogen complexes and an excess of unbound plasminogen converting to plasmin with the development of hyperplasminemia. In this situation, it is necessary to increase the dose of streptokinase 2 times (up to 200 thousand units per hour).

With a high initial tolerance for streptokinase and insufficient prolongation of TB in the course of thrombolytic therapy, it is necessary to increase the dose of streptokinase.

If it is not possible to perform a test for streptokinase tolerance, the dose of streptokinase can be adjusted by determining the lysis of euglobulins (fibrinolysis characteristic), plasminogen concentration, alpha2-antiplasmin (an indirect indicator of plasmin activity, D-dimers (fibrin proteolysis products by plasmin).

A less than twofold increase in the lysis of euglobulins, an increase in the concentration of fibrinogen / fibrin degradation products (less than 100 μg / ml) is evidence of an insufficient thrombolytic effect. The pronounced decrease in fibrinogen concentration with a high content of degradation products and a low content of D-dimers indicates a predominance of fibrinogenolysis over fibrinolysis and a high risk of hemorrhagic complications.

Streptokinase is obtained from bacteria, so it has antigenic properties. Human blood always contains antibodies against streptokinase due to frequent streptococcal infections. The titer of antibodies against streptokinase rapidly increases within a few days after its administration and reaches a peak in a few weeks. This peak can be 1000 times the basal level; Only after 6 months of the antibody titers to streptokinase return to the original (before the introduction) values. Therefore, repeated injection of streptokinase within 6 months after treatment can be dangerous.

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

Streptodeaca - streptokinase immobilized on water-soluble dextran. The drug has an extended action. The half-life of streptodeacase reaches 80 h, which allows the administration of the drug once in the form of a bolus. The gradual release of the enzyme from the complex with dextran provides a significant increase in fibrinolytic activity of the blood for 3-14 days without a noticeable decrease in plasma concentrations of fibrinogen and other coagulation factors of the blood system.

The procedure for treatment with streptocyst

The total dose of streptodease is 3,000,000 units. Preliminarily 1,000,000-1,500,000 units of the drug are diluted in 10 ml of isotonic sodium chloride solution and administered intravenously in the form of a bolus of 300,000 units (3 ml of solution), in the absence of adverse reactions after 1 hour, the remaining 2,700,000 units of the drug are diluted in 20-40 ml of isotonic sodium chloride, for 5-10 minutes. Repeated injection of streptodeases is possible not earlier than 3 months.

At present, streptodedesis-2 is produced, more effective than streptodedesis.

Urokinase is an enzyme that directly converts plasminogen to plasmin. Found for the first time in human urine, is also found in the blood. It is obtained from the culture of kidney cells of the human embryo.

Urokinase is injected intravenously in a dose of 2,000,000 units for 10-15 minutes (dissolved in 20 ml isotonic sodium chloride solution). You can enter 1,500,000 units in the form of a bolus, then 1,000,000 units in the form of infusion for 1 hour.

The most popular method for the introduction of urokinase is as follows: during the first 15-30 minutes, 4400 U / kg body weight of the patient is injected intravenously, followed by administration at a dose of 4400 VD / kg / h with a dose adjustment according to the results of control determinations of TB and concentration of fibrinogen. In the treatment of urokinase, allergic reactions are much less common than with streptokinase.

Actylase (alteplase) - recombinant tissue plasminogen activator, identical to the human tissue plasminogen activator, does not possess 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 a solvent is attached. Entered intravenously drip 100 mg for 2 hours.

Prourokinase single-chain urokinase plasminogen activator, obtained by recombinant method, is administered intravenously drip in a dose of 40-70 mg for 1-2 hours. When complicating thrombolytic therapy with bleeding, it is necessary to stop the injection of thrombolytic and transfuse intravenously fresh frozen plasma, and also inject intravenously the inhibitor of fibrinolysis of tracerol in a dose of 50 thousand units.

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

Administration of activated plasmin

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

Fibrinolysin is injected intravenously with 80,000-100,000 units in 300-400 ml of isotonic sodium chloride solution, while heparin - 10,000 units per 20,000 units of fibrinolysin is added to the solution. 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 at present.

In the process of thrombolytic therapy there is a danger of thrombolytic complications in the early period after the end of thrombolytics due to the expressed consumption of plasminogen. To prevent thrombosis, heparin therapy is indicated. It is very important to determine the timing of onset of heparin therapy after the end of thrombolytics.

Too early onset of heparin therapy is aggravated by hypocoagulation caused by fibrinogen / fibrin degradation products resulting from the use of thrombolytics. Postponement of heparin therapy increases the risk of repeated thrombosis.

In contrast to myocardial infarction with PE, along with thrombolytics, heparin is not administered.

Heparin therapy can be started if, after the end of thrombolytic therapy, the fibrinogen concentration is not lower than 1 g / l (norm 2-4 g / l) and TV is elongated no more than 2 times. Usually treatment with heparin is connected 3-4 hours after the end of thrombolytic therapy.

[15], [16]

Anticoagulant therapy

Treatment with heparin begins immediately after the diagnosis of PE (in the absence of contraindications), if thrombolytic therapy is not performed, or 3-4 hours after its termination. An adequate dose of heparin is selected individually. The optimal dose is considered, in which the coagulation time and the APTT are 2 times longer than in the original ones. The most common method of heparin therapy is the following: immediately inject intravenously with 10,000 IU of heparin, and then a continuous intravenous infusion of 1-2 thousand units of heparin per hour for 7-10 days begins. Rich (1994) recommends the administration of 5000-10,000 units of heparin intravenously at a time, followed by a constant infusion of 100-15 units / kg / min. If the APTT is more than 2-3 times higher than the initial, the rate of infusion of heparin decreases by 25%.

Less often, heparin is administered in the form of injections under the skin of the stomach 5-10 thousand units 4 times a day.

4-5 days before the proposed cancellation of heparin, indirect anticoagulants (anti-vitamin K) -pheniline up to 0.2 g / day or pelentine are prescribed up to 0.9 g / day. The adequacy of the dose of indirect anticoagulants is controlled by determining prothrombin time. S. Rich (1996) recommends the use of warfarin in a dose of 10 mg per day for 2 days, then the dose is regulated depending on the prothrombin time (optimal is its reduction to 50%). For at least 5 days, taking warfarin should be combined with heparin, as warfarin first reduces the level of protein C, which can cause thrombosis.

Thus, within 4-5 days, a patient with pulmonary embolism 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 inhibitors of coagulation), which can contribute to thrombosis.

The minimal duration of therapy with indirect anticoagulants is 3 months, after a recurrence of phlebotrombosis or pulmonary thromboembolism 12 months. After repeated relapses of thrombosis of the main veins of the lower extremities and in case of failure to perform surgical prevention of pulmonary embolism, anticoagulant therapy is prescribed for life.

In connection with the need for prolonged reception of indirect anticoagulants, it is important to consider their interaction with other drugs.

With thromboembolism of segmental and small branches of the pulmonary artery, one can confine oneself only to anticoagulant therapy with heparin and antiplatelet agents.

Assign tiklid - 0.2 g 2-3 times a day, trental - at first 0.2 g 3 times a day (2 tablets 3 times a day) after eating, when the effect is achieved (after 1-2 weeks), the dose is reduced to 0.1 g 3 times a day. When taking Trental it is possible dizziness, nausea, redness of the facial skin.

As an antiaggregant also used acetylsalicylic acid (aspirin) in small doses - 150 mg per day (such doses inhibit the production of prostaglandin thromboxane and reduce the aggregation of platelets). Treatment with antiaggregants lasts 3 months.

Preventing secondary continued thrombosis in the pulmonary artery system, such treatment contributes to the recovery of pulmonary blood flow under the influence of endogenous fibrinolysis.

[17], [18]

Coping pain and collapse

It is produced in the same way as in the prehospital stage, but in addition to the intravenous infusion of rheopolyglucinum, an intravenous drip of dopamine is used to fight the collapse.

Dopamine (dopamine) - stimulates the myocardial receptors, as well as the alpha receptors of blood vessels. Depending on the speed of infusion and dose, the drug has a predominantly cardiotonic or vasoconstrictive effect. With a sharp drop in blood pressure, dopamine is administered intravenously Drip with a gradual increase in the infusion rate from 10 to 17-20 μg / kg per minute.

Method of conducting dopmin. 4 ml (160 mg) of the drug is dissolved in 400 ml of rheopolyglucin. Thus, in 1 ml of the resulting solution, 400 μg of dopamine will be contained, and in 1 drop, 20 MCG. If the patient's body weight is 70 kg, the infusion rate of 10 μg / kg per minute will correspond to 700 μg per minute, i.е. 35 drops per minute. The infusion rate of 70 drops per minute will correspond to 20 μg / kg per minute.

Therefore, adjusting the number of drops per minute, you can adjust the dose of dopminas entering the vein, depending on the level of blood pressure.

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

[19], [20]

Reduction of pressure in a small circle of blood circulation

To reduce pressure in a small circle of blood circulation, intravenous injections of papaverine hydrochloride or no-shpas are prescribed for 2 ml every 4 hours. The drugs reduce the pressure in the pulmonary artery and reduce spasm in the pulmonary arterioles, bronchi. However, it is possible to reduce pressure in a large circle, so treatment with papaverine (no-shpoy) is done under the control of arterial pressure in the brachial artery. It should also be remembered about possible bladder paresis with the administration of large doses of papaverine.

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

In addition, intravenously drip euphillin - 10 ml of 2.4% solution per 200 ml of isotonic sodium chloride solution. Euphyllin reduces pressure in the pulmonary artery, causes bronchodilating effect. Euphyllin is administered under the control of blood pressure. At a systolic blood pressure level below 100 mm Hg. Art. From the introduction of euphyllin should be refrained.

Long-term oxygen therapy

Inhalations of moistened oxygen through nasal catheters are an essential component of therapy at the inpatient stage.

Antibiotic therapy

Antibiotic therapy is prescribed for the development of infarct-pneumonia.

Surgery

Emergency embopexemia is absolutely indicated for thromboembolism of the pulmonary trunk or its main branches with an extremely severe degree of pulmonary perfusion disorder accompanied by pronounced hemodynamic disorders: persistent systemic hypotension, low blood circulation hypertension (systolic pressure in the right ventricle 60 mm Hg and above, final diastolic - 15 mm Hg).

With conservative therapy, the survival probability of patients is very small, 75% of these patients die in the acute stage of the disease.

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

In the absence of conditions for emergency connection of the device of artificial circulation, embolectomy can be performed in conditions of temporary occlusion of the hollow veins or without stopping blood circulation through one of the main pulmonary arteries (with unilateral localization of thromboembols). Catheter, endovascular embobectomy is also used.

GP Shorokh and AA Baeshko (1994) point out the need for individualization of therapeutic tactics in PE due to perfusion scanning of the lungs. This method is based on the 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 thorax with a scintillation gamma camera or scanner.

Patients with a perfusion deficiency exceeding 50% are indicated with thrombolytic therapy. The most pronounced effect can be obtained with non-occlusive lesion of lobar and segmental arteries. Patients with the same volume of obstruction, but unstable hemodynamics and angiographically proven lesion of the main branches of the pulmonary artery, it is necessary to produce embolectomy.

Patients with a perfusion deficiency of less than 50% showed anticoagulant therapy.