Body therapy. Symptoms and treatment of pulmonary embolism. Symptoms of dangerous occlusion: what are the manifestations

Pulmonary embolism is a syndrome that develops as a result of occlusion of the pulmonary artery trunk or its branches by thrombotic masses. Tela is a formidable, life-threatening condition.

Despite the improvement in the diagnostic and treatment capabilities of modern medicine, the mortality rate from pulmonary embolism remains high and averages about 25% of the total number of registered cases, i.e. Every fourth person dies. Mortality from pulmonary embolism is in third place among diseases of the cardiovascular system.

Causes of pulmonary embolism

The main cause leading to pulmonary embolism is deep vein thrombosis of the lower extremities. Of particular danger are floating blood clots that have a free, mobile area that exceeds the diameter of the base in size. Much less often, the source of embolism can be other venous vessels from the inferior vena cava system, veins of the upper extremities, and the right side of the heart.

According to the recommendations of the European Society of Cardiology, PE risk stratification is divided into high risk (risk of early death in hospital or within 30 days after thromboembolism) - more than 15%, moderate (less than 15%) and low risk (less than 1%).

High risk factors for pulmonary embolism according to the recommendations of the European Society of Cardiology include:

• Phlebitis, thrombosis and embolism, history of varicose veins;
• Elderly and senile age (>40 years, risk doubles every 10 years);
• Physical inactivity, obesity, long-term fixed uncomfortable position of the legs;
• Temperature changes (hypothermia, dehydration);
• Female gender (twice as often as men);
• Cardiovascular diseases: atrial fibrillation, chronic cardiac and respiratory failure, ventricular aneurysm (paradoxical embolism through a patent foramen ovale in the presence of mitral regurgitation or through a ventricular septal defect);
• Malignant neoplasms;
• Infectious diseases, chronic inflammation of the pelvic organs;
• Perioperative period;
• Injuries;
• Hormonal therapy (steroids, hormonal contraceptives), chemotherapy;
• Pregnancy and postpartum period;
• Hereditary and acquired thrombophilias;
• Iatrogenic pathology: uncontrolled use of procoagulants, diuretics and laxatives; appointment of antagonistswithout prior heparin therapy; complications of venous catheterization.

In clinical practice, a revised, simplified version is often used Geneva PE risk score:

Pathogenesis of pulmonary embolism

When a pulmonary artery is occluded by a thrombus, the pressure in the pulmonary circulation increases and the load on the right ventricle increases. Due to a decrease in preload, the ejection fraction decreases, blood pressure drops, which, along with a significant deterioration in ventilation-perfusion relationships, an increase in dead space and the volume of shunted blood in the lungs, leads to hypoxia of internal organs: the brain, myocardium, and kidneys. The severity of pathophysiological manifestations directly correlates with the diameter of the blocked blood vessel. When the trunk of the pulmonary artery is blocked, death occurs almost instantly. Sudden closure of the lumen of the pulmonary arteries is aggravated by the development of generalized vasoconstriction in the pulmonary circle and reflex bronchospasm. Sufficiently prolonged arterial occlusion leads to hemorrhagic pulmonary infarction, accompanied by a perifocal inflammatory reaction. Severe overload of the right side of the heart, in combination with myocardial ischemia, leads to cardiac arrhythmia and the appearance of life-threatening arrhythmias. The most common cause of mortality in pulmonary embolism is ventricular fibrillation.

Classification of pulmonary embolism

Based on the volume of the arterial vascular bed excluded from the bloodstream during thrombotic occlusion, two main forms are distinguished: massive (over 45%) and non-massive (less than 45%) PE, expressed as a percentage, based on the fact that the basin of the right pulmonary artery is 55 %, each of the lower lobe branches – 20-25% of the pulmonary circulation.

Downstream (P. M. Zlochevsky, Pulmonary embolism, 1978):

• fulminant pulmonary embolism (or syncope);
• acute thromboembolism - death occurs within a few tens of minutes;
• I'll make it more acute – death within a few hours or days;
• chronic form of pulmonary embolism, with progression of right ventricular failure over several months or years;
• recurrent, with repeated thromboembolisms;
• erased, latently leaking.

Symptoms of pulmonary embolism

The clinical picture can be different, and mainly depends on the diameter of the affected artery and premorbid background. The most characteristic is a triad of symptoms: shortness of breath, chest pain, increased heart rate. The most constant sign of pulmonary embolism is acute shortness of breath or its significant, sudden increase in conditions accompanied by tachypnea. Shortness of breath is mixed, shallow breathing, with a frequency of 30 per minute or more, often accompanied by cough and hemoptysis.

Chest pain is a common but inconsistent symptom of thromboembolism, usually of a pleural nature. They may also be associated with cardiac causes: myocardial ischemia and increased load on the right ventricle with localization behind the sternum. Pain in the epigastrium and right hypochondrium appears with reactive pleurisy with irritation of the right dome of the diaphragm and with stretching of the liver capsule in acute right ventricular failure.

The position of orthopnea is not typical for pulmonary embolism. The level of consciousness ranges from stupor to coma, sometimes - severe anxiety and agitation. Upon examination, cyanosis (cyanosis) of the skin of a diffuse, widespread nature may be detected, caused by hypoxemia or predominantly of the upper shoulder girdle, neck, face, as a result of venous stagnation. Pale, moist skin is one of the symptoms of obstructive shock, manifested by peripheral spasm.

The Kussmaul sign is positive - swelling of the veins of the neck with intensification on inspiration, as well as with careful pressure on the liver area (Plesch's test). Auscultation of the lungs during pulmonary embolism may not reveal any changes. The development of bronchospasm is accompanied by harsh breathing and dry wheezing. Pleural friction noise is heard during pleurisy. There may be a small amount of moist rales and weakening of breathing over the zone of switched off blood flow.

During auscultation of the heart, an accent and splitting of the second sound over the PA, a gallop rhythm, and arrhythmic heartbeats (ES, AF) are heard. Palpation of the abdomen in the right hypochondrium reveals an enlarged, painful liver. Blood pressure measurement can reveal varying degrees of hypotension.

Diagnosis of pulmonary embolism

Laboratory methods: since the 90s, when thromboembolism is suspected, the presence of D-dimer in the patient’s blood is determined. D-dimer is a fragment of fibrinogen that appears in the blood when a blood clot is destroyed. In its absence, the diagnosis of thromboembolism is excluded. Detection of D-dimer can be an indicator of both thrombosis, including other localizations, and a consequence of other causes. Thus, detection of fibrinogen D-dimers is used to exclude thromboembolism, but not to confirm the diagnosis. It is important to take into account the factors influencing the occurrence of false-negative and false-positive reactions.

When analyzing an ECG for pulmonary embolism, the following signs may be detected: McGean-White syndrome S I Q III T III, conduction disturbance in the system of the right Hiss bundle branch (usually RBBB), shift of the transition zone to the right with negative T V1-V4, P- “pulmonale” , decreased ST in I and aVL, various heart rhythm disturbances, most often in the form of extrasystole. With a significant load on the RV - ventricular fibrillation.

In the diagnosis of pulmonary embolism, the following are used: pulmonary radiography, CT scan of the lungs, ventilation-perfusion scintigraphy, angiopulmonography, ECHO-CG, ultrasound examination of the veins of the lower extremities.

Treatment of pulmonary embolism

• In the acute period of pulmonary embolism, strict bed rest is prescribed;
• To relieve pain during thromboembolism, narcotic analgesics are administered intravenously. The drug of choice is morphine;
• Inhalation of an oxygen-air mixture, according to indications, transition to mechanical ventilation;
• Heparin intravenously to prevent further thrombus formation;
• Eufillin for bronchospastic syndrome;
• For arterial hypotension - infusion of dopamine, with little effectiveness, simultaneously with norepinephrine;
• Thrombolytic therapy
• Embolectomy is indicated for patients with pulmonary embolism: 1) in need of cardiopulmonary resuscitation, 2) in the presence of contraindications to thrombolysis or its ineffectiveness, 3) patent foramen ovale and intracardiac thrombosis
• Treatment of complications, prevention of rethrombosis

Prevention of pulmonary embolism

• Anticoagulant therapy;
• Installation of a vena cava filter

Pulmonary embolism(PE) is one of the most severe and catastrophic acute vascular diseases, accompanied by high mortality.
PE is a blockage of the arterial bed of the lung by a thrombus formed in the venous system of the systemic circulation, the right atrium or the right ventricle of the heart.

Epidemiology. There is no domestic statistical information on pulmonary embolism. In the United States, it is diagnosed annually in 630,000 patients, of whom 200,000 die; Among the causes of mortality, it ranks 3rd.
Even massive embolic damage to the pulmonary arteries is not diagnosed intravitally in 40-70% of patients.

Etiology. The cause of pulmonary embolism is the detachment of a venous thrombus and its obstruction of part or the entire bed of the pulmonary artery.
In most cases, the source of embolism is located in the inferior vena cava basin or in the veins of the lower extremities and pelvis, less often in the right chambers of the heart and veins of the upper extremities.
Sometimes thromboembolism can result from thrombosis of the right atrium, which develops against the background of atrial fibrillation and dilated cardiomyopathy.
Embolization of the pulmonary vascular bed is also possible with tricuspid valve endocarditis and endocardial pacing complicated by thrombosis of the right heart.

Pathogenesis. Conditions conducive to the occurrence of phlebothrombosis occur with heart failure, trauma (including operating rooms), oncological, purulent-septic, neurological and other diseases, especially in bed rest.
Typically, pulmonary embolism occurs when floating thrombi are freely located in the lumen of the vessel and have a single point of fixation in their distal section.
Such a thrombus can easily be washed away by the blood flow and brought into the pulmonary circulation.
Occlusive thrombotic lesions, in which blood clots are tightly fused to the vein wall over a significant extent, are not complicated by embolism. Fundamentally, thrombosis of any localization can cause thromboembolism, meanwhile, the source of massive pulmonary embolism, which is understood as embolic damage to the pulmonary trunk and/or main pulmonary arteries, in 65% of cases is thrombosis of the ileocaval segment, in 35% - the popliteal-femoral.
Changes in the lung parenchyma in the affected area can manifest as simple transient ischemia with rapid restoration of blood flow.
With more massive or prolonged occlusion, hemorrhagic pulmonary infarction may develop, followed by an aseptic inflammatory reaction (infarction-pneumonia).

The pleural reaction to pulmonary embolism can be in the form of fibrinous pleurisy, hemorrhagic pleurisy, or the formation of transudative pleural effusion.
Pulmonary arterial occlusion partially or completely blocks blood flow in the pulmonary circle, causing generalized spasm of the pulmonary circulation vessels and bronchospasm. As a result, acute PAH, overload of the right heart, and arrhythmias develop.
A sharp deterioration in ventilation and perfusion of the lungs leads to right-to-left shunting of insufficiently oxygenated blood.
A sharp drop in CO and hypoxemia in combination with vasospastic reactions lead to ischemia of the myocardium, brain, kidneys and other organs. The cause of death in massive acute PE may be VF, which develops as a result of acute overload of the right ventricle and myocardial ischemia.

Clinical manifestations varied, can be represented by various combinations of symptoms from the following five syndromes: pulmonary-pleural, cardiac, abdominal, cerebral and renal.

Pulmonary-pleural syndrome is manifested by bronchospasm, shortness of breath, cough, hemoptysis, pleural friction noise, symptoms of pleural effusion, and changes on a chest x-ray.

Cardiac syndrome includes chest pain, tachycardia, arterial hypotension, increased central venous pressure, swelling of the jugular veins, cyanosis, accent of the second tone and murmurs (systolic and diastolic) over the pulmonary artery, pericardial friction noise, ECG changes.
Orthopnea is not common, and patients usually remain in a horizontal position.

Abdominal syndrome (pain in the right upper quadrant of the abdomen) is caused by irritation of the right dome of the diaphragm during reactive pleurisy and (or) stretching of the liver capsule, developing with acute right ventricular failure.

Cerebral (loss of consciousness, convulsions, paresis) and renal (anuria) syndromes are a manifestation of ischemia and hypoxia of organs.

In order of decreasing frequency of occurrence, the main symptoms of pulmonary embolism are arranged in the following sequence:
1) tachycardia;
2) chest pain;
3) shortness of breath;
4) hemoptysis;
5) increase in body temperature;
6) moist rales;
7) cyanosis;
8) cough;
9) pleural friction noise;
10) collapse.

Diagnostics. When examining a patient with suspected pulmonary embolism, the doctor must solve the following problems:
1) confirm the presence of pulmonary embolism, since treatment methods for this disease are quite aggressive and should not be used without strict objective grounds;
2) assess the volume of embolic damage to the pulmonary vascular bed and the severity of hemodynamic disorders in the pulmonary and systemic circulation;
3) determine the location of thromboemboli, especially when it comes to possible surgical intervention;
4) establish the source of embolization, which is extremely important for choosing a method to prevent recurrence of embolism.

Laboratory diagnostic methods make it possible to detect the presence of siderophages in sputum and moderate hypercoagulation in the blood.

On the ECG with massive pulmonary embolism, you can see signs of acute pulmonary embolism: Me Ginn-White syndrome (S1 Q3 T3), displacement of the transition zone (deep S in V5-6 in combination with negative T in V5-6), caused by an increase in the level of pressure in the pulmonary circle blood circulation over 50 mm Hg. Art. Difficulties in interpreting ECG changes arise in elderly patients with organic lesions of the coronary arteries.
However, the absence of ECG manifestations does not exclude the presence of pulmonary embolism.

Chest x-rays may show expansion of the lung root,
signs of diffuse or local oligemia and high standing of the dome of the diaphragm on the affected side, as well as pulmonary infarction, pleural effusion, basal atelectasis, expansion of the cardiac shadow.

A plain chest x-ray allows one to exclude a pulmonary pathology other than embolism that is similar in symptoms. Dilatation of the right parts of the heart with expansion of the venous inflow pathways, high standing of the diaphragm on the side of occlusion and depletion of the pulmonary vascular pattern indicate the massive nature of the embolic lesion.
In a third of patients, there are no radiographic signs of embolism at all.

The classic triangular shadow of pulmonary infarction is detected extremely rarely (less than 2%), much more often it has great polymorphism.
Ultrasound and radionuclide research methods are more informative.

Echocardiography allows you to detect the occurrence of acute LS and exclude pathology of the valve apparatus and myocardium of the left ventricle.
With its help, you can determine the severity of hypertension in the pulmonary circulation, assess the structural and functional state of the right ventricle, detect thromboembolism in the cavities of the heart and main pulmonary arteries, and visualize a patent foramen ovale, which can affect the severity of hemodynamic disorders and cause paradoxical embolism.

However, a negative echocardiography result in no way excludes the diagnosis of pulmonary embolism. Ultrasound angioscanning of the veins of the lower extremities makes it possible to detect the source of embolization.
In this case, it is possible to obtain comprehensive information about the location, extent and nature of thrombotic occlusion, the presence or absence of a threat of re-embolism.
Difficulties arise in visualizing the ileocaval segment, which may be obstructed by intestinal gas.

Perfusion scanning of the lungs, performed after intravenous administration of albumin macrospheres labeled with 997C, is recognized as the most adequate method for screening for pulmonary embolism.

If the patient's condition is stable, this method should go ahead of other instrumental studies.

The absence of disturbances in pulmonary blood flow on scintigrams performed in at least two projections (anterior and posterior) completely excludes the diagnosis of thromboembolism.
The presence of perfusion defects is interpreted ambiguously.
A highly probable criterion for embolism is a segmental absence of blood flow in the lungs, not accompanied by changes on a plain chest radiograph.
If there is no strict segmentation and multiplicity of perfusion defects on scintigrams, the diagnosis of pulmonary embolism is unlikely (disturbances can be caused by bacterial pneumonia, atelectasis, tumor, tuberculosis and other reasons), but it is not excluded, which requires angiographic verification.

A comprehensive X-ray contrast study, including probing of the right side of the heart, angioggulmonography and retrograde ileocavagraphy, remains the “gold standard” and allows one to unambiguously solve all diagnostic problems in cases of suspected pulmonary embolism.

Angiography is absolutely indicated in all cases when massive embolic damage to the pulmonary vessels cannot be ruled out (including with questionable scan data) and the issue of choosing a treatment method is being decided. It is better to perform an X-ray contrast study, if the patient’s condition allows, at the final stage of diagnosis, after a thorough analysis of the information obtained using non-invasive methods. If the doctor’s actions are limited in time by a worsening clinical and hemodynamic situation, one should immediately resort to the most reliable angiographic diagnosis.

Unfortunately, emergency angiography is currently only possible in specialized vascular surgery centers.

Flow acute, with a sudden onset of symptoms, and always, even with their rapid disappearance in the case of a favorable outcome, threatening fatal thromboembolism.
A relapsing course is common.
Forecast always serious.

Treatment. The main thing is to prevent the death of the patient in the acute stage of the disease and the development of chronic pulmonary heart disease in the long-term period.
Treatment objectives include:
1) normalization of hemodynamics;
2) restoration of patency of the pulmonary arteries;
3) preventing relapse of the disease.

Treatment of acute pulmonary embolism can be roughly divided into three stages.
Stage 1. At the first suspicion of PE, you should immediately administer 10-15 thousand units of heparin intravenously and only after that proceed to a more detailed examination. The only exception to this rule can be cases when external or internal bleeding is present or suspected.
According to indications, sedatives, oxygen, and analgesics are prescribed, after which more detailed examination and treatment begin.
It is advisable to widely use low-molecular-weight heparins (dalteparin sodium, nadroparin sodium, enoxyparin sodium), which, in comparison with conventional unfractionated heparin, are easier to dose, less likely to cause hemorrhagic complications, and have less effect on platelet function.
They have a longer action and high bioavailability when administered subcutaneously, therefore low molecular weight heparins for medicinal purposes are administered 2 times a day under the skin of the abdomen.
Their use does not require frequent laboratory monitoring of the state of the hemostatic system. The duration of heparin therapy is 5-10 days.
Before reducing the dose of heparin, indirect anticoagulants are prescribed, which, after selecting an adequate dose, the patient must take for at least 6 months to prevent relapse of phlebothrombosis and PE.

Stage 2. When the diagnosis is confirmed, fibrinolytic agents are prescribed (iv drip administration of streptokinase or its derivatives at 100,000 U/h), vasoactive drugs (verapamil - 2-4 ml of 0.25% solution IV drip to reduce pressure in the pulmonary artery), anti - acidotic therapy (100-200 ml of 3-5% sodium bicarbonate solution intravenously), with the development of asthmatic syndrome - 10 ml of 2.4% solution of aminophylline and 3-4 ml of 3% solution of prednisolone intravenously. The administration of heparin is continued at 5-10 thousand units 4 times a day, under control of blood clotting time.

The use of thrombolytics in peripheral localization of embolic occlusion in most cases is not justified based on the risk/benefit ratio.
Their pulmonary blood pressure does not approach a dangerous level, and a favorable outcome is usually beyond doubt.
At the same time, the risk of hemorrhagic and allergic complications is extremely high, and the cost of thrombolytic drugs is quite high.

For massive pulmonary embolism, thrombolytic therapy is indicated in most clinical situations.
It is absolutely necessary for patients with severe pulmonary perfusion disorders accompanied by significant hypertension in the pulmonary circulation system (more than 50 mm Hg).
Thrombolytic therapy is also justified in cases where the volume of the lesion is relatively small, but pulmonary hypertension is severe. This discrepancy may be due to previous cardiopulmonary pathology and age-related characteristics, which leads to a limitation of the body's adaptive capabilities.

In clinical practice, streptokinase drugs are most often used despite the frequent occurrence of severe allergic reactions.
It is prescribed at a dose of 100,000 units per hour.
The duration of therapeutic thrombolysis is usually 2-3 days. Under the influence of streptokinase, there is a significant acceleration of the process of restoration of pulmonary blood flow, which reduces the time of dangerous hemodynamic overload of the right ventricle.

At the same time, there is currently no strict evidence of a reduction in mortality in patients with massive pulmonary embolism during thrombolytic therapy, although a number of our observations indicate the life-saving effect of activators of endogenous fibrinolysis.

Urokinase lacks antigenic properties, but is used infrequently due to its high cost. Clinicians placed great hopes on the use of tissue plasminogen activator obtained using genetic engineering methods (alteplase).
It was believed that these drugs would be able to lyse thromboemboli even with organizational phenomena without the risk of hemorrhagic complications, which are quite common during streptokinase therapy.
Unfortunately, expectations were not fully met.
These drugs have a fairly narrow “therapeutic window”.
Recommended doses are often not effective enough, but increasing them is fraught with a significant increase in the number of hemorrhagic complications.

Stage 3. If there is no effect from stages I and II, the question of embolectomy is raised (no later than 2 hours from the onset of the disease) - in case of acute pulmonary embolism, ligation of the main vein or installation of an “umbrella” filter in the inferior vena cava - in case of its recurrent form.

Progressive deterioration in patients with massive pulmonary embolism may also require emergency surgery. Embolectomy is indicated for patients with thromboembolism of the pulmonary trunk or both of its main branches with an extremely severe degree of pulmonary perfusion impairment, accompanied by pronounced hemodynamic disorders.
These include persistent systemic hypotension, refractory to the administration of vasopressors, or a level of systolic pressure in the right ventricle above 60 mm Hg. Art.
at high end-diastolic pressure values. In such conditions, the patient has very little chance of survival even with thrombolytic therapy.
The risk of surgery is justified primarily in young people.

Three different pulmonary embolectomy techniques are currently used.
Embolectomy in conditions of temporary occlusion of the vena cava does not require complex technical support, and in case of emergency it can be successfully performed by an experienced general surgeon.

One of the most dangerous stages of such an intervention is induction of anesthesia, when bradycardia, hypotension and asystole may occur. The worsening of hemodynamic disorders is due to the fact that the sharply dilated right parts of the heart are extremely sensitive to significant fluctuations in intrapleural pressure that occur during artificial ventilation.

All manipulations to remove emboli after clamping the vena cava should last no more than 3 minutes, since this interval is critical for patients undergoing surgery under conditions of severe initial hypoxia.
Unfortunately, such an operation is accompanied by a very high mortality rate (up to 90%).

It is optimal to perform embolectomy under conditions of artificial circulation using transsternal access.
Auxiliary venoarterial perfusion should be started at the first stage of surgery (before induction of anesthesia!) by cannulating the femoral vessels.

Artificial circulation can significantly protect the safety of embolectomy in patients with severe hemodynamic disorders.
Still, the mortality rate after such interventions reaches 50%.
If we remember that every second hopeless patient manages to save life, this result cannot be called unsatisfactory.
According to relative indications for unilateral lesions, it is possible to perform surgical deobstruction of the vascular bed from a lateral thoracotomy approach, under conditions of clamping of the corresponding pulmonary artery. Now a few words about the use of warfarin in the treatment of pulmonary embolism.

Patients undergoing surgery should begin treatment with warfarin 2-3 days before surgery.
In case of acute thrombosis, treatment with warfarin should be supplemented with heparin until the effect of oral anticoagulant therapy is fully manifested (not earlier than 3-5 days of treatment). Initial doses of warfarin are 2.5-5 mg per day. The daily dose of warfarin should be taken once a day and at the same time every day.
The drug is taken orally.
If necessary, the tablet or part of it can be chewed and washed down with water.
Further dosage regimen is set individually, depending on the determination of prothrombin time or international normalized ratio (IHO).
Prothrombin time should be increased by 2-4 times from the original, and INR should reach 2.2-4.4, depending on the disease, the risk of thrombosis, the risk of bleeding and the individual characteristics of the patient.

Preventive treatment of venous thrombosis and pulmonary embolism requires achieving an INR of 2-3.
Before starting therapy, the INR is determined (corresponding to the prothrombin time, taking into account the thromboplastin sensitivity coefficient).
Subsequently, regular laboratory monitoring is carried out every 4-8 weeks.
The duration of treatment depends on the clinical condition of the patient. Treatment can be canceled immediately.

Prevention. Primary prevention of pulmonary embolism is a set of measures to prevent venous thrombosis in the inferior vena cava system. Nonspecific (physical) measures are applicable to all inpatients without exception.
They consist of elastic compression of the lower extremities, reducing the duration of bed rest, and activating patients as early as possible.
For people forced to stay in bed for a long time, it is advisable to use simple exercise equipment that simulates walking, therapeutic exercises, as well as intermittent pneumocompression of the lower extremities.
Doctors of all specialties should engage in such prevention.
Prophylactic use of enoxaparin sodium at a dose of 40 mg once a day in patients with a high risk of postoperative venous thrombosis is 2 times more effective than unfractionated heparin.
You can also use polyglucin or rheopolyglucin 400 ml intravenously infusion once a day.
Antiplatelet agents and anticoagulants (dipyridamole, ticlopedine 0.25 2 times a day, fin 0.075 g 1 time a day, acetylsalicylic acid 0.025 g 1-2 times a day) and drugs that stimulate fibrinolysis (nicotinic acid at 0.05-OD g 3 times a day and its derivatives).

Secondary prevention of pulmonary embolism is carried out in case of developed phlebothrombosis or pulmonary embolism.
It is an integral component of the treatment of pulmonary embolism, since patients often die from relapse of the disease.
For this purpose, direct anticoagulants are prescribed in therapeutic doses.
However, they only prevent the spread of thrombosis and are unable to prevent the detachment of an already formed floating thrombus.

In such cases, it is necessary to resort to surgical methods of preventing pulmonary embolism.
The optimal method is indirect transvenous implantation of vena cava filters of various designs directly below the mouths of the renal veins.
Depending on the clinical situation, for the same purpose it is possible to perform application of the inferior vena cava with a mechanical suture, thrombectomy, and ligation of the main veins.
Such operations, subject to adequate diagnosis, are feasible in general surgical hospitals.

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Pulmonary embolism (PE)

Such a beautiful name - Tela - does not belong to a girl at all, but to one of the most terrible and severe complications, the full name of which is acute pulmonary embolism. We all know that blood clots are dangerous clots in blood vessels: as a result of thrombosis, myocardial infarctions occur (death, or necrosis of a section of the heart muscle), and strokes - necrosis of part of the brain, which occurred as a result of acute oxygen starvation when the lumen of a vessel is blocked.

But it turns out there is another way - TELA. In the world, this is the third type of serious disorders in the cardiovascular system, after heart attack and stroke. So, in the USA alone, despite its highly developed medicine, more than 300 thousand people have to be hospitalized with this pathology every year - more than the number who met on the Kulikovo Field. With pulmonary embolism the mortality rate is also very high.

Thus, every sixth patient dies, or 50 thousand annually, in the USA alone. Naturally, generalizing global data, we can assume that the true incidence is several times higher. What kind of condition is this, how does it develop, what symptoms does it manifest, and how is it treated?

TELA - what is it?

Pulmonary embolism (PE) is an acute disease of the large vessels of the lungs, which bring venous blood into them for oxygenation. The meaning of the pathology is that a blood clot that appears in the human venous system enters the right half of the heart, and then through the right ventricle enters the pulmonary artery.

Before reaching the heart, the clot only entered larger and larger veins, and it was “easy to float.” And after the obstacle passes the right ventricle, then, on the contrary, the smallest capillaries are needed for oxygen enrichment, so the pulmonary artery begins to branch again into vessels of ever smaller caliber.

As a result, the pulmonary artery plays the role of a filter, which ultimately retains this blood clot. Naturally, it gets stuck in the vessel, which does not allow it to pass further. As a result, a symptom complex called pulmonary embolism develops in all underlying parts of this blocked vessel.

Causes of pulmonary embolism

As we have already said, everything that “can fly” to the right heart concerns the veins and the venous part of the systemic circulation. Therefore, the causes of pulmonary embolism, which most often lead to clinically significant manifestations, are the following:

1. Thrombosis of deep-lying veins on the thigh and in higher sections, that is, large veins of the legs and pelvis;
2. Thrombosis of deep veins located on the lower leg (with complicated thrombophlebitis varicose veins)

The degrees of risk are not comparable: 50% of all high thromboses are complicated by pulmonary embolism, and with thrombosis of the veins of the legs, only 1-5% of all cases lead to pulmonary embolism. If you combine the indicators, it turns out that in 70% of patients with pulmonary embolism, the source of blood clots is the venous vessels of the legs.

However, there is a whole list of diseases that lead to a sharp increase in the chances of pulmonary embolism. These include:

• various tumors and malignant neoplasms;
• severe cardiac pathology: congestive failure, heart attack, stroke;
• sepsis (purulent emboli in the veins);
• erythremia (Vaquez disease) - with it the blood thickens very much;
• nephrotic syndrome;
• systemic lupus erythematosus;

In addition, older age, taking oral estrogens in women, and prolonged immobility (for example, while in intensive care) increase the risk.

It is possible to list the variants of pulmonary embolism in which there is no separation and blockage by a thrombus. These options include air embolism. An air bubble can enter the pulmonary artery even with intensive rinsing of the sinuses. Also, during childbirth, amniotic fluid can enter the pulmonary veins through the uteroplacental sinuses, and this complication has a very high mortality rate.

There are variants of fatty, traumatic and septic embolism, consisting of bacteria and purulent tissue.

It is important to say right away that mortality from pulmonary embolism has stopped increasing. If the patient is not treated and this vascular catastrophe overtakes him, then the mortality rate is always 30%. And if treatment is started correctly, timely and competently, then it will decrease threefold and will be 10%. This is, of course, a good, but clearly insufficient indicator.

The cause of death is very severe pulmonary hypertension and acute failure of the right ventricle: it cannot pump blood into the lungs, therefore, roughly speaking, death occurs from suffocation, in which you can breathe and the airways are open, but blood does not flow into the lungs.

According to pathological studies, PE does not mean that one blood clot has blocked any area: often the blood clots are multiple, and blockage occurs repeatedly. Almost 2/3 of cases lead to bilateral pulmonary artery damage (that is, both lungs are affected).

• If we take into account the angle of origin and the caliber of the branches of the pulmonary trunk, then the right lung still has a high chance of being affected, and in it the lower lobes are affected more often than the upper ones.

The main damaging mechanism for pulmonary embolism is a lack of oxygen, the discharge of blood from one vessel to another, bypassing the blocked area, and various consequences of these conditions.

Thus, when a large branch is blocked, the pressure in the main trunk of the pulmonary artery increases sharply. To “pump” the blood, the right ventricle does not have enough strength, and the phenomenon of “acute cor pulmonale” or acute right ventricular failure develops.

Patients who had lung problems before PE are somewhat more “lucky”. They have right ventricular hypertrophy and its force and contractility reserves may be greater.

Symptoms of pulmonary embolism, clinical signs

Signs of pulmonary embolism are determined by the complex interaction of many components:

• degree of obstruction (blockage) of the pulmonary artery;
• resulting cardiac output of the right ventricle;
• its initial hypertrophy;
• the presence of concomitant pulmonary pathology.

What are the main symptoms that indicate the development of pulmonary embolism? Symptoms of pulmonary embolism can be noticeable. So, the following manifestations are considered the earliest:

• shortness of breath and chest pain;
• cough and hemoptysis;
• feeling of panic;
• tachypnea (increased breathing rate over 20 per minute);
• the appearance of wheezing in the lungs;
• when listening with a phonendoscope, an accent of 2 tones appears above the pulmonary artery (the right ventricle makes every effort to “break through the blockage”);
• high temperature occurs: fever over 37.5%.

Of course, there are other signs, but they are all grouped into several main syndromes:

• Pulmonary infarction(completely similar to myocardial infarction, only occurs in the lung): shortness of breath, pain, hemoptysis.
• Acute cor pulmonale: cyanosis, fainting, and a sharp drop in pressure in the left ventricle appear.
• Chronic pulmonary hypertension. Occurs if a blood clot “leaks a little” through, but stays there for a long time. As a result, the neck veins swell, venous congestion occurs throughout the large circle, and the liver enlarges.

Diagnosis of pulmonary embolism - techniques

Despite the extremely characteristic clinical picture of pulmonary embolism, instrumental diagnostics are necessary. After all, all of the listed symptoms are nonspecific, that is, they can be determined by different diseases. In addition, routine blood and urine tests, including biochemical tests, are usually normal, even in severe lesions.

Therefore, diagnostic measures are necessary: ​​pneumonia, heart attack, bronchial asthma, lung cancer, severe asthma, sepsis, rib fractures and many other diseases may resemble pulmonary embolism.

The following methods are used to diagnose PE:

• Determination of the gas composition of arterial blood: the partial pressure of oxygen is less than 90 mm. Hg st;
• Electrocardiography. An ECG rather helps to exclude a heart attack, since ECG signs of PE are nonspecific: deviation of the electrical axis of the heart to the right and right bundle branch block often develop. If we take into account that rhythm disturbances can develop against the background of severe pulmonary embolism of large branches, then the ECG can record both atrial and ventricular extrasystole, as well as atrial fibrillation and flutter;
• X-ray of the lungs and chest. This must be done to rule out cancer and pneumonia, tuberculosis and emphysema. If there are no signs of these diseases, but congestion of the roots and central structures of the lungs, atelectasis, a sudden “break” along the vessel, infiltrative artifacts or the appearance of pleural effusion is visible, then this may indirectly indicate “in favor of pulmonary embolism”.

However, the “gold standard” for emergency diagnosis of pulmonary embolism is considered to be CT – angiography of the pulmonary vessels, or angiopulmonography.

To do this, it is enough to insert a catheter into a peripheral vein (as with a regular blood draw) and inject contrast. Then a CT scan of the lungs is performed, and in the case of a positive diagnosis, a “sudden” break in the branch (there was a contour and disappeared) of the pulmonary artery will immediately be visible, and you can even see the contours of a blood clot that has blocked the lumen of the vessel.

As you can see, almost all methods, except angiopulmography, exclude other diagnoses, but do not confirm them, that is, they are used in differential diagnosis. And only a CT scan can make a diagnosis. Therefore, you need to know that you need to take patients taken by ambulance only to places where there is an emergency computed x-ray tomograph that operates around the clock. How are these patients helped?

PE - emergency care and treatment

Treatment of pulmonary embolism begins at the prehospital stage, that is, by an ambulance doctor. Alas, do-it-yourself first aid is ineffective. The first thing that comes to mind is that giving aspirin to “dissolve” a blood clot can do a bad job, since doctors will do the same thing, but by other means. Alas, the only thing relatives and friends can do is to put the patient to bed, ventilate the room, and call an ambulance.

Emergency care for pulmonary embolism will consist of the following measures:

• Intravenous injection of heparin (this is performed by an emergency physician);
• Upon admission to the hospital, against the background of an urgent and regular determination of PTT (partial thromboplastin time), treatment with indirect anticoagulants - warfarin, under the control of INR;
• Currently, in those centers that have the opportunity, thrombolytic therapy is used: alteplase, urokinase, streptokinase. By “opportunity” we mean a whole range of modern requirements and a high level of the center, which has permission to provide this most high-tech and modern type of assistance. This therapy is aimed at quickly dissolving the blood clot with special enzymes;
• Surgical methods for removing a blood clot. These are high-risk methods, and surgical intervention is used in conditions of hypoxia and reduced tissue perfusion only if attempts to “dissolve” it are ineffective;
• Continuing treatment, after eliminating the obstruction to blood flow in the lungs, a special cava filter is usually placed in the inferior vena cava (the word “cava” means a literal translation from the Latin word “hollow”), which is designed to catch repeated blood clots.

Treatment prognosis and prevention of thromboembolism

There are a number of conditions in which the risk of pulmonary embolism increases significantly. Therefore, when performing them, it is necessary to promptly carry out primary prevention through the administration of heparin and warfarin. Thus, high-risk operations include:

• Various operations on the legs, including orthopedic (for example, endoprosthetics, or replacement with an artificial joint);
• Surgeries for hip fractures (here crushed lumps of adipose tissue enter the lumen of the vein - fat embolism). By the way, it will not be possible to dissolve a fat embolus. Need to operate;
• Gynecological operations for the removal of cancerous tumors.

In order to avoid symptoms of pulmonary embolism and the need for emergency care, you need to think about such a serious complication in advance. Thus, the usual wearing of compression hosiery can relieve this formidable complication of varicose veins and thrombophlebitis, in cases where, for example, the administration of anticoagulants is contraindicated.

– occlusion of the pulmonary artery or its branches by thrombotic masses, leading to life-threatening disorders of pulmonary and systemic hemodynamics. Classic signs of pulmonary embolism are chest pain, suffocation, cyanosis of the face and neck, collapse, and tachycardia. To confirm the diagnosis of pulmonary embolism and differential diagnosis with other conditions similar in symptoms, an ECG, pulmonary radiography, echocardiography, pulmonary scintigraphy, and angiopulmonography are performed. Treatment of pulmonary embolism involves thrombolytic and infusion therapy, oxygen inhalation; if ineffective, thromboembolectomy from the pulmonary artery.

General information

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, the venous bed of the systemic circulation and carried with the bloodstream. As a result of pulmonary embolism, the blood supply to the lung tissue is cut off. 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 correctly diagnosed and did not receive the necessary treatment. Among the causes of death of the population from cardiovascular diseases, pulmonary embolism ranks third after ischemic heart 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%.

Causes 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 artery disease, active phase of rheumatism with the presence of mitral stenosis and atrial fibrillation, hypertension, infective endocarditis, cardiomyopathies and 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

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 certain medications (oral contraceptives, hormone replacement 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);
• surgery and intravascular invasive procedures (eg, central catheter in a 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

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 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, and right ventricular failure is mild
• massive(the volume of disconnected pulmonary blood flow is more than 50%) - there is loss of consciousness, hypotension, tachycardia, cardiogenic shock, 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 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.
• sharp, in which there is a rapidly increasing obstruction of the main branches of the pulmonary artery and part 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 the sharp, sudden onset in the absence of other visible causes of this condition (cardiovascular failure, myocardial infarction, pneumonia, etc.). The classic version of PE is characterized by a number of syndromes:

1. Cardiovascular:

• acute 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.

2. 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, chest pain on the affected side, 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.

3. Fever syndrome- subfebrile, febrile body temperature. Associated with inflammatory processes in the lungs and pleura. The duration of fever ranges from 2 to 12 days.

4. Abdominal syndrome 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.

5. Immunological syndrome(pulmonitis, recurrent pleurisy, urticaria-like skin rash, eosinophilia, appearance of circulating immune complexes in the blood) develops at 2-3 weeks of the disease.

Complications

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 the compensatory capabilities of the cardiovascular system and worsen the prognosis.

Diagnostics

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:

• careful 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)
• Dynamic ECG (to exclude myocardial infarction, pericarditis

  Treatment of pulmonary embolism

  Patients with thromboembolism are admitted to the intensive care unit. In an 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. Massive infusion therapy is carried out 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 the development of massive pulmonary embolism and the ineffectiveness of thrombolysis, vascular surgeons perform surgical thromboembolectomy (removal of a blood clot). As an alternative to embolectomy, catheter thromboembolic fragmentation is used. For recurrent pulmonary embolism, it is practiced to place a special filter in the branch of the pulmonary artery, the inferior vena cava.

  Prognosis and prevention

  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.

Sudden onset of shortness of breath, dizziness, pale skin, chest pain are alarming symptoms in themselves. What could it be - an attack of angina, a hypertensive crisis, an attack of osteochondrosis?

Maybe. But among the expected diagnoses there should be one more, formidable and requiring emergency medical care - pulmonary embolism (PE).

What is pulmonary embolism and why does it develop?

PE - blockage of the lumen of the pulmonary artery. An embolism can also be a relatively rare condition caused by the entry of air into an artery (air embolism), foreign bodies, fat and tumor cells, or amniotic fluid during a pathological birth.

Most often, the culprits of blockage of the pulmonary artery are detached blood clots - one or several at once. Their size and quantity determine the severity of the symptoms and the outcome of the pathology: in some cases, a person may not even pay attention to his condition due to the absence or mild severity of symptoms, in others he may end up in intensive care or even die suddenly.

Risk areas for the likelihood of blood clots include:

• Deep vessels of the lower extremities;
• Veins of the pelvis and abdomen;
• Vessels of the right heart;
• Veins of the arms.

In order for a blood clot to appear in a vessel, several conditions are necessary: ​​blood thickening and stagnation in combination with damage to the wall of a vein or artery (Virchow’s triad).

In turn, the above conditions do not arise out of nowhere: they are a consequence of deep disturbances in the blood circulation system, its coagulability, as well as in the functional state of blood vessels.

What are the reasons?

The variety of factors that can cause thrombus formation forces experts to still debate regarding the trigger mechanism for the development of pulmonary embolism, although the main causes of blockage of the pulmonary artery veins are considered to be the following:

• Congenital and rheumatic heart defects;
• Urological diseases;
• Oncopathologies in any organs;
• Thrombophlebitis and thrombosis of leg vessels.

Pulmonary embolism most often develops as a complication of existing vascular or oncological diseases, but it can also occur in completely healthy people - for example, in those who are forced to spend a lot of time on air travel.

With generally healthy vessels, prolonged stay in an airplane seat causes circulatory disturbances in the vessels of the legs and pelvis - stagnation and thickening of the blood. Although very rare, a blood clot can form and begin its fatal journey even in those who do not suffer from varicose veins, blood pressure or heart problems.

There is another category of people with a high risk of developing thromboembolism: patients who have suffered injuries (most often a hip fracture), strokes and heart attacks - that is, those who have to adhere to strict bed rest. Poor care aggravates the situation: in immobilized patients, blood flow slows down, which ultimately creates the preconditions for the formation of blood clots in the vessels.

Pathology also occurs in obstetric practice. Pulmonary embolism as a severe complication of childbirth is most likely in women with a history of:

• Varicose veins of the legs;
• Damage to the pelvic veins;
• Obesity;
• More than four previous births;
• Preeclampsia.

The risk of developing PE is increased by cesarean section for emergency reasons, childbirth before 36 weeks, sepsis that develops as a result of purulent tissue lesions, long-term immobilization indicated for injuries, as well as air travel lasting more than six hours right before childbirth.

Dehydration (dehydration) of the body, which often begins with uncontrollable vomiting or uncontrolled use of laxatives to combat constipation, which is so common in pregnant women, leads to thickening of the blood, which can cause the formation of blood clots in the vessels.

Although extremely rare, pulmonary embolism is diagnosed even in newborns: the causes of this phenomenon can be explained by extreme prematurity of the fetus, the presence of congenital vascular and cardiac pathologies.

So, pulmonary embolism can develop at almost any age - if only there were prerequisites for this.

Classification of pulmonary embolism

As mentioned above, clots of different sizes can clog the pulmonary artery or its branches, and their number may also vary. The greatest danger is from blood clots attached to the vessel wall on only one side.

A blood clot breaks off when coughing, sudden movements, or straining. The detached clot passes through the vena cava, the right atrium, bypasses the right ventricle of the heart and enters the pulmonary artery.

There it can remain intact or break against the walls of the vessel: in this case, thromboembolism of small branches of the pulmonary artery occurs, since the size of the clot pieces is quite sufficient to thrombose small-diameter vessels.

If there are a lot of blood clots, blockage of the artery lumen by them leads to an increase in pressure in the vessels of the lungs, as well as the development of heart failure due to an increase in the load on the right ventricle - this phenomenon is known as acute cor pulmonale, one of the undoubted signs of massive pulmonary embolism.

The severity of thromboembolism and the patient’s condition depends on the extent of vascular damage.

The following degrees of pathology are distinguished:

• Massive;
• Submassive;
• Small.

Massive pulmonary embolism means that more than half of the vessels are affected. Submassive pulmonary embolism refers to thrombosis of one third to one half of large and small vessels. Minor thromboembolism is a condition in which less than a third of the pulmonary vessels are affected.

Clinical picture

Manifestations of pulmonary thromboembolism can have varying degrees of intensity: in some cases it goes almost unnoticed, in others it has a violent beginning and a catastrophic ending after just a few minutes.

The main symptoms that make a doctor suspect the onset of pulmonary embolism include:

• Shortness of breath;
• (significant acceleration of heart rate);
• Chest pain;
• The appearance of blood in the sputum when coughing;
• Temperature increase;
• Wet wheezing;
• Blueness of lips (cyanosis);
• Coughing;
• Pleural friction noise;
• A sharp and rapid drop in blood pressure (collapse).

Symptoms of the pathology are combined in a certain way, forming entire symptom complexes (syndromes), which can manifest themselves with varying degrees of thromboembolism.

Thus, small and submassive thromboembolism of pulmonary vessels is characterized by pulmonary-pleural syndrome: patients develop shortness of breath, pain in the lower chest, cough with or without sputum.

Massive embolism occurs with pronounced cardiac syndrome: chest pain similar to angina pectoris, a sharp and rapid drop in pressure, followed by collapse. You can see swollen veins on the patient's neck.

Doctors who arrived on call note in such patients an increased cardiac impulse, a positive venous pulse, an emphasis of the second tone on the pulmonary artery, and an increase in blood pressure in the right atrium (CVP).

Pulmonary embolism in older people is often accompanied by cerebral syndrome - loss of consciousness, paralysis, convulsions.

All of these syndromes can be combined in different ways.

How to spot the problem in time?

The variety of symptoms and their combinations, as well as their similarity with the manifestations of other vascular and cardiac pathologies, significantly complicate diagnosis, which in many cases leads to a fatal outcome.

What is it common to differentiate thromboembolism from? It is necessary to exclude diseases that have similar symptoms: myocardial infarction and pneumonia.

Diagnosis of suspected pulmonary embolism must be quick and accurate in order to take timely measures and minimize the severe consequences of pulmonary embolism.

For this purpose, hardware methods are used, including:

• Computed tomography;
• Perfusion scintigraphy;
• Selective angiography.

ECG and radiography have less potential in diagnosing pulmonary embolism, so the data obtained from these types of studies are used to a limited extent.

Computed tomography (CT) allows you to reliably diagnose not only pulmonary embolism, but also one of the most severe consequences of vascular thrombosis of this organ.

Magnetic resonance imaging (MRI)- is also a completely reliable research method that can even be used to diagnose pulmonary embolism in pregnant women due to the absence of radiation.

Perfusion scintigraphy- a non-invasive and relatively cheap diagnostic method that makes it possible to determine the likelihood of an embolism with an accuracy of more than 90 percent.

Selective angiography reveals unconditional signs of the development of pulmonary embolism. With its help, not only confirmation of the clinical diagnosis is carried out, but also identification of the site of thrombosis, as well as monitoring of blood movement in the pulmonary circulation.

During the angiography procedure, the thrombus can be disturbed using a catheter, and then therapy can begin: this technique allows us to subsequently obtain reliable criteria by which the effectiveness of the treatment is assessed.

Qualitative diagnosis of the condition of patients with signs of pulmonary embolism is impossible without obtaining an angiographic severity index. This indicator is calculated in points, indicating the degree of vascular damage during embolism. The level of blood supply insufficiency, which in medicine is called perfusion deficiency, is also assessed:

• An index of 16 points or lower, a perfusion deficit of 29 percent or less corresponds to a mild thromboembolism;
• An index of 17-21 points and a perfusion deficit of 30-44 percent indicates a moderate degree of impairment of the blood supply to the lungs;
• An index of 22-26 points and a perfusion deficit of 45-59 percent are indicators of severe pulmonary vascular damage;
• An extremely severe degree of pathology is estimated at 27 or more points of the angiographic severity index and over 60 percent of perfusion deficiency.

Pulmonary embolism is difficult to diagnose not only because of the variety of symptoms inherent in it and their deceptiveness. The problem also lies in the fact that the examination must be carried out as quickly as possible, since the patient’s condition can worsen right before our eyes due to repeated thrombosis of the pulmonary vessels at the slightest load.

For this reason, diagnosis of suspected thromboembolism is often combined with therapeutic measures: before the examination, patients are given an intravenous dose of heparin of 10-15 thousand units, and then conservative or surgical therapy is carried out.

How to treat?

Treatment methods, unlike methods for diagnosing pulmonary embolism, are not particularly diverse and consist of emergency measures aimed at saving the lives of patients and restoring vascular patency.

For this purpose, both surgical and conservative treatment methods are used.

Surgical treatment

Pulmonary embolism is a disease, the success of treatment of which directly depends on the severity of vascular blockage and the general severity of the patient’s condition.

Previously used methods for removing emboli from affected vessels (for example, Trendelenburg surgery) are now used with caution due to the high mortality of patients.

Experts prefer catheter intravascular embolectomy, which allows the blood clot to be removed through the chambers of the heart and blood vessels. This operation is considered more gentle.

Conservative treatment

Conservative therapy is used to liquefy (lysis) blood clots in the affected vessels and restore blood flow in them.

For this purpose, fibrinolytic drugs, direct and indirect anticoagulants are used. Fibrinolytics help thin blood clots, and anticoagulants prevent blood thickening and re-thrombosis of the pulmonary vessels.

Combination therapy for pulmonary embolism is also aimed at normalizing cardiac activity, relieving spasms, and correcting metabolism. During treatment, antishock, anti-inflammatory, expectorant drugs, and analgesics are used.

All medications are administered through a nasal catheter, intravenously. Patients can receive some medications through a catheter inserted into the pulmonary artery.

Minor and submassive degrees of pulmonary embolism have a good prognosis if diagnosis and treatment were carried out in a timely manner and in full. Massive thromboembolism ends in the rapid death of patients if they are not given a fibrinolytic in time or provided with surgical assistance.