Sudden accelerated and rapid breathing, dizziness, pale skin, chest discomfort can indicate not only angina pectoris, hypertension, osteochondrosis, but also a blockage of the pulmonary artery by a thrombus moving in it. This condition of impossibility of blood flow in a vessel is called pulmonary embolism (PE) ICD code 10.

The causes of pulmonary embolism can be an air bubble, the ingress of objects from outside, or amniotic fluid during a difficult birth. But the risk of blocking a vessel with a blood clot is much higher than all of the above methods. Moreover, a person may not even notice that a thrombus embolism is developing in some area of ​​his body. After all, a clot that comes off and stops in some place can be of different sizes or in different quantities. The severity of the disease depends on this. If there is a very dense and severe blockage of the pulmonary artery, the patient may suddenly die.

Typically, a healthy person cannot develop PE disease. Disturbances in the cardiovascular system and blood clotting can lead to severe thickening, as a result, thrombus formation. Its greatest likelihood of occurrence is noted in the vessels of the extremities, right heart, pelvis and abdomen.

The main reasons for the formation of blood clots in veins and vessels are identified:

• abnormalities of the heart structure, existing from birth or acquired, characterized by changes in the valves and chambers of the heart.
• problems of the genitourinary system;
• benign and malignant tumors in different organs;
• inflammation of the venous walls with the formation of blood clots and blockage of blood vessels, impeding the flow of blood in the legs.

But still, there are exceptions. A person who does not suffer from cardiovascular diseases can experience pulmonary embolism (ICD 10). A sedentary lifestyle can lead to this. For example, with frequent and long-term air travel and constant sitting in an airplane seat, circulatory disorders develop in the form of stagnation. Thus, forming a blood clot.

In pregnant women after childbirth, with varicose veins, obesity, or if this is not the first birth, as well as with insufficient fluid in the body, the risk of developing the disease increases.

The syndrome can take a person by surprise at any age, even a newborn.

Depending on the number of vessels affected by blood clots, pulmonary embolism is classified:

• Massive– when more than 50% of the vascular system is affected;
• Submassive– from one third to half;
• Small– less than one third of vessels with pathology.

Symptoms

The main symptoms of pulmonary embolism, by which it can be determined that the patient has a pulmonary embolism:

• Rapid and difficult breathing;
• Accelerated work of the heart muscle;
• Painful manifestations in the chest area;
• When you cough, blood appears;
• Increased temperature;
• Wet, hoarse sounds when breathing;
• Blue lip color;
• Severe cough;
• Friction noise of the membrane covering the lungs and the wall of the chest cavity;
• A sharp and rapid decrease in blood pressure.

Depending on the number of vessels affected by blood clots, the signs of the disease vary. For example, with massive thromboembolism, blood pressure drops, which leads to sudden cardiovascular failure, even with loss of consciousness, severe pain in the chest area. If emergency assistance is not provided, there is a risk of death. Externally, this can be seen by the strongly prominent veins.

With minor and submassive symptoms, shortness of breath, cough, and chest pain develop.

In older people, it is often accompanied by convulsions and paralysis. In addition, a combination of symptoms can be combined.

Pulmonary embolism is very difficult to diagnose. Since its manifestations are also characteristic of other diseases, for example, myocardial infarction or pneumonia.

Therefore, in order to understand the direction of treatment, the most effective methods are used, such as: CT, perfusion scintigraphy, selective angiography.

Computed tomography can accurately determine thromboembolism. The second method (perfusion scintigraphy) is quite cheap, but contributes 90% to the diagnosis of this disease. And finally, angiography. Thanks to this method, the diagnosis is determined, the location of thrombosis is determined, and blood movement is monitored.

Other, less effective ways to diagnose pulmonary embolism include:

• Electrocardiography. For most patients, this diagnostic method does not bring the desired results. Symptoms indicating the presence of pulmonary embolism may be absent. Here they pay attention to signs of overload of the atria and ventricles, that is, this may be an increase or change in their shape, in addition, the tilt of the cardiac axis changes. But such changes in the heart can also be present in other diseases.
• Radiography chest organs. Symptoms of the disease are changes in the shape of the lung system: abnormally elevated unpaired muscle separating the thoracic and abdominal cavities of the body, expansion of the lungs, pulmonary artery and some others.
• Echocardiography. Here they look at changes in the right ventricle of the heart, its expansion or displacement of the septum closer to the left. What can indicate the presence of a blood clot in the heart?
• Spiral CT. Monitor the movement of blood in the branches of the pulmonary artery. To carry out this diagnostic method, it is necessary to inject a special drug into the patient, which will be visible to the sensor. On a computer, with the help of the latter, a picture is created in which you can see delays in blood movement and their causes.
• Ultrasound examination deep veins of the lower limb. The presence of a blood clot in peripheral arteries is determined in two ways. Compression and Doppler examination. In the first case, an image of the patient’s large vessels is first obtained, then the skin is illuminated with ultrasound. Where there is no clearance there is a thrombosed area. In the second case, the speed of blood flow is determined by changing the frequency and wavelength of the radiation perceived by the transmitter. This way, it becomes clear where the blockage occurred. Methods are combined - ultrasonography.

Also, the disease can be determined using a laboratory method. Blood is sampled for d-dimer content. The presence of this element indicates that not so long ago, a blood clot formed in the vessel. But an increase in the content of the element can also indicate other diseases.

As mentioned above, in order to accurately assess the patient’s condition, it is necessary to know the degree of pathogenicity of the vessels, this is helped by the determination of a contrast radiological index of severity and the level of blood deficiency - perfusion deficiency (the product of the defect area by the degree of reduction in the fixation of the radiopharmaceutical drug in the studied area).

The severity index is calculated by points:

• 16 points and below, perfusion deficiency of 29% - minor embolism;
• 17-21 points, a deficit of 30-44%, the blood supply to the lungs is somewhat impaired;
• 22-26 points and a perfusion deficit of 45-59% are indicators of massive embolism;
• 27 points and 60% deficiency, a sign of extreme severity of the patient’s condition.

Treatment

The patient’s condition can disappear very quickly, so you need to hurry with the treatment of pulmonary embolism. As soon as the specialist understands that he is dealing with the formation of a blood clot in the pulmonary artery, a drug is administered that prevents blood clotting. Then treatment is carried out in one of two ways: surgical and conservative.

In the first case, the clot is removed surgically through the chambers of the heart and blood vessels. In the second, the blood clot is diluted using special drugs. Due to this, the blood clot dissolves and blood moves freely further through the vessel.

There are two groups of such drugs for blood clots:

• Fibrinolytics– act directly on the blood clot itself, diluting it.
• Anticoagulants– do not allow the blood to thicken, as a result, the risk of an incident is reduced.

All drugs that can improve the patient’s condition and alleviate symptoms are administered intravenously or using a nasal or pulmonary catheter.

But we must not forget that the easier the stage of pulmonary embolism, the more successful the treatment is. With massive embolism, the prognosis is worse. If first aid is not provided at the right time - administer absorbable, thinning drugs or do not operate, the patient will die.

Resume

In recent decades, despite the emergence of modern drugs for the prevention of pulmonary embolism in the clinic, the number of patients with this pathology has been growing. The presented material describes in detail the pathogenesis, clinical picture and treatment of this suffering. Modern recommendations for the management of patients with various forms of pulmonary embolism are presented.

Keywords

pulmonary embolism, diagnosis, treatment.

Pulmonary embolism (PE) is an acute blockage of the branches of the pulmonary artery by emboli separated from blood clots formed in the veins of the systemic circulation.

Most cases of pulmonary embolism are due to deep venous thrombosis (DVT). PE and GVT are two clinical manifestations of venous thromboembolism (VTE). 50% of patients with proximal HVT (above the knee) develop PE, often asymptomatic and detected on lung scans. On the other hand, 70% of patients with PE are found to have GVT of the lower extremities.

In the United States, the prevalence of PE in hospitalized patients is 0.4%. Every year in the United States, from 600 thousand to 2 million cases of pulmonary embolism are registered. In general, according to American and European observations, the number of cases of lifetime diagnosis of pulmonary embolism ranges from 6 to 53 cases per 100,000 population per year. Moreover, repeated episodes of pulmonary embolism are observed 3 times more often after initial pulmonary embolism than after HVT (60 and 20%, respectively). Acute cases of pulmonary embolism are fatal in 7-11% of patients. However, the true prevalence of pulmonary embolism can be judged from pathological studies. Thus, according to M. Nodstrom and B. Lindblant (1998, Sweden), VTE was found in 25% of autopsies, including PE - in 18%, in 13.1% of cases PE was the cause of death. At the same time, pulmonary embolism diagnosed during life was only 2%. In Ukraine, pulmonary embolism is the cause of 10% of deaths in surgical and orthopedic hospitals.

In 80% of cases, pulmonary embolism occurs in the presence of predisposing factors(secondary pulmonary embolism). However, according to the International Cooperative Pulmonary Embolism Registry (1999), unprovoked idiopathic pulmonary embolism is observed in 20% of cases. The occurrence of pulmonary embolism and VTE is generally determined by the interaction dependent(from the patient) and independent situational risk factors (Tables 1, 2), however, this division is rather arbitrary. The average age of patients with pulmonary embolism is 62 years. Surgery remains the most significant cause of PE, but a recent analysis (ENDORSE, 2008) of 358 hospitals in 32 countries showed that only 39.5% of patients at risk of VTE received adequate prophylaxis. Heredity also plays a role in the development of VTE, although specific genes have not yet been identified. At the same time, the presence of VTE in relatives allows us to consider this as a predisposing factor.

Among the diseases encountered in the practice of a therapist, an increased risk of pulmonary embolism is represented by: heart failure and myocardial infarction, stroke, nephrotic syndrome, polycythemia, systemic lupus erythematosus.

Largest risk of development PE is observed after surgery for 2 weeks, but persists for 2-3 months. Most patients with symptoms of HVT have proximal thrombi, which are complicated in 40-50% of cases by pulmonary embolism, often asymptomatic. PE, as a rule, occurs 3-7 days after HVT, and the appearance of the “clinic” leads to death within the first hour in 10% of cases. The clinical presentation of PE in 5-10% of patients is hypotension, in half of the cases shock develops with signs of right ventricular failure. Without anticoagulants, 50% of patients develop recurrent thrombosis within 3 months.

Pathophysiology TELA includes the following effects:

1. Increased pulmonary vascular resistance due to vascular obstruction or platelet secretion of neurohumoral factors, including serotonin.

2. Impaired gas exchange due to increased alveolar dead space due to vascular obstruction, hypoxemia due to alveolar hypoventilation relative to perfusion in the intact lung, right-to-left shunting, and impaired carbon monoxide transport due to decreased respiratory surface area.

3. Alveolar hyperventilation due to reflex stimulation of irritative receptors.

4. Increased airway resistance due to constriction of the airways distal to the main bronchi.

5. Decreased lung mobility due to pulmonary edema, pulmonary hemorrhages and loss of surfactant.

PE is stratified by risk of early death(in-hospital or 30-day mortality) based on risk markers determined clinically (using echocardiography (EchoCG), computed tomography (CT)) or laboratory:

1. Clinical markers- shock, hypotension (systolic blood pressure< 90 мм рт.ст. или падение ≥ 40 мм рт.ст. за 15 мин, если не возникли аритмия, гиповолемия или сепсис).

2. Right ventricular dysfunction:
- dilatation, hypokinesia or pressure overload on echocardiography and/or CT;
- increased levels of BNP (brain natriuretic peptide; brain natriuretic peptide) or NT-proBNP;
- increased pressure in the right ventricle (RV) during catheterization.

3. Myocardial damage- increased levels of cardiac troponins T and I.

Risk markers are used for risk stratification in order to select appropriate diagnostic and treatment tactics (Table 3).

In 90% of cases, the assumption of pulmonary embolism is based on clinical symptoms(Table 4). Shortness of breath usually appears suddenly, can be isolated, but sometimes progresses over a week or more. Syncope (fainting, loss of consciousness) is an uncommon but important initial sign of pulmonary embolism, indicating a critical decrease in hemodynamic reserve. Pleural chest pain, with or without shortness of breath, is the most common clinical manifestation of PE. Pain is most often associated with distal emboli and pleural reaction to pulmonary infarction, sometimes combined with hemoptysis. The development of cyanosis of the upper part of the body, the appearance of an accent of the second tone on the pulmonary artery and various rales in the lungs during auscultation are possible.

Isolated, acute shortness of breath in combination with acute hemodynamic disturbances is characteristic of central pulmonary embolism. However, with central PE, retrosternal pain resembling myocardial infarction is also possible; it can also be a consequence of RV ischemia. Analysis of predisposing factors helps in making a diagnosis.

Laboratory and instrumental studies include:

1. X-ray- pathological, but usually nonspecific:
- high and sedentary position of the diaphragm dome;
- disc-like atelectasis;
- expansion of the shadow of the superior vena cava;
- bulging of the second arch along the left contour of the cardiac shadow;
- infiltrates of lung tissue (zones of pulmonary infarction).

X-rays can often rule out other causes of shortness of breath or chest pain.

2. Determination of the partial pressure of gases in the blood— PE in 80% of cases is associated with blood hypooxygenation (decreased PaO2).

3. ECG- signs of pancreatic overload are determined: inversion of “T” in V 1 -V 4, QR in V 1, classic - deepening S I, Q III, T III, as well as incomplete or complete blockade of the right bundle branch, especially valuable for diagnosis for the first time arisen. Sinus tachycardia is typical, new-onset atrial fibrillation is possible, often the α angle > 90°.

4. D-dimer- fibrin degradation product. Increased in plasma in the presence of acute thrombus due to stimulation of coagulation and fibrinolysis.

A normal D-dimer level makes the diagnosis of PE or HVT unlikely, and in combination with clinical data (Wells scale, Table 5) allows you to completely exclude VTE. However, an elevated D-dimer level does not confirm PE, since fibrin is produced in many conditions (cancer, inflammation, infection, necrosis, etc.). The specificity of the test is reduced in the elderly and in periods > 3 days after thrombosis. In general, the specificity of the test for pulmonary embolism is 40-50%. The norm (upper limit) when determined by the enzyme immunoassay method (ELISA) is 500 ng/ml, but may vary among different kit manufacturers (250, 300 ng/ml). When determined by the calorimetric method/latex test - > 0.5 mg/l (500 μg/l).

5. Compression ultrasonography and CT venography. In 90% of cases, the cause of PE is HVT of the lower extremities. Compression ultrasonographic venography detects hyperventilation in 70% of patients with pulmonary embolism. Can be used as an additional procedure or in case of contraindications to the use of contrast. CT venography detects HVT in up to 90% of patients with pulmonary embolism. Moreover, both methods have a specificity of ≈ 95%.

6. Ventilation-perfusion scintigraphy. The intravenous administration of radioactive technetium Ts-99 is used. Currently used on a limited basis.

7. Spiral CT angiography of the pulmonary artery in combination with intravenous administration of contrast (usually 100 ml into the cubital vein - 3-4 ml/s).

The diagnostic value largely depends on the technique used. With a single-detector tomograph - 53% and specificity - 73%, and with a multi-detector technique (with contrast), sensitivity and specificity increase to 100%. Allows you to see blood clots in the PA at the subsegmental level.

8. Magnetic resonance imaging (with contrast enhancement), it is inferior in diagnostic value to multidetector CT and comparable to single-detector CT. It can be used in cases of intolerance to iodine-containing contrasts (gadolin is used), renal failure, and also in pregnant women as it does not have “radiation exposure”.

9. Pulmonary angiography. In use since 1960. Direct pulmonary angiography can detect thrombi measuring 1-2 mm in subsegmental arteries. It also makes it possible to identify indirect signs of pulmonary embolism, such as a slowdown in contrast flow, regional hypoperfusion, cessation of venous flow, etc. IV administration of contrast poses some danger, with a mortality rate of 0.2%. Previously, it was considered the gold standard for diagnosing pulmonary embolism, but has recently begun to give way to multi-CT, which provides the same information, but does not lead to complications. This reliable but invasive, expensive and sometimes difficult to interpret test may be used when CT findings are equivocal.

10. EchoCG. Dilatation of the pancreas is detected in more than 25% of patients with pulmonary embolism; the appearance of this sign is used for risk stratification. Echo criteria used to diagnose PE are tricuspid regurgitation, ejection velocity, and RV size. Sensitivity - 60-92%, specificity - 78-92%. A negative test does not exclude pulmonary embolism, since echo criteria may also be present for other diseases of the heart and lungs. In patients with suspected pulmonary embolism, they help manage critically ill patients.

In patients with shock or hypotension, the absence of echocardiographic evidence of RV overload or dysfunction excludes PE.

Basic Echo-Doppler criteria:

A. Criteria for RV overload:

1. Right-sided cardiac thrombosis.

2. Change in the RV in diastole (parasternal view) > 30 mm or RV/LV > 1.

3. Systolic fluttering of the interventricular septum.

4. Acceleration time< 90 мс или трикуспидальная недостаточность с градиентом давления ≤ 60 мм рт.ст. при отсутствии ПЖ-гипертрофии.

B. Sign “60/60”: acceleration of RV ejection time< 60 мс при наличии трикуспидальной недостаточности и градиента давления ≤ 60 мм рт.ст.

C. McConnel sign: normokinesia and/or hypokinesia of the apical segment of the free wall of the pancreas, despite hypokinesia and/or akinesia of the rest of the free wall of the pancreas.

Concomitant EchoCG signs of pressure overload require excluding a false diagnosis of acute pulmonary embolism in patients with hypokinesia and/or akinesia of the free wall of the pancreas, corresponding to pancreatic infarction.

Today, multidetector CT is the standard for diagnosing pulmonary embolism.

Clinical classification of pulmonary embolism (ICD-10 - I26)

A. According to the severity of development of the pathological process:
- spicy;
- subacute;
- chronic (recurrent).

B. By the volume of vascular damage:
— massive (accompanied by shock/hypotension);
— submassive (accompanied by right ventricular dysfunction without hypotension);
- non-massive (no hemodynamic disturbances or signs of right ventricular failure).

B. According to the presence of complications:
- with the development of pulmonary infarction (I26);
— with the development of cor pulmonale (I26.0);
- without mention of acute cor pulmonale (I26.9).

D. By etiology:
- associated with deep venous thrombosis;
- amniotic, associated:
- with abortion (O03-O07);
- ectopic or molar pregnancy (O00-O07, O08.2);
- pregnancy and childbirth (O88);
- idiopathic (without an established cause).

Modern diagnostic strategy is based on dividing patients into two categories depending on the risk of early death from pulmonary embolism: patients with high and low risk (Table 3).

Diagnosis of PE in the presence of highly suggestive features, especially in association with shock or hypotension, is based on the use of multidetector CT. It should be noted that, despite the clinical need for an urgent CT scan, this is not always possible due to the severity of the patient’s condition (impossibility of transportation). In such cases, immediate bedside echocardiography is necessary. If signs of pancreatic overload are detected and it is impossible to perform a CT scan, the patient should be treated as a patient with diagnosed PE. If the CT results are negative, the doctor should look for other causes of shock.

When a low risk is determined, the clinical likelihood of pulmonary embolism is assessed using an analysis of symptoms and predisposing factors. There are several different tables for this, the most common are the Geneva score and Wells score (Table 5).

When establishing a low risk, ESC (2008) proposes a diagnostic algorithm that takes into account two-level and three-level clinical probability. When the risk is low but the clinical probability is high, the diagnostic strategy is based on CT. If the CT result is negative, compression ultrasonographic venography is performed to determine HVT. In case of low or intermediate clinical probability, it is considered most appropriate to determine the level of D-dimer and, in case of increased levels, CT. If D-dimer levels are normal and CT scans are negative, no treatment is given.

Treatment

For suspected or established PE with shock or hypotension, hemodynamic and ventilatory support is required. Acute pancreatic failure with low systemic output leads to the death of patients.

Patients with massive and submassive pulmonary embolism should be hospitalized in the intensive care unit (ward).

Hemodynamic and respiratory support

In patients with pulmonary embolism and reduced cardiac output, arterial hypotension or shock, non-glycoside agents with a positive inotropic effect, vasopressors (dobutamine, dopamine, norepinephrine, etc.) and the introduction of plasma substitutes are used mainly.

1. Use of blood substitutes is a necessary condition for shock or hypotension. Quite fast (≈ 20 ml/min) intravenous administration, usually ≤ 500 ml of a plasma substitute (reopolyglucin, isotonic sodium chloride solution, etc.) can increase the cardiac index from 1.6 to 2.0 l/min/m2, predominantly in patients with normal blood pressure. However, aggressive volume loading for pulmonary embolism may worsen RV function due to increased preload and worsen hemodynamic compromise. Therefore, fluid administration to patients with pulmonary embolism must be carried out under the control of the cardiac index.

2. Inotropic support also necessary for severe pulmonary embolism. At the same time, the ESC recommendations (2008) consider the use of the following drugs possible:

— Dobutamine and dopamine— the main drugs used for inotropic support for pulmonary embolism. They increase cardiac output and improve O2 transport and tissue oxygenation with stable arterial PaO2. Indicated for pulmonary embolism with low cardiac output and moderate hypotension. Can be used either alone or in combination 1:1 IV drip.

The use of dobutamine/dopamine may be discussed in patients with low SI and normal BP. However, an increase in CI above the physiological norm can increase ventilation-perfusion discrepancies with further redistribution of blood flow for obstructed (partially) and non-obstructed vessels.

Dobutamine - IV infusion 5-20 mcg/kg/min.

Dopamine - IV infusion 5-30 mcg/kg/min.

— Norepinephrine used limitedly in hypotensive patients. Improves pancreatic function through a direct positive inotropic effect, improves coronary perfusion of the pancreas through stimulation of peripheral vascular α-adrenergic receptors and an increase in systemic blood pressure. Administration of norepinephrine (2-30 mcg/min, intravenous drip) is indicated only for massive pulmonary embolism with a significant decrease in blood pressure (systolic blood pressure< 70 мм рт.ст.).

— Adrenalin combines the positive properties of norepinephrine and dobutamine in the absence of systemic vasodilation. In patients with pulmonary embolism it may have a positive effect.

— Isoproterenol, in addition to its inotropic effect, induces pulmonary vasodilation, but this positive effect is often offset by peripheral vasodilation.

3. Vasodilators reduce pulmonary arterial pressure and pulmonary vascular resistance. However with the development of acute right ventricular failure use of vasodilators (nitrates, sodium nitroprusside, etc.) and diuretics contraindicated, because they, by reducing preload and cardiac output, can lead to severe systemic hypotension.

Inhalation administration allows one to overcome this limitation. There is some evidence of the effectiveness of aerosol administration prostacyclin in the treatment of pulmonary hypertension secondary to pulmonary embolism. Inhalation nitric oxide improves hemodynamics and gas exchange in patients with pulmonary embolism.

Preliminary usage data available levosimendan- a drug from the group of non-glycoside cardiotonic drugs that restores the interaction between the pancreas and the pulmonary artery in acute pulmonary embolism as a result of a combination of pulmonary vasodilation and increased contractility of the pancreas. Levosimendan leads to a dose-dependent increase in cardiac output and stroke volume, a dose-dependent decrease in pulmonary capillary pressure, mean blood pressure and total peripheral vascular resistance.

Levosimendan (Syndax) - intravenous infusion 0.05-0.2 mcg/kg/min, 24 hours.

There is increasing interest in the use of endothelin antagonists and phosphodiesterase-5 inhibitors in PE, which reduce the severity of pulmonary hypertension in PE. Usage sildenafil reduces the increase in pressure in the LA. However, in Ukraine today only the oral form of the drug is registered, which has proven itself in chronic pulmonary hypertension, but does not allow the drug to be used effectively in shock.

Sildenafil citrate (revacio) - 0.02 3 times / day.

4. Correction of hypoxemia and hypocapnia often required in patients with pulmonary embolism, although in most cases these changes are of moderate severity. Hypoxemia usually treated with nasal oxygen and rarely mechanical ventilation. Oxygen consumption should be minimized with measures to reduce fever and agitation, and mechanical ventilation at elevated RR. When performing mechanical ventilation, it is necessary to limit its side hemodynamic effect. In particular, positive intrathoracic pressure induced by mechanical ventilation may reduce venous return and worsen RV failure in patients with massive PE. Therefore, positive expiratory pressure (end-expiratory) can be applied. A low tidal volume (≈ 6 ml/kg body weight) can be used to achieve an end-inspiratory pressure plateau below 30 cmH2O.

5. Anesthesia— adequate analgesic therapy (using fentanyl, morphine, promedol) eliminates/prevents the development of reflex pain shock, reduces fear and agitation, improves the patient’s adaptation to hypoxia.

6. Thrombolytic therapy promotes rapid resolution of thrombolytic obstruction and has a positive effect on hemodynamic parameters. In 80% of cases, the cardiac index increases and in 40% the pressure in the pulmonary artery decreases 72 hours after treatment with streptokinase.

100 mg of recombinant tissue plasminogen activator (rtPA) at the end of a 2-hour infusion period causes a 30% decrease in PA pressure and a 15% increase in CI, a decrease in vascular obstruction, and a decrease in RV end-diastolic volume, while the administration of heparin does not produce changes. Urokinase and streptokinase give similar results after an infusion period of >12–24 hours. 100 mg rtPA administered over 2 hours produces faster angiographic and hemodynamic results than urokinase 4400 U/kg/hour, but the differences disappear by 24 hours.

Direct administration of rtPA into the PA does not provide any advantage over systemic administration. Rapid (15 min) administration of rtPA has advantages over two-hour administration.

Heparin is not a competitor to thrombolytic therapy, but necessarily complements it.

Overall, 92% of patients with PE are classified as requiring thrombolysis in the first 36 hours. Significant effect is observed up to 48 hours, after which the effectiveness progressively deteriorates, but thrombolysis can be performed in patients with PE within 6-14 days. Providing thrombolysis one week after the episode results in improvement, but differences in effectiveness with heparin appear to be negligible.

There is a risk of bleeding with thrombolysis, especially in those with intercurrent illnesses (13%). Intracerebral hemorrhages occur in 1.8% of patients after thrombolysis. Therefore, contraindications must be taken into account.

Contraindications to fibrinolytic therapy

1. Absolute:

- History of hemorrhagic (or unknown origin) stroke.

— Ischemic stroke in the previous 6 months.

- Recent major trauma/surgery/head injury (3 weeks).

— Gastrointestinal bleeding for 1 month.

- Other known bleeding events.

2. Relative:

— Transient ischemic attack within 6 months.

— Oral anticoagulant therapy.

— Pregnancy and 1 week. after childbirth.

- Unclosed wounds.

— Traumatic resuscitation.

— Refractory hypertension (SBP > 180 mm Hg).

- Severe liver diseases.

- Infective endocarditis.

- Active peptic ulcer.

Thrombolytic therapy is the first line of treatment for patients at high risk of PE starting with cardiogenic shock and/or hypotension, with very few absolute contraindications.

For intermediate risk patients, thrombolysis is discussed taking into account research results and relative contraindications.

If the risk is low, thrombolysis is not indicated.

7. Surgical pulmonary embolectomy useful in patients with absolute contraindications to thrombolysis or in case of its ineffectiveness. Despite the high effectiveness of thrombolytic therapy, it is important to note that 30-40% of patients with pulmonary embolism have relative contraindications, and 20% develop various bleedings, with 3% of patients having intracerebral bleeding.

8. Percutaneous catheter embolectomy and fragmentation performed in the presence of proximal pulmonary thrombi as an alternative to surgical treatment. The operation is performed only on large vessels (main and lobar) and is not performed on segmental pulmonary arteries.

9. Regarding compression bandages There is no reliable data on their effectiveness in pulmonary embolism, but in HVT, wearing elastic stockings reduces the number of new cases of pulmonary embolism with significant differences after 2 years. When a diagnosis of HVT is made, wearing elastic stockings for 1 year reduces the number of recurrent cases of proximal HVT.

10. Initial anticoagulation.

Anticoagulant therapy (ACT) has played a major role in the management of patients with PE since 1960, when D.W. Barrit and S.C. Jordan proved the need for the use of anticoagulation in the prevention of death and recurrence.

Rapid anticoagulation can only be achieved with parenteral agents: IV unfractionated heparin (heparin), SC low molecular weight heparin (LMWH), or fondaparinux sodium.

The regimen for IV heparin is based on the aPTT (activated partial thromboplastin time), which should be determined 4-6 hours after the initial bolus and then 3 hours after each dose change or daily after achieving the target dose. As a rule, intravenous heparin administration begins with a bolus of 80 U/kg, followed by an infusion of 18 U/kg/h, changing the administration mode depending on the aPTT (Table 7).

When prescribing unfractionated heparin, it is not the dose that is fixed, but the coagulation parameters!

LMWHs are often used for pulmonary embolism and are much more convenient to use. They should not be used in severely ill patients with a “high risk of death”, hemodynamically unstable, with renal failure with GFR< 30 мл/мин (гепарин не выводится почками). Это же относится к синтетическому ингибитору Ха-фактора — фондапаринуксу.

To date, not all LMWHs have been tested for pulmonary embolism; in addition, not all of them are registered in Ukraine (Table 8).

Other LMWHs can be successfully used for HVT.

Parenteral ACT is prescribed for 5-7 days, and with HVT and/or heparin - 10-14 days. The target level of anticoagulation is to achieve an international normalization ratio (INR) in the range of 2.0-3.0. If this level is maintained for at least 2 days, you can switch to oral anticoagulants (warfarin) in accordance with the recommended ESC (2008) tactics of “Long-term anticoagulation and secondary prevention.” It is best to start warfarin with a dose of 10 mg in otherwise healthy people under 60 years of age and with 5 mg in the elderly. Subsequently, warfarin doses are adjusted depending on the INR with a target level of 2.5.

A number of new oral anticoagulants, in particular Xa and IIa inhibitors, do not require monitoring; they are currently at the stage of completing clinical trials.

ACT should begin without delay in patients with established pulmonary embolism, as well as in high and moderate probability, as soon as the examination begins.

Patients with a high risk of bleeding and severe renal failure are prescribed only unfractionated heparin.

Treatment strategy

Patients at high risk of pulmonary embolism. Patients with PE and shock or hypotension (suspected massive PE) are at high risk of in-hospital death within the first hours. After diagnosis, such patients are treated with thrombolysis and/or heparin. In case of absolute contraindications/ineffectiveness of thrombolysis, surgical embolectomy (catheter thrombofragmentation) is performed.

Low risk of pulmonary embolism. Normotensive patients with a low risk of pulmonary embolism have a favorable short-term prognosis. In most cases (absence of chronic renal failure and high risk of bleeding), LMWH or fondaparinux subcutaneously are used, taking into account weight, without monitoring.

Intermediate the risk of pulmonary embolism is determined upon admission in hemodynamically stable patients, but with evidence of RV dysfunction and/or myocardial damage. Thrombolysis is indicated, but if heparin treatment was started earlier, then thrombolysis does not make sense.

Short the risk is determined in patients with the absence of fundamental risk factors associated with pulmonary embolism, for whom early discharge from the hospital is planned.

Treatment for high risk of pulmonary embolism

- ACT with heparin should be started without delay.

— Thrombolytic therapy should be used immediately in patients with cardiogenic shock and/or hypotension.

— Systemic hypotension must be corrected to prevent progression of RV failure and death.

— Vasopressor agents are used in hypotensive patients.

— Oxygen should be prescribed in patients with hypoxemia.

— Dobutamine and dopamine can be used in patients with pulmonary embolism with normal blood pressure and low cardiac output.

— Catheter embolectomy or fragmentation of proximal PA thrombi can be performed as an alternative to surgical treatment in patients with absolute contraindications to thrombolysis or when it is ineffective.

Treatment for low risk of pulmonary embolism

-Initial ACT should be continued for at least 5 days and then replaced with vitamin K antagonists only after achieving the target INR for at least 2 consecutive days.

— In patients with intermediate risk, ACT should begin simultaneously with the beginning of the diagnosis of pulmonary embolism and be carried out in parallel with it.

— In patients with a high risk of bleeding and with severe renal dysfunction, use unfractionated heparin with a target APTT of 1.5-2.5 times normal.

Long-term anticoagulation and secondary prevention

Long-term ACT in patients with pulmonary embolism is intended to prevent fatal and non-fatal recurrent cases of VTE.

Vitamin K antagonists are the most widely used, but LMWHs may be an effective and safe alternative in cancer patients. The target dose of vitamin K antagonists is determined by INR ≈ 2.5 (2.0-3.0). A statistically significant decrease in the number of recurrent pulmonary embolisms is observed after 4-6 weeks of treatment. Therefore, the duration of treatment cannot be less than 4-9 weeks. Discontinuation of treatment leads to a return of the risk of pulmonary embolism. Negative determination of D-dimer after 1 month. after cessation of warfarin treatment indicates the persistence and positive effect of treatment.

Sodium warfarinate (warfarin) - volume 1; 2.5; 3; 5 mg orally 1 time per day.

It should be remembered that the effect of warfarin is enhanced in combination with other drugs, and in particular with non-steroidal anti-inflammatory drugs, antibacterial drugs, ethyl alcohol, etc. Regular determination of the INR is an inconvenience for patients.

When performing long-term ACT, the risk of bleeding increases.

Currently, studies are underway on promising anticoagulants, oral factor Xa inhibitors (rivaroxaban and apixaban).

Venous filters. Installation of a filter into the inferior vena cava as a method of preventing pulmonary embolism was first proposed by Trousseau in 1868. But venous filters became available only after 1960, when the percutaneous technique for their placement became possible. Typically, filters are located in the infrarenal part of the inferior vena cava (cava filters).

Vava filters are divided into temporary(set for the period of childbirth, surgery, course of thrombolytics) and permanent(installed in case of venous thrombosis with the risk of blood clots breaking off). In this case, the detached blood clot does not enter the heart, but is retained by the filter. In Ukraine, the most commonly used vena cava filters are “Osot”.

Venous filters are especially recommended:
- with absolute contraindications to long-term ACT and a high risk of recurrent VTE;
— established proximal GVT;
- planned surgery with a high risk of bleeding;
— recurrent VTE, despite ongoing anticoagulation.

Permanent filters contribute to the lifelong prevention of pulmonary embolism, but they are associated with complications, including recurrent hypertension and the development of post-thrombotic syndrome.

Possible complications:
- early - intercalary thrombosis (10% of patients);
— late — recurrent HVT (20% of patients), postthrombotic syndrome (40%).

In general, occlusion of the inferior vena cava (complete or partial) develops in 22% of patients within 5 years, in 33% within 9 years, depending on the use and duration of ACT.

Routine installation of filters in patients with pulmonary embolism is not recommended.

References

1. Compendium 2008 - drugs / Ed. V.N. Kovalenko, A.P. Viktorova. - K.: MORION, 2008. - 2270 p.

2. Mostovoy Yu.M., Konstantinovich T.V. Pulmonary embolism: diagnostic and therapeutic tactics. Therapist's view // Health of Ukraine. - 2006. - No. 2. http://urgent.health-ua.com/article/27.html

3. Order of the Ministry of Health of Ukraine No. 329 dated June 15, 2007. “On the confirmation of clinical protocols for the provision of medical assistance for the prevention of thrombotic complications in surgery, orthopedics and traumatology, obstetrics and gynecology.” - K., Ministry of Health. — 11 s.

4. Parkhomenko A.N. Pulmonary embolism and inertia of the doctor’s thinking // Health of Ukraine. - 2007. - No. 7. - P. 14-15.

6. Cohen A.T., Tapson V.F., Bergmann J.F., Goldhaber S.Z., Kakkar A.K., Deslandes B. et al. Venous thromboembolism risk and prophylaxis in the acute hospital care setting (ENDORSE study): a multinational cross-sectional study // Lancet. - 2008. - 371. - 387-394.

7. Qaseem A., Snow V., Barry P. et al. Current Diagnosis of Venous Thromboembolism in Primary Care: A Clinical Practice Guideline from the American Academy of Family Physicians and the American College of Physicians // Ann. Fam. Med. - 2007. - 5. - 57-62.

8. Goldhaber S.Z., Visani L., De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER) // Lancet. - 1999. - V. 353. - P. 1386-1389.

9. Goldhaber S.Z., Morrison R.B. Pulmonary Embolism and Deep Vein Thrombosis // Circulation. - 2002. - 106. - 1436-1438.

10. Goldhaber S.Z. Pulmonary Thromboembolism // Harrison’s principles of internal medicine / Ed. by T.R. Harrison. — 16th edition. - 2005. - P. 1561-1565.

11. Grifoni S., Olivotto I., Cecchini P., Pieralli F. et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction // Circulation. - 2000. - V. 101. - P. 2817-2822.

12. Guidelines on the diagnosis and management of acute pulmonary embolism European Society of Cardiology (ESC) // European Heart Journal. - 2008. - 29. - P. 276-2315.

13. Hansson P.O., Welin L., Tibblin G., Eriksoon H. Deep vien thrombosis and pulmonary embolism in the general population // Arch. Intern. Med. - 199. - V. 157. - P. 1665-1670.

14. Meune C., Aissaoui N., Martins-Meune E., Mouly S., Weber S. Is bed rest recommendation in the management of patients with pulmonary embolism and/or deep vein thrombosis evidenced-based medicine: a meta-analysis // Circulation. - 2007. - 116. - II 698-II 699.

15. Kucher N., Goldhaber S.Z. Management of Massive Pulmonary Embolism // Circulation. - 2005. - 112. - e28-e32.

16. Kurzyna M., Torbicki A., Pruszczyk P., Buracowska A. et al. Disturbed right ventricular ejection pattern as a new Doppler echocardiographic sign of acute pulmonary embolism // Am. J. Cardiol. — 2002. — V. 90. — P. 507‑ 511.

17. Snow V., Qaseem A., Barry P. at al. Management of Venous Thromboembolism: A Clinical Practice Guideline from the American College of Physicians and the American Academy of Family Physicians // Ann. Fam. Med. - 2007. - 5. - 74-80.

18. McConnel M.V., Solomon S.D., Rayan M.E., Come P.C. et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism // Am. J. Cardiol. - 1996. - V. 78. - P. 469-473.

19. Nodstrom M., Lindblant B. Autopsy-verified venous thromboembolism within a defined urban population - the city of Malmo, Sweden // APMIS. - 1998. - 106. - 378-384.

20 Anderson F.A. Preventing Deep Vein Thrombosis and Pulmonary Embolism A Practical Guide to Evaluation and Improvement. http://www.outcomes-umassmed.org/dvt/best_practice/Dec. 2008

21. Samuel Z. Goldhaber, MD; John Fanikos. Prevention of Deep Vein Thrombosis and Pulmonary Embolism // Circulation. - 2004. - 110. - e445-e447.

22. Pulmonary embolism. http://en.wikipedia.org/wiki/Pulmonary_embolism/Dec. 2008

23. Segal J.B., Eng J., Tamariz L.J., Bass E.B. Review of the Evidence on Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism // Ann. Fam. Med. - 2007. - 5. - 63-73.

24. Wells P. S., Anderson D. R., Rodger M., Ginsberg J. S., Kearon C., Gent M. et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the Simply RED D-dimer // Thromb. Hoemost. - 2000. - 83. - 416-420.

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Thromboembolism code according to ICD-10

The large number of diseases detected in humans, the need for a common approach to diagnosis and accurate recording of diseases became the reason for the creation of a special international classification (ICD). The lists were compiled by WHO medical experts, who meet once every 10 years to review and correct the previous version. Now all doctors work with ICD-10, which presents all possible diseases and diagnoses detected in humans.

Arterial thrombosis in the classification of diseases

Cardiac and vascular pathology, which occurs in adults and children, is located in the section called “Diseases of the circulatory system.” Arterial thromboembolism has several variants, code I, and includes the following main vascular problems that occur in children and adults:

• pulmonary thromboembolism (I26);
• various types of thrombosis and embolism of cerebral vessels (I65 – I66);
• blockage of the carotid artery (I63.0 – I63.2);
• embolism and thrombosis of the abdominal aorta (I74);
• cessation of blood flow due to thrombosis in other parts of the aorta (I74.1);
• embolism and thrombosis of the arteries of the upper extremities (I74.2);
• embolism and thrombosis of the arteries of the lower extremities (I74.3);
• thromboembolism of the iliac arteries (I74.5).

If necessary, the doctor will always be able to find any, even rare, code for arterial thromboembolic conditions that occur in the vascular system, both in children and adult patients.

Venous thrombosis in ICD 10 revision

Venous thromboembolism can cause serious complications and conditions that are often encountered in medical practice. In the statistical list of diseases of the venous system, acute blockage of blood vessels has the code I80 - I82, and is represented by the following diseases:

• various variants of inflammation of the veins with thrombosis in the lower extremities (I80.0 – I80.9);
• portal vein thrombosis (I81);
• embolism and thrombosis of the liver veins (I82.0);
• thromboembolism of the vena cava (I82.2);
• obstruction of the renal vein (I82.3);
• thrombosis of other veins (I82.8).

Venous thromboembolism often complicates the postoperative period during any surgical intervention, which can lengthen the number of days a person spends in the hospital. That is why proper preparation for surgery and careful implementation of preventive measures for varicose veins of the lower extremities are of great importance.

Aneurysms in ICD-10

A large place in the statistical list is allocated for a variety of options for dilating and enlarging blood vessels. ICD-10 coding (I71 – I72) includes the following types of severe and dangerous conditions:

Each of these options is dangerous to human health and life, therefore, when this vascular pathology is detected, surgical treatment is required. When any type of aneurysm is detected, the doctor must, together with the patient, decide in the near future on the need and possibility of surgical intervention. If problems and contraindications arise for surgical correction of the aneurysm, the doctor will give recommendations and prescribe conservative treatment.

How a doctor uses ICD-10

At the end of the treatment process, regardless of the days the sick person is in the hospital or undergoing a course of therapy in the clinic, the doctor must make a final diagnosis. For statistics, a code is needed, not a medical report, so the specialist enters the diagnosis code found in the International Classification of the 10th revision into the statistical coupon. Subsequently, after processing information coming from different medical institutions, it is possible to draw a conclusion about the frequency of occurrence of various diseases. If cardiovascular pathology begins to increase, then you can notice it in time and try to correct the situation by influencing the causative factors and improving medical care.

The International Statistical Classification of Diseases and Related Health Problems, 10th revision, is a simple, understandable and convenient list of diseases used by doctors around the world. As a rule, each narrow specialist applies only that part of the ICD that lists diseases according to his profile.

In particular, the codes from the section “Diseases of the circulatory system” are most actively used by doctors in the following specialties:

Thromboembolic conditions occur against the background of various diseases, not always associated with diseases of the heart and blood vessels, therefore, although rare, thrombosis and embolism codes can be used by doctors of almost all specialties.

The information on the site is provided for informational purposes only and cannot replace the advice of your attending physician.

Pulmonary embolism Classification (ICD, x revision, WHO, 1992):

I26 Pulmonary embolism

Abortion (O03-O07), ectopic or molar pregnancy (O00-O07, O08.2)

Pregnancy, childbirth and the postpartum period (O88.-)

I26.0 Pulmonary embolism with mention of acute cor pulmonale

I26.9 Pulmonary embolism without mention of acute cor pulmonale

Definition: Pulmonary embolism (PE) is an acute occlusion of one or more branches of the pulmonary artery by a thrombus or embolus. PE is a component of the syndrome of thrombosis of the superior and inferior vena cava system (usually thrombosis of the pelvic veins and deep veins of the lower extremities), therefore in foreign practice these two diseases are combined under the general name - "venous thromboembolism".

Diagnostic criteria:

M.Rodger and P.S.Welis (2001) proposed a preliminary score for the probability of pulmonary embolism:

Presence of clinical symptoms of thrombosis of the deep veins of the leg – 3 points

When carrying out differential diagnosis of pulmonary embolism, the most probable is 3 points

Forced bed rest for 3 – 5 days – 1.5 points

Hemoptysis – 1 point

Oncological process – 1 point

Low probability of having PE includes patients with a score of  2 points, moderate - from 2 to 6 points, high -  6 points

On the ECG in 60 - 70% of cases there is a “triad” SI, QIII, TIII (negative). With massive pulmonary embolism - a decrease in the ST segment (systolic overload of the right ventricle), diastolic overload (dilatation) is manifested by blockade of the right bundle branch, the appearance of a pulmonary P wave is possible

Radiographic signs of pulmonary embolism:

High, sedentary position of the diaphragm dome – 40%

Depletion of the pulmonary pattern (Westermarck's symptom)

Pulmonary tissue infiltrates – infarction-pneumonia

Expansion of the shadow of the superior vena cava

Bulging of the third arch along the left contour of the cardiac shadow

American researchers have proposed a formula for confirming or excluding PE:

Where: A – swelling of the neck veins – yes –1, no – 0

B – shortness of breath – yes – 1, no – 0

B – deep vein thrombosis of the lower extremities – yes – 1, no – 0

D – ECG – signs of overload of the right heart – yes – 1, no – 0

D – radiographic signs – yes – 1, no – 0

Laboratory signs: an increase in the level of fibrinogen degradation (N  10 μg/ml) and, in particular, the concentration of fibrin D-dimer more than 0.5 mg/l;

Leukocytosis up to without a shift to the left, with pneumonia - more with a shift to the left, with MI - less with eosinophilia.

Increased levels of glutamine oxalate transaminase, lactate dehydrogenase, bilirubin levels

Scintigraphy and angiopulmonography to assess the volume, location and severity of pulmonary embolism.

Body classification (European Society of Cardiology, 1978):

By volume of damage:

According to the severity of development:

According to clinical symptoms:

“Infarction pneumonia” - thromboembolism of small branches

“Acute cor pulmonale” - thromboembolism of large branches

“Unmotivated shortness of breath” - recurrent pulmonary embolism of small branches

Examples of diagnosis formulation:

Ileofemoral thrombosis of the left limb, acute pulmonary embolism, non-massive, right-sided infarction-pneumonia, moderate severity, stage 1 ARF.

Chronic thrombosis of the popliteal vein on the left, post-thrombotic syndrome, chronic venous insufficiency, chronic recurrent pulmonary embolism of small branches, chronic compensated pulmonary hypertension of vascular origin, stage II chronic pulmonary hypertension of the restrictive type.

To continue downloading, you need to collect the image:

Pulmonary embolism - description, causes, symptoms (signs), diagnosis, treatment.

Brief description

Pulmonary embolism (PE) is the closure of the lumen of the main trunk or branches of the pulmonary artery by an embolus (thrombus), leading to a sharp decrease in blood flow in the lungs.

Code according to the international classification of diseases ICD-10:

• I26 Pulmonary embolism

Statistics. PE occurs with a frequency of 1 case per year in the population. It ranks third among the causes of mortality after ischemic heart disease and acute cerebrovascular accidents.

Reasons

Etiology. In 90% of cases, the source of pulmonary embolism is located in the basin of the inferior vena cava. Iliac-femoral venous segment. Veins of the prostate gland and other veins of the small pelvis. Deep veins of the legs.

Risk factors Malignant neoplasms Heart failure MI Sepsis Stroke Erythremia Inflammatory bowel diseases Obesity Nephrotic syndrome Estrogen intake Physical inactivity APS Primary hypercoagulation syndromes Antithrombin III deficiency Insufficiency of proteins C and S Dysfibrinogenemia Pregnancy and the postpartum period Injuries Epilepsy Postoperative period.

The pathogenesis of pulmonary embolism causes the following changes: Increase in vascular pulmonary resistance (due to vascular obstruction) Deterioration in gas exchange (due to a decrease in respiratory surface area) Alveolar hyperventilation (due to stimulation of receptors) Increase in airway resistance (as a result of bronchoconstriction) Decreased elasticity of the lung tissue (due to hemorrhage in lung tissue and a decrease in surfactant content) Hemodynamic changes in pulmonary embolism depend on the number and size of blocked vessels. With massive thromboembolism of the main trunk, acute right ventricular failure (acute pulmonary heart) occurs, usually leading to death. With thromboembolism of the branches of the pulmonary artery, as a result of an increase in the resistance of the pulmonary vessels, it increases tension in the wall of the right ventricle, leading to its dysfunction and dilatation. At the same time, the ejection from the right ventricle decreases, and the end-diastolic pressure in it increases (acute right ventricular failure). This leads to a decrease in blood flow into the left ventricle. Due to the high end-diastolic pressure in the right ventricle, the interventricular septum bends towards the left ventricle, further reducing its volume. Arterial hypotension occurs. As a result of arterial hypotension, left ventricular myocardial ischemia can develop. Myocardial ischemia of the right ventricle may be a consequence of compression of the branches of the right coronary artery. With minor thromboembolism, the function of the right ventricle is slightly impaired and blood pressure may be normal. In the presence of initial right ventricular hypertrophy, the stroke volume of the heart usually does not decrease, and only severe pulmonary hypertension occurs. Thromboembolism of small branches of the pulmonary artery can lead to pulmonary infarction.

Symptoms (signs)

The symptoms of pulmonary embolism depend on the volume of pulmonary vessels excluded from the bloodstream. Its manifestations are numerous and varied, and therefore PE is called the “great camouflage” Massive thromboembolism Shortness of breath, severe arterial hypotension, loss of consciousness, cyanosis, sometimes pain in the chest (due to damage to the pleura) Dilatation of the neck veins, enlargement of the liver In most cases in the absence of emergency assistance, massive thromboembolism leads to death. In other cases, signs of pulmonary embolism may include shortness of breath, chest pain that increases with breathing, cough, hemoptysis (with pulmonary infarction), arterial hypotension, tachycardia, sweating. In patients, moist rales, crepitus, and pleural friction noise may be heard. A low-grade fever may appear after a few days.

Symptoms of pulmonary embolism are nonspecific. There is often a discrepancy between the size of the embolus (and, accordingly, the diameter of the blocked vessel) and clinical manifestations - slight shortness of breath with a significant size of the embolus and severe pain in the chest with small blood clots.

In some cases, thromboembolism of the branches of the pulmonary artery remains unrecognized or pneumonia or MI is mistakenly diagnosed. In these cases, the persistence of blood clots in the lumen of the vessels leads to an increase in pulmonary vascular resistance and an increase in pressure in the pulmonary artery (the so-called chronic thromboembolic pulmonary hypertension develops). In such cases, shortness of breath during physical exertion, as well as rapid fatigue and weakness, come to the fore. Then right ventricular failure develops with its main symptoms - swelling of the legs, enlargement of the liver. During examination in such cases, a systolic murmur is sometimes heard over the pulmonary fields (a consequence of stenosis of one of the branches of the pulmonary artery). In some cases, blood clots lyse on their own, which leads to the disappearance of clinical manifestations.

Diagnostics

Laboratory data In most cases, the blood picture is without pathological changes. The most modern and specific biochemical manifestations of pulmonary embolism include an increase in the concentration of plasma d-dimer of more than 500 ng/ml. The gas composition of the blood in pulmonary embolism is characterized by hypoxemia and hypocapnia. When a heart attack or pneumonia occurs, inflammatory changes appear in the blood.

Classic ECG changes in PE Deep S waves in lead I and pathological Q waves in lead III (S I Q III syndrome) P - pulmonale Incomplete or complete blockade of the right branch of the His bundle (impaired conduction through the right ventricle) Inversion of T waves in the right precordial leads (result right ventricular ischemia) Atrial fibrillation Deviation of EOS by more than 90° ECG changes in PE are nonspecific and are used only to exclude MI.

X-ray examination Used primarily for differential diagnosis - excluding primary pneumonia, pneumothorax, rib fractures, tumors. In case of PE, X-ray can be detected: high position of the dome of the diaphragm on the affected side, atelectasis, pleural effusion, infiltrate (usually it is located subpleurally or has a cone-shaped shape with the apex facing to the hilum of the lungs) rupture of the vessel (symptom of “amputation”) local decrease in pulmonary vascularization (Westermarck’s symptom) congestion of the roots of the lungs; possible bulging of the trunk of the pulmonary artery.

EchoCG: with pulmonary embolism, dilatation of the right ventricle, hypokinesis of the right ventricular wall, bulging of the interventricular septum towards the left ventricle, and signs of pulmonary hypertension can be detected.

Ultrasound of peripheral veins: in some cases helps to identify the source of thromboembolism - a characteristic sign is the non-collapse of the vein when pressed on it with an ultrasound sensor (there is a blood clot in the lumen of the vein).

Lung scintigraphy. The method is highly informative. A perfusion defect indicates the absence or reduction of blood flow due to occlusion of a vessel by a thrombus. A normal lung scintigram can exclude pulmonary embolism with 90% accuracy.

Pulmonary angiography is the “gold standard” for diagnosing pulmonary embolism, as it allows one to accurately determine the location and size of the thrombus. The criteria for a reliable diagnosis are a sudden break in the branch of the pulmonary artery and the contours of a blood clot; the criteria for a probable diagnosis are a sharp narrowing of the branch of the pulmonary artery and slow washout of contrast.

Treatment

With massive pulmonary embolism, hemodynamic restoration and oxygenation are necessary.

Anticoagulation therapy The goal is to stabilize the blood clot and prevent its increase. Heparin is administered at a dose of 5000 units intravenously as a bolus, then its administration is continued intravenously at a rate of 1000–1500 units/hour. Activated PTT during anticoagulation therapy should be increased by 1.5–2 times relative to the norm. Low molecular weight heparins can also be used (calcium nadroparin, sodium enoxaparin and others at a dose of 0.5–0.8 ml subcutaneously 2 times a day ). The administration of heparin is usually carried out for 5–10 days with the simultaneous administration of an oral indirect anticoagulant (warfarin, etc.) from the 2nd day. Treatment with an indirect anticoagulant is usually continued for 3 to 6 months.

Thrombolytic therapy - streptokinase is administered at a dose of 1.5 million units over 2 hours into a peripheral vein. During the administration of streptokinase, it is recommended to suspend the administration of heparin. Its administration can be continued if the activated PTT is reduced to 80 s.

Surgical treatment An effective method of treatment for massive PE is timely embolectomy, especially in case of contraindications to the use of thrombolytics. If the source of thromboembolism is proven from the inferior vena cava system, the installation of caval filters (special devices in the inferior vena cava system to prevent the migration of detached blood clots) is effective, as with already developed acute pulmonary embolism, and for the prevention of further thromboembolism.

Prevention of pulmonary embolism. The use of heparin in a dose of 5000 units every 8–12 hours for the period of restriction of physical activity, warfarin, and intermittent pneumatic compression (periodic compression of the lower extremities with special cuffs under pressure) are considered effective.

Complications Pulmonary infarction Acute cor pulmonale Recurrence of deep vein thrombosis of the lower extremities or PE.

Forecast. In unrecognized and untreated cases of pulmonary embolism, the mortality rate of patients within 1 month is 30% (with massive thromboembolism it reaches 100%). Overall mortality within 1 year is 24%, with repeated PE - 45%. The main causes of death in the first 2 weeks are cardiovascular complications and pneumonia.

Classification, causes, symptoms, diagnosis and treatment of pulmonary embolism

Pulmonary embolism is a life-threatening condition. If blood circulation in the lungs is impaired, the patient experiences characteristic symptoms, but they may resemble other acute diseases. To establish an accurate diagnosis and identify the severity of the disorders, a full examination is necessary. If clinical signs of thromboembolism appear, a person is advised to receive emergency medical care and further treatment in the intensive care unit.

Pulmonary embolism (ICD-10 code - I26) is a condition in which sudden blockage of the branches or trunk of the pulmonary artery occurs with a thrombus formed and torn off from the right ventricle or atrium of the heart, the venous bed of the systemic circulation and brought along with the blood flow.

PE can occur rapidly and is life-threatening. Moreover, in 9 out of 10 people, death occurs due to incorrect diagnosis and lack of timely treatment. Among all common causes, pulmonary embolism ranks 3rd in the number of deaths.

Classification of pulmonary embolism is performed according to the localization of the thromboembolic process:

• massive (circulatory disturbance occurs in the main trunk or main branches of the pulmonary artery);
• blockage of segmental or lobar branches;
• embolism of small branches.

According to the degree of damage and the volume of disconnected arterial blood flow, the pathological condition in medicine is divided into the following forms:

1. 1. Small (blood circulation is impaired in less than 25% of the pulmonary vessels). With this form, a person experiences shortness of breath.
2. 2. Submassive (the volume of violations ranges from 30 to 50%). In addition to shortness of breath, the patient exhibits insufficiency of the right stomach.
3. 3. Massive (blood flow stops in more than 50% of the vessels of the lungs). This form is dangerous as it leads to loss of consciousness, tachycardia, prolonged low blood pressure, acute right ventricular failure, pulmonary hypertension and cardiogenic shock.
4. 4. Fatal (the volume of circulatory disorders is 75% of all pulmonary vessels).

The forms of pathology are divided according to clinical course:

1. 1. Acute. The blockage occurs at lightning speed, the patient experiences respiratory failure, ventricular fibrillation, respiratory arrest and collapse. Death usually occurs within a few minutes without pulmonary infarction.
2. 2. Acute. With this form of pulmonary embolism, blockage of the main trunk and main branches of the pulmonary artery occurs gradually. The onset of the condition is also sudden and rapidly developing, which occurs with symptoms of respiratory, cerebral and heart failure. Duration of acute PE days with the development of pulmonary infarction.
3. 3. Subacute. In this form, thromboembolism can continue for several weeks, gradually affecting the lungs with multiple infarctions. The progression of the condition is slow, but progresses to cardiac and respiratory failure. There is a possibility of repeated thromboembolism with a sharp exacerbation of clinical manifestations, often leading to death.
4. 4. Chronic. In another way, this form of thromboembolism is called recurrent, since repeated thromboses of lobar and/or segmental branches are observed. The patient experiences repeated pulmonary infarctions and pleurisy, the development of right ventricular failure and gradually increasing hypertension in the pulmonary circulation. Often chronic thromboembolism is a consequence of surgical interventions, cancer and pathologies of the cardiovascular system.

The main cause of thromboembolism is blockage of the arteries of the lungs by a blood clot. The pathogenesis of the latter can be observed against the background of:

• stagnation of blood in the venous vessels;
• thrombophlebitis - inflammation of the vein wall;
• increased blood clotting.

The following factors lead to stagnation:

• varicose veins;
• diabetes mellitus;
• obesity;
• heart failure;
• compression of blood vessels during bone fractures;
• impaired outflow in the presence of tumors, enlarged uterus;
• smoking.

Stagnation is often observed with low physical activity of a person. It may be associated with professional activity (sedentary work) or prolonged stay in bed (patients in cardiac intensive care units, intensive care units, etc.).

There is an increase in blood clotting in several cases:

1. 1. Increased fibrinogen concentration. This protein is directly involved in blood clotting.
2. 2. Presence of a blood tumor. For example, with polycythemia, the number of red blood cells and platelets increases.
3. 3. Cancerous tumors. With malignant tumors, blood clotting increases, so thromboembolism is often a symptom of cancer.
4. 4. Taking medications that have increased blood clotting as side effects.
5. 5. Hereditary diseases.

The risk of blood clots forming in blood vessels also increases with an increase in blood viscosity, which ultimately leads to hemodynamic disturbances. This can be triggered by dehydration or uncontrolled use of diuretics, leading to disruption of the body’s water-salt balance.

Thrombophlebitis is usually observed against the background of viral and bacterial infections, oxygen starvation or systemic inflammatory reactions. Stenting and catheter placement can lead to inflammation of the veins.

With pulmonary embolism, the following clinical signs are noted:

• acute pain in the chest, worsening with deep inspiration;
• discharge of sputum with blood when coughing;
• shortness of breath, which is observed even at rest and worsens under the influence of physical activity;
• increase in body temperature.

When blood vessels become blocked, vital signs change. A person’s breathing and heart rate increases, blood pressure decreases, and oxygen saturation of cells and tissues deteriorates.

With further development of the pathological condition, the following consequences appear:

• a gradual increase in the frequency of heartbeat and breathing, which occurs due to the body’s attempt to compensate for oxygen deficiency;
• dizziness;
• death - when the pulmonary artery is completely blocked by a thrombus.

The pathological condition has no special clinical signs, which is why it is often confused with myocardial infarction, pneumothorax and other diseases. To establish an accurate diagnosis when symptoms appear, it is necessary to conduct electrocardiography in a clinical setting, but even this does not provide 100% accuracy. Thromboembolism is judged indirectly by heart performance. It is indicated by overload of the right atrium and ventricle and sinus tachycardia.

For greater information, radiography is necessary. Typically, the image clearly shows the dome of the diaphragm, which becomes enlarged on the side of the artery blockage. Thromboembolism is also indicated by an increase in the right side of the heart and clogged pulmonary arteries.

For a more accurate diagnosis, the following types of examination are used:

1. 1. Determination of the concentration of the fibrin breakdown product - d-dimer. If the rate is below 500 µg/l, then PE is rarely diagnosed.
2. 2. Echocardiography. It can identify abnormalities in the right ventricle of the heart, detect a blood clot in the heart itself, and identify a patent foramen ovale, which may explain the cause of the circulatory disorder.
3. 3. Computed tomography. It is carried out with the introduction of a contrast agent to the patient. Allows you to make a three-dimensional image of the lungs and identify the location of the blood clot.
4. 4. Ultrasonography. Used to study the speed of blood flow in the veins of the lower extremities by considering the cross section of the vessels.
5. 5. Scintigraphy. Allows you to identify areas of the lungs in which blood circulation is impaired. In 90% of cases it helps to establish an accurate diagnosis. Used when it is impossible to use CT.
6. 6. Angiography of the pulmonary vessels is the most accurate method for detecting narrowed vessels and localizing blood clots. The procedure is carried out through invasion, so there are certain risks.

When signs of pulmonary embolism appear, a person needs urgent help (the use of folk remedies and self-medication is strictly prohibited). It consists of carrying out resuscitation measures:

Emergency care should be aimed at normalizing blood circulation in the lungs, preventing sepsis and the formation of chronic pulmonary hypertension.

In case of massive thromboembolism, the list of actions is different:

1. 1. Cardiopulmonary resuscitation is performed. The patient is given chest compressions or defibrillation and connected to a ventilator.
2. 2. If the oxygen content in the body is low, the patient is prescribed oxygen therapy - inhalation of a gas mixture enriched with oxygen up to 40-70%. The procedure is performed by inserting a catheter into the nose.
3. 3. Saline solutions with drugs that increase blood pressure by narrowing the lumen of blood vessels are administered intravenously: Adrenaline, Dobutamine, Dopamine.

In case of thromboembolism, the patient is placed in the intensive care unit, where the main treatment is carried out. During therapy, the patient must remain in bed to prevent the risk of complications.

To reduce blood clotting, the following drugs are prescribed:

1. 1. Heparin sodium, nadroparin calcium, enoxaparin sodium. The active substance of the drugs inhibits thrombin, which is one of the main enzymes involved in blood clotting.
2. 2. Warfarin. Affects the synthesis of proteins in the liver, which increase blood clotting.
3. 3. Fondaparinux. Suppresses the functions of substances involved in blood clotting.

The patient is given substances to dissolve blood clots:

1. 1. Streptokinase. The drug breaks down the blood clot due to the activation of plasmin, which is able to penetrate into cholesterol formations. Streptokinase is designed to dissolve newly formed blood clots.
2. 2. Urokinase. The effect of the drug is similar, but unlike Streptokinase, the risk of allergic reactions is lower.
3. 3. Alteplase. Just like the first two drugs, it activates plasmin, which causes blood clots to break down. Alteplase is distinguished by the absence of antigenic properties and allergic reactions, and it can be reused.

Indications for surgical intervention are:

• massive thromboembolism;
• a sharp decrease in blood pressure;
• chronic recurrent pulmonary embolism;
• severe disruption of blood circulation in the lungs;
• deterioration of the patient's condition despite ongoing drug therapy.

The patient may undergo removal of an embolus - a substance that has blocked a vessel, or the inner wall of an artery with a blood clot attached to it. Surgery is quite difficult. The patient's body must be cooled to 28 degrees, only then the chest should be opened, the sternum should be cut and access to the artery should be gained. During the operation, an artificial circulatory system is organized.

PE tends to recur, therefore, after experiencing thromboembolism, patients need to follow preventive measures aimed at preventing serious complications. To a greater extent, recurrent course is observed in persons:

• over 40 years old;
• have had a stroke or heart attack;
• overweight;
• with operations performed on the pelvic organs, abdominal cavity and chest;
• with a history of leg vein thrombosis or pulmonary embolism.

• Perform periodic ultrasound of the leg veins;
• compress the veins of the lower leg with special cuffs;
• bandage the legs tightly;
• ligate large veins of the legs;
• regularly administer Heparin, Reopoliglyukin and Fraxiparin;
• give up bad habits;
• follow a diet;
• increase mobility and physical activity.

As a preventive measure, it is possible to install a vena cava filter - a special mesh implanted into the lumen of the inferior vena cava to prevent a detached blood clot from entering the pulmonary artery and heart. Establishing barriers to cholesterol plaques is carried out both in advance and after pulmonary embolism. The surgical intervention takes place under anesthesia, so the patient does not experience any discomfort.

The prognosis for pulmonary embolism depends on several factors. The outcome is influenced by the presence of concomitant diseases, timely diagnosis and treatment. According to statistics, 10% of people die within an hour after the development of a pathological condition, 30% - after a second attack. In addition, the type of lesion influences mortality. When the pulmonary artery is blocked, accompanied by a sharp drop in blood pressure, death occurs in 30-60% of cases.

All information on the site is provided for informational purposes. Before using any recommendations, be sure to consult your doctor.

Full or partial copying of information from the site without providing an active link to it is prohibited.

Pulmonary embolism (PE) is the occlusion of one or more pulmonary arteries by blood clots that form elsewhere, usually in the large veins of the lower extremities or pelvis.

Risk factors are conditions that impair venous flow and cause endothelial damage or dysfunction, especially in patients with hypercoagulable states. Symptoms of pulmonary embolism (PE) include shortness of breath, pleuritic chest pain, cough, and in severe cases, fainting or cardiac and respiratory arrest. Detected changes are vague and may include tachypnea, tachycardia, hypotension, and increased pulmonary component of the second heart sound. Diagnosis is based on ventilation-perfusion scanning, CT angiography, or pulmonary arteriography. Treatment of pulmonary embolism (PE) involves anticoagulants, thrombolytics, and sometimes surgery to remove the clot.

Pulmonary embolism (PE) affects approximately 650,000 people and causes up to 200,000 deaths per year, accounting for approximately 15% of all hospital deaths per year. The prevalence of pulmonary embolism (PE) in children is approximately 5 per 10,000 admissions.

ICD-10 code

I26 Pulmonary embolism

I26.0 Pulmonary embolism with mention of acute cor pulmonale

I26.9 Pulmonary embolism without mention of acute cor pulmonale

Causes of pulmonary embolism

Almost all pulmonary emboli are the result of thrombosis in the lower extremities or pelvic veins (deep venous thrombosis [DVT]). Blood clots in any system can be silent. Thromboemboli can also occur in the veins of the upper extremities or in the right side of the heart. Risk factors for deep venous thrombosis and pulmonary embolism (PE) are similar in children and adults and include conditions that impair venous inflow or cause endothelial damage or dysfunction, especially in patients with an underlying hypercoagulable state. Bed rest and limited walking, even for several hours, are common precipitating factors.

Once deep venous thrombosis develops, the clot may break off and travel through the venous system to the right side of the heart, then lodge in the pulmonary arteries, where it partially or completely occludes one or more vessels. The consequences depend on the size and number of emboli, the reaction of the lungs and the ability of the person’s internal thrombolytic system to dissolve the clot.

Small emboli may have no acute physiological effects; many begin to lyse immediately and dissolve within hours or days. Large emboli may cause a reflex increase in ventilation (tachypnea); hypoxemia due to ventilation-perfusion (V/P) mismatch and shunting; atelectasis due to alveolar hypocapnia and surfactant disturbances and increased pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction. Endogenous lysis reduces most emboli, even large ones, without treatment, and physiological responses decrease within hours or days. Some emboli are resistant to lysis and can organize and persist. Sometimes chronic residual obstruction leads to pulmonary hypertension (chronic thromboembolic pulmonary hypertension), which can develop over years and lead to chronic right ventricular failure. When large emboli occlude large arteries or when many small emboli occlude more than 50% of the distal arteries of the system, pressure in the right ventricle increases, causing acute right ventricular failure, failure with shock (massive pulmonary embolism (PE)), or sudden death in severe cases. The risk of death depends on the degree and frequency of increased pressure in the right side of the heart and on the patient's previous cardiopulmonary status; higher blood pressure is more common in patients with pre-existing heart disease. Healthy patients can survive pulmonary embolism that occludes more than 50% of the pulmonary vascular bed.

Risk factors for deep venous thrombosis and pulmonary embolism (PE)

• Age > 60 years
• Atrial fibrillation
• Cigarette smoking (including secondhand smoke)
• Estrogen receptor modulators (raloxifene, tamoxifen)
• Limb injuries
• Heart failure
• Hypercoagulable states
• Antiphospholipid syndrome
• Antithrombin III deficiency
• Factor V Leiden mutation (activated protein C resistance)
• Heparin-induced thrombocytopenia and thrombosis
• Hereditary defects in fibrinolysis
• Hyperhomocysteinemia
• Factor VIII increase
• Factor XI increase
• Increased von Willebrand factor
• Paroxysmal nocturnal hemoglobinuria
• Protein C deficiency
• Protein S deficiency
• Gene defects of prothrombin G-A
• Tissue factor pathway inhibitor
• Immobilization
• Placement of venous catheters
• Malignant neoplasms
• Myeloproliferative diseases (increased viscosity)
• Nephrotic syndrome
• Obesity
• Oral contraceptives/estrogens replacement therapy
• Pregnancy and postpartum period
• Previous venous thromboembolism
• Sickle cell anemia
• Surgery in the previous 3 months

Pulmonary infarction occurs in less than 10% of patients diagnosed with pulmonary embolism (PE). This low percentage is attributed to the dual blood supply to the lungs (i.e., bronchial and pulmonary). Infarction is typically characterized by a radiographic infiltrate, chest pain, fever, and occasionally hemoptysis.

Nonthrombotic pulmonary embolism (PE)

Pulmonary embolism (PE), which develops from a variety of nonthrombotic sources, causes clinical syndromes that are distinct from thrombotic pulmonary embolism (PE).

An air embolism occurs when a large amount of air is injected into the systemic veins or into the right heart, which then moves into the pulmonary arterial system. Causes include surgery, blunt or barotrauma (eg, mechanical ventilation), use of defective or uncovered venous catheters, and rapid decompression after diving. The formation of microbubbles in the pulmonary circulation can cause endothelial damage, hypoxemia and diffuse infiltration. With a large-volume air embolism, obstruction of the pulmonary outflow tract may occur, which can lead to rapid death.

Fat embolism is caused by the entry of fat or bone marrow particles into the systemic venous circulation and then into the pulmonary arteries. Causes include long bone fractures, orthopedic procedures, capillary occlusion or bone marrow necrosis in patients with sickle cell disease crisis and, rarely, toxic modification of native or parenteral serum lipids. Fat embolism causes a pulmonary syndrome similar to acute respiratory distress syndrome, with severe, rapid-onset hypoxemia, often accompanied by neurological changes and petechial rash.

Amniotic fluid embolism is a rare syndrome caused by amniotic fluid entering the maternal venous system and then into the pulmonary arterial system during or after childbirth. The syndrome can sometimes occur during prenatal manipulation of the uterus. Patients may have cardiac shock and respiratory distress due to anaphylaxis, vasoconstriction causing acute severe pulmonary hypertension, and direct pulmonary capillary damage.

Septic embolism occurs when infected material enters the lungs. Causes include drug use, infective endocarditis of the right valves, and septic thrombophlebitis. Septic embolism causes symptoms and manifestations of pneumonia or sepsis and is initially diagnosed by the identification of focal infiltrates on chest radiography, which may increase peripherally and abscess.

Foreign body embolism is caused by the entry of particles into the pulmonary arterial system, usually due to the intravenous administration of inorganic substances, such as talc by heroin addicts or mercury by patients with mental disorders.

Tumor embolism is a rare complication of malignant neoplasms (usually adenocarcinoma), in which tumor cells from the tumor enter the venous and pulmonary arterial system, where they linger, multiply and impede blood flow. Patients typically present with symptoms of shortness of breath and pleuritic chest pain, as well as signs of cor pulmonale, which develop over weeks to months. The diagnosis, which is suspected in the presence of fine nodular or diffuse pulmonary infiltration, can be confirmed by biopsy or sometimes by cytological examination of aspirated fluid and histological examination of pulmonary capillary blood.

Systemic gas embolism is a rare syndrome that occurs during barotrauma during mechanical ventilation with high airway pressure, which leads to the breakthrough of air from the lung parenchyma into the pulmonary veins and then into the systemic arterial vessels. Gas emboli cause central nervous system lesions (including stroke), cardiac lesions, and livedo reticularis in the shoulders or anterior chest wall. The diagnosis is based on the exclusion of other vascular processes in the presence of established barotrauma.

Symptoms of pulmonary embolism

Most pulmonary emboli are small, physiologically insignificant, and asymptomatic. Even when present, symptoms of pulmonary embolism (PE) are nonspecific and vary in frequency and intensity depending on the extent of pulmonary vascular occlusion and preexisting cardiopulmonary function.

Large emboli cause acute shortness of breath and pleuritic chest pain and, less commonly, cough and/or hemoptysis. Massive pulmonary embolism (PE) causes hypotension, tachycardia, syncope, or cardiac arrest.

The most common symptoms of pulmonary embolism (PE) are tachycardia and tachypnea. Less commonly, patients have hypotension, a loud second heart sound (S2) due to an increase in the pulmonary component (P), and/or crackles and wheezes. In the presence of right ventricular failure, there may be clearly visible swelling of the internal jugular veins and bulging of the right ventricle, and a gallop rhythm of the right ventricle may be heard (third and fourth heart sounds)

We recommend reading

• Description of calorie content of different types of cheese
• Ex-governor Nikita Bely received eight years in prison
• How to properly brew delicious Turkish coffee at home, recipes
• Environmental problems of emergency zones