Pulmonary embolism is the occlusion of the pulmonary artery or its branches by thrombotic masses, leading to life–threatening disorders of pulmonary and systemic hemodynamics. Classic signs of PE are pain behind the sternum, suffocation, cyanosis of the face and neck, collapse, tachycardia. To confirm the diagnosis of pulmonary embolism and differential diagnosis with other similar symptomatic conditions, ECG, lung radiography, EchoCG, lung scintigraphy, angiopulmonography are performed. Treatment involves thrombolytic and infusion therapy, oxygen inhalation; if ineffective, thromboembolectomy from the pulmonary artery.
I26 Pulmonary embolism
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 large circulation and brought with the blood flow. As a result of PE, the blood supply to the lung tissue stops. The development of PE often occurs rapidly and can lead to the death of the patient.
0.1% of the world’s population dies from PE every year. About 90% of patients who died from PE were not correctly diagnosed during the time, and the necessary treatment was not carried out. Among the causes of death of the population from cardiovascular diseases, PE is in third place after coronary heart disease and stroke. PE can lead to death in non-cardiological pathology, arising after operations, injuries, childbirth. With timely optimal treatment of PE, there is a high rate of reduction in the mortality rate to 2 – 8%.
Causes of pulmonary embolism
The most common causes of the development of PE are:
- deep vein thrombosis (DVT) of the lower leg (in 70-90% of cases), often accompanied by thrombophlebitis. There may be thrombosis of both deep and superficial veins of the lower leg
- 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, infectious endocarditis, cardiomyopathy and non-rheumatic myocarditis)
- septic generalized process
- oncological diseases (more often pancreatic, stomach, lung cancer)
- thrombophilia (increased intravascular thrombosis in violation of the hemostasis regulation system)
- antiphospholipid syndrome — the formation of antibodies to phospholipids of platelets, endothelial cells and nervous tissue (autoimmune reactions); manifested by an increased tendency to thrombosis of various localizations.
Risk factors for venous thrombosis and PE are:
- prolonged state of immobility (bed rest, frequent and prolonged air travel, travel, paresis of the extremities), chronic cardiovascular and respiratory failure, accompanied by a slowdown in blood flow and venous stagnation.
- taking a large number of diuretics (massive loss of water leads to dehydration, increased hematocrit and blood viscosity);
- malignant neoplasms – some types of hemoblastosis, true polycythemia (a high content of erythrocytes and platelets in the blood leads to their hyperagregation 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 (hyperlipidoproteinemia, obesity, diabetes mellitus, thrombophilia);
- surgical operations and intravascular invasive procedures (for example, a central catheter in a large vein);
- arterial hypertension, congestive heart failure, strokes, heart attacks;
- spinal cord injuries, fractures of large bones;
- pregnancy, childbirth, postpartum period;
- smoking, old age, etc.
Depending on the localization of the thromboembolic process , the following variants of PE are distinguished:
- massive (thrombus 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 (more often bilateral)
Depending on the volume of disconnected arterial blood flow, forms are distinguished in PE:
- small (less than 25% of pulmonary vessels are affected) – accompanied by shortness of breath, the right ventricle functions normally
- submassive (submaximal – the volume of the affected vessels of the lungs from 30 to 50%), in which the patient has shortness of breath, normal blood pressure, right ventricular insufficiency is poorly expressed
- 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 disconnected blood flow in the lungs is more than 75%).
PE can occur in severe, moderate or mild form.
The clinical course of PE may be:
- acute (lightning-fast), when there is an instant and complete blockage of the main trunk or both main branches of the pulmonary artery by a thrombus. Acute respiratory failure, respiratory arrest, collapse, ventricular fibrillation develops. The fatal outcome occurs in a few minutes, a lung infarction does not have time to develop.
- acute, in which there is a rapidly increasing obturation of the main branches of the pulmonary artery and part of the lobular or segmental. It begins suddenly, progresses rapidly, symptoms of respiratory, cardiac and cerebral insufficiency develop. Lasts for a maximum of 3 – 5 days, complicated by the development of a lung infarction.
- subacute (prolonged) with thrombosis of large and medium branches of the pulmonary artery and the development of multiple lung infarcts. It lasts for several weeks, progresses slowly, accompanied by an increase in respiratory and right ventricular insufficiency. Repeated thromboembolism may occur with exacerbation of symptoms, in which a fatal outcome often occurs.
- chronic (recurrent), accompanied by recurrent thrombosis of the lobular, segmental branches of the pulmonary artery. It is manifested by repeated lung infarctions or repeated pleurisy (more often bilateral), as well as gradually increasing hypertension of the small circulatory circle and the development of right ventricular failure. It often develops in the postoperative period, against the background of existing oncological diseases, cardiovascular pathologies.
Symptoms of pulmonary embolism
The symptoms of PE depend on the number and size of the thrombosed pulmonary arteries, the rate of development of thromboembolism, the degree of blood supply disorders of the lung tissue, the initial condition of the patient. In PE, a wide range of clinical conditions is observed: from an almost asymptomatic course to sudden death.
The clinical manifestations of PE are nonspecific, they can be observed in other pulmonary and cardiovascular diseases, their main difference is a sharp, sudden onset in the absence of other visible causes of this condition (cardiovascular insufficiency, myocardial infarction, pneumonia, etc.). A number of syndromes are characteristic of PE in the classical version:
- acute vascular insufficiency. There is a drop in blood pressure (collapse, circulatory shock), tachycardia. The heart rate can reach more than 100 beats. per minute.
- acute coronary insufficiency (in 15-25% of patients). It is manifested by sudden severe pain behind the sternum of various nature, lasting from several minutes to several hours, atrial fibrillation, extrasystole.
- acute pulmonary heart. Caused by massive or submassive PE; manifested by tachycardia, swelling (pulsation) of the cervical veins, positive venous pulse. Edema in acute pulmonary heart does not develop.
- acute cerebrovascular insufficiency. There are general cerebral or focal disorders, cerebral hypoxia, in severe form – cerebral edema, cerebral hemorrhages. It is manifested by dizziness, tinnitus, deep fainting with convulsions, vomiting, bradycardia or a comatose state. Psychomotor agitation, hemiparesis, polyneuritis, meningial symptoms may be observed.
- acute respiratory failure is manifested by shortness of breath (from a feeling of lack of air to very pronounced manifestations). The number of breaths is more than 30-40 per minute, cyanosis is noted, the skin is ash-gray, pale.
- moderate bronchospastic syndrome is accompanied by dry wheezing.
- lung infarction, infarct pneumonia develops on the 1st – 3rd day after PE. There are complaints of shortness of breath, cough, chest pain from the lesion, which increases with breathing; hemoptysis, an increase in body temperature. Small bubbly wet wheezes, the noise of pleural friction become audible. Patients with severe heart failure have significant effusions into the pleural cavity.
3. Febrile syndrome – subfebrile, febrile body temperature. It is associated with inflammatory processes in the lungs and pleura. The duration of fever is from 2 to 12 days.
4. Abdominal syndrome is caused by acute, painful swelling of the liver (in combination with intestinal paresis, irritation of the peritoneum, hiccups). It is manifested by acute pain in the right hypochondrium, belching, vomiting.
5. Immunological syndrome (pulmonitis, recurrent pleurisy, urticaria-like skin rash, eosinophilia, the appearance of circulating immune complexes in the blood) develops at 2-3 weeks of the disease.
Acute PE can cause cardiac arrest and sudden death. When compensatory mechanisms are triggered, the patient does not immediately die, but in the absence of treatment, secondary hemodynamic disorders progress very quickly. The cardiovascular diseases present in the patient significantly reduce the compensatory capabilities of the cardiovascular system and worsen the prognosis.
In the diagnosis of PE, the main task is to locate blood clots in the pulmonary vessels, assess the degree of damage and severity of hemodynamic disorders, identify the source of thromboembolism to prevent relapses.
The complexity of the diagnosis of PE dictates the need to find such patients in specially equipped vascular departments that have the widest possible opportunities for special research and treatment. All patients with suspected PE are examined as follows:
- a thorough history collection, assessment of risk factors for DVT / PE and clinical symptoms
- general and biochemical blood and urine tests, blood gas composition study, coagulogram and D-dimer study in blood plasma (a method for diagnosing venous thrombi)
- ECG in dynamics (to exclude myocardial infarction, pericarditis, heart failure)
- lung x-ray (to exclude pneumothorax, primary pneumonia, tumors, rib fractures, pleurisy)
- echocardiography (to detect increased pressure in the pulmonary artery, overload of the right heart, blood clots in the cavities of the heart)
- lung scintigraphy (violation of blood perfusion through the lung tissue indicates a decrease or absence of blood flow due to PE)
- angiopulmonography (to accurately determine the location and size of the thrombus)
Ultrasound of the veins of the lower extremities, contrast phlebography (to identify the source of thromboembolism)
Treatment for pulmonary embolism
Patients with thromboembolism are placed in the intensive care unit. In an emergency, the patient is resuscitated in full. Further treatment of PE is aimed at normalization of pulmonary circulation, prevention of chronic pulmonary hypertension.
In order to prevent relapses of PE, strict bed rest must be observed. To maintain oxygenation, constant inhalation of oxygen is carried out. Massive infusion therapy is carried out to reduce blood viscosity and maintain blood pressure.
In the early period, the appointment of thrombolytic therapy is indicated in order to dissolve the thrombus as quickly as possible and restore blood flow in the pulmonary artery. In the future, heparin therapy is performed to prevent relapses of PE. With the phenomena of infarction-pneumonia, antibacterial therapy is prescribed.
In cases of massive PE and ineffectiveness of thrombolysis, vascular surgeons perform surgical thromboembolectomy (removal of a blood clot). As an alternative to embolectomy, catheter fragmentation of thromboembol is used. In case of recurrent PE, a special filter is placed in the branches of the pulmonary artery, the inferior vena cava.
Prognosis and prevention
With the early provision of a full volume of care to patients, the prognosis for life is favorable. With severe cardiovascular and respiratory disorders against the background of extensive PE, the mortality rate exceeds 30%. Half of the relapses of PE develop in patients who have not received anticoagulants. Timely, properly conducted anticoagulant therapy halves the risk of recurrence of PE. To prevent thromboembolism, early diagnosis and treatment of thrombophlebitis, the appointment of indirect anticoagulants to patients from risk groups are necessary.
- Pulmonary embolism. Yee KC. Lancet. 2004 Jul 17-23;364(9430):243; author reply 244. link
- Pulmonary embolism. Fortunat S, Röggla G. Lancet. 2004 Jul 17-23;364(9430):243; author reply 244. link
- Pulmonary embolism. Habib-ur-Rehman. Lancet. 2004 Jul 17-23;364(9430):243-4; author reply 244. link
- Pulmonary embolism. Konotey-Ahulu FI. Lancet. 2004 Jul 17-23;364(9430):244-5. link
- Pulmonary embolism. Robinson G. Lancet. 2004 Jul 17-23;364(9430):244. link