Pulmonary embolism is a severe form of damage to the pulmonary circulation. It develops as a result of embolization of the branches of the pulmonary artery with a gas bubble or bone marrow, amniotic fluid, thrombus. And pulmonary embolism (PE) is the most common type of obstruction (more than 60%) of the arteries of the pulmonary circulation, although against the background of other cardiovascular diseases it has a low frequency (about 1 case per 1000 people). But the high mortality before the first medical contact and the difficulty in diagnosis and treatment make this disease extremely dangerous for the patient.
What is TELA
Thromboebolism is a blockage of the lumen of a blood vessel by a blood clot, a thrombus. And in the case of pulmonary embolism, the clinic, the diagnosis and treatment of which will be discussed in the publication, this blockage occurs in the arteries of the pulmonary circulation. The thrombus enters the pulmonary artery through the veins from the systemic circulation. In 95-98% of massive PE, a large thrombus is formed in the veins of the legs or small pelvis, and only in 2-3% - in the veins of the upper half of the body and in the pool of the jugular veins. In the case of recurrent PE, many small blood clots form in the cavities of the heart. This is most common with atrial fibrillation or right heart thromboendocarditis.
Pulmonary embolism is a clinical syndrome, a set of symptoms resulting from a blood clot entering the arteries of the pulmonary circulation. This is an extremely life-threatening disease that develops and proceeds suddenly. Distinguish between massive, submassive and recurrent PE, as well as heart attack-pneumonia - a consequence of active PE. In the first case, the thrombus is so large that it blocks the pulmonary artery either at the site of its bifurcation or proximally.
Submassive pulmonary embolism develops as a result of obstruction of the lobar pulmonary artery, and recurrent - as a result of frequent embolism of small blood clots that block the lumen of small-diameter arteries. In the case of massive and submassive PE, the clinical picture (hereinafter referred to as the clinic) is bright and develops immediately, and the disease can lead to sudden death. Recurrent PE is characterized by a gradual increase in shortness of breath over several days and the development of a cough, sometimes coughing up a small amount of blood.
Patterns of development of PE
For the development of PE, it is sufficient to have a source of thrombosis in any part of the venous bed of the systemic circulation or in the right parts of the heart. Occasionally, thrombi during paradoxical movement through the open oval window of the interatrial septum can also enter from the left atrium. Then, even with left-sided endocarditis, the development of PE is possible, although such situations are extremely rare and are considered casuistic. And in order to provide unambiguous information that will not cause discrepancies and will not mislead the patient, this publication will not touch on the topic of the paradoxical movement of blood clots from the left heart.
As soon as a mobile thrombus forms in the veins of the systemic circulation or in the right heart, there is a high probability of its drift into the pulmonary artery. The most common source of blood clots are varicose veins of the lower extremities and small pelvis. In the region of the venous valves, due to stagnation of blood, a parietal thrombus gradually forms, which initially attaches to the subendothelial lining of the vein. As it grows, part of the clot breaks off and travels to the right side of the heart and lungs, where it causes thromboembolism of the pulmonary artery or its branches.
Mechanism for the development of TELA
Through the right atrium and right ventricle, the thrombus enters the trunk of the pulmonary artery. Here it irritates the receptors, causing pulmonary-cardiac reflexes: an increase in heart rate, an increase in the minute volume of blood circulation. That is, to a signal about irritation of receptorspulmonary artery, the body responds with an increase in cardiac activity, which is necessary to push the thrombus into narrower sections of the arterial bed and minimize the consequences of the disaster. This complex of disorders is already called pulmonary embolism, the symptoms and severity of which linearly depend on the size of the thrombus.
In a certain area of the pulmonary basin, despite the attempts of the cardiovascular system to push the clot further, the latter will certainly get stuck. As a result, systemic arteriolospasm instantly develops, blood flow in the affected area of the lung is blocked. With massive PE, it is impossible to push a large thrombus into a small-caliber artery, and therefore a total obstruction develops.
As a result, the blood supply to the main parts of the pulmonary circulation is blocked, and therefore oxygenated blood does not flow to the left parts of the heart - a collapse of the systemic circulation develops. The patient instantly loses consciousness due to cerebral hypoxia and shock, arrhythmic activity of the heart is provoked, ventricular extrasystole develops, or ventricular fibrillation starts.
Signs of massive and submassive embolism
The above example demonstrates an acute pulmonary embolism that is rarely treated. As a rule, such clinical situations occur in postoperative or long-term immobilized patients after the first standing up. Outwardly, it looks like this: the patient gets to his feet, because of whichthe venous outflow from the veins of the lower extremities is accelerated and the separation of the thrombus is provoked. It travels up the inferior vena cava and causes a pulmonary embolism.
The patient cries out in pain and shock, loses consciousness and falls, ventricular fibrillation develops, breathing stops, clinical death occurs. As a rule, it is very difficult to stop ventricular fibrillation in PE, as it is associated with myocardial hypoxia. Its elimination with massive embolism is almost impossible, which is why it is impossible to help the patient with total obstruction and the development of arrhythmia even with an immediate diagnosis and initiation of therapy. In addition, the rate of development of arrhythmias is so high that clinical death develops even before people in the same room with the patient have time to call for help.
Subtotal PE
In the case of subtotal PE, the rate of development of symptoms is much less, but this does not reduce the danger to life. Here, the branch of the lobar pulmonary artery is obturated, and therefore initially the volume of the lesion is much smaller. The patient does not lose consciousness abruptly, and the arrhythmia does not develop suddenly. However, due to the development of reflex reactions of arteriolospasm and the appearance of symptoms of shock, the patient's condition deteriorates sharply, severe shortness of breath develops, and the severity of acute heart and respiratory failure increases.
If pulmonary embolism is not treated and thrombolysis is not possible, the chance of death is about95-100%. Relatives of the patient should understand that such a patient needs emergency thrombolytic therapy, and therefore it is impossible to delay contacting the EMS. For comparison, with thromboembolism of the branches of the pulmonary artery, where small-caliber vessels are obturated, the patient can survive without medical care.
To survive, because we are not talking about a quick recovery, but about survival with current disorders in the cardiovascular and respiratory systems. The severity of his condition will gradually increase as shortness of breath, hemoptysis and the development of infarction pneumonia worsen. If these symptoms appear, you should immediately contact the emergency room of a hospital or an ambulance.
Causes of PE
Any phenomenon that provokes the development of thrombosis of the veins of the lower extremities or the small pelvis, as well as the formation of small blood clots in the right atrium or on the right atrioventricular valve, can cause pulmonary embolism. The causes of PE are as follows:
- varicose disease of the legs with phlebothrombosis, acute thrombophlebitis without taking anticoagulants;
- paroxysmal or permanent atrial fibrillation without anticoagulant therapy;
- right heart infective endocarditis;
- prolonged immobilization of the patient;
- traumatic surgery;
- long-term oral contraceptive course;
- cancer of the kidneys, metastases in the inferior vena cava and renal vein, oncohematological diseases;
- hypercoagulation,thrombophilia, DIC;
- recent fractures of the pelvis or tubular bones of the body;
- pregnancy and childbirth;
- obesity, metabolic syndrome, diabetes mellitus;
- smoking, high blood pressure, sedentary life.
These reasons can lead to pulmonary embolism. Diagnosis and treatment of these diseases, as well as taking anticoagulants, can eliminate or significantly reduce the risk of PE. For example, the standards for the treatment of fractures during rehabilitation after their fusion, as well as after surgical operations and delivery, include anticoagulants.
These drugs are also indicated for atrial fibrillation and infective endocarditis with vegetations on the heart valves. Such conditions are more likely to cause thromboembolism of small branches of the pulmonary artery, rather than massive and submassive PE. However, these are still serious diseases that require medical attention. The most effective drugs for prevention are new oral anticoagulants (NOACs). They do not require INR control. They also have a permanent anticoagulant effect that is independent of nutrition, as is the case with Warfarin.
Prehospital diagnosis
Regardless of the qualifications of medical personnel in massive pulmonary embolism, the clinic, diagnosis and treatment can fit in the first 30 minutes, especially in the case of rapid development of arrhythmia and clinical death. Then the patient quickly dies, although the diagnosis itself is not in doubt. Often, PE is detected at the SMP stage, and the main diagnostic symptoms are:
- complaints of sudden severe pressing and stabbing "dagger" pains in the chest, after which the patient cries out and sometimes falls unconscious;
- dramatically appeared shortness of breath, severe feeling of lack of air and squeezing in the chest;
- increased heart rate with the development of pain in the heart, non-rhythmic contraction of the heart;
- sudden appearance of first dry cough against the background of full he alth, and then with bloody sputum;
- abruptly developed cyanosis (bluish-bluish color) of the lips, gray (earthy) complexion, swelling of the veins of the neck;
- decrease in blood pressure with massive or a sharp increase in blood pressure with submassive and recurrent PE, fainting or loss of consciousness.
The main goal of diagnosis with such symptoms is to exclude myocardial infarction. If the ECG does not show signs of transmural infarction, then with a high degree of probability the current condition should be interpreted as PE and appropriate emergency care should be provided. With PE, the ECG may show: inversion of the T wave and the appearance of a Q wave in lead III, the appearance of an S wave in lead I. One of the diagnostic criteria is the expansion of the P wave and the growth of its voltage in the initial segment. Also, ECG changes are "volatile", that is, they can change over a short period of time, which indirectly confirms PE and reduces the number of convincing criteria in favor of myocardial infarction.
With recurrent pulmonary embolism, the symptoms, treatment and diagnosis are somewhat different, which is associated with a much smaller lesion. For example, if with massive PE, the size of the thrombus is approximately 8-10 mm in width and from 5-6 to 20 cm in length, then with recurrent PE, many small clots 1-3 mm in size enter the lung. Because of this, the symptoms are much poorer and include mild to moderate shortness of breath, cough, sometimes with a small amount of blood, hypertension. These symptoms build up over time, mimicking pneumonia or progressive angina, especially if not accompanied by hemoptysis.
Prehospital treatment
Treatment includes oxygen therapy with 100% oxygen, preferably mechanical ventilation, narcotic pain relief (morphine or fentanyl, neuroleptanalgesia is allowed), anticoagulant therapy with unfractionated heparin 5000-10000 IU, thrombolysis with "Streptokinase 250,000 IU" with a preliminary introduction of "Prednisolone 90 mg".
In addition to this treatment of pulmonary embolism, infusion therapy and compensation for existing disorders are required: defibrillation for the corresponding arrhythmia and cardiotonic drugs for hypotension. The indicated treatment is highly effective, but it will not help to completely dissolve the clot - hospitalization in the intensive care unit is required.
It is important to understand that the cost of a prehospital error may not be critical to the patient's prognosis. For example, if changes appear on the ECG,characteristic of a heart attack against the background of developing pulmonary embolism, narcotic pain relief and anticoagulant therapy with similar drugs are also indicated. Only the appointment of nitrates can cause harm, which will accelerate the fall in blood pressure.
The patient and EMS staff also need to remember that in case of myocardial infarction with low blood pressure (less than 100\50 mmHg) or suspected PE, nitrates should not be taken. Thus, the care of a patient with PE is almost the same as with myocardial infarction with left ventricular failure against the background of hypotension. This means that an EMS employee will have additional time for diagnosis against the background of effective treatment for PE.
Diagnosis of PE at the hospital stage
Diagnosis and treatment of pulmonary embolism at the hospital stage is more effective than at the pre-hospital one. In part, this is a purely statistical conclusion, because due to massive thromboembolism, they often do not even get to the hospital due to high pre-hospital mortality. And in the case of submassive pulmonary embolism, myocardial pneumonia and recurrent pulmonary embolism, the disease “gives time” for high-quality diagnosis and treatment. The identified symptoms are similar to those that occurred during the diagnosis at the prehospital stage.
The exclusion of a heart attack on the ECG and the appearance of signs of an overload of the right parts of the heart immediately orients the doctor in the direction of pulmonary embolism. To confirm the diagnosis, an x-ray is performed, an emergency laboratory test: a quantitative analysis for D-dimers, troponin T, CPK-MB, myoglobin. With PEsignificantly increased D-dimers with a normal troponin level (a marker of myocardial infarction).
The gold standard for diagnosing PE is the rarely available method of angiopulmonography or perfusion scanning. It is able to reliably confirm or refute the diagnosis of thromboembolism, however, such a study is not possible in most hospitals, or due to the severity of the condition, the patient dies before it is carried out. Assistance in the diagnosis is also provided by echocardiography, ultrasound of the veins of the lower extremities, dopplerography. Right atrial catheterization and pressure testing can be done intraoperatively to confirm pulmonary hypertension.
Hospital Therapy
Hospital treatment of PE requires careful monitoring of the patient's condition in the intensive care unit. After confirming the diagnosis, it is necessary to start thrombolytic therapy with tissue plasminogen proactivators - Tenecteplase or Alteplase. These are new thrombolytic drugs, the main advantage of which is the absence of clot crushing. They lyse it in layers, unlike Streptokinase.
Thrombolytic therapy (TLT) is designed to dissolve the clot if possible. However, if it is impossible to perform TLT, surgical thromboextraction can be performed - the most difficult operation for the patient in conditions of autonomous blood circulation, which should be resorted to only in cases where the patient will certainly die without intervention.
It is important to note that no suchthe concept of “auxiliary strengthening treatment” popular among the population of the CIS simply cannot exist in this situation. Here it is important not to interfere with the staff and follow medical recommendations. Pulmonary embolism is a disease that until recently in the case of submassive or massive embolism was always fatal and incurable.
All activities in the course of treatment are now aimed at effective thrombolysis and intensive therapy: adequate oxygen therapy, cardiotonic support, infusion therapy, parenteral nutrition. By the way, PE is a disease where each appointment is literally “written in blood” due to the total mortality that took place earlier. Therefore, any experiments of the patient and his relatives, as well as unmotivated transfers from departments and he alth care institutions, at the insistence, should be excluded.
