Lung infarction

Pulmonary vascular thrombosis is caused by stagnation and slowing of blood flow in the lungs, stable pulmonary hypertension, and pulmonary vasculitis. Vascular obturation, reflex spasm in the pulmonary artery system, as well as vasoconstriction due to the release of biologically active substances from platelets (serotonin, thromboxane, histamine) lead to acute pulmonary hypertension and overload of the right heart. There is a violation of diffusion and arterial hypoxemia, which is aggravated by shunting iedookislennoy blood through arteriovenous anastomoses in the lungs and intersystem anastomoses.

Lung infarction often occurs against the background of existing venous congestion and is usually hemorrhagic in nature due to the outpouring of blood from the bronchial arteries into the lung tissue, flowing through intersystem anastomoses, as well as the reverse flow of blood from the pulmonary veins.

A lung infarction is formed a day after obturation of the pulmonary vessel; its full development ends by the 7th day. Infection of pulmonary infarction leads to the development perifocal pneumonia (bacterial, kandidozny) often with abscess formation; subpleural location of infarction occurs more often fibrinous or hemorrhagic pleural effusion.

Symptoms and course of a lung Infarction

They are determined by the caliber, localization and number of obturated vessels, the state of compensatory mechanisms, and the initial pathology of the lungs and heart.

The most frequent signs are: sudden shortness of breath (or suddenly increased); chest pain (acute, resembling angina at the time of embolism; increasing when breathing and coughing with pleurisy); pallor with an ashen skin tone, less often cyanosis; tachycardia with a heart rate of more than 100 in 1 min, sometimes – heart rhythm disorders (extrasystole, less often atrial fibrillation); arterial hypotension up to collapse; cerebral palsy disorders (fainting, convulsions, coma); fever, cough with mucous or bloody sputum, hemoptysis in the formation of a lung infarction.

At the time of embolism, there is often a discrepancy between pronounced shortness of breath and a meager auscultative picture in the lungs; during the formation of a lung infarction, there may be a blunt percussion sound, weakened breathing, pleural friction noise, small-bubbled wet wheezes in a limited area; unilateral exudative pleurisy. Occasionally, there is an abdominal syndrome, manifested by acute pain in the right hypochondrium, intestinal paresis, pseudo-positive symptoms of peritoneal irritation, leukocytosis, persistent hiccups, vomiting (the syndrome is caused by damage to the diaphragmatic pleura, sharp swelling of the liver).

Signs of acute pulmonary hypertension and overload of the right heart (increased cardiac impulse, the outward displacement of the right border of the heart, pulsation in the second intercostal space to the left, accent and splitting II tone, systolic murmur at the pulmonary arteries, signs of right heart failure) are observed only during obturation of the large trunks of the pulmonary arteries.

Signs of peripheral phlebothrombosis may indicate a possible source of PE. A variety of combinations of these signs and their varying degrees of severity are possible, which makes the diagnosis of PE and lung infarction sometimes difficult.

Diagnosis helps identify ECG signs of acute overload of the right heart (high pointed prong R in leads II, III, aVF, sign Mak-Gina-white – deep prong 5 in standard lead I, deep Q wave in lead III, incomplete blockage of right bundle branch block).

X-ray examination can be defined extension the root of the lung, its obnovlennom and strain, the depletion of vessels in the area of lung tissue (symptom Westermark), darkening of triangular shape (due to infiltration of the surrounding pulmonary infarction tissue can take a rounded, irregular shape), the presence of pleural effusion and signs of acute pulmonary heart – the expansion of the superior Vena cava, the shadow of the heart to the right, bulging cone pulmonary trunk.

Ultrasound Doppler examination of the veins of the lower extremities allows you to diagnose deep vein thrombosis of the lower extremities, echocardiography reveals signs of overload of the right ventricle.

A crucial role in the diagnosis of pulmonary embolism play a radioisotope lung scan to detect the characteristic reduction of lung perfusion (selection method) and angioplasty revealing vnutriarterialno filling defects or obstruction ("open") branches of the pulmonary artery.

Treatment of lung Infarction

In cases of suspected pulmonary embolism is shown urgent hospitalization. At the pre-hospital stage, heparin is administered (10,000 UNITS). Heparin ie dissolves the blood clot, but suspends the thrombotic process and prevents the growth of a blood clot distal and proximal to the embolus. By weakening the vasoconstrictor and bronchospatic action of thoromocytic serotonin and histamine, heparin reduces the spasm of pulmonary arterioles and bronchioles. Favorably affecting the course of phlebothrombosis, the most common cause of thromboembolism, heparin serves to prevent relapses of PE.

When expressed pain syndrome and also for unloading of the pulmonary circulation and reduction of dyspnea using opioids (for example, 1 ml of 1% morphine solution in/in fractional); this allows not only effectively to stop pain and reduce the characteristic pulmonary embolism shortness of breath.

In the development of infarct pneumonia, chest pain may be pleural in nature; if it is associated with breathing, coughing, body position, it is more appropriate to use non-narcotic analgesics (for example, intravenous administration of 2 ml of 50% analgin solution). If the disease is complicated by right ventricular failure, shock is treated with vasopressors (dopamine, dobutamine).

In cases of bronchospasm and stable blood PRESSURE (systolic not less than 100 mm Hg), slow (jet or drip) administration of 10 ml of 2.4% eufillin solution is indicated. In addition to its bronchodilating effect, eufillin reduces pressure in the pulmonary arteries and has antiaggregational properties. In the hospital, continue heparin therapy (daily dose-30,000 UNITS) under the control of activated partial thromboplastin time (APTT); it is possible to use low-molecular heparin (dalteparia, enoxaiarin, fraxiparin). Heparin therapy is performed for 7-10 days.

Long-term therapy with indirect anticoagulants is indicated for recurrent phlebothrombosis and PE; in this case, a few days before the cancellation of heparin, the patient is transferred to phenylin therapy under the control of prothrombin time. The duration of therapy with indirect anticoagulants for recurrent PE or repeated development of phlebothrombosis is from 3 to 12 months. the withdrawal criterion is the disappearance or reduction of the potential threat of thrombosis and thromboembolism.

In the case of thromboembolism of small branches of the pulmonary arteries and the absence of relapses of PE, preventive therapy with antiplatelet agents is sufficient and safer than indirect anticoagulants. For this purpose, use aspirin, ticlopidin (of ticlid), trental.

When infarction pneumonia develops, antibiotics are added to therapy. After confirming the diagnosis for massive PE, right ventricular hypokinesis and persistent hypotension, thrombolytic agents are used (streptokinase, etc.); if indicated, surgical treatment is performed (thrombectomy, installation of a filter in the inferior Vena cava, etc.).

Prognosis of lung Infarction

It depends on the underlying disease, the size of the heart attack.