Pulmonary embolism

Pulmonary embolism

Pulmonary embolism (PE) is a mechanical obstruction of blood flow in the pulmonary artery system when a blood clot enters it, which leads to spasm of the branches of the pulmonary artery, the development of an acute pulmonary heart, a decrease in cardiac output, a decrease in blood oxygenation and bronchospasm. Frequency

    • In Russia, PE is registered in 4.4-14.7% of all autopsies
    • After 5 million operations, PE occurs in approximately 150,000 cases with a fatal outcome in 8,000 cases. The predominant age is over 40 years.

Etiology. In 90% of cases, the source of PE is located in the basin of the inferior vena cava

    • Iliofemoral venous segment
    • Veins of the prostate and other veins of the small pelvis
    • Deep veins of the legs.

Risk factors

    • Malignant neoplasms
    • Heart failure
    • THEM
    • Sepsis
    • Stroke
    • erythremia
    • Inflammatory Bowel Disease
    • Obesity
    • nephrotic syndrome
    • Estrogen intake
    • Hypodynamia
    • Antiphospholipid Syndrome
    • Syndromes of primary hypercoagulation
    • Antithrombin III deficiency
    • Deficiency of proteins C and S
    • Dysfibrinogenemia
    • Pregnancy and postpartum period
    • Injuries
    • Epilepsy
    • postoperative period. Pathogenesis
    • Pulmonary hypertension, right ventricular failure and shock
    • With occlusion of more than 30-50% of the pulmonary arterial branches, significant pulmonary hypertension occurs (sometimes up to 100 mm Hg, the norm is below 25 mm Hg)
    • Decrease in the total cross-sectional area of ​​the vascular bed
    • Pulmonary vasoconstriction
    • Release of serotonin and prostaglandins from platelet aggregates
    • With an increase in pulmonary vascular resistance, the right ventricle loses its ability to maintain cardiac output with the development of arterial hypotension.
    • Tachypnea and hyperventilation
    • Stimulation of juxtacapillary receptors leads to active vagal afferentation and stimulation of respiratory neurons in the medulla oblongata
    • Reflex bronchospasm in response to hypocapnia.
    • Arterial hypoxemia
    • Perfusion and reduced vascular resistance in unaffected lung segments causes right-to-left intrapulmonary shunting with inadequate blood oxygenation
    • Uneven ventilation-perfusion relationship
    • Depletion of surfactant leads to restrictive disorders.
    • Pulmonary infarction develops against the background of the initial left ventricular failure due to the failure of collateral blood flow through the bronchial arteries.

Clinical picture

    • Pulmonary-pleural syndrome
    • Dyspnea associated with impaired perfusion and ventilation of the lungs
    • Cyanosis of the face, neck and upper body is a characteristic symptom of a massive embolism.
    • Pain is also a common symptom of PE, is acute and localized in the posterior-lower chest (in 20-87% of patients)
    • Cough (in 20% of patients) is traditionally accompanied by hemoptysis
    • physical

data – dullness of percussion sound with infarct pneumonia or pleural effusion, moist rales in the lung and pleural friction rub – are traditionally unstable and are detected on 3-4 days due to the development of pulmonary infarction.

    • Cardiac syndrome is manifested by pain and discomfort behind the sternum, tachycardia, rhythm disturbances and arterial hypotension, up to the collaptoid state.
    • Abdominal syndrome (less commonly observed) is characterized by pain in the upper right abdomen and, obviously, depends on irritation of the right dome of the diaphragm with pleural effusion or stretching of the Glisson capsule with the development of right ventricular failure.
    • Cerebral syndrome (observed more often in older people) is characterized by loss of consciousness, hemiplegia and convulsions.
    • Renal syndrome (secretory anuria) is more often observed after the removal of patients with pulmonary embolism from shock.
    • Note. The classic clinical picture of PE (shortness of breath, cyanosis, anginal pain, arterial hypotension) is noted only in 16% of patients.

Laboratory research

    • hypoxemia
    • Hypercapnia. Special Studies
    • Chest X-ray
    • Atelectasis
    • Plethora of the roots of the lungs
    • Sudden interruption of the course of the vessel – symptoms of amputation
    • A local decrease in pulmonary vascularization is a symptom of Wöstermarck.
    • Ventilation-perfusion lung scintigraphy
    • High probability of PE – decreased perfusion in one or more segments with normal ventilation
    • Low probability – subsegmental or small damage to the blood supply. Note. The information content of the method decreases with concomitant COPD, lung tumors, suffered in the past by PE.
    • Pulmonary angiography is a classic diagnostic method for suspected PE based on the clinical picture and ventilation-perfusion scintigraphy data.
    • Criteria for a reliable diagnosis – a sudden breakage of a branch of the pulmonary artery and the contours of a thrombus
    • The criteria for a probable diagnosis are a sharp narrowing of the branch of the pulmonary artery and a slow washout of the contrast.
    • ECG to exclude MI and determine indirect signs of PE
    • Syndrome of deep teeth S,, Qm, Tsh in 25% of cases
    • EOS deviation to the right
    • Incomplete blockade of the right leg of the bundle of His
    • P-pulmonale – with thromboembolism of large branches
    • Various cardiac arrhythmias (for example, atrial or ventricular extrasystoles, atrial fibrillation or flutter) are a variable symptom.

Differential Diagnosis

    • Pneumonia
    • THEM
    • Heart failure
    • Pericarditis
    • Pneumothorax
    • Bronchial asthma
    • rib fracture
    • Psychogenic hyperventilation
    • Non-thrombotic pulmonary embolism (amniotic, fatty, septic, tumor).


Tactics of conducting

    • With normal blood pressure
    • For thromboembolism of small or medium branches of the pulmonary artery – heparin, then indirect anticoagulants
    • With thromboembolism of large branches of the pulmonary artery, with acute right ventricular failure – heparin or fibrinolytic agents
    • In pulmonary infarction with hemoptysis – heparin, then indirect anticoagulants
    • PE in patients with contraindications to the administration of heparin and fibrinolytic agents – installation of a filter in the inferior vena cava (caval filter).
    • With arterial hypotension
    • dobutamine dopamine, epinephrine hydrochloride
    • With the preservation of arterial hypotension, despite the replenishment of the BCC, the introduction of fibrinolytic agents.
    • With recurrent PE
    • Acetylsalicylic acid
    • Installation of a cavafilter
    • Indirect anticoagulants. Drug therapy
    • Heparin 5,000-10,000 IU IV by bolus, then continuous infusion at a dose of 10-15 IU/kg/min under PTT control after 4 hours until it increases by 1.5-2 times, then 1 r/day. With an increase in PTT by more than 2 times, the infusion rate is reduced by 25%.
    • Indirect anticoagulants are prescribed 1-2 r / day (for 5 days you will need a combination with heparin)
    • The PTT should correspond to International Normalized Ratio (INR) values ​​of 2.0 to 3.0 (see Atrial Flutter]
    • Indirect anticoagulants are taken for 3-6 months (if risk factors are eliminated) or for life (if risk factors are unlikely to be eliminated).
    • Fibrinolytic agents are injected into a peripheral vein or directly into the pulmonary artery
    • Streptokinase 250,000 IU IV for 30 minutes, then 100,000 IU/h for 1 day
    • Urokinase 4400 IU for 30 minutes, then 4400 IU/kg/h for 12-24 hours
    • Contraindications
    • Recent intracranial hemorrhage
    • Threat of bleeding (peptic ulcer, hematuria, recent abdominal surgery)
    • Control
    • chtv
    • TV
    • The level of fibrinogen and fibrin destruction products
    • Notes
    • If there are no laboratory signs of thrombus lysis, the infusion rate is doubled
    • Thrombolytics should not be administered simultaneously with heparin
    • If, after the termination of the thrombolytic infusion, the PTT exceeds the initial value by less than 2 times, a transition to heparin is possible,


    • Embolectomy
    • Closed embolectomy with suction catheter
    • Open embolectomy under cardiopulmonary bypass. Note. Mortality is 20-30%
    • Installation of a caval filter to create an obstacle to the migration of a thrombus from the basin of the inferior vena cava.


    • lung infarction
    • Acute cor pulmonale
    • Recurrent deep vein thrombosis or PE. Course and forecast
    • With timely and adequate treatment, mortality is less than 10%, without treatment – more than 30%
    • The prognosis is worse in people with pre-existing heart or lung disease.
    • Chronic pulmonary hypertension develops in 1% of cases. Prevention
    • Before surgery in the presence of risk factors
    • Pneumatic compression
    • Elastic stockings
    • Small doses of heparin (5,000 IU sc)
    • After surgical treatment in the presence of risk factors
    • Heparin in small doses of 5,000 IU s / c every 8-12 hours for 7 days
    • Small doses of indirect anticoagulants under the control of 1NR in the range of 2.0-3.0
    • Repeated PE
    • Anticoagulants
    • Cavafilter
    • Elastic stockings
    • Pregnancy
    • Prenatal period (physical activity, elastic stockings)
    • Childbirth (pneumatic compression, low dose heparin)
    • Postpartum period (indirect anticoagulants for 6 weeks, elastic stockings).

See also Secondary Pulmonary Hypertension, Primary Pulmonary Hypertension, Pulmonary Infarction, Antiphospholipid Syndrome. Adult Respiratory Distress Syndrome, Deep Vein Thrombosis of the Lower Extremities Reduction. PE – pulmonary embolism of the ICD. 126 Pulmonary embolism


  • 336:231-236
  • Massive pulmonary embolism. Saveliev VS et al. M.: Medicine, 1990

Leave a Comment

Your email address will not be published. Required fields are marked *