41. Pulmonary embolism

What is a pulmonary embolism

Pulmonary embolism (PE) = blockage of an artery in the lungs by substance that has moved from elsewhere in the body through the bloodstream (embolus)

Thromboembolism = consequence of thrombus formation within a deep vein of the body

What is the origin of tthe thrombus

• Lower extremity veins (most common!)

• Pelvic veins

• Abdominal veins

• Upper extremity veins

• Head + cervical veins

• Right heart

• Left heart (septal defect or patent foramen ovale)

What causes thrombus formation

• Venous stasis

• Hypercoagulability

• Vascular wall injury

What are the inherited risk factors of PE

• Antithrombin III deficiency

• Protein C deficiency

• Protein S deficiency

• Factor V Leiden mutation

What are the acquired risk factors

• Immobilization, trauma, chronic venous insufficiency, malignancy, surgery

• Oral contraceptives, obesity, stroke, age (>40 y/o), HF, smoking, pregnancy

What is the vascular pathology of PE

• partial or complete blockage of peripheral pulmonary blood flow

• has dual blood supply- rare necrosis

What are the haemodynamics of a PE

• Thrombus blocks vessel → causes mechanical obstruction of blood flow + blood clot releases vasoconstrictor material causing further decrease in perfusion

• Makes it difficult to pump blood from the right heart to the lung → causes backflow → eventually get insufficient filling of the left heart → circulatory collapse which can almost cause immediate death

What happens to the V/Q in normal regions of the lung

• Hyperperfusion as the blood cannot go to where the embolism is

• diverted to the normal parts of the lungs

• ↓V/Q ratio

• functional shunt increases (more perfusion than ventilation)

• hypoxemia (↓PaO2)

What happens to the V/Q in the affected region of the lung

• Hypoperfusion → ↑V/Q ratio (↑alveolar dead space)

  • In normal conditions, V/Q = 0.8, meaning that Q is more than V

  • Decreasing Q will therefore increase the V/Q ratio

• Hypocapnic bronchoconstriction (→ decreased ventilation = increase in CO2)

• Atelectatic/necrosis due to reduced production of surfactant

What are the triad of symptoms

• dyspnea

• pleuritic chest pain

• hemoptysis

What are the clinical forms

What is the diagnostic algorithm of PE

What is the diagnostics in patients with haemodynamic instability 

What is seen on a CXR

• non specific

• can be normal

• abnormal non specific findings

  • atelelectasis

  • enlarged pulmonary artery

  • pleural effusion

  • elevated hemidiaphragm

What can be seen on an ECG in PE

• can be normal

• Abnormal- non specific

  • ST depression

  • sinus tachycardia

  • negative T in V1-2

  • SVA

What are the lab fiindings in PE

• D dimer increase

  • negative predictive value

  • excludes PE

• In pulmonary infarct

  • increased WBC, FVC, CRP

• increased troponin, LDH, serum HCO3-, SGOT

What can be seen on blood gas analysis

• decreased PaO2

• decreased PaCO2

  • due to hyperventilation

• increased pH

  • respiratory alkalosis

What can be seen on a CT angiography

• The first choice for imaging the pulmonary vasculature in patients suspected with PE

• It allows adequate visualization of the pulmonary arteries down to at least the segmental level

Ventilation- perfusion scintigraphy

• Labeled with technetium

• Detects vessel occlusion > 3mm

• Normal perfusion excludes pulmonary embolism

• Specificity: tumor, pneumonia, hypoxic vasoconstriction

• To be evaluated only with CXR

What are the indications of pulmonary antiography

• Reference method – definitive diagnosis

• Failure of other studies

• Thrombolytic or anticoagulant therapy is contraindicated

What are the relative contraindications of pulmonary angiography

• Contrast material hypersensitivity

• Severe congestive HF, pulmonary hypertension