Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) · MU Plovdiv

11. Pulmonary embolism

Inside: 19 sections · 2 labelled pictures · 10 tables · 13 flashcards · 27 min

Topic 16 of 68 in the MU Plovdiv syllabus for Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) (Medicine, Year 4). The free AceMed note covers it in 16 sections, about 3,227 words (27 min of reading), with 13 flashcards.

In this note

  1. Essay 11- Pulmonary embolism
  2. Definition
  3. Etiology
  4. Risk factors of PTE
  5. Pathophysiology
  6. Types of PTE
  7. Symptoms
  8. Physical exam
  9. Signs
  10. Diagnosis
  11. Management of large pulmonary embolism
  12. Risk factors
  13. Classification
  14. Clinical presentation
  15. Treatment
  16. Complications and prognosis

Definition

  • Entity of peripheral vein thrombosis followed by embolisation of the thrombus into a branch of the pulmonary artery leading to hypertension and necrosis of pulmonary parenchyme!

Etiology

  • Most often appears as a result of acute PTE
  • Sources of thrombi include:
  • Pelvic and abdominal veins
  • DVT
  • Hypercoagulable states
  • Amniotic emboli
  • Fat emboli from long bones
  • ARDS

Risk factors of PTE

  • Acquired- age, immobilization, traumas, estrogens, weight, COPD, HF, sepsis, neoplasms, polychemotherapy, nephrotic syndrome
  • Genetic- deficiency of antithrombine, protein C and S, hyperhomocysteinemia, high conc of factors VIII, IX, XI

Pathophysiology

  • The deep venous thrombi of legs and pelvis are the most usual origin of pulmonary thromboemboli
  • They embolise into the pulmonary arteries and cause hemodynamic and gas exchange disturbances
  • Sudden increase of RV afterload can cause RV dilation and hypokinesia, tricuspid regurgitation and then RV failure
  • The decreased RV output and septal shift to left in diastole impedes LV filling
  • Changes of coronary circulation are due to a reduced transcoronary pressure gradient (which is due to aortic hypotension and increased RA pressure)
  • This reduces myocardial blood flow and hypoperfusion of RV endocardium
  • Lung perfusion is decreased but perfusion is the same
  • Increased dead space and impaired gaseous exchange
  • After some hours, the non-perfused lung no longer produces surfactant so alveolar collapse occurs

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