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Lecture Notes

Lecture Notes. Chapter 7: Pulmonary Thromboembolic Disease (PTE). Objectives. State the frequency and mortality of PTE List the predisposing factors for development of PTE Recognize signs and symptoms of PTE Describe the diagnostic studies used to confirm the presence of PTE

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Lecture Notes

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  1. Lecture Notes Chapter 7: Pulmonary Thromboembolic Disease (PTE)

  2. Objectives • State the frequency and mortality of PTE • List the predisposing factors for development of PTE • Recognize signs and symptoms of PTE • Describe the diagnostic studies used to confirm the presence of PTE • List the treatment and prevention strategies for PTE

  3. PulmonaryThromboembolic Introduction • Vascular obstruction of the pulmonary vessels by thrombi from the venous system • PTE is relatively common • 500,000 cases/year • 200,000 deaths/year

  4. Etiology: Virchow’s Triad • Associated with formation of deep venous thrombi (DVT) • Hypercoagulability • Deficiency of antithrombin III, protein S, protein C, lupus anticoagulant • Endothelial wall damage (trauma) • Fractures, surgical procedures, trauma • Venostasis • Immobilization, prolonged illness

  5. Etiology • Risk Factors for DVT • Age > 70 • Obesity • Congestive heart failure • Malignancy • Burns • Estrogen-containing drugs • Postoperative and postpartum

  6. Etiology • Thrombi originate at the site of turbulent flow • Venous valves • Sites of endothelial damage • Most thrombi originate in deep veins of lower extremities and pelvic region • Rarely from heart or upper extremities • Embolic risk higher if thrombosis above the knee • Highest risk of PTE within 72 hours of development of DVT

  7. Pathology • Pathologic changes related to • Magnitude of occlusion • Compromise of pulmonary blood flow • Small PTE may cause little or no injury to distal lung • Large thrombi may cause lung parenchymal injury (infarction) • ~10% of PTE cause infarctions • Most emboli cause physiological disruption due to release of vasoactive mediators in the clot

  8. How Pulmonary ThromboembolicOccurs??

  9. Pathophysiology: PTE Pulmonary vascular occlusion After 24 hours ↓ Pulmonary perfusion ↓ Surfacant production V>Q (dead space) ↓ Pulmonary compliance Release platelet mediators(Serotonin, Histamine, Prostaglandins) Atelectasis Local alveolar hypocapnia and hypoxemia Bronchoconstriction V/Q mismatching Hypoxemia

  10. Pathophysiology

  11. Clinical Features: History • Nonspecific and may occur without symptoms • If risk factors present = high index of suspicion • Transient acute dyspnea • Most common symptom • Pleuritic chest pain • Hemoptysis • Syncope • Suggestive of large clots

  12. Clinical Features: Physical Examination • Tachypnea, tachycardia, mild fever • Exam most often normal • If PTE is severe = signs of RV failure (JVD) • Lower extremities • Often normal • May reveal swelling and tenderness (DVT) • Breath sounds • May be normal • Localized wheezing, crackles, pleural friction

  13. Clinical Features • Physical Examination • Chest percussion and auscultation usually normal • Cardiac auscultation • Loud P2 (pulmonic valve closure) • S2 (second heart sound) splitting • Possible S3 or S4

  14. Clinical Features: Hemodynamic Evaluation • Increased CVP • Increased PAP • Normal PCWP • Low PCWP suggests significant vascular occlusion

  15. Clinical Features • Arterial Blood Gases • ABGs do not play major role in diagnosis • Uncompensated respiratory alkalosis • Mild to moderate hypoxemia • Increased alveolar-arterial gradient

  16. Clinical Features • Electrocardiogram • Rule out MI • Most often normal or nonspecific ST and T wave abnormalities • Laboratory Evaluation • “D-dimer” release (> 500ng/mL) • Result of clot formation • Inflammatory conditions

  17. Clinical Features • Radiography: • Often normal • Nonspecific abnormalities such as: • Signs of loss volume • Subsegmental atelectasis • Small pleural effusion • Westernmark’s sign indicate local vascular narrowing • Doppler ultrasound of the leg veins with positive results reveal a reason to treat with anticoagulant

  18. Clinical Features • Ventilation/Perfusion Scan • High probability V/Q scan • Normal ventilation in the presence of at least 2 segmental defects or 1 lobar defect in perfusion

  19. Clinical Features • Pulmonary Angiography • Gold standard • Determines extent of vascular involvement • Signs of PE • Abrupt cut-off of a vessel • Intraluminal filling defects • CAT Scan • Less invasive and smaller contrast load

  20. Treatment: Pharmacological Agents • Aim of treatment: • Treating vascular occlusion & preventing reocrrence • Anticoagulant Therapy • Prevention of new clot formation and growth of existing thrombi • IV Heparin • Subcutaneous low-molecular-weigh heparin (LMWH) • Unfractionated heparin • Inactivates thrombin and clotting factor X • Inhibits platelet aggregation • Monitored with PTT

  21. Treatment: Pharmacological Agents • Anticoagulant Therapy • Oral anticoagulants • Long-term therapy • Coumarinderivates [Warfarin] • Inactivate K-dependent clotting factors • Monitored with PT

  22. Treatment: Pharmacological Agents • Thrombolytic therapy [streptokinase, urokinase, TPA] • Dissolve fresh clot & restore vascular patency • Increase risk of bleeding • Indicated when significant hemodynamic compromise • Most effective during first 5 days of thrombi formation • Usually followed by heparin and warfarin therapy

  23. Treatment: Surgery • Surgical removal of emboli • Not more effective than thrombolytic therapy • Mortality rate post procedure ~60% • Inferior vena cava interruption • Less frequently performed • Used if emboli recur post anticoagulation

  24. Treatment: Supportive Care • Oxygen • Intubation and mechanical ventilation if respiratory failure present • Volume expansion and dopamine if hypotension occurs

  25. Treatment: Prevention • Prophylaxis for patients at high risk • Low-dose SC LMWH • Sodium warfarin • Venous compression devices

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