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