1. Chapter 7: Pulmonary Thromboembolic Disease (PTE)
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. Pulmonary Thromboembolic 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 Thromboembolic Occurs??

9. Pathophysiology: PTE ↓ Pulmonary perfusion ↓ Surfacant production
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 ↑ PVR ↓ RV output = ↓ LV output
When ≥ 50% vascular occlusion + vasoconstriction
↑ PVR
↓ RV output = ↓ LV output
Systemic hypotension
Cardiovascular collapse

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 Signs of PE CAT Scan
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
Coumarin derivates [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