Chapter 7: Pulmonary Thromboembolic Disease (PTE) 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 List the treatment and prevention strategies for PTE

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

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

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

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

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

How Pulmonary Thromboembolic Occurs??

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

Pathophysiology ↑ PVR ↓ RV output = ↓ LV output When ≥ 50% vascular occlusion + vasoconstriction ↑ PVR ↓ RV output = ↓ LV output Systemic hypotension Cardiovascular collapse

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

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

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

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

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

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

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

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

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

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

Treatment: Pharmacological Agents Anticoagulant Therapy Oral anticoagulants Long-term therapy Coumarin derivates [Warfarin] Inactivate K-dependent clotting factors Monitored with PT

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

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

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

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