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Chapter 26 Pulmonary Vascular Disease

Chapter 26 Pulmonary Vascular Disease. Learning Objectives. State how many patients develop venous thromboembolism each year. Describe how and where thromboemboli originate. Describe how pulmonary emboli alter lung and cardiac function.

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Chapter 26 Pulmonary Vascular Disease

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  1. Chapter 26Pulmonary Vascular Disease

  2. Learning Objectives • State how many patients develop venous thromboembolism each year. • Describe how and where thromboemboli originate. • Describe how pulmonary emboli alter lung and cardiac function. • Identify the clinical features and diagnostic findings associated with pulmonary embolism (PE).

  3. Learning Objectives (cont.) • Describe how PE is diagnosed and managed. • Describe the hemodynamic findings associated with pulmonary hypertension. • Describe the possible mechanisms believed to be responsible for the onset of IPAH. • State who is at risk of the development of IPAH.

  4. Learning Objectives (cont.) • Identify the clinical features associated with IPAH. • Describe the treatment used to care for patients with IPAH. • Describe the pathogenesis and management of pulmonary hypertension associated with COPD.

  5. Introduction • Pulmonary Vascular Disease • Pulmonary vasculature is affected by pulmonary & nonpulmonary disorders • Degree of pulmonary hypertension is determined by severity of underlying disease • Nonpulmonary causes include • Heart disease • Connective tissue diseases • Venous thromboembolic disease

  6. Introduction (cont.) • Venous Thromboembolic Disease • Includes deep vein thrombosis (DVT) & pulmonary emboli (PE) • Major national health problem • Up to 300,000 new cases annually (U.S.) • 1/3 die in first hour of onset of symptoms (PE) • >70% of patients who die of PE are not suspected before death

  7. Pathogenesis • PEs are most often detached portions of venous thrombi • Most often (86%), thrombi form in deep veins (DVT) of legs or pelvis • Conditions that favor thrombus formation (factors known as Virchow’s triad) • Venous stasis: i.e., immobilization in hospital • Hypercoagulable states • Vessel wall abnormalities

  8. The three components that make up Virchow’s Triad are:

  9. Pathology • Stasis in conjunction with trauma or presence of toxins results in thrombi • Thrombus fragment travels to lungs resulting in PE • PE is most frequent in lower lobes & right lung • Pulmonary hemorrhage or infarction are rare (<10%) • Bronchial circulation provides collateral circulation limiting risk of infarction

  10. Pathophysiology • Massive PE causes death by cardiovascular failure, not respiratory failure • Emboli obstruct blood flow resulting in • Alveolar deadspace • Bronchoconstriction • Decreased surfactant production • Hypoxemia • Pulmonary hypertension • Shock (saddle embolus)

  11. Clinical Features • No specific signs or symptoms • Anticoagulation is started on suspicion of PE & stopped only when PE is ruled out • Most common symptom is dyspnea

  12. Clinical Features (cont.)

  13. What are the most common symptoms associated with PE?

  14. Clinical Features: Chest Film • Rules out other life-threatening conditions • Radiograph is abnormal in 80% of cases • Enlargement of right pulmonary artery (66%) • Elevation of diaphragm (61%) • Cardiomegaly (55%) • Small pleural effusion (50%) • Patchy or rounded infiltrates next to pleural surface are less common but characteristic of PE

  15. Clinical Features: ECG & ABGs • ECG rules out other life-threatening conditions • ECG often abnormal but nonspecific • Tachycardia, ST-segment depression most common • ABG findings most commonly show hypoxemia & hypocapnia • 15% to 25% of patients have PO2 >80 mm Hg

  16. Clinical Features: D-dimers • Sensitivity of 97% to 100% for PE • Specificity of 39%, so its use with comorbidities is limited • Level <500 mg/L rules out PE (98%)

  17. Diagnosis of DVT • Testing for lower extremity DVT • Venography • Standard diagnostic tool • Injection of dye • Impedance plethysmography • Noninvasive, sensitive, & specific • Compression ultrasonography • Noninvasive, sensitive, & specific • Test of choice for diagnosis of DVT

  18. Diagnosis of DVT (cont.)

  19. Diagnosis of PE • Three tests available • V/Q scan • Helical/Spiral CTA • Pulmonary angiography

  20. The most commonly used (definitive) test for diagnosing a PE is:

  21. Diagnosis of PE: V/Q Scan . . • Ventilation scan: Radioactive gas inhaled • Perfusion scan: IV push of radioisotope-tagged albumin • Gamma radiation produced by radioisotopes show distribution of blood flow & ventilation • Areas with blood flow or ventilation scan “hot” • Areas with ventilation (hot) but no perfusion (cold) suggest presence of PE

  22. . . V/Q Diagnosis of PE: Helical/Spiral CTA • Principal diagnostic tool when used with IV contrast • Equal to scan if combined with D-dimer • Generally unable to detect smaller PE • Advantage of helical/spiral CTA is its ability to provide alternate diagnoses

  23. Diagnosis of PE: Helical/Spiral CTA (cont.)

  24. Diagnosis of PE: Helical/Spiral CTA (cont.)

  25. . . V/Q Diagnosis of PE: Pulmonary Angiography • Used if scan & spiral CT fail to identify PE • Low risk-to-benefit ratio justifies use of procedure • Catheter is threaded so tip passes through right heart & into pulmonary artery • Radiopaque dye is injected

  26. Diagnosis of PE: Pulmonary Angiography (cont.) • Fluoroscope monitors progress of dye • Abnormalities include filling defects & abrupt ending of arteries

  27. Treatment: Prophylaxis of DVT • High mortality justifies prophylactic treatment • Moderate- to high-risk patients include those • Undergoing joint replacement • With acute spinal injury or ischemic stroke • With myocardial infarction or heart failure • Who are MICU patients (i.e., pneumonia) • Treatment is anticoagulant therapy • Heparin or fondaparinux is most commonly used

  28. Management of DVT • Heparin is standard therapy • Immediate action • Does not lyse existing clots but prevents clot growth & formation • Thrombolytic agents • Streptokinase, urokinase, TPA • Actually lyse or destroy PE • Not routinely used • High risk of limb gangrene • Risks & benefits not well established

  29. Management of PE • Similar regimen to DVT • First-line heparin followed by oral coumarin • Supportive measures include • Oxygen therapy • Analgesia • Hypotension & shock are treated with vasopressors & fluids • In persistent hypotension due to massive PE, thrombolytics are indicated

  30. Pulmonary Hypertension • Pulmonary arterial hypertension (PAH) • Mean pulmonary artery pressure (MPAP) >25 mm Hg at rest ORMPAP >30 mm Hg with exercise, with increased pulmonary vascular resistance (PVR) & normal left ventricular function • Associated with congenital heart disease, collagen vascular disease, liver cirrhosis, etc • Idiopathic pulmonary arterial hypertension (IPAH) if no identifiable cause is found

  31. Pathogenesis: IPAH • Development of IPAH • Genetic predisposition probably required • Follows insult to arterial endothelium • Damage results in vasoconstriction • May be caused by abnormal transport of potassium & calcium

  32. Epidemiology: IPAH • 3 times more common in women than men • 7% of cases are familial • Most common between ages 20 & 50 years • As only 33% of patients are alive in 5 years, it is important to identify & aggressively treat this disorder

  33. Clinical Features: Symptoms of IPAH • Symptoms are vague, so misdiagnosis is common • Initial symptom: dyspnea (60%) • Angina (50%) • Syncope (8%) • Other symptoms include • Cough, hemoptysis, hoarseness, & Reynaud’s phenomenon

  34. Clinical Features: Symptoms of IPAH (cont.)

  35. Management of Pulmonary Hypertension • Supplemental oxygen (SaO2 >90%) • Anticoagulation with coumarin • Adjust to keep INR ~2 • Vasodilators (calcium channel blockers) • May use digoxin & diuretics to manage side effects • Nitric oxide is preferred • Very short half life • Does not affect cardiac output • Enhances V/Q mismatching

  36. Management of Pulmonary Hypertension (Cont.) • Prostanoids is increasingly used as substitute for inhaled nitric oxide • Epoprostenol • Treprostinil • Iloprost • Surgical Therapy • Atrial Septostomy • Lung transplantation is option for severe hypertension

  37. Pulmonary Hypertension in COPD • ~50% of elderly with COPD have significant pulmonary hypertension • Alveolar hypoxia causes vasoconstriction & eventually medial hypertrophy, fibrosis, & lumen narrowing • Leads to hypertension • Severity of COPD correlates with severity of hypertension • Long term oxygen therapy is only treatment that improves survival among this patient population

  38. The main mechanism for PHTN in COPD patients is:

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