chapter 26 pulmonary vascular disease
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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. - PowerPoint PPT PresentationTRANSCRIPT
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
Chapter 26
Pulmonary Vascular Disease
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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).
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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.
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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.
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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
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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
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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
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The three components that make up Virchow’s Triad are:
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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
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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)
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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
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Clinical Features (cont.)
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What are the most common symptoms associated with PE?
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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
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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
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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%)
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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
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Diagnosis of DVT (cont.)
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Diagnosis of PE
Three tests available1. V/Q scan
2. Helical/Spiral CTA
3. Pulmonary angiography
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The most commonly used (definitive) test for diagnosing a PE is:
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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
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.. ..
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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
V/Q V/Q . . . .
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Diagnosis of PE: Helical/Spiral CTA (cont.)
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Diagnosis of PE: Helical/Spiral CTA (cont.)
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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
V/QV/Q . . . .
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Diagnosis of PE: Pulmonary Angiography (cont.)
Fluoroscope monitors progress of dye Abnormalities include filling defects & abrupt
ending of arteries
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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
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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
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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
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Pulmonary Hypertension
Pulmonary arterial hypertension (PAH) Mean pulmonary artery pressure (MPAP) >25 mm
Hg at rest OR MPAP >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
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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
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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
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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
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Clinical Features: Symptoms of IPAH (cont.)
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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
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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
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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
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The main mechanism for PHTN in COPD patients is: