Chapter 26 Pulmonary Vascular Disease

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Transcript Chapter 26 Pulmonary Vascular Disease

Chapter 26
Pulmonary Vascular Disease
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Learning Objectives
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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.)
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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.)
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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
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Pulmonary Vascular Disease
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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.)
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Venous Thromboembolic Disease
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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
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PEs are most often detached portions of
venous thrombi
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Most often (86%), thrombi form in deep veins
(DVT) of legs or pelvis
Conditions that favor thrombus formation
(factors known as Virchow’s triad)
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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
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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%)
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Bronchial circulation provides collateral circulation
limiting risk of infarction
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Pathophysiology
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Massive PE causes death by cardiovascular
failure, not respiratory failure
Emboli obstruct blood flow resulting in
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Alveolar deadspace
 Bronchoconstriction
 Decreased surfactant production
 Hypoxemia
 Pulmonary hypertension
 Shock (saddle embolus)
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Clinical Features
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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
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Rules out other life-threatening conditions
Radiograph is abnormal in 80% of cases
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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
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ECG rules out other life-threatening
conditions
ECG often abnormal but nonspecific
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Tachycardia, ST-segment depression most
common
ABG findings most commonly show
hypoxemia & hypocapnia
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15% to 25% of patients have PO2 >80 mm Hg
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Clinical Features: D-dimers
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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
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Testing for lower extremity DVT
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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
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Three tests available
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2.
3.
V/Q scan
Helical/Spiral CTA
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
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Ventilation scan: Radioactive gas inhaled
Perfusion scan: IV push of radioisotopetagged albumin
Gamma radiation produced by radioisotopes
show distribution of blood flow & ventilation
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Areas with blood flow or ventilation scan “hot”
Areas with ventilation (hot) but no perfusion (cold)
suggest presence of PE
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Diagnosis of PE: Helical/Spiral CTA
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Principal diagnostic tool when used with IV
contrast
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V/Q
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Equal to
scan if combined with D-dimer
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Generally unable to detect smaller PE
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Advantage of helical/spiral CTA is its ability to
provide alternate diagnoses
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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
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Used if V/Q 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
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Diagnosis of PE: Pulmonary
Angiography (cont.)
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Fluoroscope monitors progress of dye
Abnormalities include filling defects & abrupt
ending of arteries
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Treatment: Prophylaxis of DVT
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High mortality justifies prophylactic treatment
Moderate- to high-risk patients include those
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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
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Heparin or fondaparinux is most commonly used
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Management of DVT
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Heparin is standard therapy
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Immediate action
Does not lyse existing clots but prevents clot
growth & formation
Thrombolytic agents
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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
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Similar regimen to DVT
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First-line heparin followed by oral coumarin
Supportive measures include
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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
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Pulmonary arterial hypertension (PAH)
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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
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Development of IPAH
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Genetic predisposition probably required
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Follows insult to arterial endothelium
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Damage results in vasoconstriction
• May be caused by abnormal transport of potassium &
calcium
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Epidemiology: IPAH
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3 times more common in women than men
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7% of cases are familial
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Most common between ages 20 & 50 years
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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
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Symptoms are vague, so misdiagnosis is
common
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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
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Supplemental oxygen (SaO2 >90%)
Anticoagulation with coumarin
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Adjust to keep INR ~2
Vasodilators (calcium channel blockers)
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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.)
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Prostanoids is increasingly used as substitute
for inhaled nitric oxide
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Epoprostenol
Treprostinil
Iloprost
Surgical Therapy
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Atrial Septostomy
Lung transplantation is option for severe
hypertension
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Pulmonary Hypertension in COPD
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~50% of elderly with COPD have significant
pulmonary hypertension
Alveolar hypoxia causes vasoconstriction &
eventually medial hypertrophy, fibrosis, & lumen
narrowing
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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:
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