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
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).
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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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.
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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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.
Copyright © 2013, 2009, 2003, 1999, 1995, 1990, 1982, 1977, 1973, 1969 by Mosby, an imprint of Elsevier Inc.
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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 available
1.
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
Ventilation scan: Radioactive gas inhaled
Perfusion scan: IV push of radioisotopetagged 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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Diagnosis of PE: Helical/Spiral CTA
Principal diagnostic tool when used with IV
contrast
. .
V/Q
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
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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 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.)
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:
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