Pulmonary Embolism
and COPD
Fall Semester
Pulmonary Embolism
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Obstruction of pulmonary artery or branch by blood
clot (most common & usually arises from
peripheral vein), air, fat, amniotic fluid, or septic
thrombus
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Obstructed area has diminished or absent blood flow
◦ Although area is ventilated, no gas exchange occurs
(dead space)
Inflammatory process causes regional blood vessels,
bronchioles to constrict, further increasing
pulmonary vascular resistance, pulmonary arterial
pressure, right ventricular workload
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Ventilation-perfusion imbalance, right ventricular
failure, shock
Risk Factors:
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Venous stasis: Prolonged immobility,
Hypercoagulabilty
Venous endothelial disease: DVT &
thrombophlebitis
Certain disease states: heart disease (HF),
trauma (fracture of hip), postoperative (orthopedic,
abdominal) /postpartum, diabetes mellitus (DM),
COPD.
Other conditions:Advance age (>50 years),
pregnancy, obesity, oral contraceptive use,
constrictive clothing, history of PE, DVT, &
thrombophlebitis
Review chart 23-8 page, 582
Clinical Manifestation: depend on the
size of thrombus and the area occluded
 Dyspnea
most frequent symptoms
 Tachypnea most frequent sign
 Chest pain (sudden, substernal,
pleuritic in origin)
 Anxiety, fever, tachycardia, cough,
apprehension, hemoptysis,
diaphoresis and syncope
Diagnostic Finding
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Death occurs within one hour
CXR ( show infiltrate, atelectasis, elevation
of diaphragm on the affected side, pleural
effusion)
ECG (sinus tachycardia, PR interval
depression,
ABG’s ( hypoxemia, hypocapnia from
tachypnea)
V\Q scan: second choice, evaluate
different areas in the lungs and compare
the V/Q in each area after IV
administration of contrast agent and scan.
Diagnostic Finding
 CT scan for the lung
 D-diamer assay: blood test for evidence of
blood clot. ↑ indicates clotting abnormality
such as (hypercoagulability)
 Pulmonary angiography, (first choice):
injection of dye under fluoroscopy through a
catheter that goes to vena cava (right side of
the heart) to discover the thrombus
Prevention
◦ Exercises to avoid venous stasis
◦ Early ambulation
◦ Anticoagulant therapy (heparin, and low molecular
weight heparin: Enoxaparin)
◦ Sequential compression devices (SCDs) as elastic
stocking: prevent venous stasis,
◦ Review chart 23-9 p 584.
(Prevention of recurrent pulmonary embolism)
Medical Management:
Purpose to lyse the emboli and prevent new
one from forming
General measures to improve respiratory and
vascular status
 Anticoagulant therapy: (Heparin and Warfarin)
 Thrombolytic therapy: ( streptokinase, urokinase)
 Check PTT, INR, HCT, & platelets count
 Surgical intervention: (embolectomy) done for Pts
who fail to improve with medications or
medications were contraindicated

Nursing Management
Minimize the risk of PE
 Preventing thrombus formation:
- Early ambulation after surgery,
- Leg exercises to avoid venous stasis, avoid dangling of legs,
and feet should rest on floor.
- Care of IV devices,
 Assessing potential of PE: risk factors
 Monitoring thrombolytic therapy
 Managing O2 therapy
 Relieving anxiety
 Providing post op care: VS, UO, elevation of legs, isometric
exercise, elastic stocking, and avoid sitting to prevent hip
flexion
 Monitoring for complications

Chronic obstructive pulmonary disease,
COPD

A disease state characterized by airflow
limitation that is not full reversible (GOLD: Global
initiative for chronic obstructive lung disease).

COPD is currently the 4th leading cause of death
and the 12th leading cause of disability in US.

COPD includes diseases that cause airflow
obstruction (emphysema, chronic bronchitis) or a
combination of these disorders.

Asthma is now considered a separate disorder
but can coexist with COPD.
Pathophysiology
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Airflow limitation is progressive and associated with
abnormal inflammatory response of the lungs to
noxious agents or gases
Inflammatory response occurs throughout the
airways, lung parenchyma, and pulmonary
vasculature.
Scar tissue and narrowing occur in airways.
Substances activated by chronic inflammation
(proteinase and antiproteinase) damage the
parenchyma of lungs.
Inflammatory response causes changes in pulmonary
vasculature.
Chronic Bronchitis
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Cough with sputum production on most days for 3
months of a year for 2 consecutive years.
Smoke and air pollutants irritation of airways results in
inflammation and hypersecretion of mucus.
Hallmark goblet cell and mucus glands increase in
number & size
Ciliary function is reduced (more mucus produced),
bronchial walls thicken (due to infiltration of the
bronchial wall with inflammatory cell), bronchial
airways narrow, and mucus may plug airways
Alveoli become damaged and fibrosed, and alveolar
macrophage function diminishes.
The patient is more susceptible to respiratory
infections.
Pathophysiology of Chronic Bronchitis
Emphysema
Abnormal distention of air spaces beyond the terminal
bronchioles with destruction of alveoli walls

Decreased alveolar surface area causes an increase in
“dead space” & impaired O2 diffusion (hypoxemia).
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Reduction of the pulmonary capillary bed increases
pulmonary vascular resistance and pulmonary artery
pressures.
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Hypoxemia is the result of these pathologic changes.
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Increased pulmonary artery pressure may cause
right-sided heart failure (cor pulmonale).
Changes in Alveolar Structure with Emphysema
Risk Factors for COPD
(see chart 24-1, )
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Tobacco smoke causes 80-90% of COPD cases!
Passive smoking
Occupational exposure
Ambient air pollution
Genetic abnormalities
◦ Alpha1-antitrypsin deficiency: enzyme that
protect the lungs’ tissues from destruction
Clinical Manifestation
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1.
2.
3.
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3 primary symptoms:
Chronic cough
Sputum production
Dyspnea on exertion
Wt loss
Barrel chest (A-P diameter/ Transverse diameter :
2/1)
Retraction in the supraclavicular area on inspiration
Shrug shoulder
Abdominal muscle contraction on inspiration.
Typical Posture of a Person with COPD
Diagnostic finding
 Health history (exposure to risk factor, past
medical history, family Hx)
 Pulmonary function test
 Spirometry (FEV1\FVC) = <70%
 ABG’s (PaO2, PaCo2) hypoxemia
 CXR seldom used
 Screening for Alpha1-antitrypsin deficiency
Medical Management
 Risk reduction especially smoking
 Pharmacologic therapy ( bronchodilators and
corticosteroids)
 Management of exacerbation (worsening of
the S&S)
 O2 therapy gradually because of hypercapnia
 Pulmonary rehabilitation
Nursing Process
Assessment:
• Health history
• Inspection and exam findings
• See Chart 24-2 and Chart 24-3
• Review of diagnostic tests
Nursing Process: The Care of Patients with
COPD- Diagnoses

Impaired gas exchange R\t V\Q inequality
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ineffective airway clearance R\t increased mucous secretion
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Ineffective breathing pattern R\t bronchospasm, mucus
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Activity intolerance R\t fatigue, hypoxemia
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Deficient knowledge regarding self care
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Ineffective coping R\t anxiety, lower activity level
Collaborative Problems
 Respiratory insufficiency or failure
 Atelectasis
 Pulmonary infection
 Pneumonia
 Pneumothorax
 Pulmonary hypertension: Cor pulmonale-
(Rt side heart failure)
Planning
 Promote smoking cessation
 Improve gas exchange
 Maintain airway clearance
 Improve breathing pattern
 Improve activity tolerance
 Increase knowledge
 Enhance individual coping mechanism
Improving Gas Exchange
- Proper administration of bronchodilators and
corticosteroids
- Reduction of pulmonary irritants
- Directed coughing (“huff” cough after deep
breathing)
- Chest physiotherapy
- Breathing exercises to reduce air trapping
◦ Diaphragmatic breathing
◦ Pursed-lip breathing
- Use of supplemental oxygen
Improving Activity Tolerance
 Focus on rehabilitation activities to improve
ADLs and promote independence.
 Pacing of activities
 Exercise training
 Walking aides
 Utilization of a collaborative approach
Other Interventions
 Set realistic goals
 Avoid extreme temperatures
 Enhancement of coping strategies
 Monitor for and management of
potential complications
Patient Teaching
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Disease process
Medications
Procedures
When and how to seek help
Prevention of infections
Avoidance of irritants; indoor and outdoor
pollution and occupational exposure
Lifestyle changes, including cessation of
smoking
Bronchiectasis and
Asthma
Chapter 24
Bronchiectasis
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A chronic, irreversible dilation of the bronchi and
bronchioles.
Under the new definition of COPD, it is considered a
separate disease process from COPD (NIH,2001).
It may be caused by a variety of conditions, including:
Airway obstruction
Diffuse airway injury
Pulmonary infections and obstruction of the bronchus
or complications of long-term pulmonary infections
Genetic disorders such as cystic fibrosis
Abnormal host defense (eg, ciliary dyskinesia or humoral
immunodeficiency)
Idiopathic causes
Pathophysiology

The inflammatory process associated with
pulmonary infections damages the
bronchial wall, causing a loss of its
supporting structure and resulting in thick
sputum that ultimately obstructs the
bronchi.

The walls become permanently distended
and distorted, impairing mucociliary
clearance. The inflammation and infection
extend to the peribronchial tissues;
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Bronchiectasis is usually localized, affecting a
segment or lobe of a lung, most frequently the
lower lobes.

The retention of secretions and subsequent
obstruction ultimately cause the alveoli distal to
the obstruction to collapse (atelectasis).
Inflammatory scarring or fibrosis replaces
functioning lung tissue.

In time the patient develops respiratory
insufficiency with reduced vital capacity,
decreased ventilation, and an increased ratio of
residual volume to total lung capacity.
There is impairment in the matching of ventilation
to perfusion (ventilation–perfusion imbalance)
and hypoxemia.
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Clinical Manifestations
Characteristic symptoms of Bronchiectasis include:
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Chronic cough
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Production of purulent sputum in copious amounts.
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Many patients with this disease have hemoptysis.
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Clubbing of the fingers also is common because of
respiratory insufficiency.
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Repeated episodes of pulmonary infection.
Assessment and Diagnostic Findings
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Bronchiectasis is not readily diagnosed because the
symptoms can be mistaken for those of simple
chronic bronchitis.
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A definite sign is offered by the prolonged history of
productive cough, with sputum consistently
negative for tubercle bacilli.
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The diagnosis is established by a computed
tomography (CT) scan, which demonstrates either
the presence or absence of bronchial dilation.
Medical Management
Treatment objectives are to:
- Promote bronchial drainage
- Clear excessive secretions from the affected portion
of the lungs
- Prevent or control infection.
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Postural drainage: draining the Bronchiectasis areas by
gravity reduces the amount of secretions and the
degree of infection.
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Sometimes mucopurulent sputum must be removed by
bronchoscopy.
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Chest physiotherapy, including percussion and postural
drainage, is important in secretion management.

Smoking cessation: smoking impairs bronchial drainage
…by paralyzing ciliary action, increasing bronchial
secretions, causing inflammation of the mucous
membranes, & hyperplasia of the mucous glands.

Infection is controlled: antimicrobial therapy (based on
sensitivity studies & sputum culture). A year-round regimen
of antibiotic agents (different types of antibiotics) may be
prescribed at intervals. It may be prescribed throughout the
winter (or when acute upper respiratory tract infections
occur).

Vaccination against influenza & pneumococcal pneumonia
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Bronchodilators: assist with secretion management.
Surgery: to conserve normal pulmonary tissue & avoid
complications
Nursing Management

Focuses on alleviating symptoms & to clear pulmonary
secretions.

Patient teaching: smoking & other factors that increase
the production of mucus and hamper its removal
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Patient and family teaching: to perform postural
drainage & to avoid exposure to others with upper
respiratory or other infections.
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Teaching pt: early signs of respiratory infection &
progression of disease (so appropriate treatment can
be implemented promptly).
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Assess pt nutritional status, & teach pt strategies to
ensure adequate diet and energy conservation