1. Pulmonary Embolism and COPD
Fall Semester

2. Pulmonary Embolism
Obstruction of pulmonary artery or branch by blood clot (most common & usually arises from peripheral vein), air, fat, amniotic fluid, or septic thrombus
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
Ventilation-perfusion imbalance, right ventricular failure, shock

3. Risk Factors: 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

5. 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

6. Diagnostic Finding 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.

7. 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

8. 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)

9. General measures to improve respiratory and vascular status
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
PTT: partial thromboplastin sec; INR international ratio” appropriateness bw dose and PT

10. 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

11. 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.

12. Pathophysiology
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.

13. Chronic Bronchitis
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.

14. Pathophysiology of Chronic Bronchitis

15. 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).
Reduction of the pulmonary capillary bed increases pulmonary vascular resistance and pulmonary artery pressures.
Hypoxemia is the result of these pathologic changes.
Increased pulmonary artery pressure may cause right-sided heart failure (cor pulmonale).

16. Changes in Alveolar Structure with Emphysema

18. Risk Factors for COPD (see chart 24-1, )
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
Tobacco smoke causes 80-90% of COPD cases! Damage the scavenger and cilliary cleansing mechanism, and increase goblet cells so increase mucous production.

19. Clinical Manifestation
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.

21. Typical Posture of a Person with COPD

22. 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

23. 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

24. Nursing Process Assessment: Health history
Inspection and exam findings
See Chart 24-2 and Chart 24-3
Review of diagnostic tests

25. Nursing Process: The Care of Patients with COPD- Diagnoses
Impaired gas exchange R\t V\Q inequality
ineffective airway clearance R\t increased mucous secretion
Ineffective breathing pattern R\t bronchospasm, mucus
Activity intolerance R\t fatigue, hypoxemia
Deficient knowledge regarding self care
Ineffective coping R\t anxiety, lower activity level

26. Collaborative Problems
Respiratory insufficiency or failure
Atelectasis
Pulmonary infection
Pneumonia
Pneumothorax
Pulmonary hypertension: Cor pulmonale- (Rt side heart failure)

27. Planning Promote smoking cessation Improve gas exchange
Maintain airway clearance
Improve breathing pattern
Improve activity tolerance
Increase knowledge
Enhance individual coping mechanism

28. 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

29. 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

30. Other Interventions Set realistic goals Avoid extreme temperatures
Enhancement of coping strategies
Monitor for and management of potential complications

31. Patient Teaching 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

32. Bronchiectasis and Asthma
Chapter 24

33. Bronchiectasis
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

34. 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;

35. 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.

38. Clinical Manifestations
Characteristic symptoms of Bronchiectasis include:
Chronic cough
Production of purulent sputum in copious amounts.
Many patients with this disease have hemoptysis.
Clubbing of the fingers also is common because of respiratory insufficiency.
Repeated episodes of pulmonary infection.

39. Assessment and Diagnostic Findings
Bronchiectasis is not readily diagnosed because the symptoms can be mistaken for those of simple chronic bronchitis.
A definite sign is offered by the prolonged history of productive cough, with sputum consistently negative for tubercle bacilli.
The diagnosis is established by a computed tomography (CT) scan, which demonstrates either the presence or absence of bronchial dilation.

40. Medical Management Treatment objectives are to:
- Promote bronchial drainage
- Clear excessive secretions from the affected portion of the lungs
- Prevent or control infection.
Postural drainage: draining the Bronchiectasis areas by gravity reduces the amount of secretions and the degree of infection.
Sometimes mucopurulent sputum must be removed by bronchoscopy.
Chest physiotherapy, including percussion and postural drainage, is important in secretion management.

41. 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
Bronchodilators: assist with secretion management.
Surgery: to conserve normal pulmonary tissue & avoid complications

42. 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
Patient and family teaching: to perform postural drainage & to avoid exposure to others with upper respiratory or other infections.
Teaching pt: early signs of respiratory infection & progression of disease (so appropriate treatment can be implemented promptly).
Assess pt nutritional status, & teach pt strategies to ensure adequate diet and energy conservation