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69 Cards in this Set

  • Front
  • Back
Characterized by presence of airflow obstruction
Caused by emphysema or chronic bronchitis or both
Generally progressive
May be accompanied by airway hyperreactivity
May be partially reversible
4th leading cause of death in U.S
Exposure to tobacco smoke is the Primary cause of COPD in the U.S.
Abnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles without obvious fibrosis
Presence of chronic productive cough for
3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded
chronic bronchitis
Cigarette Smoking most significant cause of COPD
Clinically significant airway obstruction develops in 15% of smokers
80% to 90% of COPD deaths in the U.S. are related to tobacco smoking
More than one out of every five deaths in the U.S. is the result of cigarette smoking
Approximately 4000 chemicals and gases are inhaled into the lungs when smoking
Nicotine acts as a stimulant to the sympathetic nervous system
Compounds problems in a person with CAD
¯ Ciliary activity -can't clear mucous well
Possible loss of ciliated cells
Increased HR and BP-peripheral vasoconstriction
Production of mucus -more mucus and smaller airway to clear secretions
Reduction in airway diameter
Increased difficulty in clearing secretions
Abnormal dilation of the distal air space
Alveolar wall destruction
Stimulatory effect of nicotine increases the heart’s demand for O2
Cellular hyperplasia
Carbon monoxide-from smoking
¯ O2 carrying capacity
Impairs psychomotor performance and judgment

Involuntary smoke exposure (secondhand smoke) associated with:
¯ Pulmonary function
­ Risk of lung cancer
­ Mortality rates from ischemic heart disease
Major contributing factor to the aggravation and progression of COPD
Recurring infections occur more in people with COPD
Recurring infections impair normal defense mechanisms
COPD infection
protein normally stop prolytic enzyme from being so rough on lungs
a-Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD
AAT deficiency accounts for < 1% of COPD in the U.S.
AAT is a produced by the liver and normally found in the lungs
Leads to premature emphysema
Emphysema results in lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages
Level of AAT is controlled by a pair of autosomal codominant genes
People with this type of emphysema are primarily of northern European origin
COPD heredity
Some degree of emphysema is common
Gradual loss of elastic recoil
Lungs become rounded and smaller
Loss in alveolar supporting structures
Loss of intraalveolar septum decreases number of functional alveoli
Thinner alveolar walls contribute to loss of septal tissue and alveolar capillaries
Arterial O2 levels decrease
Thoracic cage changes from osteoporosis and calcification of costal cartilages
decrease compliance of chest wall; increase work of breathing
COPD and Aging
Hyperinflation of alveoli
Destruction of alveolar walls
Destruction of alveolar capillary walls
Narrowed airways
Loss of lung elasticity

Destruction of alveolar walls allow to breathe in but not out so have air trapping so can't exhale as efficiently as should d/t loss of lung elasticity and narrowed airways
Two types:
emphysema patho
ones closer to bronchus are ones trapping air
Respiratory bronchioles enlarge
Walls are destroyed
Bronchioles become confluent
Often associated with chronic bronchitis
More common than panlobular
Centrilobular emphysema
)-all alveoli are trapping air
Affects bronchioles, alveolar ducts and sacs, and alveoli
Progressive loss of lung tissue
¯ Alveolar-capillary surface area
Usually found in persons with AAT deficiency
Panlobular emphysema
Difficult to distinguish the two types
Two types may exist at the same time
severe emphysema
Small bronchioles become obstructed as a result of mucus
Smooth muscle spasm
Inflammatory process
Collapse of bronchiolar walls
Recurrent infectious processes lead to increased production and stimulation of neutrophils and macrophages
Proteolytic enzymes released by neutrophils and macrophages
Destruction of alveolar tissue ®
Exudate formation
Elastin and collagen are destroyed
Results in no pull or traction on the walls of the bronchioles
Air goes into the lungs but is unable to come out on its own and remains in the lung
Causes bronchioles to collapse
Trapped air ® hyperinflation and overdistention-air is trapped d/t lack of recoil. air can't get out b/c of bad airways
As more alveoli collapse, blebs and bullae may develop-bleb=airfilled space
Surface area for O2 diffusion in the blood decreases
Compensation is done by increasing respiratory rate to increase alveolar ventilation
Hypoxemia usually develops late in disease
as more air comes in bronchioles collapse causing less airspace
mucus secreting glands overproducing in trachea and bronchi-normal alveoli
Hyperplasia of mucus-secreting glands
in the trachea and bronchi
Increase in goblet cells
Disappearance of cilia-no cilia to get rid of extra mucus
Chronic inflammatory changes and narrowing of small airways
Altered function of alveolar macrophages leading to increased bronchial infections
Frequently airways are colonized with microorganisms
Excess amounts of mucus are found and may occlude small bronchioles
Chronic bronchitis patho
Alveolar structures and capillaries are normal-but airways get thicker
Chronic inflammation
Primary pathologic mechanism in causing changes
Causes vasodilation, congestion, mucosal edema
Mucous glands become hyperplasic -alveolar walls full of mucus
Causes narrowing of airway lumen and diminished airflow
chronic bronchitis patho
Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
Mucus is a physical barrier to ventilation
Tendency to hypoventilate and retain CO2
Frequently patients require O2 both at rest and during exercise
Peribronchial fibrosis may also result from the healing process secondary to inflammation
Cough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretions
Bronchospasm frequently develops
Usually more common with history of smoking or asthma
chronic bronchitis patho
can have emphysema for years before dyspnea becomes significant
Progresses in severity
Patient will first complain of dyspnea on exertion and progress to interfering with ADLs and rest
Minimal coughing with no to small amounts of sputum
Overdistention (barrel chest) of alveoli causes diaphragm to flatten and AP diameter to increase
Patient becomes chest breather, relying on accessory muscles
Ribs become fixed in inspiratory position
Patient is characteristically underweight even when the patient has adequate calorie intake Protein-calorie malnutrition with loss of lean muscle mass and subcutaneous fat
Clinical Manifestations
Earliest symptoms:
Frequent, productive cough during winter
Frequent respiratory infections
Bronchospasm can occur at end of paroxysms of coughing
Cough usually exacerbated by respiratory irritants or cold air
Dyspnea on exertion
History of smoking is almost always present
Normal weight or heavyset
Ruddy appearance
Hypoxemia and hypercapnia
Result from hypoventilation and ­ airway resistance in addition to problems with alveolar gas exchange
Hemoglobin may reach 20 g/dl or more-causes ruddy appearance body produces more RBCs-polycythemia
Clinical Manifestations
Cor pulmonale-right sided heart failure
Pulmonary hypertension-causes heart failure d/t HTN

Right side of the heart must increase to push blood into the lungs
Right-sided heart failure develops
Subsequent intravascular volume expansion b/c blood can't be pumped to lungs
Systemic venous congestion
Heart sound changes to the second heart sound, right-sided ventricular diastolic S3 gallop, and early ejection click along left sternal border
Distended neck veins
Hepatomegaly with upper quadrant tenderness
Epigastric distress
Peripheral edema
Weight gain
COPD complications
Acute exacerbations of chronic bronchitis
Acute respiratory failure
Can be caused by cor pulmonale or discontinuation of bronchodilator or corticosteroid medication- R.sided heart failure
b-adrenergic blockers may exacerbate respiratory failure in patient with asthmatic component
Indiscriminate use of sedatives and narcotics may suppress respiratory drive and lead to respiratory failure

Peptic ulcer disease and GERD-occur with steroids pt. is on.
COPD complications
Chest x-rays early in the disease may not show abnormalities-later will show flat diaphram and larger airspace
History and physical exam
Pulmonary function studies
Typical findings include reduced FEV(forced expiratory velocity) /FVC(forced vital capacity) and increased residual volume and total lung capacity-d/t air trapping
Ratio of < 70% suggests presence of obstructive lung disease
COPD diagnostic studies
¯ PaO2-d/t decreased area for gas exchange
­ PaCO2 d/t air trapping making you acidotic
¯ pH respiratory acidosis
­ Bicarbonate level found in late stages COPD b/c can't compensate anymore
COPD diagnostic studies
Exercise test to determine O2 saturation in the blood and pulse oximetry
ECG can show signs of right ventricular failure
Goal: increased ventilation-reduce complication
COPD diagnostic studies
Smoking cessation
Accelerated decline in pulmonary function slows and function usually improves
Most significant factor in slowing the progression of the disease
COPD collaborative care
¯ Airway resistance and hyperinflation
Reduction in dyspnea and ­ in FEV
Given as maintenance therapy
b-adrenergic agonists
MDI or nebulizer
Preferred route of administration
Inhaled anticholinergics 1st line ex: albuterol, atrovent
Minimal side effects-increased HR, stimulates beta receptors on SNS, headaches, tremors-dry mouth headache, dry cough
Best taken on a regular basis
COPD drug therapy
¯ Airway resistance and hyperinflation
Reduction in dyspnea and ­ in FEV
Given as maintenance therapy
MDI or nebulizer
Preferred route of administration
b-adrenergic agonists
Minimal side effects-increased HR, stimulates beta receptors on SNS, headaches, tremors-dry mouth headache, dry cough
Best taken on a regular basis
1st line ex: albuterol, atrovent
Inhaled anticholinergics
Raises PO2 in inspired air
Treats hypoxemia
Classified as high- or low-flow systems
Simple Face Mask for Oxygen Administration
Plastic Face Mask with Reservoir Bag for Oxygen Administration
Humidification is commonly used
because O2 has a drying effect on the mucosa
Nebulizers provide humidified O2
O2 therapy
Deliver flows (15 to 20 L/min) of warm, humidified air through a nasal cannula or a transtracheal cannula
Increases exercise tolerance
CO2 narcosis-stop drive to breathe
O2 toxicity
Absorption atelectasis
complications of oxygen therapy
Improved prognosis
Improved neuropsychologic function
Increased exercise intolerance
Decreased hematocrit
Reduced pulmonary hypertension
Benefit of therapy should be evaluated when patient’s condition has stabilized
Short-term home O2 may be indicated for persisting hypoxemia after discharge
Long-term O2 therapy
Patients may receive O2 only during exercise and/or sleep
Periodic reevaluations are necessary for the patient who is using chronic supplemental O2 every 30 to 90 days
chronic O2 therapy at home
Nasal cannula
Reservoir cannula
Store O2 in a small reservoir during exhalation and can reduce flow requirements by 50%
Encourage patient to remain as active as possible
oxygen delivery systems
Lung volume reduction surgery
Lung transplantation
Single lung is most common technique
Prolongs life
Improves functional capacity
Enhances quality of life
Rejection and effects of immunosuppressive
therapy are obstacles
surgical therapy
Breathing retraining
Pursed-lip breathing-inhale through nose; exhale w/lips pursed (like whistling)
Prolongs exhalation and prevents bronchiolar collapse and air trapping
Diaphragmatic breathing
Focuses on using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rate
Can be achieved by assuming semi- Fowler’s position and placing one hand on the abdomen and the other on the chest and observing which moves
Lay back in semifowlers one hand on abdomen and one on chest-abd. out when inhale and hand on stomach should rise
respiratory therapy
Huff coughing-cough during exhalation-helps clear secretions
Can easily be taught
May help clear secretions ineffective coughing patterns do not
effective coughing
Postural drainage-uses gravity to rid secretions
Helps bring secretions into larger, more central airways
Postural drainage
Uses gravity to assist in bronchial drainage
Drainage positions are determined by involved areas of lung
Chest physiotherapy
-hands cupped and loosen secretions
Performed in the appropriate postural drainage position
Hands in a cup-like position, creating an air pocket between the patient’s chest and the hand
Hollow sound should be heard with flexion and extension of the wrist
Facilitates movement of thick mucus
Should not be performed over kidneys, sternum, spinal cord, or any tender area
Tensing the hand and arm muscles repeatedly
Pressing mildly with the flat of the hand on the affected area while the patient slowly exhales a deep breath
Facilitates movement of secretions to larger airways
Mild vibration tolerated better than percussion
Flutter mucus clearance device-used more with patients wtih CF
Handheld device
Provides expiratory pressure treatment for patients with mucus-producing conditions
Works by vibrating the airways, loosening the mucus from airway walls
Intermittently increases interbronchial pressure, helping to maintain the patency of the airway
Accelerates expiratory airflow
Used in place of CPT in patients where it is contraindicated
should breathe slow and deep with meds-cough when done
Powered by a compressor air or O2 generator
Medication is nebulized depending on factors such as droplet size
Aerosol-nebulization therapy
Full stomachs press on diaphragm causing dyspnea and discomfort
Difficulty eating and breathing at the same time leads to inadequate amounts being eaten
Decrease dyspnea and conserve energy
Rest at least 30 minutes prior to eating-right up until meals
Use bronchodilator
Select foods that can be prepared in advance
Patient should eat 5-6 small meals to avoid feeling bloated (caused by swallowing air)
Avoid foods that require a great deal of chewing
Avoid exercises and treatments 1 hour before and after eating
Avoid gas-forming foods
High-calorie, high-protein diet is recommended
Avoid high carbohydrate diet to prevent increase in CO2 load
Fluids (intake of 3L/day) should be taken between meals
nutritional therapy
Health History
Exposure to chemical pollution
Respiratory irritants
Recurrent respiratory infections
Family history of respiratory disease
nursing assessment COPD
Weight loss or gain
Inability to perform ADLs
Swelling of the feet
Progressive dyspnea
Recurrent cough, sputum
Constipation, gas, bloating
Insomnia, sitting up to sleep
nursing assessment COPD
Rapid, shallow breathing
Inability to speak
Pursed-lip breathing
Wheezing, rhonchi, crackles
Use of accessory muscles
Cor pulmonale
Abnormal ABGs
nursing assessment COPD
Ineffective airway clearance
Impaired gas exchange
Imbalanced nutrition: less than body requirements
Disturbed sleep pattern
Risk for infection
nursing diagnosis COPD
Return of baseline respiratory function
Ability to perform ADLs
Relief from dyspnea
No complications related to COPD
Knowledge and ability to implement long- term regimen
Overall improved quality of life
Nursing Management

Avoiding or controlling exposure to occupational and environmental pollutants and irritants
Early detection of small-airway disease
Early diagnosis of respiratory tract infections
Awareness of family history of COPD and AAT deficiency
Health care workers should avoid smoking while caring for patients, as odor is offensive to patients
health promotion COPD
watch for complications
Required for complications like pneumonia, cor pulmonale, and acute respiratory failure
Once crisis is resolved, assess degree and severity of underlying respiratory problem
acute intervention COPD
Pulmonary rehabilitation-often very effective-structured prgram can attend
Control and alleviate symptoms of pathophysiologic complications of respiratory impairment
Teach patient how to achieve optimal capability in carrying out ADLs
Physical therapy
ambulatory and home care COPD
Activity considerations
Exercise training of upper extremities to help improve function and relieve dyspnea
Alternative methods of ADLs explored
Encourage patient to sit while
performing activities
Coordinated walking
Slow, pursed-lip breathing
After exercise, wait 5 minutes before using b-adrenergic agonist MDI
Keep diary of activity to see progress
Sexual activity
Plan during part of day when breathing is best
Slow, pursed-lip breathing
Refrain from activity after eating or other strenuous activity
Do not assume dominant position
Do not prolong foreplay
Nasal saline sprays
Nasal steroid inhalers
Long-acting theophylline
Decreases bronchospasm and airway obstruction
ambulatory and home care COPD
Psychosocial considerations
Social isolation
Use relaxation techniques and support groups
Discourage moving to places above 4000 ft.
No significant benefit to moving to a different climate
psychological considerations COPD
Expected outcomes
Normal breath sounds
Effective coughing
Return of PaO2 to normal range for patient
Improved mental status
Maintenance of normal body weight
Normal serum protein levels
Feeling of being rested
Improvement in sleep pattern
Awareness of need to seek medical attention
Behaviors minimizing risk of infection
No infection
nursing management COPD
Not disease, a condition caused by something else

Results from inadequate gas exchange
Insufficient O2 transferred to the blood
Hypoxemia-not enough O2 to tissues (PaO2 < 60mmHg on 60% O2)
Inadequate CO2 removal
Hypercapnia-can't get rid of CO2 (PaCO2 > 45mmHg and pH < 7.35)
Not a disease but a condition
Result of one or more diseases involving the lungs or other body systems
Hypoxemic respiratory failure
Hypercapnic respiratory failure
Acute respiratory failure
Causes: tramua, emphysema, asthma, pulmonary edema, pneumonia
hypoxemic respiratory failure
PaO2 of 60 mm Hg or less
Inspired O2 concentration of 60% or greater
hypoxemic respiratory failure
Causes: COPD, drug overdose, CNS disease, MS, gamorea

PaCO2 above normal (>45 mm Hg)
Acidemia (pH <7.35)
Hypercapnic Respiratory Failure
V/Q mismatch-V=ventilation Q=perfussion should be equal. Air in alveoli & blood going into alveolus
COPD-ventilation-makes alveoli walls collapse
Pneumonia-ventilation-mucus & infection in way of air exchange
Pulmonary embolus-perfussion
causes hypoxemic respiratory failure
Shunt-blood goes through heart but doesn't get oxygenated.
Anatomic shunt-septal defect-blood R--> L side heart
Intrapulmonary shunt-pulmonary capillaries with no gas exchange
Extreme V/Q mismatch
causes hypoxemic respiratory failure
Diffusion limitation-problem in ARDS
Severe emphysema
Recurrent pulmonary emboli-no gas diffusion d/t thicker walls
Pulmonary fibrosis-thick alveoli & perfussion cant' take place
Hypoxemia present during exercise
cause hypoxemic respiratory failure
Alveolar hypoventilation
Restrictive lung disease
CNS disease
Chest wall dysfunction
Neuromuscular disease
causes hypoxemic respiratory failure
Interrelationship of mechanisms
Combination of two or more physiologic mechanisms
causes hypoxemic respiratory failure
getting rid of CO2 is problem; gets enough O2

Airways and alveoli-obstuction and airtrapping can't get rid of CO2
Chronic bronchitis
Cystic fibrosis
cause of hypercapnic respiratory failure
getting rid of CO2 is problem; gets enough O2
Imbalance between ventilatory supply and demand
Airways and alveoli-obstuction and airtrapping can't get rid of CO2
Chronic bronchitis
Cystic fibrosis
Central nervous system-suppress drive to breathe not breathing off CO2
Drug overdose
Brainstem infarction
Spinal cord injuries
Chest wall-can't expand fully-don't have unresticted movement so can't breathe out fully.
Flail chest
Mechanical restriction
Muscle spasm
Neuromuscular conditions
Muscular dystrophy
Multiple sclerosis
Hypercapnic Respiratory Failure
Etiology and Pathophysiology
Major threat is the inability of the lungs to meet the oxygen demands of the tissues or tissue can't use oxygen you are getting
tissue oxygen needs
Sudden or gradual onset-sudden onset poorly tolerated
A sudden ¯ in PaO2 or rapid ­ in PaCO2 is a serious condition
When compensatory mechanisms fail, respiratory failure occurs
Signs may be specific or nonspecific- decreased LOC, restlessness
Severe morning headache-d/t increased CO2, vasodilation & more blood in head causing HA
Late sign
Tachycardia and mild hypertension
Early signs
Consequences of hypoxemia and hypoxia
Metabolic acidosis and cell death
¯ Cardiac output
Impaired renal function- d/t decreased O2 to kidneys
Specific clinical manifestations
Rapid, shallow breathing pattern as you decompensate it will slow down
Tripod position
Pursed-lip breathing
Change in I:E ratio
Clinical manifestations respiratory failure
Physical assessment--crackles, absent lung sounds, rubs
ABG analysis- increased CO2, decreased O2
Chest x-ray-COPD, pneumonia, trauma
Serum electrolytes
V/Q lung scan
Pulmonary artery catheter (severe cases)
cultures-sputum, blood
Diagnostic studies respiratory failure
Nursing Assessment
Past health history-TB, pneumonia, COPD
Sleep pattern changes
nursing assessment and management respiratory failure