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COPDDescriptionCOPDDescription
Characterized by presence of airflow obstruction
Caused by emphysema or chronic bronchitis
Generally progressive May be accompanied by airway
hyperreactivity May be partially reversible
Characterized by presence of airflow obstruction
Caused by emphysema or chronic bronchitis
Generally progressive May be accompanied by airway
hyperreactivity May be partially reversible
Emphysema DescriptionEmphysema Description
Abnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles
Abnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles
Chronic Bronchitis DescriptionChronic Bronchitis Description
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
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
COPDCausesCOPDCauses
Cigarette smoking Primary cause of COPD*** Clinically significant airway obstruction
develops in 15% of smokers 80% to 90% of COPD deaths are related
to tobacco smoking > 1 in 5 deaths is result of cigarette
smoking
Cigarette smoking Primary cause of COPD*** Clinically significant airway obstruction
develops in 15% of smokers 80% to 90% of COPD deaths are related
to tobacco smoking > 1 in 5 deaths is result of cigarette
smoking
COPDCausesCOPDCauses
Cigarette smoking Nicotine stimulates sympathetic nervous
system resulting in: HR Peripheral vasoconstriction BP and cardiac workload
Cigarette smoking Nicotine stimulates sympathetic nervous
system resulting in: HR Peripheral vasoconstriction BP and cardiac workload
COPDCausesCOPDCauses Cigarette smoking
Compounds problems in a person with CAD Ciliary activity Possible loss of ciliated cells Abnormal dilation of the distal air space Alveolar wall destruction Carbon monoxide
O2 carrying capacity Impairs psychomotor performance and judgment
Cellular hyperplasia Production of mucus Reduction in airway diameter Increased difficulty in clearing secretions
Cigarette smoking Compounds problems in a person with CAD Ciliary activity Possible loss of ciliated cells Abnormal dilation of the distal air space Alveolar wall destruction Carbon monoxide
O2 carrying capacity Impairs psychomotor performance and judgment
Cellular hyperplasia Production of mucus Reduction in airway diameter Increased difficulty in clearing secretions
COPDCausesCOPDCauses
Secondhand smoke exposure associated with: Pulmonary function Risk of lung cancer Mortality rates from ischemic heart
disease
Secondhand smoke exposure associated with: Pulmonary function Risk of lung cancer Mortality rates from ischemic heart
disease
COPDCausesCOPDCauses
Infection Major contributing factor to the aggravation
and progression of COPD Heredity
-Antitrypsin (AAT) deficiency (produced by liver and found in lungs); accounts for < 1% of COPD cases
Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages
Infection Major contributing factor to the aggravation
and progression of COPD Heredity
-Antitrypsin (AAT) deficiency (produced by liver and found in lungs); accounts for < 1% of COPD cases
Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages
Emphysema PathophysiologyEmphysema Pathophysiology
Hyperinflation of alveoli Destruction of alveolar walls Destruction of alveolar capillary walls Narrowed airways Loss of lung elasticity
Hyperinflation of alveoli Destruction of alveolar walls Destruction of alveolar capillary walls Narrowed airways Loss of lung elasticity
Emphysema PathophysiologyEmphysema Pathophysiology
Two types: Centrilobular (central part of lobule)
Most common
Panlobular (destruction of whole lobule)
Usually associated with AAT deficiency
Two types: Centrilobular (central part of lobule)
Most common
Panlobular (destruction of whole lobule)
Usually associated with AAT deficiency
Emphysema PathophysiologyEmphysema Pathophysiology
Structural changes are: Hyperinflation of alveoli Destruction of alveolar capillary walls Narrowed, tortuous small airways Loss of lung elasticity
Structural changes are: Hyperinflation of alveoli Destruction of alveolar capillary walls Narrowed, tortuous small airways Loss of lung elasticity
Emphysema PathophysiologyEmphysema Pathophysiology
Small bronchioles become obstructed as a result of
Mucus Smooth muscle spasm Inflammatory process Collapse of bronchiolar walls
Recurrent infections production/stimulation of neutrophils and macrophages release proteolytic enzymes alveolar destruction inflammation, exudate, and edema
Small bronchioles become obstructed as a result of
Mucus Smooth muscle spasm Inflammatory process Collapse of bronchiolar walls
Recurrent infections production/stimulation of neutrophils and macrophages release proteolytic enzymes alveolar destruction inflammation, exudate, and edema
Emphysema PathophysiologyEmphysema Pathophysiology
Elastin and collagen are destroyed Air goes into the lungs but is unable to
come out on its own and remains in the lung
Causes bronchioles to collapse
Elastin and collagen are destroyed Air goes into the lungs but is unable to
come out on its own and remains in the lung
Causes bronchioles to collapse
Emphysema PathophysiologyEmphysema Pathophysiology
Trapped air hyperinflation and overdistention
As more alveoli coalesce, blebs and bullae may develop
Destruction of alveolar walls and capillaries reduced surface area for O2 diffusion
Compensation is done by increasing respiratory rate to increase alveolar ventilation
Hypoxemia usually develops late in disease
Trapped air hyperinflation and overdistention
As more alveoli coalesce, blebs and bullae may develop
Destruction of alveolar walls and capillaries reduced surface area for O2 diffusion
Compensation is done by increasing respiratory rate to increase alveolar ventilation
Hypoxemia usually develops late in disease
EmphysemaClinical ManifestationsEmphysemaClinical Manifestations
Dyspnea Progresses in severity Patient will first complain of dyspnea
on exertion and progress to interfering with ADLs and rest
Dyspnea Progresses in severity Patient will first complain of dyspnea
on exertion and progress to interfering with ADLs and rest
Emphysema Clinical ManifestationsEmphysema Clinical Manifestations
Minimal coughing with no to small amounts of sputum
Overdistention of alveoli causes diaphragm to flatten and AP diameter to increase
Minimal coughing with no to small amounts of sputum
Overdistention of alveoli causes diaphragm to flatten and AP diameter to increase
Emphysema Clinical ManifestationsEmphysema Clinical Manifestations
Patient becomes chest breather, relying on accessory muscles
Ribs become fixed in inspiratory position
Patient becomes chest breather, relying on accessory muscles
Ribs become fixed in inspiratory position
Emphysema Clinical ManifestationsEmphysema Clinical Manifestations
Patient is underweight (despite adequate calorie intake)
Patient is underweight (despite adequate calorie intake)
Chronic BronchitisPathophysiologyChronic BronchitisPathophysiology
Pathologic lung changes are: Hyperplasia of mucus-secreting glands
in trachea and bronchi Increase in goblet cells Disappearance of cilia Chronic inflammatory changes and narrrowing
of small airways Altered fxn of alveolar macrophages
infections
Pathologic lung changes are: Hyperplasia of mucus-secreting glands
in trachea and bronchi Increase in goblet cells Disappearance of cilia Chronic inflammatory changes and narrrowing
of small airways Altered fxn of alveolar macrophages
infections
Chronic BronchitisPathophysiologyChronic BronchitisPathophysiology
Chronic inflammation Primary pathologic mechanism
causing changes Narrow airway lumen and reduced
airflow d/t hyperplasia of mucus glands Inflammatory swelling Excess, thick mucus
Chronic inflammation Primary pathologic mechanism
causing changes Narrow airway lumen and reduced
airflow d/t hyperplasia of mucus glands Inflammatory swelling Excess, thick mucus
Chronic BronchitisPathophysiologyChronic BronchitisPathophysiology
Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
Chronic BronchitisPathophysiologyChronic BronchitisPathophysiology
Bronchioles are clogged with mucus and pose a physical barrier to ventilation
Hypoxemia and hypercapnia d/t lack of ventilation and O2 diffusion
Tendency to hypoventilate and retain CO2
Frequently patients require O2 both at rest and during exercise
Bronchioles are clogged with mucus and pose a physical barrier to ventilation
Hypoxemia and hypercapnia d/t lack of ventilation and O2 diffusion
Tendency to hypoventilate and retain CO2
Frequently patients require O2 both at rest and during exercise
Chronic Bronchitis PathophysiologyChronic Bronchitis Pathophysiology
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 More common with history of smoking
or asthma
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 More common with history of smoking
or asthma
Chronic BronchitisClinical ManifestationsChronic BronchitisClinical Manifestations
Earliest symptoms: Frequent, productive cough during
winter Frequent respiratory infections
Earliest symptoms: Frequent, productive cough during
winter Frequent respiratory infections
Chronic BronchitisClinical ManifestationsChronic BronchitisClinical Manifestations
Bronchospasm at end of paroxysms of coughing Cough Dyspnea on exertion History of smoking Normal weight or heavyset Ruddy (bluish-red) appearance d/t
polycythemia (increased Hgb d/t chronic hypoxemia)) cyanosis
Bronchospasm at end of paroxysms of coughing Cough Dyspnea on exertion History of smoking Normal weight or heavyset Ruddy (bluish-red) appearance d/t
polycythemia (increased Hgb d/t chronic hypoxemia)) cyanosis
Chronic BronchitisClinical ManifestationsChronic BronchitisClinical Manifestations
Hypoxemia and hypercapnia Results from hypoventilation and
airway resistance + problems with alveolar gas exchange
Hypoxemia and hypercapnia Results from hypoventilation and
airway resistance + problems with alveolar gas exchange
COPDComplicationsCOPDComplications
Pulmonary hypertension (pulmonary vessel constriction d/t alveolar hypoxia & acidosis)
Cor pulmonale (Rt heart hypertrophy + RV failure)
Pneumonia Acute Respiratory Failure
Pulmonary hypertension (pulmonary vessel constriction d/t alveolar hypoxia & acidosis)
Cor pulmonale (Rt heart hypertrophy + RV failure)
Pneumonia Acute Respiratory Failure
COPDDiagnostic StudiesCOPDDiagnostic Studies
Chest x-rays early in the disease may not show abnormalities
History and physical exam Pulmonary function studies
reduced FEV1/FVC and residual volume and total lung capacity
Chest x-rays early in the disease may not show abnormalities
History and physical exam Pulmonary function studies
reduced FEV1/FVC and residual volume and total lung capacity
COPDDiagnostic StudiesCOPDDiagnostic Studies
ABGs PaO2
PaCO2 (especially in chronic bronchitis) pH (especially in chronic bronchitis) Bicarbonate level found in late stages
COPD
ABGs PaO2
PaCO2 (especially in chronic bronchitis) pH (especially in chronic bronchitis) Bicarbonate level found in late stages
COPD
COPDCollaborative CareCOPDCollaborative Care
Smoking cessation Most significant factor in slowing the
progression of the disease
Smoking cessation Most significant factor in slowing the
progression of the disease
COPDCollaborative Care: Drug TherapyCOPDCollaborative Care: Drug Therapy
Bronchodilators – as maintenance therapy -adrenergic agonists (e.g. Ventolin)
MDI or nebulizer preferred Anticholinergics (e.g. Atrovent)
Bronchodilators – as maintenance therapy -adrenergic agonists (e.g. Ventolin)
MDI or nebulizer preferred Anticholinergics (e.g. Atrovent)
COPDCollaborative Care: Oxygen Therapy
COPDCollaborative Care: Oxygen Therapy
O2 therapy
Raises PO2 in inspired air Treats hypoxemia Titrate to lowest effective dose
O2 therapy
Raises PO2 in inspired air Treats hypoxemia Titrate to lowest effective dose
COPD Collaborative Care: Oxygen Therapy
COPD Collaborative Care: Oxygen Therapy
Chronic O2 therapy at home Improved prognosis Improved neuropsychologic function Increased exercise tolerance Decreased hematocrit Reduced pulmonary hypertension
Chronic O2 therapy at home Improved prognosis Improved neuropsychologic function Increased exercise tolerance Decreased hematocrit Reduced pulmonary hypertension
COPDCollaborative Care: Respiratory Therapy
COPDCollaborative Care: Respiratory Therapy
Breathing retraining Pursed-lip breathing
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
See text re how to teach
Breathing retraining Pursed-lip breathing
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
See text re how to teach
COPDCollaborative Care: Respiratory Therapy
COPDCollaborative Care: Respiratory Therapy
Huff coughing (Table 28-21) Chest physiotherapy – to bring secretions
into larger, more central airways Postural drainage Percussion Vibration
Huff coughing (Table 28-21) Chest physiotherapy – to bring secretions
into larger, more central airways Postural drainage Percussion Vibration
COPDCollaborative CareCOPDCollaborative Care
Encourage patient to remain as active
as possible
Encourage patient to remain as active
as possible
COPDCollaborative CareCOPDCollaborative Care
Surgical Therapy Lung volume reduction surgery Lung transplant
Surgical Therapy Lung volume reduction surgery Lung transplant
COPDCollaborative CareCOPDCollaborative Care
Nutritional therapy Full stomachs press on diaphragm causing
dyspnea and discomfort Difficulty eating and breathing at the same time
leads to inadequate amounts being eaten
Nutritional therapy Full stomachs press on diaphragm causing
dyspnea and discomfort Difficulty eating and breathing at the same time
leads to inadequate amounts being eaten
COPDCollaborative CareCOPDCollaborative Care
Nutritional therapy To decrease dyspnea and conserve energy Rest at least 30 minutes prior to eating Use bronchodilator before meals Select foods that can be prepared in advance 5-6 small meals to avoid bloating Avoid foods that require a great deal of chewing Avoid exercises and treatments 1 hour before and
after eating
Nutritional therapy To decrease dyspnea and conserve energy Rest at least 30 minutes prior to eating Use bronchodilator before meals Select foods that can be prepared in advance 5-6 small meals to avoid bloating Avoid foods that require a great deal of chewing Avoid exercises and treatments 1 hour before and
after eating
COPDCollaborative CareCOPDCollaborative Care
Nutritional therapy Avoid gas-forming foods High-calorie, high-protein diet is
recommended Supplements Avoid high carbohydrate diet to prevent
increase in CO2 load
Nutritional therapy Avoid gas-forming foods High-calorie, high-protein diet is
recommended Supplements Avoid high carbohydrate diet to prevent
increase in CO2 load
Nursing ManagementNursing DiagnosesNursing ManagementNursing Diagnoses
Ineffective airway clearance Impaired gas exchange Imbalanced nutrition: less than body
requirements Disturbed sleep pattern Risk for infection
Ineffective airway clearance Impaired gas exchange Imbalanced nutrition: less than body
requirements Disturbed sleep pattern Risk for infection
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Health Promotion STOP SMOKING!!! Avoid or control exposure to occupational
and environmental pollutants and irritants Early detection of small-airway disease Early diagnosis of respiratory tract
infections
Health Promotion STOP SMOKING!!! Avoid or control exposure to occupational
and environmental pollutants and irritants Early detection of small-airway disease Early diagnosis of respiratory tract
infections
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Acute Intervention Required for complications like pneumonia,
cor pulmonale, and acute respiratory failure
Acute Intervention Required for complications like pneumonia,
cor pulmonale, and acute respiratory failure
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Pulmonary rehabilitation
Control and alleviate symptoms of pathophysiologic complications of respiratory impairment
Ambulatory and Home Care Pulmonary rehabilitation
Control and alleviate symptoms of pathophysiologic complications of respiratory impairment
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Teach patient how to achieve optimal capability
in carrying out ADLs Physical therapy Nutrition Education
Activity considerations Exercise training of upper extremities to help
improve function and relieve dyspnea
Ambulatory and Home Care Teach patient how to achieve optimal capability
in carrying out ADLs Physical therapy Nutrition Education
Activity considerations Exercise training of upper extremities to help
improve function and relieve dyspnea
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
n Ambulatory and Home Care n Explore alternative methods of ADLs
Encourage patient to sit while
performing activities Coordinated walking
n Ambulatory and Home Care n Explore alternative methods of ADLs
Encourage patient to sit while
performing activities Coordinated walking
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Slow, pursed-lip breathing After exercise, wait 5 minutes before
using -adrenergic agonist MDI
Ambulatory and Home Care Slow, pursed-lip breathing After exercise, wait 5 minutes before
using -adrenergic agonist MDI
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Sexual activity
Plan during part of day when breathing is best Slow, pursed-lip breathing Refrain after eating or other strenuous
activity Do not assume dominant position Do not prolong foreplay
Ambulatory and Home Care Sexual activity
Plan during part of day when breathing is best Slow, pursed-lip breathing Refrain after eating or other strenuous
activity Do not assume dominant position Do not prolong foreplay
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Sleep
Nasal saline sprays Decongestants Nasal steroid inhalers Long-acting theophylline
Decreases bronchospasm and airway obstruction
Ambulatory and Home Care Sleep
Nasal saline sprays Decongestants Nasal steroid inhalers Long-acting theophylline
Decreases bronchospasm and airway obstruction
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
Ambulatory and Home Care Psychosocial considerations
Guilt Depression Anxiety Social isolation Denial Dependence Use relaxation techniques and support groups
Ambulatory and Home Care Psychosocial considerations
Guilt Depression Anxiety Social isolation Denial Dependence Use relaxation techniques and support groups