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Chronic Obstructive Pulmonary Disease (COPD)
COPDDescriptionCharacterized by presence of airflow obstructionCaused by emphysema or chronic bronchitisGenerally progressive May be accompanied by airway hyperreactivityMay be partially reversible
Emphysema DescriptionAbnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles
Chronic Bronchitis DescriptionPresence 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
COPDCausesCigarette smokingPrimary cause of COPD***Clinically significant airway obstruction develops in 15% of smokers80% to 90% of COPD deaths are related to tobacco smoking> 1 in 5 deaths is result of cigarette smoking
COPDCausesCigarette smokingNicotine stimulates sympathetic nervous system resulting in: HR Peripheral vasoconstriction BP and cardiac workload
COPDCausesCigarette smokingCompounds problems in a person with CAD Ciliary activity Possible loss of ciliated cellsAbnormal dilation of the distal air spaceAlveolar wall destructionCarbon monoxide O2 carrying capacityImpairs psychomotor performance and judgmentCellular hyperplasia Production of mucus Reduction in airway diameterIncreased difficulty in clearing secretions
COPDCausesSecondhand smoke exposure associated with: Pulmonary function Risk of lung cancer Mortality rates from ischemic heart disease
COPDCausesInfectionMajor contributing factor to the aggravation and progression of COPDHeredity-Antitrypsin (AAT) deficiency (produced by liver and found in lungs); accounts for < 1% of COPD casesEmphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages
Pathophysiology of Chronic Bronchitis and EmphysemaFig. 28-7
Emphysema Pathophysiology
Hyperinflation of alveoliDestruction of alveolar wallsDestruction of alveolar capillary wallsNarrowed airwaysLoss of lung elasticity
Emphysema PathophysiologyTwo types:Centrilobular (central part of lobule)Most common
Panlobular (destruction of whole lobule)Usually associated with AAT deficiency
Emphysema PathophysiologyStructural changes are:Hyperinflation of alveoliDestruction of alveolar capillary wallsNarrowed, tortuous small airwaysLoss of lung elasticity
Emphysema PathophysiologySmall bronchioles become obstructed as a result of MucusSmooth muscle spasmInflammatory processCollapse of bronchiolar wallsRecurrent infections production/stimulation of neutrophils and macrophages release proteolytic enzymesalveolar destruction inflammation, exudate, and edema
Emphysema PathophysiologyElastin and collagen are destroyedAir goes into the lungs but is unable to come out on its own and remains in the lungCauses bronchioles to collapse
Emphysema PathophysiologyTrapped air hyperinflation and overdistentionAs more alveoli coalesce, blebs and bullae may developDestruction of alveolar walls and capillaries reduced surface area for O2 diffusion Compensation is done by increasing respiratory rate to increase alveolar ventilationHypoxemia usually develops late in disease
EmphysemaClinical Manifestations
Dyspnea Progresses in severityPatient will first complain of dyspnea on exertion and progress to interfering with ADLs and rest
Emphysema Clinical ManifestationsMinimal coughing with no to small amounts of sputum
Overdistention of alveoli causes diaphragm to flatten and AP diameter to increase
Emphysema Clinical Manifestations
Patient becomes chest breather, relying on accessory musclesRibs become fixed in inspiratory position
Emphysema Clinical ManifestationsPatient is underweight (despite adequate calorie intake)
Chronic BronchitisPathophysiologyPathologic lung changes are:Hyperplasia of mucus-secreting glands in trachea and bronchiIncrease in goblet cellsDisappearance of ciliaChronic inflammatory changes and narrrowing of small airwaysAltered fxn of alveolar macrophages infections
Chronic BronchitisPathophysiologyChronic inflammation Primary pathologic mechanism causing changesNarrow airway lumen and reduced airflow d/t hyperplasia of mucus glandsInflammatory swellingExcess, thick mucus
Chronic BronchitisPathophysiology
Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
Chronic BronchitisPathophysiology Bronchioles are clogged with mucus and pose a physical barrier to ventilationHypoxemia and hypercapnia d/t lack of ventilation and O2 diffusionTendency to hypoventilate and retain CO2Frequently patients require O2 both at rest and during exercise
Chronic Bronchitis PathophysiologyCough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretionsBronchospasm frequently developsMore common with history of smoking or asthma
Chronic BronchitisClinical ManifestationsEarliest symptoms: Frequent, productive cough during winter Frequent respiratory infections
Chronic BronchitisClinical ManifestationsBronchospasm at end of paroxysms of coughingCoughDyspnea on exertion History of smokingNormal weight or heavyset Ruddy (bluish-red) appearance d/t polycythemia (increased Hgb d/t chronic hypoxemia))cyanosis
Chronic BronchitisClinical ManifestationsHypoxemia and hypercapnia Results from hypoventilation and airway resistance + problems with alveolar gas exchange
COPDComplicationsPulmonary hypertension (pulmonary vessel constriction d/t alveolar hypoxia & acidosis)Cor pulmonale (Rt heart hypertrophy + RV failure)PneumoniaAcute Respiratory Failure
COPDDiagnostic StudiesChest x-rays early in the disease may not show abnormalitiesHistory and physical examPulmonary function studiesreduced FEV1/FVC and residual volume and total lung capacity
COPDDiagnostic StudiesABGs PaO2 PaCO2 (especially in chronic bronchitis) pH (especially in chronic bronchitis) Bicarbonate level found in late stages COPD
COPDCollaborative CareSmoking cessationMost significant factor in slowing the progression of the disease
COPDCollaborative Care: Drug Therapy
Bronchodilators as maintenance therapy -adrenergic agonists (e.g. Ventolin)MDI or nebulizer preferredAnticholinergics (e.g. Atrovent)
COPDCollaborative Care: Oxygen TherapyO2 therapyRaises PO2 in inspired airTreats hypoxemiaTitrate to lowest effective dose
COPD Collaborative Care: Oxygen TherapyChronic O2 therapy at homeImproved prognosis Improved neuropsychologic functionIncreased exercise toleranceDecreased hematocrit Reduced pulmonary hypertension
COPDCollaborative Care: Respiratory TherapyBreathing retrainingPursed-lip breathingProlongs exhalation and prevents bronchiolar collapse and air trappingDiaphragmatic breathingFocuses on using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rateSee text re how to teach
COPDCollaborative Care: Respiratory TherapyHuff coughing (Table 28-21)Chest physiotherapy to bring secretions into larger, more central airwaysPostural drainagePercussionVibration
Positions for Postural DrainageFig. 28-16Positions for Postural Drainage
COPDCollaborative CareEncourage patient to remain as active as possible
COPDCollaborative CareSurgical TherapyLung volume reduction surgeryLung transplant
COPDCollaborative CareNutritional therapyFull stomachs press on diaphragm causing dyspnea and discomfortDifficulty eating and breathing at the same time leads to inadequate amounts being eaten
COPDCollaborative CareNutritional therapyTo decrease dyspnea and conserve energyRest at least 30 minutes prior to eatingUse bronchodilator before mealsSelect foods that can be prepared in advance5-6 small meals to avoid bloatingAvoid foods that require a great deal of chewingAvoid exercises and treatments 1 hour before and after eating
COPDCollaborative Care
Nutritional therapyAvoid gas-forming foodsHigh-calorie, high-protein diet is recommendedSupplementsAvoid high carbohydrate diet to prevent increase in CO2 load
Nursing ManagementNursing DiagnosesIneffective airway clearanceImpaired gas exchangeImbalanced nutrition: less than body requirementsDisturbed sleep patternRisk for infection
Nursing ManagementNursing Implementation
Health PromotionSTOP SMOKING!!!Avoid or control exposure to occupational and environmental pollutants and irritants Early detection of small-airway diseaseEarly diagnosis of respiratory tract infections
Nursing ManagementNursing Implementation
Acute InterventionRequired for complications like pneumonia, cor pulmonale, and acute respiratory failure
Nursing ManagementNursing Implementation
Ambulatory and Home CarePulmonary rehabilitationControl and alleviate symptoms of pathophysiologic complications of respiratory impairment
Nursing ManagementNursing Implementation
Ambulatory and Home Care Teach patient how to achieve optimal capability in carrying out ADLsPhysical therapy NutritionEducationActivity considerationsExercise training of upper extremities to help improve function and relieve dyspnea
Nursing ManagementNursing Implementation
Ambulatory and Home Care Explore alternative methods of ADLs Encourage patient to sit while performing activitiesCoordinated walking
Nursing ManagementNursing Implementation
Ambulatory and Home CareSlow, pursed-lip breathingAfter exercise, wait 5 minutes before using -adrenergic agonist MDI
Nursing ManagementNursing Implementation
Ambulatory and Home CareSexual activityPlan during part of day when breathing is bestSlow, pursed-lip breathingRefrain after eating or other strenuous activityDo not assume dominant positionDo not prolong foreplay
Nursing ManagementNursing Implementation
Ambulatory and Home CareSleepNasal saline sprays DecongestantsNasal steroid inhalers Long-acting theophylline Decreases bronchospasm and airway obstruction
Nursing ManagementNursing Implementation
Ambulatory and Home CarePsychosocial considerationsGuilt DepressionAnxiety Social isolation DenialDependenceUse relaxation techniques and support groups
Nursing ManagementNursing Implementation
Ambulatory and Home CareDiscourage moving to places above 4000 ft.