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.