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COPD Ms. Gardner NUR - 224

COPD Ms. Gardner NUR - 224. COPD. Chronic Obstructive Pulmonary Disease a slowly progressive obstruction of the airways currently is 4th leading cause of death the 12th leading cause of disability.

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COPD Ms. Gardner NUR - 224

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  1. COPDMs. GardnerNUR - 224

  2. COPD Chronic Obstructive Pulmonary Disease • a slowly progressive obstruction of the airways • currently is 4th leading cause of death • the 12th leading cause of disability. • 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.

  3. COPD -Pathophysiology • Airflow limitation is progressive and is associated with abnormal inflammatory response of the lungs to noxious agents. • This process causes airways to narrow  resistance to airflow increases and expiration becomes difficult or slow. • The result is a mismatch between alveolar ventilation and blood flow or perfusion  impaired gas exchange.

  4. COPD versus Asthma • Asthma is now considered a separate • reversible disorder • No longer under the diagnosis of COPD • Uncontrolled asthma over a • lifetime may result in COPD • COPD is not reversible

  5. CHRONIC BRONCHITIS • A disorder of excess bronchial mucus secretion • Productive cough • Cigarette smoking • Inhaled irritants • Mucous-secreting glands and goblet cells increase in number. • Ciliary function is reduced, bronchial walls thicken, bronchial airways narrow, and mucous may plug airways.

  6. PATHO – CHRONIC BRONCHITIS

  7. EMPHYSEMA • Impaired oxygen/carbon dioxide exchange • Decreased alveolar surface area • Hypoxemia result.

  8. EMPHYSEMA • Alveoli walls continue to breakdown, pulmonary capillary bed is reduced resistance to pulmonary blood flow is increased  forcing the ( R) ventricle to maintain a higher pressure in the pulmonary artery. • Increased pulmonary artery pressure may cause right-sided heart failure (corpulmonale).

  9. TYPICAL POSTURE-EMPHYSEMA

  10. RISK FACTORS • More common in Whites than Blacks • Affect men more frequently than women • Affects middle-aged and older adults • Tobacco smoke causes 80-90% of COPD cases! • Occupational exposure • Genetic abnormalities Alpha1-antitrypsin deficiency

  11. Cigarette Smoking • affect’s the respiratory tract ciliary cleansing mechanism • airflow is obstructed • irritation of the goblet cells/mucous glands  increase mucous production

  12. CLINICAL MANIFESTATIONS 3 primary symptoms • chronic cough • sputum production • dyspnea • Weight loss • Barrel chest • Pursed lip breathing

  13. CHARACTERISTICS CHEST WALL

  14. ASSESSMENT/DIAGNOSTIC FINDINGS • Health history • Pulmonary function test • Spirometry • ABG- PCO2 >45 / PaO2 60-80 • Screening – alpha 1 – antitrypsin deficiency • CBC – RBC/Hct. • Key factor dx. – patient’s history/responsiveness to bronchodilators

  15. COLLABORATIVE COMPLICATIONS • Respiratory insufficiency • Pneumonia • Chronic atelectasis • Pulmonary arterial hypertension (cor pulmonale)

  16. MEDICAL MANAGEMENT Risk reduction – • smoking cessation / most cost - effective intervention nicotine replacement – gum, inhaler, nicotine patch, positive reinforcement/patient teaching • immunization against pneumococcal pneumonia/influenza vaccine  reduce the risk of respiratory infection • Pharmacologic Therapy

  17. MEDICAL MANAGEMENT Bronchodilators • Delivered – meter-dose inhalers dry powder inhalers spacer holding chambers nebulizers

  18. DRUG THERAPYBronchodilators • Beta2-Adrenergic agonists Proventil (albuterol) Alupent (metaproterenol) Brethine (terbutaline) • Anticholinergics Atrovent (ipratropium bromide) • Methylxanthines Aminophylline (Phyllocontin) Theophylline (Slo-bid; Theo-Dur) • Combination meds

  19. DRUG THERAPY Corticosteriods • May improve the symptoms of COPD  do not slow the decline of lung function • Short term therapy may improve pulmonary function and exercise tolerance . • Long term therapy not recommended Other medications • antibiotics, mucolytic agents, antitussive agents,

  20. OXYGEN THERAPY • Long term continuous therapy, during exercise, prevent acute dyspnea, during exacerbation • Goal to improve mental functioning and quality of life and reduce the work load of breathing • O2 sat -90% • Low flow devices most common • COMPLICATIONS of O2 THERAPY to much O2  CO2 retention

  21. COPDOTHER TREATMENTs Surgical Management Bullectomy Lung Volume Reduction Surgery (LVRS) Transplant

  22. PATIENT EDUCATION • Breathing exercises • Activity pacing • Oxygen therapy • Nutrition therapy • Coping measures

  23. COpdNursing diagnoses • Ineffective airway clearance • Impaired gas exchange • Imbalanced nutrition • Risk for infection

  24. Home/ Community • Knowledge of s/s of infection • Increase exercise tolerance and prevent further loss of pulmonary function • Avoid extremes of heat and cold • Avoid stress/emotional disturbances • Demonstrate how to use MDI prior to discharge • Smoking cessation • Utilize resources – home care, support groups, organizations -> American Lung Association

  25. ASTHMA • Chronic inflammatory disease of the airways  episodes of wheezing, breathlessness, chest tightness, and coughing. • Most episodes of asthma ”attacks” are brief • Acute episodes usually reverse either spontaneously or with treatment

  26. ASTHMA • Affects more than 22 million people • Accounts for more than 497, 000 hospitalizations annually • Common chronic disease of children – occurs at any age • More common in women than men • Patients may experience symptom – free periods alternating with acute exacerbations  last from minutes to hours, to days.

  27. ASTHMA Pathophysiology • airways are in a persistent state of inflammation • during this period, neutrophils, and lymphocytes play a role in the inflammation of asthma. • when activated they produce chemicals that enhance the inflammatory response  increase blood flow, vasoconstriction • inflammation progresses  airway edema, bronchoconstriction and mucous secretion - narrows the airway

  28. ASTHMA CONT’D • resistance increases, limiting airflow and increasing the work of breathing. • trapped air mixes with inspired air in the alveoli  affecting gas exchange  hypoxemia • hypoxemia  hyperventilation  decrease in PaCO2  respiratory alkalosis

  29. ASTHMA • Predisposing factors/Triggers: • exposure to allergens • inhaled irritants • respiratory tract infection • stress, medications, exercise

  30. ASTHMA Clinical manifestations • Chest tightness, non-productive cough, dyspnea, wheezing • Often occurs at night or early in morning • Onset • Attack may subside rapidly or persist for hours/days • During an attack

  31. ASTHMA Assessment/Diagnostic findings • Episodic symptoms of airflow obstruction • Positive family history • Pulmonary function test • ABGs

  32. ASTHMA Preventive Measures • Avoiding allergens/environmental triggers • Modifying home environment • Early treatment of respiratory tract infection

  33. ASTHMA Medical Management /Medications therapy • Quick relief medications • Long acting medications

  34. ASTHMA Quick relief medications • Beta2- agonists • albuterol (Proventil) /levalbuterol (Xopenex) • Administered by MDI/DPI • Act within minutes • Tachycardia, nervousness and muscle tremors • Monitor v/s prior to, during, and after treatment

  35. ASTHMA Anticholinergic medications • Prevent bronchoconstriction • Ipratropium bromide (Atrovent), Tiotropium bromide (Spriva) • Administered by MDI/inhaler • Act more slowly than adrenergic stimulants

  36. ASTHMA Systemic Corticosteroids • Solu-Medrol, Prednisone • very potent and effective anti-inflammatory • alleviate symptoms, improve airway function • initially used – inhaled form  side effect thrush • side effects

  37. ASTHMA Long-term medications Methylxanthines -Theophylline • Relaxes bronchial smooth muscle • Monitor serum theophylline levels (10-20ug/mL) Mast Cell Stablizers • Cromolyn sodium(Intal), nedrocromil(Tilade) • Decreases inflammation, prevents bronchospasm effects • Monitor for coughing, skin rash, unpleasant taste

  38. ASTHMA Leukotriene Modifiers • Montelukast (Singulair), zafirlukast (Accolate) • Oral medications – reduces the inflammatory response in asthma, improves lung function • Affects the metabolism and secretion of other medication – warfarin, theophylline • May cause liver toxicity • Administer with meals

  39. ASTHMA Management of Exacerbations • Early treatment and education • Quick – acting beta 2 adrenergic agonist • Systemic corticosteroids’ • Oxygen supplementation • Antibiotics • Peak Flow Monitoring

  40. ASTHMA Peak expiratory flow monitoring • measures the highest airflow during a forced expiration • establishes the patient’s personal best or normal PERF • value is used to evaluate the severity of airway obstruction • Traffic signals are used for simplicity – green (80 to 100%) yellow 50-80% red 50 % or less

  41. ASTHMA Nursing management – depends on severity of symptoms • Acute asthma attacks cause – fear as breathing becomes more difficult  hypoxemia • Priority during an attack – improve airway clearance and reduce fear and anxiety • Teach about prevention of future attacks and home management

  42. ASTHMA • Ineffective airway clearance • Anxiety • Community based - care

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