Copd

21
COPD

description

NSG

Transcript of Copd

  • COPD

  • DefinitionA disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema; the airflow obstruction is generally progressive, may be accompanied by airflow hyperactivity, and may be viewed as partially reversible.Includes emphysema and chronic bronchitis

  • Types of COPDEmphysemaPermanent and destructive enlargement of airspaces distal to the terminal bronchioles without obvious fibrosis and with loss of normal architectureAlways involves clinically significant airflow limitation.pink pufferChronic BronchitisPresence of a cough productive of sputum not attributable to other causes on most days for at least 3 months over 2 consecutive yearsMay be present in the absence of airflow limitation.blue bloater

  • COPD

  • Pathogenesis of COPDIncreased number of activated polymorphonuclear cells and macrophages produce elastases (such as human leukocyte elastase), resulting in lung destruction.Increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells

  • Pathogenesis of COPD (cont.)Emphysema3 morphologic patterns:Centricacinar:focal destruction limited to the respiratory bronchioles and the central portions of acinus associated with cigarette smoking most severe in the upper lobes Panacinar:involves the entire alveolus distal to the terminal bronchiole develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency most severe in the lower lung zones Distal acinar:Also called paraseptalleast common form involves distal airway structures, alveolar ducts, and sacs localized to fibrous septa or to the pleura and leads to formation of bullae (can result in pneumothorax)Chronic BronchitisMucus gland enlargementAirway atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening Respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucous plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis Airway walls to deform and narrow the airway lumen

  • Risk FactorsSMOKING!48 million smokers in the U.S.3000 new people take up smoking dailyNearly all patients with symptomatic COPD are current or former smokers10-20% of smokers will develop symptomatic COPD.In men who smoke one pack/day, the drop in FEV1 per year was 9 mL more than in non-smokersOccupational ExposuresDusts, gases, fumesAlpha1-antitrypsin deficiencyAlpha1-antitrypsin is an important protease inhibitor that usually presents elastases from causing lung destruction

  • SymptomsDyspneaCough (usually worse in morning, sputum production)WheezingCyanosisRight heart failureWeight loss, anorexia

  • Physical ExamRR, HR, O2 saturationGen: Barrel-chest, accessory muscle useCV: Quiet heart soundsResp: Decreased breath sounds, wheezing, rhonchi, crackles

  • LabsCBC: Hgb/HctABG: pH, pCO2Chemistry: HCO3

  • Emphysema

  • Diagnosis of COPDLook for secondary polycythemia: Hct >52% in males, Hct>47% in femalesMeasure alpha1-antitrypsin levels in all patients 40 years or younger, or in those with family history.Hyperinflation see on chest x-rayBullae seen on Chest x-ray or CT scan

  • Pulmonary Function Tests

  • Diagnosis of COPD Pulmonary Function Tests Forced Expiratory Volume for 1 second (FEV1)FEV1/FVC (Forced Vital Capacity) ratio Total Lung Capacity (TLC) Forced Residual Capacity (FRC) Residual Volume (RV) Vital Capacity (VC)

  • Pulmonary Function Tests

  • COPD ExacerbationTypically manifest as increased sputum production, more purulent sputum and worsening of dyspnea.Although infectious etiologies account for most exacerbations, exposure to allergens, pollutants or inhaled irritants may also play a role. Bacterial infection is a factor in 70 to 75 percent of exacerbations, with up to 60 percent caused by Streptococcus pneumoniaeHaemophilus influenzaeMoraxella catarrhalis Antibiotic therapy has a small but important effect on clinical recovery and outcome. Respiratory fluoroquinolone (Levofloxacin, Moxifloxacin)Ceftriaxone + azithromycinShort courses of systemic corticosteroids may provide important benefits in patients with exacerbations of COPD. Oxygen therapy to keep saturation Between 90-93%Non-invasive ventilation such as BiPAP can be helpful in avoiding intubation/mechanical ventilation.

  • Treatment of COPDSMOKING CESSATION!Short-acting bronchodilatorsalbuterolLong-acting bronchodilatorsalmeterolCombination of anti-cholinergic and -agonist bronchodilatorIpratropium + albuterol (combivent)Tiotropium (spiriva)Methylxanthines (Theophylline)Has anti-inflammatory affect, and improves respiratory muscle function, stimulates the respiratory center, and promotes bronchodilation Adverse effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and seizures Inhaled corticosteroidsFluticasone (Flovent), budesonide (Pulmicort)Combination of Inhaled corticosteroid and long-acting -agonist Fluticasone + salmeterol (Advair)Oral Corticosteroids

  • Treatment of COPD (cont.)Oxygen TherapyContinous oxygen has been shown to cut mortality in half or decrease morbidity when compared with non-continous oxygenContinuous (24 hours/day)Resting Pa02 of 55 mm HG, or Resting oxygen saturation < 88%Resting Pa02 of 56-59 mmHg or Oxygen Sat. 56)NoncontinuousDuring exercise when PaO2 is < 55 mmHg or Oxygen sat. < 88% with low level of exercise.During sleep if Pa02 is < 55 mmHg or Sa02 less than 88% with associated complications such as pulmonary hypertension, daytime somnolence, cardiac arrythmias.

  • Treatment of COPD (cont.)Pulmonary RehabilitationAimed at keeping patient conditioned with exercise, perception of dyspnea, quality of life and self-efficacy.SurgeryBullectomy Resection of large bullae compressing normal lung Lung volume reduction surgeryPneumonectomy of nonuniform emphysematous lungDouble lung transplantationCan be life-saving, but is costly, can be lack of donor availability and requires lifelong immunosuppression.

  • Treatment of COPD

  • Stages of COPD

    StageFEV1/FVC RatioFEV1 %Clinical FindingsAt Risk>0.7Patients who smoke, patients exposed to high pollutants, and patients with recurrent respiratory symptoms/infections. Give influenza and pneumonia vaccines.Mild < 0.7>80Add short-acting bronchodilator as neededModerate