Gold Guideline

COPD Definition and Overview

4/25/2013 2:36:00 PM

Persistent airflow limitation associated with chronic inflammatory ( major contributing factor) response in airways and lung to noxious particles or gases. Irreversible disease. Exacerbations and comorbidities contribute to severity

Inhaled cigarette smoke or other noxious particles. o Induce parenchymal tissue destruction ( emphysema) destruction of lung parenchyma by inflammatory processes leads to loss alveolar attachment (gas exchanging surface) and decrease lung elastic recoil and increased in compliance. Irreversible enlargement of airspace (ACINAR) Destruction of walls w/o any obvious fibrosis spirometry test is useful for lung function reduced FEV1 and gas trapping during expiration causing hyperinflation. Reduces inspiratory capacity due to increase in residual volume. Increased dyspnea and impairment of intrinsic contractile properties of respiratory muscles. Bronchodilators reduce air trapping and decrease symptoms. Centrilobular: central/proximal part of acinar affected. More common and severe in upper lobes. Common among heavy smoker and more associated with chronic bronchitis Panacinar-distal region => poor outcome loss of septa ( decreased elastic recoil) goblet cell metaplasia more mucous production inflammatory infiltration ( neutrophils) more proteases which destroy alveolar smooth muscle hypertrophy pulmonary capillary destruction- pushing same amount of blood to smaller region. Not enough ventilation cause vasoconstriction since it matches perfusion with ventilation. o disrupt normal repair and defense mechanism ( small airway fibrosis or chronic bronchitis). Presence of cough and sputum production for 3 months in each of two consecutive years. Physiologic changes:

Mucus hypersecretion causing chronic productive cough might accompany by limiting airflow. Increases inflammation. Hypersecretion increased due to increase in goblet cell and proteases. Not all COPD pt have symptomatic mucus hypersecretion. Spirometry test for lung function might be normal Increase the risk/association: heart failure, lung cancer, Cor pulmonale Vagus nerve exposed; smooth muscle hypertrophy, airway hyperresponsivnes -> asthma components

Pertain to COPD in general: even though emphysema and chronic bronchitis have distinct anatomic/clinical characteristic. They are typically present in combinations in pt. Gas exchange abnormalities. Hypoxemia and hypercapnia due to worsening oxygen and CO2 transfer. Increase in CO2 retention Pulmonary hypertension. Develop late in COPD due to hypoxic vasoconstriction of small pulmonary arteries. This then cause structural changes like hyperplasia and smooth muscle hypertrophy/hyperplasia. Loss of pulmonary capillary bed in emphysema also contribute to pulmonary hypertension which leads to Right ventricular hypertrophy and eventually right cardiac failure Exacerbations: triggered by bacteria or viruses, environmental or unknown factors. Bacterial/viral infection have increased inflammation. Exacerbation has increased hyperinflation and gas trapping leading to dyspnea. Worsening VA/Q leading to hypoxemia. Other conditions ( pneumonia, thromboembolism, and acute cardiac failure) mimic/aggravate exacerbation. Systemic features: COPD have impact on hyperinflation, cardiac function, and gas exchange. Skeletal muscle wasting or dysfynction, cachexia, and initiate or worsen IHD, HF, osteoporosis, diabetes, metabolic syndrome, and depression (cant breath, stop activities, lead to depress), weight loss More prone to infection: not moving the secretions Expiration takes more energy for gas exchange.

Alter eating pattern; cant eat large meals -> nutritional abnormalities

Physical/anatomical changes due to COPD Hyperinflation of the lung due to trap air Chronic inflammation Change to chest wall configuration Airway hyperplasia and lead to atrophy of other tissue Stress muscle and atrophy Diaphragm become flat due to stress/trap air

Factors influencing development and progression Cigarette smoking is the best and most contributing risk factor o Dose related: age started, pack years, current smoking status Gene Alpha-1 antitrypsin, inhibitor of serine proteases. No antitrypsin = protease destroying/breaking down airway Oxidative stress not associated with initiation of problem but contribute to problem once it started. NO + production of free radicals forming proxinitrite Age and gender women are more susceptible to effect of tobacco than male. Age is cumulative of exposure throughout life Lung growth and development less birth weight, lower FEV1 Exposure to particles - cigarette smoker have higher prevalence. Other type of tobacco/soking are also risk factors. Second hand smoke. Smoking during pregnancy pose risk to fetus affecting lung growth and development and priming immune system o Occupational exposure, dusts and fumes. Wood, animal dung, indoor air pollution, urban air pollution. Socioeconomic status poverty might be due to nutrition, crowding, infections , or other things . Infections history of sever childhood respiratory infection Signs/symptoms: o ASK: occupation, live, history of repiratory infection, premature, a few years of sputum, color, mother smoke, smoke while pregnant, weight loss (progressively), fatigue, cough at night, chest tightness, pleuritic chest pain (pain during inhalation), Work/home area with pollution or chemical fumes, interfere with work, activities, sleep, etc. Depression (QOL). Smoking still, spirometery, taking or hospitalized for the symptoms, comordbities, family support, compliance, pulmonary rehab program

Diagnosis Consider COPD if these occur in pt age >40. Symptoms may precede airflow limitation for many years. Conversely, airflow limitation may occur w/o chronic symptoms o Dyspnea progressive, worse w/ exercise, persistent. Increased breathe, heaviness, air hunger, gasping o chronic cough may be intermittent and unproductive. Often first symptom. o sputum production any pattern of sputum indicate COPD. Sputum purulent reflect increase in inflammatory mediator -> onset of bacterial exacerbation o risk of factors for disease- smoke/heatin fuel/occupation dust/chemicals o FEV1/FVC <0.7 required for diagnosis and assessement for severity of COPD Other symptoms o Chest tightness/wheezing not symptom to exclude/confirm diagnosis of COPD. Increase in intercostal/accessory muscles. o Additional features in sever disease fatigue, weight loss in severe COPD and other disease (tuberculosis/lung cancer). Depression and/or anxiety common in COPD leads to increased risk of exacerbation or poorer health status. o o not a lot of abnormal detected results. - Cyanosis of blueness in the gums, mouth, oral, etc. but this is severe and late stage. o o - Clubbing- knuckle is bubbled up and prevent fingernails from touching. - Sign of lack of oxygen and can happen to those with heart or lung disease o o o o - Barrel chest- respiratory rate is higher -Accessory muscles are used due to diaphragm not functioning as well. - Need Spirometry tests -Increase baseline respiratory rate due to high in CO2 and needing to remove it faster hyperventilation -Persed lips to breath out to increase respiratory pressure to remove more CO2 expiratory Medical history assess

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Exposure to risk factor PMH asthma, allergy, sinusitis, nasal polyps or respiratory infection ar FH COPD or chronic respiratory disease History of exacerbation or previous hospitalization for respiratory disorder. Presence of comorbidities heart disease or osteoporosis Alpha-1 antitrypsin deficiency screening Oximetry and arterial blood gas measurement To see if they have CO2 retention and see what the O2 level is O2- just get saturation number ( if less than 90% then you will then youll need an arterial blood gas. (never in clinic)

Other diagnosis and assessment o o

Assessment Assessment of symptoms o mMRC or CAT Severity of the disease Airflow limitation

Table 2.5: Classification of Severity of Airflow Limitation in COPD (2013 GOLD Guidelines, page 14) Characteristics (POST-bronchodilator) FEV1 80% predicted FEV1 50-79% predicted FEV1 30-49% predicted FEV1 <30% predicted

Stage

In patients with FEV1/FVC < 70%: GOLD 1: Mild GOLD 2: Moderate GOLD 3: Severe GOLD 4: Very Severe

*first assess symptoms, then assess risk for gold classification and exacerbation history. Place patient on whichever is more severe. Hopistalization for COPD is automatic high risk* Impact of health status Risk of future events ( exacerbation, hospital admission, death) o Exacerbation- worsening of pts respiratory symptom beyond normal day-to-day variation. Worsening airflow limitation is associated with an increasing prevalence of exacerbation and risk of death. Comorbidities o Weight loss, nutritional abnormalities and skeletal muscle dysfunction (loss of cells and abnormal function of remaining cells). o CVD, metabolic, depression, lung cancer, osteoporosis Therapeutic Options key points o o o smoking cessation is important pharmacologic therapy reduce COPD symptoms and exacerbation no medication for COPD shown to modify long-term decline in lung function o influenza and pneumococcal vacs should offered to every COPD patient Pharmacologic Therapy for Stable Chronic COPD Reduce symptoms, frequency, severity of exacerbation. Does not help long term decline of lung function.

Treatment regimen depends on severity of symptoms, airflow limitation, severity of exacerbation, cost, and availability. Inhalation route inhalation technique is essential Nebulization only use when pt reports clear symptomatic benefit/severely overinflated/low flowrate Bronchodilators ( Beta-agonist, ACholinergic) o Increase FEV1, improve emptying of lungs, reduce dynamic hyperinflation. Given as needed or regular basis o Inhaled are preferred, choice of bronchodilators depends on patient response. o LABA are more effective than SABAs. Combined of bronchodilator from different classes may improve efficacy o Beta2-agonist Use of SABA as prn in patient who already have LABA has not supported evidence for additional benefit. Do not recommend Improve FEV, lung volume, dyspnea, health-related quality of life and exacerbation rate. No effect on mortality and rate of decline of lung function Indacaterol is better than salmeterol/formoterol but similar to tiotropium Adverse: tachycardia, tremors, arrhythmia, hypokalemia w/ thiazide o Anticholinergic Longer bronchodilation effect than Beta agonist Tiotropium is 24 hr and reduce exacerbation, hospitalization, symptoms, health status. Higher affinity for M1 and M3 Ipratropium: M1, M2, and M3 Adverse: ANTI-SLUDGE GI: reduction in gastric acid secretion and motility ( dyspepsia), constipation Oral: cough, bad taste, dryness of mouth Ocular: mydriasis, increase in intraocular pressure CV: increase HR( PNS is predominant tone) Respiratory: Upper Respiratory tract infection, sinusitis, rhinitis, epistaxis Hypersensitivity reaction

Respimat soft mist shown to increase risk of mortality.

** atropine (tertiary crosses CNS) Theophylline small therapeutic window, benefit near toxic dose. Seizures, cardiac arrhythmias. LAST LINE: do not USE IT

Methylxanthines

Corticosteroids Inhaled corticosteroids: show improves symptoms, lung function, and quality of life, and reduces frequency of exacerbation. Withdrawal from treatment lead to exacerbations. ICS increased risk of pneumonia Mono therapy inhaled corticosteroid if FEV1 <50% Combination ICS + Bronchodilator ICS + LABA more effective in pts with moderate very severe COPD. No mortality change PDE4 main cAMP-metabolizing enzyme in inflammatory and immune cells. PD4 has anti-inflammatory properties which inhibit release of mediators S/E ** KNOW IT** : diarrhea, nausea, decrease in appetite, back painm muscle spasm, headache, uncontrollable shaking of part of your body, dizziness Vaccine Influenza live/inactivated are recommended for COPD Pneumococcal vaccine are recommended for ALL COPD patient due to ICS Roflumilast reduces moderate/severe exacerbation in patient with ONLY CHRONIC BRONCHITIS PD4 inhibitor suppresses chronic mediator: neutrophils/macrophage

Non-Pharmacologic Therapies Goal: reduce symptom, improve quality of life, increase physical and emotional pulmonary rehabilitation for exercise deconditioning, altered mood states, muscle wasting, and weight loss o improve peak workload, oxygen consumption, endurance time Other Treatments

Oxygen Therapy o long term oxygen treatment >15 hours ONLY has been shown to increase survival in pt with severe hypoxemia. Key points o Identify/reduce risk factors are important in prevention/treatment of COPD. Smoking should quit o FEV1 is inadequate for impact of disease on pts. Assessment of symptoms and future risk of exacerbation should be used to manage stable COPD o Pharmacologic therapy: reduce symptoms, frequency and severity of exacerbation, improve health status and exercise tolerance. NO IMPROVEMENT ON DECLINE LUNG FUNCTION o o o o LABA and L-ACh are preferred over short. Inhaled are preferred over oral ICS + LABA/L-Ach is recommended for high risk exacerbation NEVER USE ICS MONOTHERAPY Roflumilast may useful to reduce exacerbation for pt with FEV < 50% with chronic bronchitis and frequent exacerbation o Influenza and pneumococcal are recommended for all pts. Tobacco smoke Avoid continued occupational exposure Indoor/outdoor air pollution FEV1 is poor descriptor of disease, pt symptoms and future risk must be evaluated with it. Identify and reduce exposure to risk factors o o o Pt: SaO2 88%, pulmonary hypertension, edema -> CHF Management of stable COPD

Treatment of Stable COPD o

Monitoring and Follow-up Measure o o spirometry once a year CAT score Q 2 3 months

Symptoms every and each visit about changes in symptoms since last visit: cough, sputum, breathlessness, fatigue, activity limitation, and sleep disturbances

Smoking status monitor pharmacotherapy and other medical treatment o o inhaler technique dosages, adherence, effectiveness, side effects

monitor exacerbation history o use of ER, increased need of bronchodilator, hospitalization monitor comorbidities

Management of Exacerbations ( ACUTE) Key points: Exacerbation is an acute event characterized by worsening patients respiratory symptoms that is not normal day-to-day Precipitated by mostly viral upper respiratory tract infection Diagnosis: acute change of symptoms ( baseline dyspnea, cough, sputum production) that is beyond normal day-today variation Goal: minimize impact, prevent subsequent exacerbation Treatment: SABA w/ or w/o S-ACH are preferred bronchodilators for exacerbation Additional treatment: Systemic corticosteroid and antibiotic can shorten recovery time, improve lung function ( FEV1) and PaO2, reduce early relapse, treatment failure, and hospital stay Prevention exacerbation: smoking cessation, influenza/pneumococcal vaccination, knowledge of current therapy including inhaler techniques, treatment with long acting bronchodilator with or w/o ICS, and treatment with PD4 inhibitor Definition An exacerbation of COPD is an acute event characterized by a worsening of the patients respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication Exacerbations of COPD can be precipitated by several factors. The most common causes appear to be respiratory tract infections (viral or bacterial. 1/3 exacerbation cannot be identified Frequent exacerbators are defined as two or more per year. Increase in usage of rescue bronchodilator Relies on clinical presentation of cute change in symptom that are not day to day o o o Dyspnea Cough Sputum production

Diagnosis

Will need a panel of biomarkers to get etiologic diagnosis

uses of accessory muscle, nasal flaring, paradoxical chest movement ( stomach going in when breathing in) Central cyanosis; edema development of heart failure; deteriorated mental status; hemodynamic instability severe tachy or major hypotension.

Assessment

treatment options

Pharmacologic treatment o Three classes meds use for exacerbation Bronchodilator

SABA with or without S-ACH are preferred. No difference between metered dose or nebulizer

Corticosteroid Systemic shorten recovery time, improve FEV, PaO2, reduce relapse, length hospital stay and treatment failure EVERYONE SHOULD GET An ORAL STEROID Oxygen: -> most important for acute exacerbation. Noninvasive mechanical ventilation only Antibiotic use of antibiotic in pt with sign of bacterial infection ( sputum purulence). Only for moderately or severely ill pts who have 3 cardinal symptoms ( dyspnea, sputum volume, and purulence) , require mechanical ventilation 5 10 days therapy *****Procalcitonin III biomarker (+) meanins it is a bacterial infection****

adjunct therapies: fluid balance, anticoagulant, treatment of comorbidities and nutritional respiratory support o use when pt is hypoxemia targeting 88-92%

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use noninvasive mechanical ventilation is PREFFERED improve acidosis and decrease PaCO2

Hospital discharge and follow-up Prior to discharge, pt start on long-acting bronchodilator with/without ICS What are the criteria for discharge of a patient with COPD? o - major thing we need to do: smoking cessation, inhaler technique, prevent another exacerbaction with long term therapy and counsel or give immunizations.

 COPD and Comorbidities Key points o Comorbidities should not alter COPD treatment. Comorbidities should be treated as pt did not have COPD o o o CVD is most frequent in ppl with COPD Osteoporosis and depression are major comorbidities in COPD Lung cancer is frequently seen pt with COPD

4/25/2013 2:36:00 PM

4/25/2013 2:36:00 PM