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COPD 1 Chronic Obstructive Pulmonary Disease Definition o COPD is a disease characterized by a progressive airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Umbrella term – encompasses a number of pulmonary disease states a) Bronchitis (pg 511 DiPiro) -Condition with chronic or recurrent mucus secretion into the bronchial tree with cough that occurs on most days b) Emphysema -Condition of the lung characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles -Destruction of their walls -Without obvious fibrosis Epidemiology o COPD currently affects ~16 million Americans th Rare blood test confirms it. In general, if pt. presents with obstructive lung disease symptoms at <35 years of age, most likely have this. o 4 leading cause of death in U.S. o Burden on society (Annual cost to the nation for COPD is ~$31.9 billion) Risk factors Major Minor o Smoking (#1 risk factor) o Air pollution o Increasing age o Race (Caucasians at risk) o Male gender o Nutrition status (Poor nutrition risk) o Existing impaired lung function o Family History o Alpha 1 antitrypsin deficiency o Lower socioeconomic status o Occupation o Bronchial hyperreactivity o Respiratory tract infections Inhale particles that (frequent) aren’t normal to air Pathophysiology o Proteolytic-antiproteolytic theory Alpha 1 antitrypsin Protease inhibitor that normally inhibits trypsin and other proteases from destroying normal lung tissue Smoking is linked to a decreased activity of alpha 1 antitrypsin and stimulation of proteases Oxidants from smoking inactivate anti-proteases (responsible for protecting the lung) Proteases Destroy PROTEINS that make up lung matrix o Decrease cilia o Impair T lymphocytes (make immunologic response ) o Increase neutrophil chemotaxis (neutrophils accumulate in respiratory tract) o Increase levels IL-8 (more potentiation of inflammatory cascade) Antiproteases Protect the lung by inhibiting proteases e.g. Alpha-1 antitrypsin COPD 2 Pt. comes in with complaint of SOB. Clinical presentation (see table 27-2 pg 514 DiPiro) Predominant Predominant emphysema bronchitis Age 60+ 50+ Dyspnea severe less severe Cough After dyspnea Before dyspnea Sputum Scanty, mucoid Copius, purulent Bronchial infection Less frequent More frequent Cor pulmonale Rare Common General appearance Pink Puffer Blue Bloater Always tachypnic, expend enormous amt. of calories per day just breathing. Respiratory center responds to CO2. V/Q Mismatch (V=ventilation, Q= perfusion) Retain a lot of CO2 b/c respiratory center doesn’t respond to a lot of CO2. - + Poor ventilation (problem getting air down) Poor perfusion b/c alveolus and capillary surrounding the alveolus are destroyed Poor ventilation but perfusion is fine Pt. usually comes in with cough problem b/c problem with upper airway. Mucus accumulation in airway. Does not matter if pt. has emphysema or bronchitis. Both are treated the same. Most pts. Have some symptoms of both. DIAGNOSIS Should be considered in patients over the age of 35 who have a risk factor and who present with one of more of the following symptoms: o Exertional breathlessness -Intermittently or everyday -Present throughout the day o Chronic cough -Rarely only nocturnal o Regular sputum production o Frequent winter “bronchitis” o Wheeze o History of exposure to risk factors -TOBACCO SMOKE! o Dyspnea Dyspnea scale (progressive and persistant) GRADE DEGREE OF BREATHLESSNESS RELATED TO ACTIVITIES 1 Not troubled by breathlessness except on strenuous exercise 2 Short of breath when hurrying or walking up a slight hill Walks slower than contemporaries on level ground b/c of 3 breathlessness, or has to stop for breath when walking at own pace Stops for breath after walking about 100m or after a few minutes on 4 level ground Too breathless to leave the house, or breathless when dressing or 5 undressing Spirometry (pulmonary function test) Should be performed: o In all patients > 35y.o., current or ex-smokers, with a chronic cough o At time of diagnosis COPD 3 o To reconsider diagnosis if patient shows an exceptionally good Diagnostic Tests: Patients with COPD typically show: response to treatment -Decrease in FEV1 AND o Follow disease progression (FEV1 q yr) -Decrease in FVC -FEV1/FVC <70% and Other tests at diagnosis postbronchodilator FEV1 <80% o Chest x ray (used to rule out pneumonia, lung cancer, TB) predicted o Full CBC (ID anemia / polycythemia) o BMI (see if nutritionally stable) o ?alpha 1 antitrypsin deficiency (screen; Do they have a family h/o of this?) o ECG / echo (used to rule out CHF) o Pulse oximetry o Sputum Culture (used to rule out respiratory infection) (Bronchodilator) Reversibility testing o No longer necessary (b/c a lot of times pt would be labeled as non-responsive, but later may be responsive or chronically responsive) Differential List o Asthma (easy to rule out in younger pt., reversible, more diurnal variation) Pulmonary Fx Tests: o CHF (have crackles, x-ray, echo, edema) FVC: o Tuberculosis (around anyone recently infected with TB?) FEV1/FVC ratio Differential List for EXACERBATION -Normal >80% - <80% means obstruction o Infection (flu, pneumonia) DL: diffusion capacity o CHF exacerbation When DLCO reduced – means??? (DLCO = diffusion capacity of carbon monoxide) o PE -usually points to emphysema 2/2 diffusion capacity diminished b/c of loss of surface area available for gas exchange Disease ASSESSMENT SEVERITY Mild airflow obstruction Moderate airflow obstruction Severe airflow obstruction #1 goal for everyone with COPD is to be a non-smoker. FEV1 (after b-agonist) 50-80% predicted 30-49% predicted < 30% predicted Example: Person Managing Stable COPD who smokes 1 SMOKING CESSATION ppd for 20 yrs has a 20 pack year o Obtain smoking history history o Pack years Calculation NUMBER OF PACKS PER DAY X DURATION o Counsel to quit AND offer assistance at each provider visit o Only treatment that has been shown to prevent progression of the disease When a person tries to quit smoking, cough may actually get worse. Make sure to tell them that and that it will eventually get better. Cough might get worse b/c smoking has killed all the cilia. When stop smoking, cilia try to come back alive. More of a cough to clear the lungs. Treatment INHALED BRONCHODILATOR THERAPY Short acting beta agonist: albuterol (Beta-2 agonist) (CENTRAL to sx management) COPD 4 Never schedule Albuterol for asthma, but can for COPD. Albuterol stimulates receptors on airway smooth muscle, takes effect relatively quickly (within 1-2 min) and last s 4-6 hrs. Cholinergic nerves are going to be the main neural bronchoconstrictor pathway in the airways. Have increased tone of that in COPD pts. so if have a drug like ipratropium, it will decreade tone around the airways (relaxes muscles) Ipratropium has favorable effects on sleep. May help people who have trouble sleeping b/c cholinergic tone peaks during sleeping hours. o MOA: Bronchodilation (stimulates B2-receptors on airway smooth muscle). Smooth muscle relaxation following adenylate cyclase activation and increase in cyclic AMP production Functional antagonism of bronchoconstriction o Usual dose: 1-2 p q4 h prn SOB o Max recommended dose in COPD: A little higher than what package insert says for asthma b/c not getting a lot of good delivery of drug to site anyway b/c of perfusion and ventilation. 12 puffs a day for asthma (go a little higher for COPD) so 18-20 puffs are ok if no signs of toxicity o Place in therapy: Can be used as initial empirical treatment for relief of breathlessness FIRST LINE. Appropriate to schedule around the clock Can be used ATC for symptomatic relief Albuterol may help get some of the mucus out of o Onset of effect: 1-3 minutes the lungs ( mucocilliary clearance) o Duration of action: 4-6 hours o Reliever/rescue medication: PRN dosing In general, long acting B-agonists are much more B2 selective than o B2:B1 selectivity short-acting. Short-acting will have more adverse effect like tachycardia, Albuterol = 1375:1 muscle tremor. Salmeterol = 85,000:1 o ADR: tachycardia, skeletal muscle tremor, H/A, anxiety o Monitoring: Measure effectiveness by lung function, improvement in symptoms, activities of daily living, exercise capacity, rapidity of symptom relief o Education points: proper inhaler technique, carry with you Short acting anticholinergic: Ipratropium (Atrovent®) o MOA: Anticholinergic; relaxes muscles around bronchial tree. (nonspecific muscarinic receptor antagonist decreases airway smooth muscle tone) -Scheduled o Usual dose: 2-4 puffs q 4-6 hours prn SOB ipratropium is o Maintenance medication: 2-3 inhalations QID according to package insert acceptable (use around o Max dose: 24 puffs / day the clock) o Place in therapy: Can be used as initial empiric treatment FIRST LINE -Takes 30 min to kick in Symptomatic relief with anticholinergic ~80% will respond Symptomatic relief with SABA ~70% o Onset of action: 20-30 minutes Some say to start ipratropium even before o Duration of action: 4-6 hours albuterol. There was a study. Either will be appropriate as first line. o Usually used in combo with albuterol o Combination product (Combivent®) Fixed dose combination of albuterol and ipratropium (ipratropium bromide and albuterol sulfate) Onset of action: Albuterol: 1-3 minutes Ipratropium: 20-30 minutes Duration of action: 4-6 hrs Maintenance medication: 2-3 inhalations QID according to package insert Education: proper technique, carry with them Allergy alert: peanuts, soy lecithin Advantages: COPD 5 Cost (only need one inhaler) side effects b/c not maxing out on one drug o ADR: dry mouth, dizziness Think anticholinergic side effects DON’T use in patients with Glaucoma Urinary retention o Education points: proper inhaler technique o Clinical pearls: ALLERGY ALERT! peanut allergy, soy lecithin Long acting beta agonist: salmeterol, formoterol (serevent, foradil) o MOA: bronchodilator. Smooth muscle relaxation following adenylate cyclase If pt. is still activation and increase in cAMP production (stimulates B2-receptors on airway smooth symptomatic when muscle) on combination of Blister cap is refrigerated, short acting agents, o Usual dose: salmeterol diskus 1 p BID, formoterol 1 blister cap BID more steps than salmeterol move to longer o Maintenance medication: 1 inhalation (discus) BID acting agent. o Place in therapy: used in patients who remain symptomatic despite treatment with S.A.B.A. o Use in those that experience >2 exacerbations/ year o Onset of effect: 5 min (formoterol) 20 min (salmeterol) o Duration of action: 12+ hours o ADR: tachycardia, skeletal muscle tremor, anxiety, nervousness o Education points: don’t over use (no added effects if take more hits, just more side effects), NOT to be used for acute symptoms don’t carry as a rescue inhaler Long acting anticholinergic: tiotropium (Spiriva) o Will learn during in-service o MOA: o Usual dose: o Duration of effect: 24+ hours o Place in therapy: o ADR: Dry mouth, problematic in glaucoma patients o Education points: devise handihaler (new) Be careful if pt. has arrhythmias, CHF, liver problem, allergy to caffeine or chocolate Theophylline o MOA: not fully understood. Thought to work on cAMP / PDE (increasing cAMP in airway smooth muscle) o Usual dose: Sustained release products o Maintenance medication: qd to bid o Place in therapy: only used after trial of SABA and LABA (NOT FIRST LINE) Pt unable to use inhaled therapy o Duration of action: 12-24 hours o Monitoring: plasma level o Assess effectiveness by evaluating activities of daily living, improvement in symptoms, exercise cap, and lung function o Drug interactions (macrolides, FQ’s, smoking) COPD 6 o Other clinical pearls (see asthma handout) o Education points: limit caffeine use. Use as directed. Blood levels may be needed o Side effects of theophylline and comparative concentrations LEVEL SIDE EFFECT As level of theophylline 10-20 N/V increases, so does the severity >20 N/V/D irritable, insomnia and adverse effect >40 cardiac sx >50 seizures Long Acting Bronchodilators: Oral B2 o Oral sustained-release B2-agonist o Duration of action: 12 hrs. o Side effects: tremor, tachycardia, palpitations o Trade names: Volmax (albuterol sulfate), Proventil Repetabs (albuterol sulfate) o Use limited by side effects CORTICOSTEROIDS o INHALED MOA: anti-inflammatory Place in therapy: Flovent, Pulmicort Patients with FEV1 <50% predicted (same drugs as in Asthma handout) Those who are having >2 exacerbations / year (that require treatment with antibiotics or steroids) Moderate to sever COPD (d/c if no benefit after > 4 weeks) Goal: reduce exacerbation rates and slow decline in health status NICE guidelines: moderate to severe COPD (discontinue if no benefit > 4 weeks) Monitoring: risk of osteoporosis, cataracts If need to keep Education points: importance of compliance, onset of effect someone on oral Spacing device Patient should use a spacer corticosteroid, use lowest dose Rinse mouth with water after use possible and use o ORAL every other day. Maintenance use not generally recommended Maybe needed in those with severe dz, or those that can’t be withdrawn Have role in following an exacerbation exacerbations Risks: osteoporosis, DM, cataracts, HTN, possible mood changes (these risks are lower for inhaled corticosteroids) COMBINATION THERAPY In general, as the disease progresses, probably need add-ons. If patients remain symptomatic on monotherapy Effective combinations include o Beta2 agonists + anticholinergic o Beta 2 agonists + theophylline o Anticholinergic and theophylline o Long acting beta agonist and inhaled corticosteroid o ?long acting beta agonist + long acting anticholinergic Clinical pearl COPD 7 Not going to get more drug from nebulizer than inhaler if used correctly. o patients on long acting inhalers, will still require a short acting agent for acute symptoms of SOB/ cough Delivery Systems Inhalers (MDI, DPI (Turbuhaler, Diskus), Handihaler, Foradil blister caps Spacer (may use tidal breathing) Phasing out metered dose inhalers (don’t want drug with Nebulizer propellant anymore, too many fluorocarbons) o Those with distressing or disabling breathlessness despite maximal therapy using inhalers should be considered for neb therapy OXYGEN o Long term oxygen therapy (LTOT) indicated in patients who have decreased O2 sat and one of the following: Secondary polycythemia (increase in Hgb/Hct) Nocturnal hypoxemia Peripheral edema Evidence of complication Pulmonary HTN o To derive mortality benefits, need to use at least 15 hrs/day o Ambulatory oxygen therapy o Consider for those with exercise desaturation o Show improvement in exercise capacity or dyspnea with oxygen o Motivated to use it HEALTH MAINTENANCE Vaccinations o Pneumovax o Flu shot annually Mucolytics (water is the best mucolytic, may use Mucomyst or guaifenesin o Considered for those with chronic cough production of sputum Anti-tussives o Not recommended (don’t want to suppress cough b/c cough helps get gunk out of the lungs) HOW TO CHOOSE WHICH BRONCHODILATOR? o PRN vs. scheduled o Availability o Individual Response o Cost o Long acting – convenient o Combining bronchodilators Improve efficacy Decrease risk of ADR’s Putting it all together OTHER THERAPIES o Pulmonary rehabilitation Improve quality of life Physical wellbeing Emotional wellbeing Nutritional counseling Education (Pulmonary rehabilitation is a multidisciplinary group of physician, nurse, respiratory therapist, pharmacist, intuitionalist, and social worker.) COPD 8 1) Regular scheduled combo of SA bronchodilators (like combivent around the clock or ipratropium around the clock) 2) Regular scheduled LA inhaled bronchodilator (like servent BID, tiotropium BID) OR 3) Regularly scheduled combo of LA anticholinergic AND B-agonist Combination LABA + ICS -After trial of inhaled therapy -Pt. can’t use inhalers -Minimal drug interactions present MANAGING COMPLICATIONS OF COPD Complications Exacerbations Pulmonary HTN Cor pulmonale Arrhythmias Polycythemia RTI Acute respiratory failure Exacerbations o Definition Sustained worsening of symptoms from usual stable state which is beyond normal day-to-day variations, and is acute in onset o Etiology Infection (#1 cause), air pollution, unknown o Conditions that may mimic: Pneumonia, CHF, PE, arrhythmia, pneumothroax Staging Exacerbations: o Diagnosis Three symptoms: o Usually associated with: *Increased sputum purulence *Increased sputum volume Worsening breathlessness *Increased dypsnea symptoms MILD ONE of three MODERATE SEVERE symptoms present TWO of the three symptoms present ALL THREE symptoms present COPD 9 Increased sputum volume and purulence (sticky, thick) Changing sputum color Cough (worse) For a couple days o Treatment Initial Increase frequency of bronchodilator use – consider neb Oral antibiotics If purulent sputum Prednisone 30mg po qd for 7-14 days for all patients with significant increase in breathlessness unless contraindicated o Patients with FEV1 ≤ 50% and 2 or more exacerbations in a 12 month period are candidates for ICS PULMONARY HTN Definition o Disease in which blood pressure is abnormally high in the arteries between the heart and lungs. This condition can ultimately lead to heart failure o Mean pulmonary artery pressure (MPAP) via right heart catheterization >25mm Hg at rest >30mm Hg with exertion Etiology o Primary PAH (idiopathic) o Connective tissue disease (thickening / hardening of vessels leads to decreased contractability) o Medications (fenfluramine, phentermine) o HIV o Thromboembolic event o Chronic hypoxemia (chronic obstruction, not enough oxygen in the arteries btwn heart and lungs) Pathogenesis o Pulmonary vasoconstriction o Decrease flow in the pulmonary arterioles o Reactive pulmonary hypertension o Damaged pulmonary vasculature o Increase in vascular injury with vicious cycle perpetuating pulmonary HTN Symptoms o SOB, chest pain, syncope, fatigue, peripheral edema Diagnosis o Of exclusion 2/2 non-specific symptoms Treatment o CCB (standard of care) Diltiazem, nifedipine, amlodipine used most frequently o Anticoagulation Warfarin target INR 2-3. Patients on warfarin showed increased survival regardless of CCB efficacy o Diuretics Evidence of peripheral edema, ascites COPD 10 o Oxygen Maintain o2 sat > 90% o Prostacyclin + analogs (epoprostenol, treprostinil, beraprost, iloprost o Endothelin receptor antagonist (bosentan) o Phosphodiesterase inhibit For more information on PPH see Chest supplement, July 2004 COR PULMONALE o Definition / etiology Enlargement of the right ventricle secondary to abnormalities of pulmonary Chronic hypoxia ventilation. Leads to right sided heart failure Pulmonary HTN RetainNa/ H20 leads to development of edema End stage Cor pulmonale o Pathogenesis Normally, flow through the pulmonary vascular bed depends not only on pumping action of the RV, but also on respiratory movements and on the filling and contraction of the left ventricle o Diagnosis Subj: Peripheral edema Obj: Elevated systemic venous pressure (can cause hepatomegaly and ankle edema) Heart sounds Gallup rhythm on auscultation Loud pulmonary second heart sound Pulmonary trunk may be enlarged on xray Echo may show enlargement of RV cavity o Treatment Diuretics, Oxygen ARRYTHMIAS o Etiology: decreased O2 delivered to heart o Treatment (increase oxygen saturation (long term O2 therapy)) Reverse cause: electrolyte changes, hypoxia, theophylline toxicity POLYCYTHEMIA Definition o Increase in circulating RBC above normal Etiology o Erythropoeitin produced 2/2 kidneys sense hypoxemia. Increased production of RBC in an effort to increase oxygen carrying capacity of blood. End result; increased risk of clotting Signs / symptoms o Elevated H/H (Hematocrit 55-60) o Mental status changes (confused) o Thrombotic stroke Treatment o Chronic O2 COPD 11 o Phlebotomy (draining of the blood) o ?anticoagulation RTI Signs/symptoms o Changes in sputum color, quantity, consistency o ? fever + WBC (usual signs of infection may not be present) o increased breathlessness and cough Treatment o antibiotic ? 7-10 days ACUTE RESPIRATORY FAILURE (take pt. to physician or ER) Definition o Non COPD patient: paO2 < 50 or Pa CO2 > 50 o COPD ↓ PaO2 of 10-15 or ↑ PCO2 SO pH ≤ 7.3 o Signs/ symptoms o Restlessness, tachycardia, cyanosis, irregular breathing, mental status changes, diaphoresis (sweating), hypotension End stage COPD o Treatment -Social worker o Maximize bronchodilator -do not resuscitate order o O2 -very difficult to o Intubation extubate pt w/ end-stage COPD o Pulse steroids (pick a regimen, on 7 days, off 7 days) b/c not too much o Theophylline lung fxn left o Correct cause (infection, resp depressants) Inhaled steroids. If pt has more than 2 exacerbations/year should have trial of inhaled steroids MONITORING Smoking cessation Improvement in status Treatment / prevention of acute exacerbations Reduction in rate of progression of the disease Improvement of physical and psychological well-being of pt to maintain daily activities Reduction in days lost from work, hospitalizations and mortality FREQUENCY MILD / MODERATE At least annual SEVERE At least twice a year COPD 12 Clinical assessment Smoking status and desire to quit Adequacy of symptom control Breathlessness Exercise tolerance Estimated exacerbation frequency Presence of complications Effects of each drug treatment Inhaler technique Need for referral to specialist and therapy services Need for pulm rehab (recommend Smoking status and desire to quit Adequacy of symptom control Breathlessness Exercise tolerance Estimated exacerbation frequency Presence of cor pulmonale Need for long-term oxygen therapy Patient’s nutritional state Presence of depression Effects of each drug treatment Inhaler technique Need for social services and occupational therapy input Need for referral to specialist and therapy services Need for pulmonary rehab FEV1 and FVC BMI MRC dyspnea score for anybody with moderate-severe) Measurements to make FEV1 and FVC BMI MRC dysnea score SaO2 PATIENT EDUCATION Non pharmacologic therapy (smoking cessation) Inhaler / spacer / nebulizer technique Importance of compliance Disease progression Nutrition / exercise / psycho-social issues (anxiety or distress) Pulmonary rehabilitation ( hospitalizations, severity of exacerbation) Maintenance of MDI / spacers wash once every week in soapy dish water wash once every 2-4 weeks Prognosis Mortality rates -FEV1 >50% predicted Comparable to general population -FEV1 20% predicted Approximately 30% mortality at 1 year Approximately 95% at 10 years