?A disease state characterized by airflow limitation that is not fully reversible. Airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Symptoms, functional abnormalities, and complications of COPD can all be explained on the basis of this underlying inflammation and the resulting pathology.?



Definitions

?Chronic Bronchitis (clinical)

?Sputum production more days than not for at least 3 months a year for at least 2 years

?Emphysema (pathologic)

?Parenchymal destruction airspace walls distal to terminal bronchioles, without fibrosis

?Important: You can have either, but to have COPD you MUST demonstrate obstruction (thus the ?O? in COPD)

Epidemiology

?Fourth leading cause of death in U.S.

?100,000 American deaths each year

?15-20% of chronic smokers develop COPD

?2.5% mortality for COPD hospital admissions

?COPD with acute respiratory failure:

?24% in hospital mortality

?59% one year mortality

?If you have COPD and PaCO2 > 50mmHg:

?67% chance of being alive in 6 months

?57% chance of being alive in 12 months

Diagnosis

?Symptoms

?Dyspnea

?Sputum production (especially in the morning)

?Recurrent acute chest illnesses

?Headache in the morning ? possible hypercapnia

?Cor pulmonale (Right heart failure)

Goals Of Management

?Identifying and ameliorating (if possible) the cause of the acute exacerbation

?Optimizing lung function by administering bronchodilators and other pharmacotherapy

?Assuring adequate oxygenation and secretion clearance

?Averting the need for intubation, if possible

?Preventing complications of immobility, such as thromboemboli and deconditioning

?Addressing nutritional needs ? at the time of the acute illness, most patients are in negative nitrogen balance, which is exacerbated by steroid therapy

Diagnosis:

?Signs

?Prolonged expiratory time

?Expiratory wheezes

?Increased AP diameter of chest

?Decreased breath sounds (especially upper lung fields)

?Distant heart sounds

?End stage: accessory muscles, pursed lip breathing, cyanosis, enlarged liver and pedal edema (in case of cor pulmonale).

Diagnosis

?Radiology

?Chest X-ray

?Hyperinflated lung fields more radiolucent

?Bullae, often bilateral upper lobes in smokers

?Flat diaphragms (best seen on lateral) and retrosternal airspace can indicate air trapping

?High Resolution CT of Chest

?Most sensitive to detect above changes

?No role in routine care of COPD patients

?Can be useful for giant bullous disease surgeries or lung volume reduction surgery planning

Diagnosis

?Pulmonary Function Testing

?Spirometry: Decreased FEV1/FVC

?FEV1 percent predicted defines severity

?Lung volumes: Increased TLC, RV, RV/TLC

?DLCO: Decreased

Gold Staging Criteria

?Stage O: Normal spirometry; chronic sx

?Stage 1 (Mild):

?FEV1/FVC < 70%; FEV1 > 80% predicted

?Stage 2 (Moderate):

?FEV1/FVC < 70%; FEV1 30-80% predicted

?2A: FEV1 50-80% predicted

?2B: FEV1 30-50% predicted

Diagnosis

?Stage 3 (severe):

?FEV1/FVC < 70% AND:

?FEV1 < 30% predicted OR:

?FEV1 < 50% predicted and clinical evidence of Right heart failure

Diagnosis

American Thoracic Society ? Spirometry

?Low FEV1/FVC defines obstruction

?FEV1%predicted Category

?< 35% Very Severe

?35-50% Severe

?50-60% Moderately Severe

?60-70% Moderate

?70-80% Mild

?80-100% Mild vs. Normal variant

?> 100% Normal

Managing Stable COPD

?Smoking Cessation Is KEY!

?YOUR intervention will make a difference ? must address at each visit

?Medication

?Two therapies ONLY have been shown to improve mortality in stable COPD:

?1) Smoking Cessation

?2) Oxygen Therapy

Bronchodilator Technique

?MDI's get better drug deposition than nebs

?Use a spacer device with MDI's

?Technique is key ? important for patient and doctor

?Inadequate dosing can hamper treatment

?Sympathomimetics

?Beta-2 selectivity is good

?Some additive vs. slightly synergistic effects of combining beta-2 agonist and ipratropium (Combivent)

?Some data to support decreased H.influenzae pneumonia incidence with Serevent

Anticholinergic Agents (Atrovent, glycopyrrolate)

?Similar ability to bronchodilate (in appropriate doses) as beta-agonists

?Also reduces sputum volume; no change in viscosity

?Usually under dosed

?Recommend 2 (36 mcg) puffs qid

?glycopyrrolate which is manufactured for IV/IM use for other indications, is available only "off label" for nebulized use in COPD (1 to 2 mg every two to four hours).

?Aminophylline and theophylline are not recommended for the management of acute exacerbations of COPD. Randomized controlled trials of intravenous aminophylline in this setting have failed to show efficacy in excess of that afforded by therapy with inhaled bronchodilators and corticosteroids

Mucokinetic agents

?There is little evidence supporting the use of mucokinetic (mucolytic) agents, such as N-acetylcysteine or iodide preparations, in acute exacerbations of COPD. In fact, some drugs of this class may worsen bronchospasm.

?Oxygen. Yes.

?Demonstrated to improve exercise performance, symptom indices and mortality

?Goal in hypercapnic patients for SpO2 need not be greater than 88-90%

?Always test COPD patients for oxygenation with ambulation if baseline at rest room air SpO2 ok

?Systemic Corticosteroids

?Never demonstrated to significantly impact mortality or exercise capacity

?Slight improvements in symptom indices

?Significant side effects

?Rarely of benefit, generally of harm to your patient

?Occasionally useful in a small subset failing other therapies AND with demonstrated bronchodilator response on PFT's

?Inhaled Corticosteroids

?Jury still out

?Lots of recent research with some favorable data supporting its use

?May be part of standard regimens in the future

?Vaccines

?Pneumovax, annual flu shots

?Chronic antibiotic therapy ? BAD IDEA

?Nutritional status ? Important

?Pulmonary Rehabilitation

?Improved exercise capacity, symptom scores

?Lung Volume Reduction Surgery

?Transplant

Managing Acute Exacerbations of COPD

?Common precipitants:

?Infection ? esp viral or bacterial

?Acute bronchospasm

?Sedation

?Who To Admit?

?Countless studies, few definite answers

?Worsening hypoxemia and/or hypercapnia

?Otherwise, mostly a clinical decision

?Key points to consider:

?Oxygen

?Bronchodilators

?Steroids

?Antibiotics

?Albuterol:

?Neb or MDI ? neb MAY be better in acute setting, but MDI's have better drug deposition overall

?Continuous nebulizer treatments confer no benefit over treatments every 1-2 hours

?Generally should avoid subcutaneous beta-agonists

?BEWARE: Hypokalemia, tachycardia (occasional)

?Levalbuterol still with weak clinical data ? few situations where it is clinically indicated

?ATROVENT (anticholinergic bronchodilator)

?Bronchodilation

?May decrease secretions

?Few significant side effects

?Usually significantly under dosed ? emerging data supports much higher doses than usually used currently

?Corticosteroids ? Parenteral corticosteroids are frequently used in treating acute exacerbations of COPD. Methylprednisolone (60 to 125 mg intravenously, two to four times daily) or the equivalent glucocorticoid dose of other steroid preparations commonly is given.

?Corticosteroids Utilization in this setting was initially based upon small randomized trials in which only a minority of patients benefit and the degree of improvement is modest

?A randomized, placebo-controlled trial of 271 patients has confirmed the benefits of systemic corticosteroids given for up to 2 weeks to hospitalized patients with COPD exacerbation

?Antibiotics

??Winnipeg? Criteria (give for 2-3 of the following):

?Increased cough

?Increased purulence

?Increased sputum production

?Antibiotics accelerate improvement in peak expiratory flow rates and lessen the rate of recrudescence in this setting

?Amoxicillin, Doxycycline, TMP/SMX, Azithromycin, Clarithromycin, Levaquin for 10 days

?Mucokinetic Agents ? JUST SAY NO.

?N-acetylcysteine is actually contraindicated in patients with airway obstruction

?No significant clinical benefit ever demonstrated

?Chest PT, intermittent positive pressure breathing and postural drainage may actually be harmful in the setting of acute obstruction

?Methylxanthines (Theophylline, Aminophylline)

?Not recommended for acute exacerbations

?No significant benefit ever demonstrated in large, prospective trials

?Oxygen: YES!

?Generally a good thing ? cells like that stuff

?If requiring a significant increase in FiO2 over baseline requirement, start hunting for something other than just COPD exacerbation

?BEWARE of CO2 RETAINERS! (goal SpO2 90%, PaO2 of 60 to 65 mmHg )

?1) Altered V/Q relationships

?2) Haldane effect (Hgb*O2 holds less CO2 ? goes out into plasma)

?3) Decreased ventilatory drive (least impt mechanism)

?Non-Invasive Positive Pressure Ventilation

?BiPAP

?Set FiO2, inspiratory (IPAP) and expiratory (EPAP)

?Difference between IPAP and EPAP augments tidal volume, therefore improving minute ventilation. CO2 then gets blown off

?MORTALITY BENEFIT in patients who will tolerate

?Mechanical Ventilation

?Respiratory distress

?Acidemia that does not correct quickly with therapy

?Inability to oxygenate adequately

?Often a clinical decision relative to patient's work of breathing