copd and the gold guidelines 02 21 2005[2]

COPD and the GOLD Guidelines

Fiona R. Prabhu, MD

Assistant Professor, Family & Community Medicine

February 21, 2005

Prevalence

12.1 million adults aged 25 and over were diagnosed with COPD in 2001

24 million adults have evidence of impaired lung function → underdiagnosis

Mortality

4th leading cause of death in the United States currently

Projected to be the 3rd leading cause of death for both males and females by 2020

119,000 adults age 25 and over died from COPD in 2000

Costs

1.5 million emergency room visits in 2000 726,000 hospitalizations in 2000 Total estimated cost of COPD in 2002 was

$32.1 billion $18 billion in direct costs $14.1 billion in indirect costs

Definition

Airflow limitation that is NOT fully reversible Progressive Associated with an abnormal inflammatory

response of the lungs to noxious particles or gases

Pathogenesis

Three processes: Chronic inflammation Imbalance of proteinases and anti-proteinases Oxidative stress

Chronic Inflammation

Chronic inflammation in airways, parenchyma, pulmonary vasculature

Inflammatory cells involved are: Macrophages

leukotriene B4 T-lymphocytes (CD8) interleukin 8 Neutrophils TNF-α

Pathology

Central Airways: Enlarged mucus secreting

glands Increase in goblet cells

Mucus hypersecretion Peripheral Airways

Repeated cycles of injury and repair

Increased collagen/scarring in airway wall

Pathology

Pulmonary vascular changes

Thickening of vessel wall (intima)

Increase in smooth muscle

Infiltration of vessel wall by inflammatory cells As COPD worsens, more smooth muscle, proteoglycans and

collagen further thicken the vessel wall

Pathophysiology

Mucus hypersecretion

Ciliary dysfunction

Airflow limitation

Pulmonary hyperinflation

Gas exchange abnormalities

Pulmonary hypertension

Cor pulmonale

Mucus hyperserection & ciliary dysfunction → cough, sputum production

Diagnosis of COPD

History of Present Illness

Chronic Cough Intermittently or every day Present throughout the day;

seldom only nocturnal Chronic sputum production

Any pattern Repeated episodes of acute

bronchitis

Chronic cough and sputum production often precede development of airflow limitation by many years

Not all patients with these symptoms develop COPD

Dyspnea on exertion Progressive Persistent Worse with exercise Worse during respiratory

infections History of exposure to risk

factors Tobacco smoke Occupational dusts and

chemicals Smoke from home cooking and

heating fuels

Medical History

Exposure to risk factors, incl. intensity/duration

History of exacerbations or previous hospitalizations for respiratory disorder

Past medical history Asthma, allergies, sinusitis/nasal

polyps, respiratory infections in childhood

Presence of co-morbid conditions Heart disease Rheumatic disease

Family History COPD Other chronic respiratory diseases

Social History Impact of disease on patient’s life,

inc. activity, missed work and economic impact

Effect on family routines Depression/anxiety Social and family support available

to the patient Other:

Appropriateness of current medical treatments

Possibilities for reducing risk factors, esp. smoking cessation

Risk Factors

Tobacco Smoke Cigarettes, Pipes, cigars – lower rates than

cigarette smokers but higher than non-smokers

Occupational dusts and chemicals

Vapors, irritants, fumes Need sufficiently intense or

prolonged exposure Indoor air pollution

Biomass fuel used for cooking and heating in poorly vented dwellings

Outdoor air pollution Minor risk factor Passive

cigarette smoke exposure Respiratory infections in early

childhood Lower socioeconomic status

association with COPD May be secondary to crowding,

poor nutrition, etc.

Physical Examination

Thorax: Barrel chest

Lungs Decreased breath sounds Wheezing

Cardiac Right-sided heart failure

Edema, tender liver, distended abdomen

Physical signs are rarely apparent until significant impairment of lung

function has occurred

Diagnostic Tests

Chest X-ray Flattened diaphragms Use to exclude other diagnoses

High resolution CT Not routinely recommended If in doubt about diagnosis of

COPD If considering bullectomy or lung

volume reduction surgery CBC

May see increased hemoglobin/hematocrit secondary to hemoconcentration

ABG Spirometry

Spirometry

Measure of FVC and FEV1 FVC = forced vital capacity

Maximum volume of air forcibly exhaled from the point of maximal inhalation

FEV1 = forced expiratory volume in 1 second Volume of air exhaled in the 1st second of the FVC maneuver

Calculate the FVC/FEV1 ratio Normal ratio = 70/80% COPD ratio = <70% pre-bronchodilator FVC & FEV are COPD ratio = <80% post-bronchodilator both decreased

Essential to making the diagnosis of COPD

Spirometry

Best performed with the patient seated Optimal results:

Patient breathes in fully Patient must seal their lips around the mouthpiece Have the patient force the air out of their chest as hard and fast as

they can until their lungs are completely “empty” Exhalation must be at least 6 seconds and can take up to 15 seconds

Breathe in again and relax Need 3 technically satisfactory curves

Vary no more than 5% (or 100 mL) Ratio is calculated from the maximum FVC and FEV1 from any of

these curves.

Spirometry

Bronchodilator Reversibility Testing Perform in the initial assessment of COPD in

order to:Exclude asthmaEstablish best attainable lung functionGauge patient prognosisGuide treatment decisions

Arterial Blood Gas (ABG)

Obtain in patients with FEV1 < 40% predicted OR Clinical signs of respiratory or right heart failure

Central cyanosis, ankle swelling, increase in jugular venous pressure (JVP) OR

Respiratory Failure: PaO2 < 60 mm Hg with or without PaCO2 > 45 mm Hg

while breathing air at sea level Technique:

Obtain by arterial puncture; DO NOT USE finger or ear oximeters

Other Tests

Alpha-1 antitrypsin Consider in patients with COPD < age 45 Strong family hx of early COPD or with alpha-1

antitrypsin deficiency

Differential Diagnosis of COPD

Asthma Reversible airflow limitation Early onset (childhood) Symptoms vary day to day

Congestive heart failure Volume restriction, NOT airflow

limitation CXR with dilated heart, pulmonary

edema Bronchiectasis

Large volumes of purulent sputum Commonly associated with bacterial

infection Bronchial dilation and bronchial

wall thickening on CXR or CT

Tuberculosis Onset at all ages Chest x-ray with infiltrate or

nodular lesions Obliterative bronchiolitis

Younger patients/non-smokers May have a hx of rheumatoid

arthritis or fume exposure CT shows hypodense areas with

expiration Diffuse panbronchiolitis

Male/non-smokers Chronic sinusitis CXR and high resolution CT show

diffuse small centrilobular nodular opacities and hyperinflation

COPD Management Program

GOLD (Global Initiative for Chronic Obstructive Lung Disease)

Guidelines

Goals

Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment Cessation of cigarette smoking

Components

Assess and monitor disease Reduce risk factors Manage stable COPD Manage acute exacerbations

Assess and Monitor Disease

Initial Visit

Pattern of symptom development Exposure to risk factors History of exacerbations or previous hospitalizations for respiratory

disorder Past medical history Family history Social history

Impact of disease on patient’s life Effect on family routines Feelings of depression or anxiety Social and family support available to the patient

Possibilities for reducing risk factors, especially smoking cessation

Testing

Spirometry Initially and yearly

ABG Obtain if FEV1 < 40% predicted OR Clinical signs of respiratory or right heart failure Respiratory Failure

Alpha-1 antitrypsin If patient <45 years old or strong family history of COPD

Follow-Up Visits

Discuss new or worsening symptoms Perform spirometry if there is a substantial increase in symptoms

OR if a complication occurs ABG

Patients with an FEV1 <40% predicted Early signs of respiratory failure or CHF

Monitor pharmacotherapy Dosages Adherence Inhaler technique Effectiveness of current regimen at controlling symptoms Side effects of treatment

Follow-up Visits

Monitor co-morbid conditions Bronchial carcinoma Tuberculosis Sleep apnea Left heart failure

Obtain appropriate information through CXR, ECG whenever symptoms suggest one of these conditions

Reduce Risk Factors

Risk Factors

Tobacco smoke Occupational dusts and chemicals Indoor and outdoor air pollutants

Smoking Cessation

The single MOST effective and cost-effective intervention to reduce the risk of developing COPD and to stop its progression

Brief tobacco dependence treatment is effective Offer this at EVERY visit to the health care provider

Brief 3 minute period of counseling Three types of counseling are esp. effective:

Practical counseling Social support as part of the treatment Social support arranged outside of the treatment

Several effective medications are available and at least one of these medications should be added to counseling if necessary and if there are no contraindications

Nicotine gum, inhaler, nasal spray, trasndermal patch, sublingual tablet, lozenges Bupropion nortriptyline

Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians.

Smoking Cessation Strategy

Ask Systematically identify all tobacco users at every visit

Advise Strongly urge all tobacco users to quit, in a clear, strong, and personalized manner

Assess Determine willingness to make a quit attempt.

e.g. within the next 3 days, how willing is this person to make a quit attempt

Assist Aid the patient in quitting

e.g. quit plan, counseling, intra-treatment social support, extra-treatment social support, approved pharmacotherapy, supplementary materials

Arrange Schedule a follow-up contact, either in person or via telephone


Smoking Prevention – What you can do as a provider:

Encourage comprehensive tobacco-control policies and programs

Work with government officials to pass legislation to establish smoke-free schools, public facilities, and work environments

Encourage patients to keep smoke-free homes


Occupational Exposures

Primary prevention Eliminate or reduce exposures to various

substances in the workplace

Secondary prevention Surveillance and early detection

Indoor and Outdoor Air Pollution

Implement measures to reduce or avoid indoor air pollution from biomass fuel burned for cooking and heating in poorly ventilated dwellings

Advise patients to monitor public announcements of air quality

Avoid vigorous exercise outdoors or stay indoors during pollution episodes, depending on COPD severity

Manage Stable COPD

General Principles

Determine disease severity Implement step-wise

treatment plan Educate the patient

Improve skills Improve ability to cope with

illness Improve health status

Prescribe Treatment Pharmacologic Non-pharmacologic

Rehabilitation Exercise training Nutrition counseling education Oxygen therapy

Surgical interventions

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Stage Characteristics

0:

At Risk

Normal spirometry

Chronic symptoms (cough, sputum)

I:

Mild

FEV1/FVC < 70%

FEV1 >= 80% predicted

Usu. Chronic cough and sputum production

II: Moderate 50% <= FEV1 < 80% predicted

Progression of symptoms; dyspnea on exertion

III:

Severe

30%<= FEV1 < 50% predicted

↑ dyspnea; repeated exacerbations which have an impact on patients’ quality of life

IV

Very severe

FEV1< 30% predicted OR

FEV1<50% predicted + chronic respiratory failureQuality of life is appreciably impairedExacerbations may be life-threatening

COPD Severity

Patient Education

Smoking cessation Basic information about COPD and pathophysiology of the

disease General approach to therapy and specific aspects of medical

treatment Self-management skills Strategies to help minimize dyspnea Advice about when to seek help Self-management and decision-making in exacerbations Advance directives and end-of-life issues

Medications

Goals Prevent and control symptoms Reduce frequency and severity of exacerbations Improve health status Improve exercise tolerance

No existing medications can modify the long-term decline in lung function

Reduction of therapy once symptom control occurs is not normally possible

COPD is progressive and over time will require progressive introduction of more treatments to attempt to limit the impact of these changes

Bronchodilators

Central to symptom management Used in all stages of COPD severity

Inhaled forms are preferred Can be prescribed as needed OR regularly to prevent or reduce

symptoms Long-acting inhaled bronchodilators are more effective and convenient

(but are more expensive) Combining drugs with different mechanisms and durations of action

may increase the degree of bronchodilation for equivalent or lesser side effects

All categories of bronchodilators have been show to increase exercise capacity without necessarily producing significant changes in FEV1

Bronchodilators

Beta2-agonists Short-acting: albuterol Long-acting: salmeterol (Serevent™), formoterol (Foradil™)

Anticholinergics Short acting: ipratropium bromide (Atrovent™) Long acting: tiotropium bromide (Spiriva™)

Methylxanthines (Theophylline™) Combination bronchodilators

Fenoterol/ipratropium (Duovent™) Salbutamol/ipratropium (Combivent™)


Glucocorticosteroids

Use if FEV1 < 50% predicted and repeated exacerbations, e.g. three in the last three years

Severe COPD and Very Severe COPD Does not modify the long-term decline in FEV1 BUT does reduce the

frequency of excacerbations and improves health status The combination of a long-acting beta2-agonist and an inhaled

glucocorticosteroid is more effective than the individual components Long-term treatment with oral glucocorticoids is NOT recommended Glucocorticosteroid (inhaled) reversibility testing

Treatment trial of inhaled glucocorticosteroids for 6 to 12 weeks then repeat spirometry with and without bronchodilators

Patients most likely to respond to inhaled steroids have an FEV1 increase of 200 mL and 15% above baseline post-bronchodilator


Inhaled Glucocorticoids

Beclomethasone (Vanceril™) Budesonide (Pulmicort™) Fluticasone (Flovent™) Triamcinolone (Azmacort™)


Immunizations

Vaccines Influenza yearly

Reduces serious illness and death in COPD patients by approximately 50%

Give once yearly: autumn OR twice yearly: autumn and winter

Pneumovax Sufficient data to support its general use in COPD is

lacking, but it is commonly used

Other Medications?

Alpha-1 Antitrypsin Augmentation Therapy Only if this deficiency is present in an individual should they undergo

treatment Antibiotics

Prophylactic use is NOT recommended Can be used in the treatment of infectious exacerbations of COPD

Mucolytic agents Overall benefits are small, so currently not recommended for widespread

use Types:

Ambroxol Erdosteine (Erdostin, Mucotec) Carbocysteine (Mucodyne) Iodinated gylerol (Expigen)


Other Medications?

Antioxidant agents N-acetylcysteine (Bronkyl, Fluimucil, Mucomyst) Have been shown to reduce the frequency of exacerbations and could have a role in

the treatment of patients with recurrent exacerbations More studies are needed

Immunoregulators Not recommended at this time No reproducible studies are available

Antitussives Regular use is contraindicated in stable COPD since cough has a significant protective

role Vasodilators

Inhaled nitric oxide Can worsen gas exchange because of altered hypoxic regulation of ventilation-perfusion

balance and is contraindicated in stable COPD


Other Medications?

Respiratory stimulants Doxapram (IV) Almitrine bismesylate

Not recommended in stable COPD Narcotics

Oral and parenteral opioids are effective for treating dyspnea in patients with advanced COPD

Use this with caution; benefits may be limited to a few sensitive subjects nebulized opioids: insufficient evidence re: efficacy

Miscellaenous: Nedocromil Leukotriene modifiers Alternative healing methods

None have been adequately studied in COPD patients at this time


Stage 0: At Risk

Avoid risk factors Offer influenza vaccination

Stage I: Mild COPD

Avoid risk factors Offer vaccination Use short-acting

bronchodilators as needed

I:

Mild

FEV1/FVC < 70%

FEV1 >= 80% predicted

Usu. Chronic cough and sputum production

Stage II: Moderate COPD

Avoid risk factors Offer influenza vaccine Add short-acting

bronchodilators when needed

Add regular treatment with 1 or more long-acting bronchodilators

Add rehabilitation

II: Moderate

50% <= FEV1 < 80% predicted

Progression of symptoms; dyspnea on exertion

Stage III: Severe COPD

Avoid risk factors Offer influenza vaccine Add short-acting

bronchodilators when needed Add regular treatment with 1 or

more long-acting bronchodilators

Add rehabilitation Add inhaled glucocorticoids if

repeated exacerbations

III:

Severe

30%<= FEV1 < 50% predicted

↑ dyspnea; repeated exacerbations which have an impact on patients’ quality of life

Stage IV: Very Severe COPD

Avoid risk factors Offer influenza vaccination Add short-acting

bronchodilators as needed Add rehabilitation Add inhaled glucocorticoids if

repeated exacerbations Add long-term oxygen if chronic

respiratory failure Consider surgical treatments

IV

Very severe

FEV1< 30% predicted OR

FEV1<50% predicted + chronic respiratory failureQuality of life is appreciably impairedExacerbations may be life-threatening

Non-Pharmacologic Therapy

Rehabilitation

COPD patients at all stages of severity benefit from exercise training programs Improves both exercise tolerance and symptoms of dyspnea and fatigue

Goals Reduce symptoms Improve quality of life Increase physical and emotional participation in everyday activities

Comprehensive program should include several types of health professionals: Exercise training Nutrition counseling Education

Minimum effective length of time = 2 months Setting: inpatient OR outpatient OR home Baseline and outcome assessments of each participant should be made to quantify

individual gains and target areas for improvement Measurement of spirometry before and after a bronchodilator drug Assessment of exercise capacity Assessment of inspiratory and expiratory muscle strength and lower limb strength


Oxygen Therapy

Stage IV - Severe COPD PaO2 at or below 55 mm Hg or SaO2 at or below 88% with or without

hypercapnia OR PaO2 between 55-60 mm Hg or SaO2 89% IF pulmonary hypertension,

peripheral edema suggesting congestive heart failure, or polycythemia (Hct > 55%)

Based on awake PaO2 values GOAL

Increase baseline PaO2 to at least 60 mm Hg at sea level and rest and/or produce SaO2 at least 89%

Need to use at least 15 hours per day in patients with chronic respiratory failure to improve survival

Can have a beneficial impact on hemodynamics, hematologic characteristics, exercise capacity, lung mechanics and mental state


Surgical Treatment

Bullectomy Effective in reducing dyspnea and improving lung function in

appropriately selected patient Lung volume reduction surgery

Parts of the lung are resected to reduce hyperinflation Does not improve life expectancy Does improve exercise capacity in patients with predominantly

upper lobe emphysema and a low post-rehabilitation exercise capacity

May improve global health status in patients with heterogeneous emphysema

High hospital costs; still experimental/palliative


Surgical Treatment

Lung transplantation Improves quality of life and functional capacity

in appropriately selected patient Criteria for referral:

FEV1 < 35% predicted all fourPaO2 < 55-60 mm Hg criteria

PaCO2 > 50 mm Hg must beSecondary pulmonary hypertension present


COPD Patients and Surgery

Increased risk of post-operative pulmonary complications

Risk of complications increases as the incision approaches the diaphragm

Epidural and spinal anesthesia have a lower risk than general anesthesia

Postpone surgery if the patient has a COPD exacerbation


Manage Exacerbations

General Points

Most common causes of exacerbations are: Infection of the tracheobronchial tree Air pollution In 1/3 of severe exacerbations a cause cannot be identified

Inhaled bronchodilators, theophylline, and systemic (preferably oral) glucocorticosteroids are effective treatments

Patients with clinical signs of airway infection may benefit from antibiotic treatment Increased volume of sputum Change in color of sputum Fever

Non-invasive intermittent positive pressure ventilation (NIPPV) in exacerbations is helpful:

Improves blood gases and pH Reduces in-hospital mortality Decreases the need for invasive mechanical ventilation and intubation Decreases the length of hospital stay


Diagnosis and Assessment of Severity

History Increased breathlessness Chest tightness Increased cough and sputum Change of color and/or tenacity of

sputum Fever Non-specific:

Malaise, insomnia, sleepiness, fatigue, depression, or confusion

Assessment of Severity

Lung Function Tests PEF < 100 L/min. or FEV1 < 1

L = severe exacerbation Arterial Blood Gas

PaO2 < 60 mmHg and/or SaO2 < 90% with or without PaCO2 < 50 mmHg when breathing room air = respiratory failure

PaO2 < 50 mmHg, PaCO2 < 70 mmHg and ph < 7.3 = life-threatening episode

Chest x-ray Look for complications

Pneumonia Alternative diagnoses

ECG Right ventricular hypertrophy Arrhythmias Ischemia

Sputum Culture/sensitivity

Comprehensive Metabolic Profile

Assess for electrolyte disturbances, diabetes

Albumin to assess nutrition


Home? Hospital admission?

Floor? ICU?


Indications for Hospital Admission

Marked increase in intensity of symptoms such as sudden development of resting dyspnea

Severe background COPD Onset of new physical signs

Cyanosis, peripheral edema Failure of exacerbation to respond to initial medical management Significant co-morbidities Newly occurring arrhythmias Diagnostic uncertainty Older age Insufficient home support

Indications for ICU Admission

Severe dyspnea that responds inadequately to initial emergency therapy

Confusion, lethargy, coma Persistent or worsening hypoxemia (PaO2 < 50 mm Hg)

and/or Severe/worsening hypercapnia (PaCO2 > 70 mm Hg) and/or Severe/worsening respiratory acidosis (pH < 7.30) despite

supplemental oxygen and NIPPV

NIPPV = non-invasive positive pressure ventilation

Management of Exacerbations

Risk of dying from an exacerbation is closely related to: Development of respiratory acidosis Presence of significant co-morbidities Need for ventilatory support

Severe Exacerbation, Non Life Threatening

Assess severity of symptoms Obtain arterial blood gas and chest x-ray Administer controlled oxygen therapy

Repeat ABG after 30 minutes Bronchodilators Glucocorticosteroids Consider antibiotics Consider non-invasive mechanical ventilation Monitor fluid balance and nutrition Consider subcutaneous heparin therapy Identify and treat associated conditions (CHF, arrhythmias)

Management of COPD Exacerbations

Controlled oxygen therapy Administer enough to maintain PaO2 > 60 mmHG or

SaO2 > 90% Monitor patient closely for CO2 retention or acidosis

Bronchodilators (inhaled) Increase doses or frequency Combine ß2 agonists and anticholinergics Use spacers or air-driven nebulizers Consider adding IV methylxanthine (aminophylline) if

needed



Glucocorticosteroids (oral or IV) Recommended as an addition to bronchodilator therapy If baseline FEV1 < 50% predicted

30-40 mg oral prednisolone x 10 days OR nebulized budesonide (Pulmicort™)

Antibiotics IF breathlessness and cough are increased AND sputum is purulent

and increased in volume Choice of antibiotics should reflect local antibiotic sensitivity for the

following microbes: S. pneumoniae H. influenzae M. catarrhalis



Manual or mechanical chest percussion and postural drainage may be beneficial in patients producing > 25 mL sputum per day OR with lobar atelectasis.



Ventilatory Support Decrease mortality and morbidity Relieve symptoms Used most commonly in Stage IV, Very Severe COPD Forms:

Non-invasive using negative or positive pressure devices invasive/mechanical with oro- or naso-tracheal tube OR

tracheostomy


NIPPV

Success rates of 80-85% Increases pH, reduces PaCO2, reduces

severity of breathlessness in the first 4 hours of treatment

Decreases length of hospital stay Decreases mortality/intubation rate

NIPPV (C-PAP, Bi-PAP)

Selection criteria Moderate to severe dyspnea with use of

accessory muscles and paradoxical abdominal motion

Moderate to severe acidosis (pH < 7.35) and hypercapnia (PaCO2 > 45 mmHg)

Respiratory frequency > 25 breaths/minute

NIPPV

Exclusion criteria Respiratory arrest Cardiovascular instability

Hypotension Arrhythmias Myocardial infarction

Somnolence, impaired mental status, lack of cooperation High aspiration risk – viscous/copius secretions Recent facial or gastroesophageal surgery Cranio-facial trauma, fixed nasopharyngeal abnormalities Extreme obesity

Indications for Invasive Mechanical Ventilation

Severe dyspnea with use of accessory muscles and paradoxical abdominal motion

Respiratory rate > 35 breaths/minute Life-threatening hypoxemia: PaO2 < 40 mm Hg Severe acidosis (pH < 7.25) and hypercapnia (PaCO2 > 60 mm Hg) Respiratory arrest Somnolence, impaired mental status Cardiovascular complications

Hypotension/shock/heart failure Other complications

Metabolic abnormalities/sepsis/pneumonia/pulmonary embolism/barotrauma/massive pleural effusion

NIPPV failure

Use of Invasive Ventilation in End-Stage COPD

Hazards: Ventilator-acquired pneumonia

Increased prevalence of multi-resistant organisms Barotrauma Failure to wean to spontaneous ventilation

Mortality among COPD patients with respiratory failure is no greater than mortality among patients ventilated for non-COPD reasons

Weaning from Ventilator

Methods still debated Whatever clinical protocol is adopted, weaning is

shorted as long as a protocol is used! NIPPV used during the weaning process has

shortened weaning time, reduced stay in the ICU, decreased the incidence of nosocomial pneumonia, and improved 60-day survival rates

Discharge Criteria

Inhaled Beta2-agonist use is at most every 4 hours Patient is able to walk across the room Patient is able to eat and sleep without frequent awakening Patient has been clinically stable for 12-24 hours ABGs are stable for 12-24 hours Patient/home caregiver fully understands correct use of

medications Follow-up and home care arrangements have been

completed Patient, family, and physician are confident that patient can

manage successfully

Follow-Up Assessment after Hospital Discharge

4-6 weeks after discharge Assess:

Ability to cope in usual environment Inhaler technique Understanding of recommended treatment regimen

Measure FEV1 Determine need for long-term oxygen therapy and/or home

nebulizer (for patients with very severe COPD, Stage IV)

Follow-up after this is the same as for Stable COPD monitoring

REFERENCES

National Heart, Lung, and Blood Institute Data Fact Sheet for Chronic Obstructive Pulmonary Disease

GOLD (Global Initiative for Chronic Obstructive Lung Disease) Executive Summary, April 2001

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention. A Guide for Health Care Professionals. Updated July 2005. www.goldcopd.org – Accessed August 21, 2006.

Fiore MC, Bailey WC, Cohen SJ, et. al. Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service. October 2000.

copd and the gold guidelines 02 21 2005[2]

Health & Medicine