copd and pneu

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N522: Primary Care III

COPDBy

J. Patterson Johnson, Ed.D, FNP

Primary Source: Global Initiative for COPD,WWW.GOLDCOPD.COM (2009 expert panel’srecommendations)



OVERVIEW

COPD (chr. Obstr.pulmonary disease)

4th leading cause of death & morbidity

in the U.S.

Mortality ’s with age, men > women

Symptoms manifest after significantlung tissue damage



DEFINITION

American Thoracic Society: “Air flowobstruction caused by chronic bronchitis

or emphysema; the airflow obstructionis generally progressive,may beaccompanied by airway

hyperactivity,and may be partiallyreversible”



DEFINITIONS [CONT]

Emphysema - Abnormal permanentstretching of the alveoli with destruction

of their walls which results in airtrapping.

Chronic bronchitis - excessive sputum

production/recurrent cough on mostdays for more that 3 mons. /yr.for atleast 2 consecutive yrs.



DEFINITION [CONT.]

THE GOLD report defines COPD as “A disease state characterized by airflow

limitation that is not fully reversible.The airflow limitation is usually bothprogressive and associated with an

abnormal inflammatory response of thelungs to noxious particles or gases



CAUSES OF AIRFLOWLIMITATION

IRREVERSIBLE CAUSES:

fibrosis & narrowing of the airways

Loss of elastic recoil due to alveolardestruction

Destruction of alveolar support thatmaintains patency of small airways.



CAUSES OF AIRFLOWLIMITATION [CONT.]

Reversible:

Accumulation of inflammatory cells,

mucus, and plasma exudate in bronchi

Smooth muscle contraction in peripheraland central airways

Dynamic hyperinflation during exercise



RISK FACTORS

Cigarette smoking (primary cause)

1 -antitrypsin deficiency -- an inherited

disorder

Occupational dusts & chemical

Infections

Socioeconomic status



CLINICAL MANIFESTATIONS

Chronic cough, chronic sputumproduction, dyspnea, and history of

exposure to risk factors. As a rule cough is the earliest symptom

of COPD

chronic sputum production suggestCOPD regardless of the pattern



CLINICAL MANIFESTATION[cont.]

Dyspnea that is persistent, worsensover time, and worsens with resp.

infections or exercise is alsocharacteristic of COPD.

Even patients without dyspnea, but with

a chronic cough, sputum productionand risk factors should be screenedwith pulmonary function tests



PHYSICAL FINDINGS - Advanced Disease

Emphysema - thin, muscle wasting,increased use of accessory resp.

muscles. Reduced diaphragramaticexcursion, barrel chest diminishedbreath sounds, no clubbing no cyanosis.

Chronic bronchitis - overweight,cyanosis, copious sputum, wheezes,crackles at the bases



DIFFERENTIAL DIAGNOSIS

Asthma, TB, congestive heart failure,bronchiectasis, obliterative bronchiolitis

Studies show that COPD is most oftenmisdiagnosed for asthma



DIFFERENTIAL DIAGNOSISFeatures

COPD: Onset in mid-life

Symptoms slowly progressive

Long smoking history

Dyspnea during exercise

largely irreversible airflow limitation




ASTHMA: Onset early in life

Symptoms vary from day to day

Symptoms at night & early morning

Allergy, rhinitis, & or eczema alsopresent

Family history of asthma

largely reversible air flow




CHF: fine basilar crackles onauscultation

CXR shows dilated heart, pulmonaryedema

PFTs indicate volume restriction not

airflow limitation




BRONCHIECTASIS: Large volumes of purulent sputum

commonly associated with bacterialinfection

Coarse crackles on auscultation

CXR/CT shows bronchial wall thickening




TUBERCULOSIS: Onset all ages

CXR shows lung infiltrate or nodular

lesions

Microbial confirmation

High local prevalence of TB




OBLITERATIVE BRONCHIOLITIS:Onset in younger age, nonsmokers

May have history of rheumatoid arthritisor fume exposure

CT scan on expiration shows hypodense

areas



LABORATORY STUDIES

Pulmonary function tests - spirometry,static lung volumes, and single breath

maximal diffusion capacity of carbonmonoxide (DlCOSB)

Spirometry - FEV1, FVC, FEV1 / FVC

Static lung volume - TLC, FRC, RV



LAB. STUDIES [cont.]

DLCOSB -measures the rate at which cois taken up by hemoglobin in the

pulmonary capillaries CXR -excludes other diagnoses and

helps diagnosis if bullous disease

ABG’S Alpha-1 antitrypsin deficiency screening



CLASSIFICATIONPost-Bronchodilator

Stage I: Mild -FEV1/FVC < 0.70; FEV1 ≥ 80%predicted

Stage II: Moderate – FEV1/FVC <0.70; 50%≤ FEV1 < 80% predicted

Stage III: Severe - FEV1/FVC < 0.70; 30% ≤FEV1 <50% predicted

Stage IV: Very severe – FEV1/FVC < 0.70;FEV1 < 30% predicted or FEV1 <50%predicted, plus chronic resp. failure



DISEASE MANAGEMENT

Treatment modalities - Education,pharmacotherapy, rehabilitation,and

oxygen administration. Education - smoking cessation,

reduction of risk factors, use of

medication, recognition of exacerbation,and reduction of dyspnea



DISEASE MANAGEMENT

Education in the last stage of COPDshould include instruction on: disease

complication, oxygen therapy, and endof life decisions (advanced directives)



KEY POINTS: STRATEGIES TOHELP PT. QUIT

systematically identify all tobacco usersat every visit

strongly urge all tobacco users to quit

determine willingness to make quitattempt

Aid the patient in quitting

Schedule follow-up contact



DISEASE MANAGEMENT[cont]

Pharmacotherapy -

Note: Studies show that none of the

existing meds for COPD serve to modifythe long term decline in lung functionthat is the hallmark of the disease.

Pharmacotherapy is used to decreasesymptoms and or/complications



DISEASE MANAGEMENT[cont.]

Medications - Bronchodilators arecentral to the symptomatic

management of COPD. They are givenon an as needed basis or on a regularbasis to prevent or reduce symptoms.

Principal bronchodilator treatments arebeta2 -agonists, anticholinergics,theophylline, and combo of these drugs




Inhalation is the preferred route of bronchodilators

To improve delivery, breath-activateddevices or spacers should be used

Routine use of nebulizers for medication

administration is discouraged becauseof the added cost.




The long-acting beta2-agonistsalmeterol significantly improves health

status and is more convenient than theshort-acting eg. Albuterol

the anticholinergic ipratropium

(atrovent) also improves health statusbut requires frequent dosing




Combination therapy using a fixed ratioof short-acting beta2-agonist and

ipratropium have been shown to haveenhanced effects.

Theophylline although effective is no

longer considered a first-line drug. Thisis due the higher rate of adversereaction and toxicity.




Steroid use is controversial.Glococorticosteroids may be helpful

during exacerbation but less effectivefor routine management.

Glucocorticosteroid Reversibility Testing

glucocorticosteroid be added tobronchodilator for a 6-12 week trial




Determine benefit of steroid bycomparing FEV1 at end of trial with

baseline. Positive response = FEV1 increase of

200ml and 15% above bronchodilator

baseline




Other Meds - antibiotics (prophylacticantibiotics use is not supported in Lit.),

vaccines, alpha1- antitrypsinaugmentation.

Rehabilitation; recommended for all

stages. Components - exercise training,counseling, and education.




Oxygen therapy has been found toimprove survival as well as mental and

physical status. Should be reserved for patients with

severe COPD.

Indication is by waking PaO2 ordesaturation during activity.




Indication for O2 -

PaO2 < 55 mm Hg or SaO2 < 88% at

rest; PaO2 < 55 mm Hg or SaO2 <89%with exercise or during sleep; PaO2 bet.55- 60 mm Hg or SaO2 < 89% with

evidence of pulmonary hypertension orcor pulmonale




Surgical Intervention: Lung volumereduction surgery. A large US trial (the

national Emphysema Treatment)started in 1996 and scheduled to end in2003 is in progress.

Lung transplantation may provideopportunity for survival.




Exacerbation - Common causes includeresp. infection and air pollution

Signs of exacerbation - accessorymuscle use, worsening or new onset of central cyanosis, dev. Of peripheral

edama, hemodynamic instability, rightheart failure, decreased level of alertness




Managing Exacerbation

Increase bronchodilators, initiate

antibiotics if indicated (increasedsputum amount and purulence). Pt.Should be assessed hours after initial

treatment adaptation. If not adequatelyimproved add oral corticosteroid. If noimprovement or worsening, hospitalize



COMPLICATIONS OF COPD

Hypoxemia

Hypercapnia

Pulmonary hypertension

Cor Pulmonale

copd and pneu

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