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COPD Diagnosis, Phenotype, and Management:

Incorporating Current Guidelines

Sally K. Miller, PhD, APRNFNP-BC, AGACNP-BC, AGPCNP-BC

Associate ProfessorUniversity of Nevada Las Vegas

School of NursingNurse Practitioner

Correct Care SolutionsiCarePsychiatry

Objectives

1. Analyze the pathophysiology of COPD as it defines target of therapy

2. Analyze the mechanism of action of available pharmacotherapeutic options

3. Select pharmacotherapeutics relevant to goals of therapy

4. Discuss common phenotypical presentations

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Epidemiology

• Estimates are that < ½ of patients with COPD know they have it

• COPD is the 3rd leading cause of death in the U.S.

• COPD is the only one of the top five leading causes of death that has risen in the last 30 years

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The Rule of 50’s

• 50% of COPD patients are undiagnosed

• COPD is evident by the age of 50

• At the time of diagnosis FEV1 < 50%predicted

• 50% 5-year survival

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The Dutch Hypothesis

• OAD is based upon allergy and bronchial hyperresponsiveness; host factors are determined by heredity but modulated by environment

• Various forms of OAD have multiple overlapping features

• One form of airway disease may evolve into another (asthma COPD)

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• Cellular inflammation • including neutrophils

and macrophages• Cytokine, chemokine,

protease responses • Emphysema (lung

destruction) frequent

• Cellular inflammation with eosinophils, mast cells, T lymphocytes (neutrophils in severe disease)

• Broad inflammatory mediator responses

• Airway remodeling (epithelial injury and fibrosis)

COPDAsthma

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Risk Factors

Host Factors

• Genetic predisposition

• Alpha1 antitrypsin deficiency

• Age

• Asthma

Environment

• Smoking

• Allergens

• Pollution

• Infection **

• Socioeconomic status

**Hospitalization for respiratory infection prior to the age of 10

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Risk Factors Summary

• Predisposing host factors, including genetic factors and asthma, complicated by exposure to cigarette smoke and other irritants, provide the foundation for development of clinically significant COPD

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Pathophysiology

• Persistent and progressive airflow limitation that is not fully reversible

• The airflow limitation is usually associated with a chronic inflammatory response to noxious stimuli that renders alveoli useless

• Its pathology may or may not be characterized by chronic bronchitis or emphysmatic changes

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Pathophysiology

• Chronic bronchitis may or may not be present– A result of chronic airway injury and

narrowing– Inflammation of the small airways– Hypertrophy of large airway mucus

glands– Increased mucus production

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Pathophysiology

• Chronic bronchitis (cont.)– Normal ciliated pseudostratified

squamous epithelium is replaced by squamous metaplasia – clearance markedly diminished

– Hypertrophy and hyperplasia of submucosal glans is the prominent feature.

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Pathophysiology

• Chronic bronchitis (cont.)– Smooth muscle hypertrophy occurs– Hyperresponsiveness to nonspecific stimuli

occurs ̶ not as acute as in asthma, but more chronic and progressive

– Bronchioles are infiltrated with inflammatory cells; peribronchial fibrosis occurs.

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Pathophysiology• Emphysema may or may not be

present– A disease of lung parenchyma – not

conducting airways– Loss of elastic tissue results in loss of

recoil tension to support alveoli during expiration.

– Elastic recoil is dependent primarily on tissue elasticity.

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Pathophysiology

• Emphysema (cont.)– Tissue elasticity is maintained in the

healthy lung with a balance of elastases and antielastases.

– With the loss of antielastases, premature expiratory collapse occurs.

– Primary pathophysiology is progressive destruction of terminal respiratory units.

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Pathophysiology

• Emphysema (cont.)– Airway inflammation is not a primary

factor.

– Loss of alveolar surface area and accompanying bed decrease gas exchange producing hypoxia and dyspnea.

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Pathophysiology

• May be a consequence of – Mucus hypersecretion

– Ciliary dysfunction

– Hyperinflation

– Impaired gas exchange

– Pulmonary hypertension

– Cor pulmonale

• But the bottom line is airflow limitation18

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Normal v Emphysmatic Lung

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Emphysema

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Chronic Bronchitis

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Diagnostic Evaluation/Symptom Progression

• Chronic cough

• Chronic sputum production

• Dyspnea

• Exposure to environmental risk factors

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Physical Examination

• Not particularly useful in terms of diagnosis

• Greatest utility is in ruling out co-morbid, exacerbating factors

• Physical findings attributable to COPD must be differentiated from normal, age-related change

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Diagnostic Evaluation• Spirometry is the mainstay of laboratory

assessment is COPD• The two measures useful in terms of

diagnostic criteria are the forced expiratory volume in the first second of expiration (FEV1) and the forced vital capacity (FVC)

• These measures should be performed on every patient > 45 y.o. who is a smoker, or anyone with the key indicator symptoms described

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Spirometry Assessment

• The ratio of expiratory flow in the first second (FEV1) to the total respiratory effort (FVC) is considered the most sensitive indicator or early airflow limitation

• It declines even in patients who have not yet developed an isolated decline in FEV1 (FEV1 < 80%)

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Spirometry Assessment• As a result, a patient with a FEV1/FVC

ratio of 70% or less has spirometric evidence of obstruction, despite normal FEV1; this is diagnostic of COPD

• A patient with an FEV1/FVC of 70% and a normal FEV1 has stage mild COPD

• Subjective symptoms may or may not be present – not required for diagnosis

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Spirogram: Normal and COPD Patient

FEV1 FVC FEV1/FVC

Normal 4.150 5.200 80%

COPD 2.350 3.900 60%

0

1

2

3

4

5

1 2 3 4 5 6Seconds

Lit

er

FEV1

FEV1FVC

FVCNormal

COPD

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After the Diagnosis…How to Classify and Treat?

• Diagnostic criteria is met when the FEV1/FVC ratio is < 70%

• Now we stage the patient so that we can treat appropriately

• Staging is based on– Symptom assessment

– GOLD score (FEV1)

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GOLD Stage of COPD

STAGE FEV1

GOLD 1 (mild)

> 80% pred

GOLD 2 (moderate)

< 80% pred but > 50% pred

GOLD 3 (severe)

< 50% pred but

> 30% pred

GOLD 4 (very severe)

< 30% pred

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Symptom Assessment

• Unlike asthma, symptom assessment is conducted via standardized objective tools

• COPD Assessment Test (CAT) is one; there are several others

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COPD Assessment Test (CAT):http://catestonline.org

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Management• Reduction of risk factors• Ensure appropriate immunizations,

e.g., pneumococcal and influenza vaccines

• Pharmacotherapy depending upon GOLD stage (FEV1) and objective symptom assessment – treatment group A, B, C, or D

• Consider pulmonary rehabilitation33

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Management -- Pharmacological

• Pharmacotherapy targets improving airflow

• Foundation of pharmacotherapy include the long acting beta agonists (LABA) and the long acting muscarinic antagonists (LAMA)

• Inhaled corticosteroids for more severe disease

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Management -- Pharmacological

• LABA (Salmeterol)– Activate the sympathetic nervous

system– Maintain a steady state of

bronchodilation

• LAMA (Tiotroprium)– Antagonize the parasympathetic

nervous sytem– Decreases the ability to bronchconstrict

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Considering Bronchodilators

• Long acting bronchodilators are more effective and more convenient, but are also more expensive

• Both short and long term bronchodilators may increase anxiety, a common co-morbidity that can exacerbate dyspnea

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Long-Acting Bronchodilators in COPD: Combined Therapy

38Time on Treatment (weeks)

Cha

nge

in F

EV

1

(% b

asel

ine)

Placebo

* * *

0 4 8 12

0

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20

10

5

15

Salmeterol + Ipratropium Salmeterol

Pharmacotherapy

• Based on treatment group A, B, C, D

• Treatment groups categorized on FEV1 (GOLD stage) and symptom score

• Primary purpose is to control symptoms and reduce risk of exacerbation

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Treatment Groups

• Group A– Low risk (GOLD stage I or II = FEV1 >

50%)– Low symptom score on objective test

• Group B– Low risk (GOLD stage I or II = FEV1 >

50%) – Higher symptom score on objective test

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Treatment Groups

• Group C– High risk (GOLD stage III or IV = FEV1 <

50%)

– Low symptom score on objective test

• Group D– High risk (GOLD stage III or IV = FEV1 <

50%)

– Higher symptom score on objectivce test41

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What’s New in 2018?

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Primary Changes Are…

• LAMA is demonstrated as superior to LABA in terms of outcomes

• LABA/ICS are superior in combination as compared to either one alone

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Phenotypes

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Phenotypes

• Phenotype– A single or combination of disease

attributes that describe differences among individuals with COPD as they relate to clinically meaningful presentations and outcomes

– Numerous phenotypes have been proposed, defined, identified

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Phenotypes

• Asthma

• Bronchial hyperresponsiveness

• Bronchodilator reversibility

• Emphysema

• Hyperinflation

• Cachexia

• Chronic bronchitis

• Frequent exacerbators

• Systemic inflammation

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Phenotypes

• Perhaps more clinically relevant– Overlap or mixed COPD-asthma

– The exacerbator

– Emphysmatic-hyperinflation

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Phenotypes

• Other types– Fast decliner

– Systemic

– Alpha-1-antitrypsin deficiency

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70-year-old Male with Persistent Nocturnal

Awakening

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70 year old with persistent nocturnal awakening

• ‘Breathing problems’ since childhood

• Progressive sleep problems

• PMH - HTN• 96 pack years

smoking• PE - decreased

breath sounds

• FEV1 0.78 (25% pred) – FVC 2.21 (49% pred)– FEV1/FVC ratio 35%

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What Stage of COPD

• His FEV1/FVC ratio is approximately 30-35%

• His FEV1 is 25%

• CAT score is 22

• He is in treatment group D

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Treatment?• Textbook group D patient

– Ensure vaccines UTD– Consider pulmonary rehab– Would expect combination ICS/LABA/LAMA

therapy– He is adamant that his only concern is sleeping– He is started on Advair 250/50 b.i.d.– Sleep improves dramatically– He refused any additional therapy at every visit;

died approximately 1 year later

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Thank you!

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References

• Global Initiative for Chronic Obstructive Lung Disease (GOLD). GOLD 2017 global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, 2017 report. November 17, 2016. http://goldcopd.org/gold-2017-global-strategy-diagnosis-management-prevention-copd/ Accessed July 26, 2017.

• Mannino, D.M., & Buist, A.S. (2007). Global burden of COPD: risk factors, prevalence, and future trends. The Lancet; 370(9589) 765-73.

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References• Miravitlles, M., Calle, M., Soler-Cataluna, J.J.

(2012). Clinical phenotypes of COPD: identification, definition, and implications for guidelines. Archivos de Bronconeumologia, 48(3), 86-98.

• Van Noord, J.A., de Munck, D.R.A.J., Bantje, T.A., Hop, W.C.J., Adveld, M.L.M., & Bommer, A.M. (2000). Long-term treatment of chronic obstructive pulmonary disease with salmeterol and the additive effect of ipratroprium. European Respiratory Journal, 15, 878-85.

• Vestbo, J. (2014). COPD: definition and subtypes. Clinics in Chest Medicine, 35(1), 1-6.

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