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diAGNOSAURUS Chronic obstructive pulmonary disease (COPD) Definition = Emphysema or chronic bronchitis

Etiology of emphysema 1. Tobacco smoke 2. Alpha-1-antiprotease deficiency 3. Talcosis (from IV drug use)

DDx 1. Bronchiectasis 2. Cystic fibrosis 3. Asthma 4. Bronchiolitis 5. Recurrent pulmonary emboli

See related DDx 1. Upper airway obstruction 2. Obstruction on PFTs Pulmonary Function Tests (PFTs) |

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QUICK ANSWEARS

Key Features

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Essentials of Diagnosis History of cigarette smoking Chronic cough, dyspnea (in emphysema), and sputum production (in chronic bronchitis) Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination Airflow limitation on pulmonary function testing

:

General Considerations

Airflow obstruction due to chronic bronchitis or emphysema; most patients have features of both Obstruction

– Is progressive – May be accompanied by airway hyperreactivity – May be partially reversible

Chronic bronchitis is characterized by

months or more

excessive mucous secretions with productive cough for 3

in at least 2 consecutive years

Emphysema is abnormal enlargement of air spaces distal to terminal bronchiole, with destruction of bronchial walls without fibrosis Cigarette smoking is the most important cause – About 80% of patients have had a significant exposure to tobacco smoke

Air pollution, airway infection, familial factors, and allergy have been implicated in chronic bronchitis

1-Antiprotease deficiency

Symptoms and Signs

has been implicated in emphysema

:

Presentation

– Usually at 40–50 years of age – Cough – Sputum production – Shortness of breath

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Dyspnea initially occurs only with heavy exertion , progressing to symptoms at rest in severe disease Exacerbation of symptoms beyond normal day-to-day variation, often including increased dyspnea, an increased frequency or severity of cough, increased sputum volume, or change in sputum character

Infections (viral more commonly than bacterial) precede exacerbations in most patients

Late-stage COPD characterized by

– Hypoxemia – Pneumonia – Pulmonary hypertension – Cor pulmonale – Respiratory failure

Clinical findings may be absent early

Patients are often dichotomized as "pink puffers" or "blue bloaters" depending on whether emphysema or chronic bronchitis predominates

ddx

ASTHMA Bronchiectasis, which features recurrent pneumonia and hemoptysis , with distinct radiographic findings

BRONCHOPULMONARY MYCOSIS CENTRAL AIRFLOW OBSTRUCTION

Severe 1- antiprotease deficiency

CYSTIC FIBROSIS,

WHICH IS USUALLY FIRST SEEN IN CHILDREN AND YOUNG ADULTS

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Diagnosis

:

Laboratory Tests

Sputum examination may reveal

– Streptococcus pneumoniae – Haemophilus influenzae – Moraxella catarrhalis – Cultures correlate poorly with exacerbations

ECG shows sinus tachycardia, abnormalities consistent with cor pulmonale in severe disease, and/or supraventricular tachycardias and ventricular irritability

Arterial blood gas values –

Unnecessary unless

hypoxemia or hypercapnia is suspected

– May show only an increased A–a DO2 in early disease – Hypoxemia in advanced disease – Compensated respiratory acidosis with worsening acidemia during exacerbations

Spirometry

:

– Objectively measures pulmonary function and assesses severity

– Early changes are reductions in midexpiratory flow and abnormal closing volumes – FEV1 and FEV1/FVC are reduced later in disease – FVC is reduced in severe disease

–

Lung volume measurements show an increase in

total lung capacity (TLC),

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residual volume (RV), and an elevation of RV/TLC indicating

air trapping

1-Antiprotease level in young patients with emphysema

Imaging Studies

:

Radiographs of patients with chronic bronchitis typically show only

perivascular markings

nonspecific peribronchial and

Plain radiographs are insensitive for the diagnosis of emphysema; they show hyperinflation with flattening of the diaphragm or peripheral arterial deficiency in about half of cases

CT of the chest is more sensitive and specific than plain radiographs for the diagnosis of emphysema

Doppler echocardiography is an effective noninvasive way to estimate

pulmonary artery pressure if pulmonary hypertension is suspected

Treatment

:

Medications Supplemental oxygen

:

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– Hypoxemic patients with pulmonary hypertension, chronic cor pulmonale, erythrocytosis, impaired cognitive function , exercise intolerance, nocturnal restlessness, or morning headache are likely to benefit from home oxygen therapy

– Benefits of home oxygen therapy in patients with hypoxemia include longer survival, reduced hospitalizations, and better quality of life – Unless therapy is intended only for night-time or exercise use, 15 hours of nasal oxygen per day is required – For most patients, a flow rate of

1–3 L achieves a PaO2 > 55 mm Hg

– Medicare covers 80% of costs for patients who meet requirements

Bronchodilators are the most important pharmacologic agents –

Ipratropium bromide (2–4 puffs via MDI every 6 hours) is first-line therapy because it is longer-acting and without sympathomimetic side effects

– (

Short-acting -agonists albuterol,

metaproterenol

) have a shorter onset of action and are less expensive

– At maximal doses, bronchodilation of β-agonists is equivalent to ipratropium , but with side effects of tremor, tachycardia, and hypokalemia – Ipratropium and β-agonists together are more effective than either alone

–

(

Long-acting β -agonists formoterol , salmeterol ) and anticholinergics ( tiotropium )

appear to achieve bronchodilation that is equivalent or superior to what is experienced with ipratropium in addition to similar improvements on health status

Corticosteroids

:

– COPD is generally

not steroid responsive;

10–20% of stable outpatients have

> a 20% increase in FEV1 compared with placebo

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Oral theophylline is a third-line agent for patients

who do not respond to ipratropium or β-agonists

Antibiotics improve outcomes slightly when used to treat acute exacerbations

– Macrolides (azithromycin 500 mg followed by 250 mg daily for 5 days) – Fluoroquinolones (ciprofloxacin 500 mg every 12 hours) – Amoxicillin-clavulanate (875/125 mg every 12 hours)

Opioids : severe dyspnea in spite of optimal management may warrant a trial of an opioid

Sedative-hypnotic drugs (diazepam 5 mg three times daily orally) may benefit very anxious patients with intractable dyspnea

Surgery

:

Lung transplantation offers substantial improvement in pulmonary function and exercise performance; 2year survival is 75%

Lung volume reduction surgery in highly selected patients results in modest improvements in pulmonary function, exercise performance, and dyspnea; surgical mortality rates at experienced centers are 4–10%

Bullectomy is used for palliation of dyspnea in patients with severe bullous emphysema; most commonly pursued when a single bulla occupies at least 30–50% of the hemithorax

Therapeutic Procedures

:

Smoking cessation is the single most important goal

Cough suppressants and sedatives

should be avoided

as routine measures

Graded physical exercise programs Measure theophylline levels in hospitalized patients who have already been taking theophylline; it should not be

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Noninvasive positive pressure ventilation – Reduces the need for intubation – Shortens ICU lengths of stay – May reduce the risk of health care–associated infection and antibiotic use

Complications

:

Acute bronchitis, pneumonia, pulmonary thromboembolism, and concomitant left ventricular failure

may worsen

otherwise stable COPD

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure

are common in advanced disease

Spontaneous pneumothorax occurs in a small fraction of emphysematous patients

Hemoptysis may result from chronic bronchitis or bronchogenic carcinoma

Prevention

:

Largely preventable by eliminating chronic exposure to tobacco smoke

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Vaccination against influenza and pneumococcal infection

Prognosis

:

Median survival for severe disease (FEV1 < 1 L) is 4 years Degree of dysfunction at presentation is the A multidimensional index

most important predictor

(the BODE index),

of survival

which includes

body mass index (BMI), airway obstruction (FEV1), dyspnea (Medical Research Council dyspnea score), and exercise capacity, predicts death and hospitalization better than FEV1 alone

When to Refer

:

COPD onset occurs before the age of 40

Frequent exacerbations

(two or more a year) despite optimal treatment

Severe or rapidly progressive COPD Symptoms disproportionate to the severity of airflow obstruction Need for long-term oxygen therapy

Onset of comorbid illnesses (such as bronchiectasis, heart failure, or lung cancer )

When to Admit

:

Severe symptoms or acute worsening that fails to respond to outpatient management Acute or worsening hypoxemia, hypercapnia, peripheral edema, or change in mental status Inadequate home care, or inability to sleep or maintain nutrition/hydration due to symptoms The presence of high-risk comorbid conditions

References Ambrosino N et al. The clinical management in extremely severe COPD. Respir Med. 2007 Aug;101(8):1613â&#x20AC;&#x201C;24.

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[PMID: 17383170]

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Cote CG et al. Predictors of mortality in chronic obstructive pulmonary disease. Clin Chest Med. 2007 Sep;28(3):515–24.

17720040] Nannini L et al. Combined corticosteroid and long-acting beta-agonist in one inhaler versus placebo for chronic obstructive pulmonary disease. Cochrane Database of Syst Rev. 2007 Oct 17;(4):CD003794.

[PMID: 17943798]

Qaseem A et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2007 Nov 6;147(9):633–8.

[PMID: 17975186]

Rabe KF et al; Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med. 2007 Sep 15;176(6):532–55.

[PMID: 17507545]

Singh S et al. Inhaled anticholinergics and risk of major adverse cardiovascular events in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. JAMA. 2008 Sep 24;300(12):1439–50.

[PMID: 18812535]

Tashkin DP et al. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med. 2008 Oct 9;359(15):1543–54.

[PMID: 18836213] Torpy JM et al. JAMA patient page. Chronic obstructive pulmonary disease. JAMA. 2008 Nov 26;300(20):2448.

Wilson JF. In the clinic. Smoking cessation. Ann Intern Med. 2007 Feb 6;146(3):ITC2-1–ITC2-16.

[PMID: 19033597]

[PMID: 17283345]

Wilt TJ et al. Management of stable chronic obstructive pulmonary disease: a systemic review for a clinical practice guideline. Ann Intern Med. 2007 Nov 6;147(9):639–653.

[PMID: 17975187]

Yang IA et al. Inhaled corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database of Syst Rev. 2007 Apr 18;(2):CD002991.

[PMID: 17443520]

Content adapted from CURRENT Medical Diagnosis & Treatment 2010

Home oxygen therapy : requirements for Medicare coverage.1

Group I (any of the following): 1. PaO2 55 mm Hg or SaO2 88% taken at rest breathing room air, while awake.

2. During sleep (prescription for nocturnal oxygen use only):

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b. Decrease in PaO2 > 10 mm Hg or decrease in SaO2 > 5% associated with symptoms or signs reasonably attributed to hypoxemia (eg, impaired cognitive processes, nocturnal restlessness, insomnia).

3. During exercise (prescription for oxygen use only during exercise): a. PaO2 55 mg Hg or SaO2 88% taken during exercise for a patient whose awake, resting, room air PaO2 is 56 mm Hg or SaO2 89%, and

b. There is evidence that the use of supplemental oxygen during exercise improves the hypoxemia that was demonstrated during exercise while breathing room air.

Group II2

:

PaO2 = 56â&#x20AC;&#x201C;59 mm Hg or SaO2 = 89% if there is evidence of any of the following: 1. Dependent edema suggesting congestive heart failure.

2. P pulmonale on ECG (P wave > 3 mm in standard leads II, III, or aVF).

3. Hematocrit > 56%.

1Health Care Financing Administration, 1989.

2Patients in this group must have a second oxygen test 3 months after the initial oxygen set-up.

Patterns of disease in advanced COPD.

Type A: Pink Puffer (Emphysema Predominant)

Type B: Blue Bloater Major complaint is chronic cough, productive of mucopurulent sputum, with frequent exacerbations

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due to chest infections.

Major complaint is dyspnea, often severe, usually presenting after age 50. Cough is rare, with scant clear, mucoid sputum.

Patients are thin, with recent weight loss

History and physical examination

common.

They appear uncomfortable, with evident use of accessory muscles of respiration.

Chest is very quiet without adventitious sounds.

Often presents in late 30s and 40s.

Dyspnea usually mild, though patients may note limitations to exercise.

Patients frequently overweight and cyanotic but seem comfortable at rest.

Peripheral edema is common.

Chest is noisy, with rhonchi invariably present; wheezes are common.

No peripheral edema.

Hemoglobin usually normal (12–15 g/dL).

PaO2 normal to slightly reduced (65–75 mm Hg) but SaO2 normal at rest.

PaCO2 normal to slightly reduced (35–40 mm Hemoglobin usually elevated (15–18 g/dL).

Hg).

Chest radiograph shows hyperinflation with

Laboratory studies

flattened diaphragms.

Vascular markings are diminished , particularly at the

PaO2 reduced (45–60 mm Hg) and PaCO2 slightly to markedly elevated (50–60 mm Hg).

Chest radiograph shows increased interstitial markings ("dirty lungs"), especially at bases.

apices.

Diaphragms are not flattened.

Airflow obstruction ubiquitous.

Total lung capacity increased, sometimes markedly so.

DLCO reduced.

Pulmonary function tests

Static lung compliance increased.

Airflow obstruction ubiquitous.

Total lung capacity generally normal but may be slightly increased.

DLCO normal.

Static lung compliance normal.

Special evaluations

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/

matching

Increased perfusion to low / areas.

Cardiac output normal to slightly low.

Pulmonary artery pressures mildly elevated and increase with exercise.

Cardiac output normal.

Pulmonary artery pressures elevated, sometimes

Hemodynamics

markedly so, and worsen with exercise.

Mild to moderate degree of oxygen desaturation not usually associated with obstructive sleep apnea.

Nocturnal ventilation

Severe oxygen desaturation, frequently associated with obstructive sleep apnea.

Increased minute ventilation for level of oxygen consumption. PaO2 tends to fall, PaCO2 rises slightly.

Exercise ventilation

Decreased minute ventilation for level of oxygen consumption.

PaO2 may rise; PaCO2 may rise significantly.

DLCO, single-breath diffusing capacity for carbon monoxide; /, ventilation-perfusion.

guidance

:

COPD Management: Stable COPD

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Source: Adapted from ATS/ERS and GOLD Initiative, 2007

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COPD Management:

COPD Exacerbation

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Source: ATS/ERS

cRITICAL CARE Chronic Obstructive Pulmonary Disease Patients with COPD are at increased risk for PE.

unusually difficult.

: In addition, their preexisting respiratory compromise and

leave them particularly vulnerable to the cardiopulmonary consequences of PE . Ironically,

abnormal pulmonary vasculature

diagnosis of PE in the setting of COPD is

Patients commonly complain of

dyspnea, chest pain, cough, and anxiety, and occasionally note hemoptysis and leg swelling.

Their examinations, chest radiograms, ECGs, and arterial blood gas values are usually abnormal at baseline.

. / scans are most often unhelpful.

For example, in

PIOPED 108 patients were identified as having COPD (although objective data were available in only 43).155 Scans were intermediate probability in a full 60%. Only 20 patients (19%) had results which made pulmonary angiography unnecessary by being normal, high probability, or low probability paired with a low pretest clinical estimate. Nevertheless, for the occasional patient, /

scanning obviated pulmonary angiography.

Positive leg studies may provide a rationale for anticoagulation and obviate [= αποφεύγω ] the need for

although this approach has been called into question. 41

further investigation,

CT angiography or pulmonary angiography may be necessary to establish a diagnosis. The physician and patient may be in the unfortunate

When patients with COPD present with symptoms that are atypical for their usual exacerbation, particularly when the PaCO2 is reduced from previously elevated values, it is worth considering the diagnosis.156

position of having to repeatedly consider an invasive procedure or risk a missed diagnosis.

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In fact, it is in just this type of situation that PEs go undiagnosed. There is no simple answer to this problem and PEs will continue to be underdiagnosed until better, less invasive tests are available.

TINTINALLI Chronic Obstructive Pulmonary Disease: Management of patients

Introduction

Recent efforts to improve public awareness and research in COPD worldwide have resulted in the

with chronic obstructive

recent release of at least five sets of guidelines directed at the evaluation and treatment of

pulmonary disease (COPD) can be

COPD. 1â&#x20AC;&#x201C;6

challenging and frustrating.

According the U.S. National Heart, Lung, and Blood Institute and the World Health Organization's Global Initiative for Chronic Obstructive Lung Disease (GOLD), COPD is treatment of other disease entities characterized by airflow limitation that is not fully reversible. The airflow obstruction is have emerged over the past generally progressive and associated with an abnormal inflammatory response to noxious several decades, research and progress in the treatment of COPD particles or gases.5 Although many advances in the

remain limited.

. The diagnosis may be confirmed with spirometric A diagnosis of COPD should be evaluation: a post-bronchodilator forced expiratory volume in 1 s c o n s i d e red in any patient who (FEV1) of less than 80 percent predicted in combination with a c o m p l a i ns of chronic cough, sputum ratio of FEV1 to forced vital capacity of less than 70 percent.5 production or dyspnea, and/or exposure to risk factors for the disease

About 85 percent of patients with COPD suffer from chronic bronchitis, and 15 percent suffer primarily from emphysema.6 airspaces distal to the terminal bronchioles,

Chronic bronchitis is defined as the presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded.

Emphysema is defined as abnormal, permanent enlargement of the

accompanied by destruction of their walls and without obvious fibrosis.

In contrast, the GOLD definition does not distinguish between chronic bronchitis and emphysema. 5 Chronic bronchitis is defined in clinical terms, and emphysema is defined in terms of anatomic pathology.

Update 11/11/2008: Emergency Medicine: Management of COPD Exacerbation

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Epidemiology Chronic obstructive pulmonary disease is a major worldwide respiratory health problem. It is the sixth leading cause of death in the world, the and

fourth most common cause of death in the United States , the third most common cause of hospitalization,

the only leading cause of death that is increasing in prevalence.

In North America, COPD is rare in persons younger than 40 years but very common among older individuals, with a prevalence of

The disease is more common in men than in women, but the prevalence of COPD in women has doubled in the past few decades, a reflection of increased smoking behavior of women and increased recognition of COPD in women as a diagnostic possibility by physicians. The prevalence of COPD is highest in those

approximately 10 percent in those 55 to 85 years of age.

countries that have the greatest cigarette use.

The mortality of patients while hospitalized for a COPD exacerbation is approximately 5 to 14 percent. 7

Mortality of COPD patients admitted to an intensive care unit for exacerbation is 24 percent. For patients 65 years or older and discharged from the intensive care unit after treatment of a COPD exacerbation, the 1-year mortality is 59 percent, nearly double the expected 30 percent.

Chronic obstructive pulmonary disease is an expensive public health problem in terms of direct economic costs (such as hospital admissions and outpatient treatments), indirect economic costs (such as lost years of life, disability, and loss of working capacity), and reduction in quality of life. Estimations on the annual cost of COPD in the United States reached more than 30 billion dollars in 1995. The use of health care resources by elderly patients with COPD is immense during hospitalization and after discharge. 8

Pathophysiology

:

Cigarette smoking accounts for an estimated 80 to 90 percent of the risk of developing COPD. Age of starting, total pack-years, and current smoking status are predictive of COPD mortality.2

Of note, only 15 percent of smokers develop clinically significant COPD. A variety of other environmental risk factors, such as respiratory infections, occupational exposures, ambient air pollution, passive smoke exposure, and diet, have been suggested as other risk factors .

The only proven

genetic risk factor is 1-antitrypsin deficiency , although this accounts for fewer than

1 percent of COPD patients.

The earliest objective changes in the evolution of COPD are clinically imperceptible and are measured as small increases in peripheral airway resistance or lung compliance.

The recently released GOLD guideline stages COPD by The slow, insidious appearance severity. The use of this staging system may prove helpful in o f d y s p n e a a n d h y p e r s e c r e t i o n o f t e n diagnosing and treating COPD earlier requires several decades of disease.

The sedentary habits of many cigarette smokers result in failure to unmask exertional dyspnea, and denial results in suppression of symptoms or attribution of such symptoms to aging, poor conditioning, obesity, or allergies. Further, the respiratory consequences of cigarette smoking are

a continuum of slowly evolving and latent effects, unique to each individual, in a complex dose-response relationship.

Early in disease evolution, abstinence from smoking may eliminate symptoms and result in physiologic improvement. Once well established, however, abnormalities persist and may progress despite abstinence.

Pathologic specimens from patients with early disease demonstrate

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As disease evolves, such findings are exaggerated, acute and chronic inflammatory changes in the epithelium are more notable, and acinar expansion, destruction, and coalescence are seen.

Elements of emphysematous disease are invariably present in concert with those of bronchitic disease, although one often predominates.

Despite recognition of causative factors, what determines the clinical onset and rate of

Clearly, there is a great deal of variability in disease pattern and severity among individuals with a seemingly similar predisposition to disease.

progression of chronic airflow obstruction and the direction

The central element in the pathophysiology of chronic airflow obstruction is due to increased resistance or decreased caliber throughout the small bronchi and bronchioles. toward emphysematous or

bronchitic patterns are uncertain.

impedance [= resistance ] to airflow, especially expiratory airflow,

The majority of airway inflammation and obstruction occurs in bronchioles and lung parenchyma. Airflow obstruction results from a combination of airway secretions, mucosal edema, bronchospasm, and bronchoconstriction

from impaired elasticity.

Impedance to airflow alone accounts substantially for the abnormal physiology of the disease.

Exaggerated airway resistance

reduces total minute ventilation or increases respiratory work.

To the degree that alveolar hypoventilation occurs, hypoxemia and hypercarbia result. Even without hypoventilation, hypoxemia occurs due to ventilation-perfusion mismatching.

In addition to obstruction of peripheral airways, all forms of advanced chronic airflow obstruction involve other pathophysiologic elements to complete the overall picture.

For example, in dominantly emphysematous disease, destruction and coalescence of alveolar architecture reduce the total "matched" alveolar and capillary surface areas for diffusion of gas, and vascular destruction results in "unmatched" regions where ventilation is wasted . In addition, neurochemical

in chronic airflow obstruction may be aberrant [= παρεκκλίνων ]

and proprioceptive ventilatory responses

.

For example, ventilatory response to hypercarbia may be blunted [= αμβλυμένος ] during sleep , and VENTILATORY DRIVE AND DYSPNEA may be exaggerated despite normal pulmonary inflation.

The composition of muscle fiber types, breathing patterns, and resistance to fatigue of respiratory muscles

are also altered in advanced disease.

Moreover, pulmonary arterial hypertension supervenes as chronic airflow obstruction progresses. The right ventricle transiently hypertrophies and then dilates with the evolution of overt cor pulmonale.

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Arterial hypoxemia increases as the effects of right-to-left shunt on poorly oxygenated mixed venous blood are exaggerated.

Right ventricular pressure overload is associated with atrial and ventricular arrhythmias.

Although COPD is increasingly becoming recognized as a chronic inflammatory disease, there is no mention in the current guidelines of lower airway inflammation in the definition of COPD. 1â&#x20AC;&#x201C;6

Classification of Chronic Obstructive Pulmonary Disease by Severity

Stage

Characteristics

0. At risk

Normal spirometry

Chronic symptoms (cough, sputum production)

I. Mild

FEV1/FVC <70%

COPD FEV180% predicted With or without chronic symptoms (cough, sputum production)

II. Moderate COPD

FEV1/FVC <70%

30% FEV1 <80% predicted IIA

50% FEV1 <80% predicted

IIB

30% FEV1 <50% predicted

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With or without chronic symptoms (cough, sputum production)

III. Severe

FEV1/FVC <70%

COPD

FEV1 <30% predicted or <50% predicted plus respiratory failure or clinical signs of right heart failure

Abbreviations: COPD = chronic obstructive pulmonary disease; FEV1 = forced expiratory volume in 1 s; FVC = forced vital capacity; respiratory failure = arterial partial pressure of oxygen <60 mm Hg (8.0 kPa) with or without arterial partial pressure of carbon dioxide >50 mm Hg (6.7 kPa) while breathing air at sea level.

Source: Adapted from Pauwels RA, Buist AS, Calverley PM, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 163:1256, 2001.

Clinical Features

:

Chronic, Compensated COPD

Despite the pathophysiologic segregation [= χωβρισμός ] of chronic airflow obstruction into categories of pulmonary emphysema, chronic bronchitis, and bronchiectasis,

none of these exists as a pure entity in clinical medicine.

Most patients demonstrate a mixture of symptoms and signs. The hallmark symptoms are exertional dyspnea and cough.

Chronic, productive cough is common, and minor hemoptysis is frequent, especially in chronic bronchitis and bronchiectasis.

Physical findings include tachypnea, accessory respiratory muscle use, and pursed- lip exhalation.

Airflow obstruction causes wheezing during exhalation, especially during maximum forced exhalation, and prolongation of the expiratory time.

In dominantly bronchitic disease, coarse crackles are heard as uncleared secretions move about the central airways

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. In dominantly emphysematous disease, there is expansion of the thorax, impeded diaphragmatic motion, and global diminution of breath sounds.

Weight loss is frequent due to poor dietary intake and excessive caloric expenditure for the work of breathing.

Plethora due to secondary polycythemia and cyanosis and tremor, somnolence, and confusion due to hypercarbia may be seen in advanced disease . Findings of secondary pulmonary hypertension with or without cor pulmonale may be present.

The physical signs of ventricular dysfunction are often disguised [= συγκεκαλυμένος ]or underestimated by the seemingly more overwhelming signs of respiratory disease, or because pulmonary hyperinflation prohibits adequate auscultation.

Acute Exacerbations of COPD Decompensation is usually due to worsening of airflow obstruction resulting from superimposed respiratory infection, increased bronchospasm, or other respiratory pathology, such as pulmonary embolism, interference with respiratory drive, cardiovascular deterioration, smoking, noncompliance with medications, noxious environmental exposures, use of medications that prevent bronchorrhea, and adverse responses to medication.

Disordered ventilatory drive may a r i s e f r om misuse of oxygen therapy, Metabolic disturbances and inadequate oxygen h y p n o t i c s, or tranquilizers. delivery independent of respiratory function may cause decompensated COPD.

Exacerbations of COPD frequently result in progressive hypoxemia. Signs of hypoxemia include tachypnea, tachycardia, systemic hypertension, cyanosis, and a change in mental status. The most life-threatening feature of decompensation is hypoxemia, where

arterial saturation falls below 90 percent.

With increased work of breathing, muscle production of carbon dioxide increases, and alveolar ventilation is often unable to increase to prevent carbon dioxide retention and respiratory acidosis. Signs of hypercapnia include

mental status changes and hypopnea.

Upon presentation to the ED, patients usually complain of dyspnea and orthopnea.

The intensified effort to ventilate is further dramatized by the sitting-up-and-forward position, pursed-lip exhalation, accessory muscle use, and diaphoresis.

Pulsus paradoxus may be noted during blood pressure recording.

Complications such as pneumonia, pneumothorax, pulmonary embolism, or an acute abdomen may be neglected or minimized by the patient's generalized respiratory distress, tachypnea, or global diminution of breath sounds.

The physician should maintain a broad differential diagnosis for other disease entities that may be

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present with similar symptoms of dyspnea, such as

asthma, congestive heart failure, pneumonia, pulmonary embolism, tuberculosis, and metabolic disturbances.

Diagnosis

:

Chronic, Compensated COPD The most valuable tool in characterizing disease severity is pulmonary function testing.

In addition, examination of lung mechanics, analysis of arterial blood gases, description of ventilatory response patterns, tests of respiratory muscle performance, metabolic assessment, and noninvasive survey of hemodynamic reserve

can be performed.

The ratio of FEV1 to forced vital capacity should be used to diagnose mild COPD. However, once the disease progresses, the percentage of predicted FEV1 is a better measure of disease severity. 1â&#x20AC;&#x201C;6 Various guidelines characterize COPD severity as mild, moderate, or severe, although agreement on precise FEV1 standards remains arbitrary. 1â&#x20AC;&#x201C;6

In the early stages of COPD, arterial blood gas measurements reveal mild -to-moderate hypoxemia without evidence of hypercapnia

. As the disease progresses in severity (especially when the FEV1 falls below 1 L), hypoxemia becomes more severe and the development of hypercapnia becomes more evident. Arterial blood gas measurements worsen during acute exacerbations and may worsen during exercise and sleep.

Dominantly bronchitic disease may be associated with subtle or absent x-ray findings.

Radiographic examination is often misleading; mild chronic airflow obstruction is not likely to be radiographically apparent.

In contrast, dominantly emphysematous disease may be associated with remarkable signs of hyperaeration, such as increased anteroposterior diameter, flattened diaphragms, increased parenchymal lucency, and attenuation of pulmonary arterial vascular shadows, despite only mild-to-moderate physiologic alterations.

Right or left ventricular enlargement may not produce relative enlargement of the cardiac silhouette. Certainly, radiography is of unquestionable value in diagnosing complications such as pneumothorax, pneumonia, pleural effusion, and pulmonary neoplasia.

Diagnosing heart failure and assessing ventricular function in patients with COPD is difficult, although the use of B -natriuretic peptide may aid in this differentiation. 9

Echocardiography or gated nuclear scans to estimate ejection fractions may also be helpful. Electrocardiograms are useful to identify arrhythmias or ischemic injury but do not accurately assess the severity of pulmonary hypertension or right ventricular dysfunction.

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Acute Exacerbations of COPD Assessment of the patient with COPD exacerbation includes

1.

2.

3.

4.

5.

6.

a thorough medical history and a thorough history of the patient's recent COPD history, assessment of oxygenation, physical examination, bedside pulmonary function tests (if possible), assessment of sputum, and chest radiography.

Assessing oxygenation is essential. Although pulse oximetry may identify hypoxemia, it cannot identify hypercapnia or acid-base disturbances .

Further, unlike asthma,

a correlation between FEV1 and oxygenation does not exist.

Therefore, the spirometric criteria that have been used to eliminate the need for arterial blood gases in asthmatic patients cannot be safely applied to patients with COPD.10 A partial

pressure of oxygen, arterial (PaO2) of less than 60 mm Hg or an arterial oxygen saturation (SaO2) of less than 90 percent in room air indicates respiratory failure. In addition, a patient who is hypercapnic or who has a pH of less than 7.30 likely is experiencing a life-threatening episode of ventilatory failure and needs intensive management in the emergency department and in the intensive care unit.

Bedside pulmonary function tests can provide a rapid, objective assessment of patients and serve as a guide to the effectiveness of therapy; however, patient cooperation is essential for these tests to be reliable.

If the patient is able to cooperate, a peak expiratory Frequently, patients with COPD flow rate (PEFR) of less than 100 L per min or an FEV1 of e x a c e r b ation are too dyspneic to less than 1.00 L in a patient without chronic severe c o o p e r a te with these tests. As a result, obstruction indicates a severe exacerbation. some guidelines do not recommend using these measurements during acute Sequential measurements can be very helpful in exacerbation.3â&#x20AC;&#x201C;6 determining response to therapy.

Signs on physical examination and physician estimates of pulmonary function are highly inaccurate. 11 Measurement of FEV1 is preferred to PEFR, because FEV1 allows comparison with baseline studies and published guidelines.

Assessment of sputum includes questions about changes in volume and color, especially an increase in purulence. An increase in sputum volume and color changes suggest a bacterial etiology for the exacerbation and indicate a need for antibiotic therapy. 12 Recommendations for obtaining sputum cultures vary among various guidelines.1â&#x20AC;&#x201C;6 Radiographic abnormalities are common in COPD exacerbation and may elucidate the underlying etiology of the exacerbation, such as pneumonia, or may identify an alternative diagnosis, such as congestive heart failure. Therefore, radiographs should be strongly considered when evaluating a patient with COPD exacerbation.13

Electrocardiograms may reveal concurrent disease processes, such as ischemia or acute myocardial infarction, signs of cor pulmonale, and arrhythmias, such as multifocal atrial tachycardia. Theophylline levels should be measured in patients who take theophylline. Other tests, such as complete blood cell counts, electrolytes,

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computed tomography, and D-dimers should be obtained based on the clinical picture.

Treatment

:

Chronic, Compensated COPD The appropriate and optimal management of decompensated chronic airflow obstruction in an emergency department setting requires an appreciation of chronic day-to-day therapy.

Specific management

limits further insults to the respiratory system, treats reversible bronchospasm, and prevents or treats complications.

Healthy Lifestyle Elements include regular exercise, weight control, and smoking cessation .Pulmonary rehabilitation can improve exercise capacity Smoking cessation is the only and quality of life and is recommended in those patients with therapeutic intervention that can moderate to severe COPD. Although there is some controversy reduce the accelerated decline in lung regarding the pneumococcal vaccine in COPD patients, it is function. 14 Smoking cessation (and currently recommended by the American Thoracic Society.2 long -term oxygen therapy) has been shown to reduce COPD mortality. 1â&#x20AC;&#x201C;6

Oxygen The primary goal of long-term oxygen therapy (LTOT) is to increase baseline Pao2 to at least 60 mm Hg or an SaO2 of at least 90 percent at rest. h The use of long -term oxygen ome oxygen therapy accounts for approximately 30 percent of all therapy in patients with chronic COPD-related costs in the United States. respiratory failure has been demonstrated to reduce COPD mortality. Long-term oxygen therapy should be started in patients in whom arterial blood gases demonstrate a PaO2 of 55 mm Hg or less, an SaO2 below 88 percent, or a PaO2 between 56 and 59 mm Hg when signs of pulmonary hypertension, cor pulmonale, or polycythemia are present.5 Pharmacotherapy

Although there is no evidence that pharmacotherapy alters the progression of COPD, it is used to provide symptomatic relief, control exacerbations, improve quality of life, and improve exercise performance.

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Untitled Document Inhaled bronchodilators are used on an as - needed basis for mild to moderately obstructed patients with intermittent symptoms or on a regular basis to prevent or decrease symptoms, although they probably only chronically improve FEV1 by 10 percent in COPD.

2-Agonists relax smooth muscle by stimulating

2-adrenergic receptors. The use of long-acting inhaled

2-agonists, such as salmeterol and

The use of short-acting 2-agonists also improve exercise capacity but may be less convenient to use. formoterol, may improve overall symptoms and health status.15

In those patients with persistent symptoms, who are refractory to 2-adrenergic agents, or who are bothered by side effects, ipratropium bromide is the drug of choice . The regular use of inhaled ipratropium also has been shown to improve health status.

Anticholinergic agents facilitate bronchodilation by blocking the effect of acetylcholine on muscarinic-3 receptors.

Consideration should be given to combining 2-agonists with ipratropium, because the combination may improve bronchodilation more than either drug alone.14 With increasing

symptoms, even after optimization of the above two classes of bronchodilators, theophylline may be helpful.

Evidence is currently lacking to recommend the use of long- term systemic corticosteroid therapy for all patients with COPD.14

Only about 20 to 30 percent of patients with COPD improve when given chronic oral steroids. Initiating corticosteroid therapy requires careful analysis so as not to subject a nonresponder to the side effects unnecessarily.

Data from large trials studying the effects of inhaled corticosteroids in COPD showed that regular treatment with

inhaled corticosteroids is indicated only for patients

with a documented spirometric response to inhaled corticosteroids, those with an FEV1 of less than 50 percent, or those with predicted and recurrent exacerbations requiring antibiotic treatment or systemic corticosteroids.5 Although some studies support the use of theophylline in stable COPD patients, most current COPD guidelines consider it an adjunct therapy.1â&#x20AC;&#x201C;6

Mobilization of Secretions Assurance of generous oral fluid intake and atmospheric humidification, avoidance of antihistamine and decongestant agents, and limitation of antitussive use help mobilize respiratory secretions. The efficacy of specific expectorant products is dubious.

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Untitled Document Acute Exacerbations of COPD The goals of emergency therapy in exacerbation of COPD are to correct tissue oxygenation, alleviate reversible bronchospasm, and treat the underlying etiology of the exacerbation

Factors that influence therapy in the ED include (1) the patient's mental status; (2) degree of reversible bronchospasm; (3) recent medication usage and evidence of potential toxicity; (4) prior history of exacerbation courses, hospitalization, and intubation; (5) the presence of contraindications to any drug or class of drugs; and (6) specific causes or complications related to the exacerbation.

Oxygen The first goal in the treatment of COPD is to correct or prevent life threatening hypoxemia, aiming for a PaO2 greater than 60 mm Hg or an SaO2 greater than 90 percent.

This can be accomplished in the ED with any of the following devices: standard dual-prong nasal cannula, simple face mask, Venturi mask, and non-rebreathing mask with reservoir and one-way valve.

The need to increase PaO2 must be balanced against the possibility of producing hypercapnia, so monitoring of oxygenation and CO2 levels with arterial blood gases is imperative. Improvement after administration of supplemental oxygen may take 20 to 30 min to achieve a steady state.

If adequate oxygenation is not achieved or respiratory acidosis ensues, assisted ventilation may be required.

2-Adrenergic Agonists 2-Agonists and anticholinergic agents are first-line therapies in the management of acute, severe COPD recommended by most guidelines.1â&#x20AC;&#x201C;6 Aerosolized forms, via nebulizer or metered dose inhalers, are preferred because they minimize systemic toxicity, although limited data exist regarding the optimal dose and frequency of administration.

According to American Thoracic Society guidelines, 2-agonist agents improvement of FEV1, but the incidence of side effects is greater. 16 Side may be administered every 30 to 60 effects of 2-agonists include tremor, anxiety, and palpitations. 2-Agonists m i n , i f t o l e r a t e d . 2 Nebulized aerosols administered every 20 min may result in more rapid

should be accompanied by heart monitoring in patients known to have or are suspected of having coexisting heart disease.

Anticholinergics Anticholinergic agents, such as ipratropium and glycopyrrolate, produce similar short - term improvements in airflow obstruction measured by FEV1 and PEFR, as do 2- agonists.3â&#x20AC;&#x201C;6

Whereas some guidelines favor 2-agonists as a firstline therapy, others favor anticholinergic agents.

Ipratropium bromide given by metered dose inhaler with a spacer or as an inhalant solution by nebulization (0.5 mg or 2.5 mL of the 0.02% inhalant solution) is the usual agent of choice, although aerosolized glycopyrrolate 2 mg in 10 mL

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of saline, has been shown to be effective.

The timing of repeat doses of anticholinergic agents has not been well studied. Side effects are minimal and appear to be limited to dry mouth and an occasional metallic taste.

Evidence regarding the efficacy of the combination of a 2-adrenergic agent and an anticholinergic agent compared with a single agent alone is conflicting, although many physicians favor using this combination initially and some favor using it if the response to maximal doses of a single bronchodilator is poor.

Corticosteroids The use of a short course (7 to 14 days) of systemic steroids appears more effective than placebo in improving FEV1 in acute severe exacerbations of COPD, although their role in mild-to-moderate exacerbations needs to be delineated further.17 , 18 If used, the optimal effective dose ranges from ONE TO THREE TIMES THE MAXIMAL PHYSIOLOGIC ADRENAL SECRETION RATE (i.e., the equivalent of prednisone, 60 to 180 mg per d ). Hyperglycemia is the most common adverse effect.

Antibiotics All current guidelines recommend antibiotics for the treatment of COPD exacerbation if there is evidence of infection, such as change in volume of sputum and increased purulence of sputum.

Saint's meta-analysis demonstrated a small, but statistically significant, benefit for antibiotics in terms of resolution of obstruction and symptoms. 12 T he benefits are more apparent in more severe exacerbations. 6

Antibiotic choices should be directed at the most common pathogens known to be associated with COPD exacerbation, namely Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

There is little evidence regarding the duration of treatment; 3 to 14 days is typical in these studies.

Methylxanthines The role of methylxanthines, such as

Current evidence does not support the routine use of methylxanthines for COPD exacerbations, although most guidelines suggest their use in certain

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Untitled Document theophylline and aminophylline, in the treatment of COPD exacerbation remains controversial.

situations, such as severe exacerbation when other therapy has failed or in patients already using methylxanthines who have subtherapeutic drug levels. 3â&#x20AC;&#x201C;5 The bronchodilation effect of aminophylline is limited, and its therapeutic range is narrow.

The intravenous loading dose usually required to obtain an initial serum concentration of 8 to 12 g/mL is 5 to 6 mg/kg ideal body weight in patients not currently receiving the drug.

In patients who regularly use theophylline, a mini-loading dose should be administered: (target concentrationâ&#x20AC;&#x201C;currently assayed concentration) x volume of distribution (i.e., 0.5 times ideal body weight in liters).

With the mini-load method, the target concentration should be between 10 and 15 g/mL. The intravenous maintenance infusion rate is 0.2 to 0.8 mg/kg ideal body weight per h.

It is important to lower maintenance rates when treating patients with lower clearance rates due to congestive heart failure or hepatic insufficiency and raise maintenance rates in patients with higher clearance rates, such as smokers.

Maintenance theophylline infusion in patients on chronic oral therapy is complicated, because it is difficult to account for enteric drug yet to be absorbed.

Loading and maintenance doses may need to be reduced to minimize the risk of "summation toxicity" due to continued enteric absorption.

Standard-release preparations may continue to be absorbed for up to 6 h, and sustained-release preparations may require up to 12 h. Therefore, maintenance infusion rates should be reduced for 6 h after ingestion of a standard-release formulation and 12 h after ingestion of a sustained-release preparation (including 24-h release forms).

Theophylline and aminophylline should not be given orally in an emergency setting unless decompensation is not severe, alimentary motility is assured, and forthcoming ambulatory care is imminent.

Assisted Ventilation Mechanical ventilation is indicated in patients with COPD exacerbation if there is evidence of respiratory muscle fatigue, worsening respiratory acidosis, deteriorating mental status, and in those with clinically significant hypoxemia refractory to supplemental oxygen by usual techniques The main goals of assisted ventilation are to rest ventilatory muscles and to restore gas exchange to a stable baseline.

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Noninvasive positive pressure ventilation (NIPPV) can be delivered via a nasal mask, full face mask, or mouthpiece. No particular mode of ventilation or ventilatory device has been shown to be clearly superior.

Studies have demonstrated better outcomes in terms of intubation rates, short-term mortality rates, symptomatic improvement, and length of hospitalization in patients with respiratory failure who receive NIPPV. 19

Disadvantages of NIPPV include slower correction of gas-exchange abnormalities, risk of aspiration, inability to control airway secretions directly, and possible complications of gastric distention and skin necrosis.

Contraindications to the use of NIPPV include an uncooperative or obtunded patient, inability of the patient to clear airway secretions, hemodynamic instability, respiratory arrest, recent facial or gastroesophageal surgery, burns, poor mask fit, or extreme obesity.

Invasive ventilation should be considered in patients with ventilatory or respiratory failure who do not qualify for NIPPV. The methods most commonly used are assisted control ventilation, pressure support ventilation, or pressure support ventilation in combination with intermittent mandatory ventilation.

Adverse events associated with invasive ventilation include pneumonia, barotrauma, and failure to wean.

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Other Options There is currently little evidence to support the use of a mixture of helium and oxygen or magnesium in the treatment of acute COPD exacerbation. Factors underlying the exacerbation, comorbidities, and other etiologies of dyspnea should be identified and treated.

Future Considerations and New Therapies Bronchodilators play an important role in the long-term management of patients with COPD, but they do not alter the progression of COPD.

Major advances include the development of long -acting anticholinergic agents, such as tiotropium bromide. Tiotropium bromide has the benefit of once-daily dosing.

Inflammation is being investigated more closely in the pathogenesis of COPD, especially the role of neutrophils.

Corticosteroids, chemokine (interleukin 8) inhibitors, leukotriene B4 inhibitors, adhesion molecule inhibitors, and phosphodiesterase inhibitors are being studied with the goal of inhibiting neutrophil activity.

Surfactant replacement and lung reduction therapies are also under investigation. antiproteases, such as 1-antitrypsin.

Evidence suggests that the imbalance between proteases in COPD patients may be restored by inhibiting proteolytic enzymes, such as neutrophil elastase inhibitors, cathepsin inhibitors, matrix metalloproteinase inhibitors, and secretory leukoprotease inhibitors, or by increasing

Evidence also exists that oxidative stress is increased in patients with COPD, and that reactive oxygen species are involved in the pathogenesis of COPD. Therefore, antioxidants such as N-acetyl cysteine and spin-trap antioxidants such as -phenyl-N-tertbutyl nitrone may be useful.

Pulmonary vasodilators, such as prostacyclin analogues, nitric oxide donors, endothelial antagonists, and angiotensin antagonists,

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are being studied in the hope of preventing the progression of pulmonary hypertension and cor pulmonale.

Mucus regulators, such as tachykinin antagonists, sensory neuropeptide-release inhibitors, mediator and enzyme inhibitors, MUC gene suppressors, and mucolytic agents, may inhibit the hypersecretion of mucus, without affecting normal mucus secretion and normal mucociliary clearance.

Summary for Emergency Department Management of Exacerbations in Chronic Obstructive Pulmonary Disease

Assess severity of symptom

Administer controlled oxygen therapy Perform arterial blood gas measurement after 20â&#x20AC;&#x201C;30 min if SaO2 remains <90% or if concerned about symptomatic hypercapnia Administer bronchodilators

2-agonists and/or anticholinergic agents by nebulization or MDI with spacer Consider adding intravenous methylxanthine, if needed

Add corticosteroids Oral or intravenous

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Consider antibiotics If increased sputum volume, change in sputum color, fever, or suspicion of infectious etiology of exacerbation

Consider noninvasive mechanical ventilation Laboratory evaluation Chest x-ray CBC with differential Electrolytes Arterial blood gases ECG as needed

At all times Monitor fluid balance Consider subcutaneous heparin (venous thrombosis prophylaxis) Identify and treat associated conditions (e.g., heart failure, arrhythmias) Closely monitor condition of the patient

Abbreviations: CBC = complete blood cell count; ECG = electrocardiogram; MDI = metered dose inhaler; SaO2 = arterial oxygen saturation.

Source: Adapted from Pauwels RA, Buist AS, Calverley PM, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 163:1256, 2001.

Indications for Invasive Mechanical Ventilation

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Severe dyspnea with use of accessory muscles and paradoxical abdominal motion

Respiratory frequency >35 breaths per min

Life-threatening hypoxemia: PaO2 <50 mm Hg (<5.3 kPa) or PaO2/FIO2 <200 mm Hg Severe acidosis (pH <7.25) and hypercapnia (PaCO2 >60 mm Hg or >8.0 kPa)

Respiratory arrest Somnolence, impaired mental status Cardiovascular complications (hypotension, shock, heart failure) NIPPV failure

Abbreviations: FIO2 = fraction of inspired oxygen; NIPPV = noninvasive positive pressure ventilation; PaCO2 = partial pressure of carbon dioxide, arterial; PaO2 = partial pressure of oxygen, arterial.

Source: Adapted from Pauwels RA, Buist AS, Calverley PM, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 163:1256, 2001.

Disposition

Admission Criteria Patients who fail to improve adequately or deteriorate despite medical therapy, have significant comorbid illnesses, or are without an intact social support system at home should be hospitalized.

UNFORTUNATELY, OBJECTIVE CRITERIA REGARDING HOSPITAL ADMISSION, OBSERVATION UNIT STAY, AND ED DISCHARGE ARE LACKING. THE GOLD .GUIDELINES OFFER CRITERIA THAT MAY HELP GUIDE THE EMERGENCY PHYSICIAN'S DISPOSITION DECISION-MAKING PROCESS

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relapse and may be safely discharged home,20 current data indicate that 43 percent of patients with COPD exacerbation discharged home from the ED have ongoing symptoms at 2 weeks and 43 percent have a relapse of symptoms. 21 The primary goals of hospitalization are to manage the acute exacerbation, prevent further deterioration, and educate patients about disease management.

Discharge

If the patient is deemed stable enough for discharge to home, the following should be arranged: (1) adequate supply of home oxygen, if needed; (2) adequate and appropriate bronchodilator treatment; (3) consideration of a short course of oral corticosteroids;18 and (4) a follow-up appointment with their physician.

Indications for Hospital Admission for Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Marked increase in intensity of symptoms, such as sudden development of resting dyspnea Severe background of chronic obstructive pulmonary disease Onset of new physical signs (e.g., cyanosis, peripheral edema) Failure of exacerbation to respond to initial medical management Significant comorbidities Newly occurring arrhythmias Diagnostic uncertainty Older age Insufficient home support file:///C|/Documents%20and%20Settings/Administrator/My%20Documents/site%20finaL/copd.htm[8/13/2010 8:19:11 PM]

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Source: Adapted from Pauwels RA, Buist AS, Calverley PM, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 163:1256, 2001.

Indications for Intensive Care Admission of Patients with Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Severe dyspnea that responds inadequately to initial emergency therapy Confusion, lethargy, coma Persistent or worsening hypoxemia: PaO2 <50 mm Hg (<6.7 kPa) Severe or worsening hypercapnia: PaCO2 >70 mm Hg (>9.3 kPa) Severe or worsening respiratory acidosis (pH <7.30) despite supplemental oxygen and NIPPV

Abbreviations: NIPPV = noninvasive positive pressure ventilation; PaCO2 = partial pressure of carbon dioxide, arterial; PaO2 = partial pressure of oxygen, arterial.

Source: Adapted from Pauwels RA, Buist AS, Calverley PM, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 163:1256, 2001.

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HURST THE HEART DIAGNOSIS OF PATIENT WITHS ISCEMIC HEART DISEASE

Management of Special Categories

Systemic Arterial Hypertension

Patients with systemic arterial hypertension often have angina pectoris.

In most patients, significant coronary atherosclerosis of the epicardial blood vessels is present, but some patients with systemic arterial hypertension may have angina pectoris, or even fatal MI, without significant obstruction of the large epicardial vessels. . In many patients, treatment of the hypertension with a A major mistake is to send a blocker, calcium antagonist, or ACE inhibitor also will decrease patient for noninvasive testing when MVO2 and prevent the development of angina pectoris.

In general, efforts should be made to control the blood pressure both at rest and during exercise. It is now

the patient's hypertension has not been treated

known that many patients with an elevated systolic and/or diastolic blood pressure above the normal variation during exercise will develop severe fixed systemic arterial hypertension.

Efforts should be made to control the blood pressure both at rest and during exertion.

Chronic Obstructive Pulmonary Disease/Asthma

Blockers should be avoided in the subset of patients who have true bronchospastic lung disease; in them, the use of nitrates and calcium antagonists is preferred.

Because many of these patients receive medications for their pulmonary disease that may increase their heart rate or even produce supraventricular tachycardia, it is preferable to use a heart rate-slowing calcium antagonist such as diltiazem or verapamil.

Elderly Patients

The presence of sinus tachycardia or atrial fibrillation is In general, elderly patients such as t o l e r a t e c a l c i u m a n t a g o n i s t s b e t t er than nifedipine or amlodipine. blockers.

In such patients, diltiazem or verapamil, or even a relative contraindication to the selection of dihydropyridines

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a

blocker is preferable.

On the other hand,

blockers, verapamil, and diltiazem can exacerbate AV block, and

verapamil produces constipation in many elderly patients.

Also, some elderly patients develop postural hypotension from short-acting nitrates.

Peripheral Vascular Disease

Alternatively, the worsening symptoms may be the result of a decrease in arterial perfusion pressure.

In general, it is preferable to treat patients with chronic stable angina who have peripheral vascular disease with nitrates and a calcium antagonist.

Patients with peripheral vascular disease may have a worsening of their symptoms when they are treated with a nonselective blocker, permitting unopposed -induced vasoconstriction.

Diabetes Mellitus

If it is necessary to use a blocker, a cardioselective Patients with chronic stable agent should be chosen, because it is less likely to impair angina who have diabetes mellitus and the recognition of and recovery from insulin-induced insulin -induced hypoglycemic episodes hypoglycemia.

In most diabetics, cardioselective blockers are well tolerated. The BARI-2D randomized clinical trial is evaluating the efficacy of early myocardial revascularization in diabetes with CAD.

should probably be treated with nitrates and calcium antagonists (see Chap. 90 ).

Chronic Renal Disease

Although

blockers and calcium antagonists can normally be used effectively in patients with

chronic angina and chronic renal insufficiency, careful monitoring may be necessary, because many antagonists are excreted primarily by the kidneys.

blockers and calcium

PULMONARY HYPERTENSION

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Chronic Obstructive Airways Disease

Chronic bronchitis and emphysema (chronic obstructive pulmonary disease [COPD]) are the most common causes of cor pulmonale in patients with intrinsic pulmonary disease. 17 , 18 Cystic fibrosis is an example of A MIXED AIRWAYS AND PARENCHYMAL LUNG DISEASE in which pulmonary hypertension plays a significant role in outcome.

Cor pulmonale is encountered in two different settings: acutely in the setting of decompensation, which is often caused by an acute respiratory infection, and chronically, when progressive lung disease and worsening gas exchange lead to unremitting vascular remodeling.

Noninvasive studies, such as echocardiography, have proved useful in some centers.19 , 20

The gold standard for diagnosing pulmonary hypertension in patients with COPD is right -heart catheterization.

RV enlargement, the cardinal sign of pulmonary hypertension, can be difficult to discern in obstructive airways disease because of hyperinflation and cardiac rotation.21 Once suspicion is raised that the clinical picture of RV failure stems from gas exchange abnormalities, an arterial blood sample will

confirm that the PO2 is low (PO2 <50 mmHg) and the PCO2 is high (PCO2 >50 mmHg).

Derangement in gas exchange to this degree is rare in LV failure unless overt pulmonary edema is present.

. Because of these limitations, standard ECG criteria for ECG evidence of RV hypertrophy RV enlargement apply in about one-third of patients with is also often equivocal in patients with COPD who have cor pulmonale at autopsy.

Consecutive changes in the ECG are often more useful than a single ECG in detecting RV overload.

chronic obstructive airways disease (chronic bronchitis and emphysema, COPD) because of rotation and displacement of the heart, widened distances between electrodes and the cardiac surface, and the predominance of right -sided heart dilatation over hypertrophy

As the arterial PO2 drops to abnormal levels (e.g., <60 to 70 mmHg while awake), T waves tend to become inverted, biphasic, or flat in the right, precordial leads (V1 to V3); the mean electrical axis of the QRS shifts 30 degrees or more to the right of the patient's usual axis; ST segments become depressed in leads II, III, and aVF; and right bundle-branch block (incomplete or complete) often appears. THESE CHANGES TEND TO REVERSE AS ARTERIAL OXYGENATION IMPROVES (SEECHAP. 13 ).

Considerable improvement also may be accomplished even in the individual who has chronic pulmonary hypertension

In the patient with COPD with acute cor pulmonale precipitated by a

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by sustained (>18 h/d) breathing of oxygen-enriched air.

Once the RV has failed, inotropic agents should be used cautiously because of the threat of arrhythmias posed by arterial hypoxemia and respiratory acidosis.

bout of bronchitis or pneumonia, the goal of therapy is to maintain tolerable levels of arterial oxygenation while waiting for the upper respiratory infection to subside.

Moreover, after adequate oxygenation has been achieved, the need for digitalis and diuretics often decreases because the hemodynamic burden on the RV decreases. Even though acute cor pulmonale is largely reversible, each bout appears to leave behind a slightly higher level of pulmonary hypertension after recovery.17 Polycythemia is rarely severe enough to be a serious problem in cor pulmonale associated with bronchitis and emphysema; when it is present, it is usually indicative of suboptimal use of supplemental oxygen.

Arterial blood gas composition is the therapeutic compass to the control of pulmonary hypertension in COPD. The degree of hypoxia may be underestimated

Vasodilators recently have been tried in various types of secondary pulmonary hypertension, including that caused by COPD.22

by blood sampling while the patient is awake and at rest, as hypoxemia is more marked during sleep and with physical

They may aggravate arterial hypoxemia by exaggerating ventilationâ&#x20AC;&#x201C;perfusion abnormalities.

activity. Determinations of the oxygen saturation during sleep or with ambulation using pulse oximetry are

TO DATE, THE SAFEST AND MOST helpful in optimally prescribing EFFECTIVE APPROACH TO PULMONARY supplemental oxygen.

VASODILATATION IN OBSTRUCTIVE LUNG DISEASE WITH ARTERIAL HYPOXEMIA IS THE USE OF SUPPLEMENTAL OXYGEN. 22

CHRONIC COR PULMONALE

Incidence

Estimates of the incidence of chronic cor pulmonale, as well as estimates of morbidity and even mortality directly attributable to right-heart dysfunction secondary to lung disease, are difficult to obtain. It is difficult to separate epidemiologic data relevant to cor pulmonale from the lung disease that is its primary cause. In addition, a definitive diagnosis most often requires invasive diagnostic procedures, often at a time when treating the lung disease is the most paramount clinical issue. However, the magnitude of the clinical problem can be appreciated from data on chronic obstructive pulmonary disease (COPD), undoubtedly the most common cause of cor pulmonale.

The estimated total prevalence of COPD in the world is currently 400 million individuals. In 1999, there were 713,000 hospital discharges with a diagnosis of COPD in the United States, a discharge rate of 25.9 per 10,000 population. In the United States, there were 123,550 deaths caused by COPD in the year 2000.3 According to a WHO report, COPD accounted for 4.8 percent of all deaths in the United States in 1998. Worldwide, the problem is even more dramatic. WHO estimates that COPD accounted for 4.73 percent of all deaths in member nations (Table 73â&#x20AC;&#x201C;1). Thus, for every 100,000 people in the world, 43 died of COPD in 2001.3

WHO estimates that up to 14 percent of patients with COPD suffer from secondary PAH, whereas RV dysfunction has been found in up to 66 percent of patients with end-stage lung disease referred for lung transplantation evaluation.3 , 4 However, the incidence of severe pulmonary hypertension in COPD is 5 percent or less. 5 , 6 The fraction of patients with right side of the heart dysfunction resulting from secondary PAH is unknown. A study from the United Kingdom estimates that 0.3 percent of the population had both an arterial oxygen tension less than 55 mmHg and clear evidence of airways obstruction by pulmonary function testing.7 These data would predict 60,000 subjects in England and Wales at serious risk for secondary PAH. 7 Again, the number of these subjects who had cor pulmonale cannot be determined.

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Untitled Document It is clear from the available epidemiologic data that diseases predisposing to cor pulmonale are an enormous health problem throughout the world. Undoubtedly cor pulmonale is a major contributor to the morbidity and mortality in these diseases.

Worldwide Mortality Attributable to Chronic Obstructive Pulmonary Disease (COPD)

WHO region

Total Population

Total Deaths

COPD Deaths

COPD percent of Total Deaths

Deaths per 100,000

Africa

655,476,000

10,680,871

116,045

1.09

17.7

The Americas

837,967,000

5,910,811

221,682

3.75

26.5

493,091,000

4,156,667

88,318

2.12

17.9

Europe

874,178,000

9,702,763

284,581

2.93

32.6

Southeast Asia

1,559,810,000

14,466,690

614,555

4.25

39.4

Western Pacific

1,701,689,000

11,636,373

1,347,093

11.58

79.2

Total

6,122,211,000

56,554,175

2,672,274

4.73

43.6

Eastern Mediterranean

SOURCE: World Health Organization. Consultation on the Development of a Comprehensive Approach for the Prevention and Control of Chronic Respiratory Diseases. 3

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Chronic Lung Disease

COPD patients ascending to altitude often report increased dyspnea and reduced exercise ability. Those with hypoxemia, pulmonary hypertension, disordered control of ventilation, and sleep-disordered breathing at sea level may have greater problems at altitude because of the greater alveolar hypoxia.

The required FiO2 can be calculated by Such patients may require multiplying low-altitude FiO2 by the ratio of lows u p p l e m ental oxygen at altitude when altitude barometric pressure divided by hight h e y d o not at sea level (and avoid altitude barometric pressure. This will ensure the delivery of the same partial pressure of oxygen as at low altitude.

having to descend), and oxygendependent patients at sea level may need to increase the FiO2.

There are no data to suggest that persons with COPD are more likely to develop AMS or HAPE, although such persons may be self-selected to avoid travel to high-altitude locations.

In fact, persons with mild to moderate COPD already are partially acclimatized and may do well at modest altitude.

High altitude per se does not exacerbate asthma, and persons with chronic bronchospasm often report easier breathing at high altitude due to lower air density and/or cleaner air.

Patients with allergic asthma do better at high altitude because of reduced allergens.

DEGOWIN Chronic Obstructive Pulmonary Diseases

The obstruction is fully reversible, at least initially, in asthma and may be either fixed or partially reversible in COPD.

Airflow obstruction in expiration is the hallmark of asthma and chronic obstructive lung disease (COPD).

Expiratory airflow obstruction leads to air trapping (increased residual volume) and a sustained inspiratory position of the chest (flat diaphragm, horizontal ribs, increased anterior-posterior diameter, hyperresonance) which increases the work of breathing and decreases the inspiratory capacity. file:///C|/Documents%20and%20Settings/Administrator/My%20Documents/site%20finaL/copd.htm[8/13/2010 8:19:11 PM]

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The combination of history, physical signs, chest radiographic features and results of pulmonary function testing allow differentiation of the different syndromes [Straus SE, McAlister FA, Sackett DL, et al. The accuracy of patient history, wheezing, and laryngeal measurements in diagnosing obstructive airway disease. JAMA. 2000;283:1853â&#x20AC;&#x201C;1857 [PMID: 10770147] ; Holleman DR Jr, Simel DL. The rational clinical examination. Does the clinical examination predict airflow limitation? JAMA. 1995;273:313â&#x20AC;&#x201C;319[PMID: 7815660].

Key Syndrome Asthma Asthma is an acquired

Airway obstruction leads to air trapping and lung hyperinflation.

syndrome of increased airway

Asymptomatic patients may have active airway inflammation.

Between attacks, the patient is well and the chest findings are normal.

An asthma flair frequently begins with nonproductive cough and progressive dyspnea.

responsiveness to allergic and nonallergic stimuli, airway inflammation, bronchospasm, hyperplasia of mucous-producing cells, and bronchial smooth muscle hypertrophy.

Nocturnal awaking with attacks of coughing and chest tightness is common.

Sitting and leaning over a table or chair back improves the dyspnea. The respiratory rate does not increase, but inspiration is short while expiration is prolonged and labored; the patient is often anxious.

As air trapping increases, the chest becomes hyperresonant, the diaphragm flattens and the thorax maintains the inspiratory position. The costal margins only diverge slightly, or they may actually converge during inspiration. In severe asthma attacks, the sternocleidomastoid and platysma muscles tense and the alae nasi flare with each inspiratory effort.

Wheezing becomes less prominent as the attack worsens. Auscultation discloses decreased air movement, wheezes, and coarse crackles.

LOCALIZED ABSENCE OF BREATH SOUNDS SUGGESTS BRONCHIAL PLUGGING. As the attack subsides, clear tenacious sputum is raised, and breathing gradually becomes less labored.

Asthma can occur without wheezing.

The only sign that consistently identifies severe asthma is use of the accessory muscles of respiration.

Clinical history and bedside or home airflow measurements are useful for assessment of severity and planning management.

DDX:

Asthma can be confused with other conditions.

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When wheezing is limited to a single region, bronchial obstruction from foreign body or neoplasm should be considered.

The sudden occurrence of LV failure or mitral regurgitation may closely simulate asthma: there are wheezes and crackles, and labored breathing may limit heart auscultation.

Vocal cord dysfunction (i.e., paradoxical closure of the cords during inspiration) may be identified by examination of the glottis during an attack; it is suggested when the wheezes are loudest over the neck.

The symptoms and signs of asthma are often relieved in a few minutes by inhaled bronchodilators; reversible airway obstruction can be demonstrated with pulmonary function testing.

Key Syndrome Emphysema

Smoking leads to the destruction of alveolar walls with loss of alveolar surface area and decreased elastic recoil produces collapse with expiration.

They often exhale with pursed-lips, especially with exertion.

Patients present with progressive dyspnea, often accompanied by gradual weight loss.

The chest is hyperresonant with decreased breath sounds and prolonged expiration ( Key Sign Resonance and Hyperresonanceâ&#x20AC;&#x201D;Pulmonary Emphysema).

Wheezes and crackles are uncommon unless infection supervenes. Physical findings are poorly correlated with the severity of airflow obstruction or abnormalities of gas exchange.

Early detection of obstructive airways disease in patients with symptoms or risk factors is best accomplished by spirometry.

Key Syndrome Chronic Bronchitis

. Airways obstruction is prominent and hypoxia common.

Chronic inflammation and infection of the airways Patients present with chronic cough with >60 mL/d of s e c o n d a r y from chronic exposure to sputum (chronic bronchitis with or without bronchiectasis) and r e s u l t s progressive dyspnea. Lung examination shows diminished breath t o b a c c o s m o k e sounds and prolongation of expiration; wheezing and inspiratory crackles may be present.

Physical finding are poorly correlated with the severity of airflow obstruction or abnormalities of gas exchange.

Bronchiectasis

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Cough with purulent sputum and Severe acute or chronic occasionally hemoptysis or recurrent pneumonia pulmonary infections result in multiple is the presenting symptom. Sputum is copious and chronically infected dilatations of the smaller bronchi.

purulent.

A resonant chest with coarse basilar crackles suggests bronchiectasis. Clubbing may be present.

Chronic infection with nontuberculous mycobacteria is common. High-resolution CT imaging is diagnostic [Barker AF. Bronchiectasis. N Engl J Med. 2002;346:1383–1393 [PMID: 11986413] .

Asthma Clinical Severity Classification

Symptoms Asthma Severity

Day

Night

FEV1; Peak expiratory flow variability

Mild Intermittent

2 or less days/week

2 or less nights/month

80; <20%

Mild Persistent

>2 days/week

>2 nights/month

80; 20–30%

Moderate Persistent

Daily

> 1 night/week

60–79%; >30%

Severe Persistent

Continual

Frequent

<60%; >30%

Gold Criteria for COPD Severity

Stage

Severity

I

Mild

FEV1 (% predicted) 80

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II

Moderate

< 80

<0.7

III

Severe

< 50

<0.7

IV

Very severe

<30 or < 50 with respiratory failure or right heart failure

<0.7

HAZZARD GERIATRICS CHAPTER 83 : COPD

|

GO |

82 = AGING OF RESPIRATORY

| GO |

62. Cognitive Changes Associated with Normal and Pathological Aging

|

GO |

Chronic Obstructive Pulmonary Disease

Emphysema and chronic bronchitis obstruct airflow, resulting in hypoxemia and hypercapnia.

Deficits in verbal and visual memory, attention, abstraction, psychomotor speed, information processing speed, and IQ have all been reported.

Cognitive dysfunction is commonly observed in chronic obstructive pulmonary disease, although the specific skills affected appear to be broad and diffuse.

These changes in cognition appear to be caused by hypoxemia. The decrease in arterial oxygen partial pressure correlates with neuropsychological impairments, and most studies indicate that oxygen therapy results in modest improvements in cognition.

Depression is also common in chronic obstructive pulmonary disease and must be considered as another cognitive risk factor.

Chapter 40. Malnutrition and Enteral/Parenteral Alimentation [

GO ]

Chronic Obstructive Pulmonary Disease

Prevalence estimates of malnutrition in patients with COPD range from 20% to 70%.

Although a meta-analysis concluded that energy supplementation does not have significant effects in patients with stable COPD, another review indicated that 10

Increased inflammatory activity probably contributes to catabolic

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of 12 randomized-controlled trials have noted positive effects of nutritional support (mostly oral supplements providing 400â&#x20AC;&#x201C; 1000 kcal/d) on anthropometric, immune, muscular strength, and respiratory function outcome measures.

processes that combine with undernutrition to cause weight loss and loss of lean body mass.

Given the relative low cost and potential for benefit, nutritional support might be considered for patients with COPD and evidence of PEM.

Tests to Assess Response to Therapy for Asthma and COPD The inhaled corticosteroids used to treat asthma and COPD frequently cause thrush (or other sideeffects at high daily doses), while the long-acting BD inhalers may cause muscle cramps, tremors, insomnia, and arrhythmias.

These asthma controller medications are usually started at high doses or in combination during an exacerbation of asthma or COPD, but this therapy should be adjusted downward a few months later after maximal control is obtained.

When oral corticosteroids such as prednisone are necessary to maintain asthma control, serious morbidity frequently occurs because of ocular disease, osteoporosis, and glucose intolerance; therefore, objective measurements of the effectiveness of each newly prescribed asthma or COPD medication for each patient is highly desirable.

Two lung function tests are used as asthma therapy outcome measures in the outpatient clinic setting: the pre- or post-BD FEV1 during a clinic visit, or peak expiratory flow (PEF) measured at home in the early morning.

Pocket spirometers, which measure both FEV1 and PEF, are now available for the same cost as a mechanical peak flow meter.

Because many elderly patients become tolerant of severe, long-standing airway obstruction and consequently underreport respiratory symptoms, objective measurement of

The FEV1 is more accurate and more sensitive than peak flow for detecting narrow airways, and it is linearly related to the severity

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lung function is needed.

elderly patients.

FEV1 improvement of more than 20% and 0.20 L is necessary to be confident that the change was not merely a result of measurement noise.

The FEV1 measured 10â&#x20AC;&#x201C;30 minutes after albuterol is considered the best lung function that can be achieved on the day of the visit, and therefore, is a more stable measure in asthmatics than comparing visit-tovisit FEV1 values without prior administration of albuterol.

In the future, the availability of less expensive eNO analyzers for monitoring asthma in outpatient settings may complement or replace spirometry for this purpose.

Differential Diagnosis of Asthma and COPD The elderly are much more likely than middle-aged adults to have COPD and cardiovascular disease, both often a result of cigarette smoking, and both with symptoms that may mimic asthma, increasing the value of objective pulmonary function (PF) tests in the elderly patient.

Because intermittent airway obstruction is the primary physiologic manifestation of asthma, the first (and least expensive) PF test to perform is spirometry, especially if the patient is experiencing symptoms at the time of presentation

The differential diagnosis of asthma and COPD in elderly persons is often more difficult than in younger adults because of the higher prevalence of comorbidity.

If the FEV1/FVC ratio is below the lower limit of the normal range (assuming that appropriate reference equations for elderly patients are used and the quality of the test session was good), the patient has airway obstruction.

The degree of severity of the obstruction is then determined by the percent predicted FEV1. When compared

to younger patients with asthma, one will often be surprised by more severe airway obstruction (an

FEV1 below 50% predicted) in elderly patients with asthma.

If the patient has airways obstruction, repeat spirometry approximately 45 minutes after administration of a combination of albuterol and ipratropium (post-BD) spirometry). A positive (significant) BD response is best defined as an increase of at least a 12% (and 0.20 L) improvement in percent predicted FEV1 or FVC. With good test quality, baseline airway obstruction followed by a BD response helps to confirm asthma in a patient with a history suggesting asthma. However, the lack of a positive BD response is of no help in making the diagnosis (does not rule out asthma), because chronic asthma often leads to airways inflammation that is not acutely reversible. Furthermore, many elderly patients with a history of smoking, current symptoms suggesting asthma, baseline airways obstruction, and a "positive" BD response, still have some "fixed" obstruction (a low FEV1) following aggressive therapy for asthma.

Some guidelines consider this pattern evidence for COPD.

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Pre- and post-BD spirometry may be normal in patients with a history suggesting asthma. The patient maybe asked to return for retesting when symptoms occur; however, a methacholine challenge test (MCT) or measurement of exhaled nitric oxide (eNO) can quickly and safely detect the bronchial hyperresponsiveness (MCT) or the eosinophilic airway inflammation (eNO) characteristic of asthma.

The MCT has optimal clinical utility when the pretest probability of asthma is intermediate.

A high PC-20 (above 16 mg/mL) makes asthma highly unlikely, while a low PC-20 (below 4 mg/mL) in a patient with a history of asthma-like symptoms increases the pretest probability of asthma.

Emphysema lowers the DLCO, obstructive chronic bronchitis does not affect the DLCO, and ASTHMA FREQUENTLY INCREASES THE DLCO. A lung CT scan may also differentiate asthma from emphysema in a cigarette smoker, although both diseases may coexist

Measurement of the DLCO is quick, safe, and helps to distinguish between emphysema and other causes of chronic airway obstruction.

The role of PF tests in making a differential diagnosis of asthma versus COPD in a patient with chronic or intermittent dyspnea.

If the patient has airways obstruction, repeat spirometry approximately 45 minutes after administration of a combination of albuterol and ipratropium (post-BD) spirometry). A positive (significant) BD response is

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best defined as an increase of at least a 12% (and 0.20 L) improvement in percent predicted FEV1 or FVC. With good test quality, baseline airway obstruction followed by a BD response helps to confirm asthma in a patient with a history suggesting asthma. However, the lack of a positive BD response is of no help in making the diagnosis (does not rule out asthma), because chronic asthma often leads to airways inflammation that is not acutely reversible. Furthermore, many elderly patients with a history of smoking, current symptoms suggesting asthma, baseline airways obstruction, and a "positive" BD response, still have some "fixed" obstruction (a low FEV1) following aggressive therapy for asthma. Some guidelines consider this pattern evidence for COPD. Pre- and post-BD spirometry may be normal in patients with a history suggesting asthma. The patient maybe asked to return for retesting when symptoms occur; however, a methacholine challenge test (MCT) or measurement of exhaled nitric oxide (eNO) can quickly and safely detect the bronchial hyperresponsiveness (MCT) or the eosinophilic airway inflammation (eNO) characteristic of asthma. The MCT has optimal clinical utility when the pretest probability of asthma is intermediate. A high PC-20 (above 16 mg/mL) makes asthma highly unlikely, while a low PC-20 (below 4 mg/mL) in a patient with a history of asthma-like symptoms increases the pretest probability of asthma.

Measurement of the DLCO is quick, safe, and helps to distinguish between emphysema and other causes of chronic airway obstruction. Emphysema lowers the DLCO, obstructive chronic bronchitis does not affect the DLCO, and asthma frequently increases the DLCO. A lung CT scan may also differentiate asthma from emphysema in a cigarette smoker, although both diseases may coexist

GOODMAN GILMAN Use of Asthma Drugs in COPD

Pharmacological interventions can help patients to stop smoking.

Nicotine gum (NICORETTE), nicotine transdermal patches (NICODERM), and the antidepressant agent bupropion (ZYBAN) are moderately useful when combined with other interventions such as support groups and physician encouragement. Clonidine may be

helpful in reducing the craving for cigarettes. Treatment of nicotine addiction is

Emphysema can be prevented or its progression slowed if the patient stops smoking (Ferguson and

Cherniack, 1993 ).

discussed inChapter 23 .

For patients with emphysema who have a significant degree of

The pharmacological treatment of e s t a b l i s hed emphysema resembles that production, symptomatic use of inhaled ipratropium or a 2 adrenergic o f a s t h m a largely because the agonist may be helpful. inflammatory/bronchospastic component Ipratropium or tiotropium usually produces o f a p a t i e n t ' s d i s e a s e i s t h e a s p e c t about the same modest degree of bronchodilation a m e n a b l e t o t h e r a p y ( F e r g u s o n a n d in patients with COPD as do maximal doses of 2 C h e r n i a c k , 1 9 9 3 ) . adrenergic agonists. As in asthmatic patients, continuous use of bronchodilators is controversial, with some studies suggesting that it is associated with an unfavorable course of COPD (van Schayck et al., 1991 ). active inflammation with bronchospasm and excessive mucus

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subgroup

of

patients

may

respond

favorably

to

short

courses

of

oral

glucocorticoids. Without a treatment trial, it is not possible to predict whether a particular patient will respond to glucocorticoids.

Response to oral glucocorticoids may predict those patients who will respond to inhaled glucocorticoids.

However, except for the treatment of acute bronchospastic episodes, glucocorticoids have given mixed results in the treatment of COPD (American Thoracic Society, 1987 ;Dompeling et al., 1993 ).

In some patients, theophylline may be effective (Murciano et al., 1989 ); in others who have a profound response to 2 adrenergic agonists, theophylline fails to produce additional bronchodilation beyond that achieved by maximal doses of the inhaled adrenergic agonist.

In a minority of patients, emphysema results from a genetic deficiency of the plasma proteinase inhibitor 1-antiproteinase (also called 1-antitrypsin) (Crystal, 1990 ). Lung tissue destruction is caused by the unopposed action of neutrophil elastase and other proteinases.

Purified 1-antiproteinase (PROLASTIN) from human plasma is available for intravenous replacement.

Links : PATHOPHYSIOLOGY OF DISEASE Chapter 9. Pulmonary Disease | GO |

FAMILY M EDICINE Chapter 26. Respiratory Problems |

GO

|

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dRUG MONOGRAPHS Dyphylline and Guaifenesin | GO |

iMAGES VIDEO AND AUDIO

| GO |

CURRENT EMERNGENCIES

Asthma & Chronic Obstructive Pulmonary Disease CURRENT Diagnosis & Treatment: Emergency Medicine > Chapter 31. Pulmonary Emergencies > Immediate Management of LifeThreatening Problems

Severe Asthma, Chronic Obstructive Pulmonary Disease CURRENT Diagnosis & Treatment: Emergency Medicine > Chapter 11. Respiratory Distress > Immediate Management of LifeThreatening Problems

Asthma, Chronic Obstructive Pulmonary Disease, & Cystic Fibrosis CURRENT Diagnosis & Treatment: Emergency Medicine > Chapter 11. Respiratory Distress > Emergency Treatment of Specific Disorders > Airway Disease

HARRISON

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Chapter 254. Chronic Obstructive Pulmonary Disease

Chapter e36. Pulmonary Biomarkers in COPD

Etiology

Chronic Obstructive Lung Disease

Chronic Lung Disease Harrison's Online > Chapter 117. Health Advice for International Travel > Travel and Special Hosts > Chronic Illness, Disability, and Travel

Nontypable H. influenzae is a common cause of community-acquired bacterial pneumonia in...

file:///C|/Documents%20and%20Settings/Administrator/My%20Documents/site%20finaL/copd.htm[8/13/2010 8:19:11 PM]

Untitled Document Harrison's Online > Chapter 139. Haemophilus Infections > Haemophilus influenzae > Clinical Manifestations > Nontypable H. influenzae

CURRENT DT PULMONARY

Chapter 7. Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease (COPD) CURRENT Diagnosis & Treatment in Pulmonary Medicine > Chapter 30. Medical Conditions That Often Cause Daytime Sleepiness

Exacerbations of Chronic Obstructive Pulmonary Disease CURRENT Diagnosis & Treatment in Pulmonary Medicine > Chapter 25. Acute Ventilatory Failure > Treatment

Chronic Obstructive Pulmonary Disease CURRENT Diagnosis & Treatment in Pulmonary Medicine > Chapter 26. Chronic Ventilatory Failure > Treatment > Noninvasive Positive-Pressure Ventilation

Exacerbations of COPD (Including Emphysema) CURRENT Diagnosis & Treatment in Pulmonary Medicine > Chapter 25. Acute Ventilatory Failure > A Mechanistic Approach to Acute Ventilatory Failure > Increased Work of Breathing Due to Lung, Chest Wall, and Pleural Processes

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Pulmonary Function Tests: Interpretation in Obstructive and Restrictive Pulmonary Disease.

Tests

Units

Definition

Disease

Obstructive

Disease

Restrictive

SPIROMETRY

Forced vital capacity (FVC)

Forced expiratory volume in 1 second (FEV1) FEV1/FVC Forced expiratory flow from 25%â&#x20AC;&#x201C; 75% of the forced vital capacity (FEF 25â&#x20AC;&#x201C; 75%)

Peak expiratory flow rate (PEFR)

(MVV)

Maximum voluntary ventilation

L

The volume that can be forcefully expelled from the lungs after maximal inspiration.

L

The volume expelled in the first second of the FVC maneuver.

N or

N or

%

L/sec

L/sec

N or

N or

The maximal midexpiratory airflow rate.

The maximal airflow rate achieved in the FVC maneuver.

N or

The maximum volume that can be breathed L/minin 1 minute (usually measured for 15 seconds and multiplied by 4).

N or

LUNG VOLUMES

Slow vital capacity (SVC)

L

The volume that can be slowly exhaled after maximal inspiration.

N or

Total lung capacity (TLC)

L

The volume in the lungs after a maximal inspiration.

N or

Functional residual capacity (FRC)

L

The volume in the lungs at the end of a normal tidal expiration.

Expiratory reserve volume (ERV)

L

The volume representing the difference between FRC and RV.

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N or

N or

N or

Untitled Document Residual volume (RV)

L

RV/TLC ratio

. . .

The volume remaining in the lungs after maximal expiration.

N or

N or

See Key. N = normal; = less than predicted; = greater than predicted. Normal values vary according to subject sex, age, body size, and ethnicity.

Modified, with permission, from Tierney LM Jr, McPhee SJ, Papadakis MA (editors): Current Medical Diagnosis & Treatment 2003. McGrawHill, 2003.

Pulmonary Function Tests: Interpretation in Obstructive and Restrictive Pulmonary Disease.

Tests

Units

Definition

Disease

Obstructive

Disease

Restrictive

SPIROMETRY

Forced vital capacity (FVC)

Forced expiratory volume in 1 second (FEV1) FEV1/FVC Forced expiratory flow from 25%â&#x20AC;&#x201C; 75% of the forced vital capacity (FEF 25â&#x20AC;&#x201C; 75%)

Peak expiratory flow rate (PEFR)

(MVV)

Maximum voluntary ventilation

L

The volume that can be forcefully expelled from the lungs after maximal inspiration.

L

The volume expelled in the first second of the FVC maneuver.

N or

N or

%

L/sec

L/sec

N or

N or

The maximal midexpiratory airflow rate.

The maximal airflow rate achieved in the FVC maneuver.

N or

The maximum volume that can be breathed L/minin 1 minute (usually measured for 15 seconds and multiplied by 4).

N or

LUNG VOLUMES

Slow vital capacity (SVC)

L

The volume that can be slowly exhaled after maximal inspiration.

N or

Total lung capacity (TLC)

L

The volume in the lungs after a maximal inspiration.

N or

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Untitled Document Functional residual capacity (FRC)

L

The volume in the lungs at the end of a normal tidal expiration.

Expiratory reserve volume (ERV)

L

The volume representing the difference between FRC and RV.

Residual volume (RV)

L

The volume remaining in the lungs after maximal expiration.

RV/TLC ratio

. . .

N or

N or

N or

N or

N or

See Key. N = normal; = less than predicted; = greater than predicted. Normal values vary according to subject sex, age, body size, and ethnicity.

Modified, with permission, from Tierney LM Jr, McPhee SJ, Papadakis MA (editors): Current Medical Diagnosis & Treatment 2003. McGrawHill, 2003.

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