COPD

Presenting findings [6]

• Chronic cough with expectoration (expectoration typically occurs in the morning)

• Dyspnea and tachypnea
o Initial stages: only on exertion
o Advanced stages: continuously
• Pursed lip breathing
o The patient breathes in through the nose and breathes out slowly
through pursed lips.
o This style of breathing increases airway pressure and prevents
bronchial collapse during the last phase of expiration.
o More commonly seen in patients with emphysema
• Prolonged expiratory phase, end-expiratory wheezing, crackles, muffled breath
sounds, and/or coarse rhonchi on auscultation
• Cyanosis due to hypoxemia
• Tachycardia

Features of advanced COPD [15]

• Congested neck veins

• Barrel chest: This deformity is most commonly seen in individuals
with emphysema.
• Asynchronous movement of the chest and abdomen during respiration
• Use of accessory respiratory muscles due to diaphragmatic dysfunction
• Hyperresonant lungs, reduced diaphragmatic excursion, and relative cardiac
dullness on percussion
• Decreased breath sounds on auscultation: “silent lung”
• Peripheral edema (most often ankle edema)
• Right ventricular hypertrophy with signs of right heart failure and cor pulmonale
• Hepatomegaly
• Often weight loss and cachexia
• Secondary polycythemia
• Confusion: due to hypoxemia and hypercapnia
• Nail clubbing in the case of certain comorbidities (e.g., bronchiectasis, pulmonary
fibrosis, lung cancer) [16]
 Nail clubbing is not a finding specific to COPD; its presence usually suggests
comorbidities such as bronchiectasis, pulmonary fibrosis, or lung cancer.

Pink puffer and blue bloater [15]

According to their clinical appearance, patients with COPD are often categorized as
either “Pink Puffer” or “Blue Bloater”.

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Pink puffer vs. blue bloater

Pink Puffer Blue Bloater

Main pathomechanism • Emphysema • Chronic bronchitis

• Noncyanotic
• Productive cough
• Cachectic
Clinical features • Overweight
• Pursed-lip breathing
• Peripheral edema
• Mild cough

PaO2 • Slightly reduced • Markedly reduced

PaCO2 • Normal (possibly in late hypercapnia) • Increased (early hypercapnia)

Emphysema subtypes
Emphysema is characterized by the destruction of lung parenchyma and is often seen in
patients with advanced pulmonary disease. The presence of emphysema does not
necessarily correlate with spirometric findings. Emphysema can be divided into the
following subtypes: [1][17]

• Centrilobular emphysema (centriacinar emphysema)

o Most common type of emphysema
o Classically seen in smokers
o Characterized by the destruction of the respiratory bronchiole (central
portion of the acinus); spares distal alveoli
o Usually affects the upper lobes
 • Panlobular emphysema (panacinar emphysema)
o Rare type of emphysema
o Associated with AATD
o Characterized by the destruction of the entire acinus (respiratory
bronchiole and alveoli)
o Usually affects the lower lobes
• Other subtypes
o Cicatricial emphysema
▪ Mainly caused by exposure to quartz dust
▪ Results in chronic inflammation and nodular scar formation
o Giant bullous emphysema
▪ Characterized by large bullae (congenital or acquired) that
extrude into the surrounding tissue
▪ Bullae may rupture, leading to pneumothorax.
▪ Depending on the shape of the bullae, resection should be
considered.
o Senile emphysema
▪ Loss of pulmonary elasticity with age may lead to
an emphysematous lung.
▪ Considered a normal consequence of aging
▪
“Smoke rises up:” Centriacinar emphysema is associated with smoking and primarily
involves the upper lobes of the lungs.
Diagnostics

Initial tests [1][2]

• Spirometry
o FEV1:FVC < 70% after bronchodilator inhalation confirms the
diagnosis.
o ↓ FEV1 (FEV1% of the predicted value determines the GOLD
spirometric grade.)
o Normal or ↓ FVC
• Serum AAT level: Screen all patients with confirmed COPD for AATD upon initial
diagnosis.
“A COP with low FEVer”: FEV1 for COPD patients.
Additional testing
Advanced pulmonary function testing
Characteristic changes are observed in patients with significant emphysema and
small airway abnormalities.

• Body plethysmography
o ↑ Total lung capacity (TLC)
o ↑ Functional residual capacity (FRC)
o ↑ Residual volume (RV)
• Single-breath diffusing
capacity: ↓ DLCO
• Postbronchodilator test: A negative response (change in FEV1 < 12%) is more
common in patients with COPD than asthma (see “COPD vs. asthma”). [1][19][20]
Reversibility of bronchoconstriction is not a reliable factor for differentiating between
COPD and asthma. [1]

Assessment for respiratory failure

• Pulse oximetry
o Obtain in patients with signs of respiratory distress or signs of right
heart failure.
o Measure at rest and on ambient air or usual oxygen prescription.
• ABG
o Obtain in patients with SO2 < 92% and/or acute illness (e.g., altered
mental status, AECOPD).
o Findings
▪ May show hypoxemic respiratory failure (↓ PO2) with or
without hypercapnic respiratory failure (↑ PCO2)
▪ Chronic hypercapnia due to CO2 trapping is common in
patients with severe COPD.
Chest imaging [1][2]
Chest imaging is not needed for diagnosis; consider based on clinical context to assess
for alternative diagnoses, comorbidities, or complications.

• Chest x-ray findings in COPD

o Signs of pulmonary hyperinflation
▪ Increased anteroposterior diameter (barrel chest)
 Pushed down and flattened diaphragm
▪
▪ Horizontal ribs and widened intercostal spaces
▪ Hyperlucency of lung tissue (decreased lung markings)
▪ Long and narrow heart shadow
o Signs of bullous emphysema: parenchymal bullae or pulmonary blebs
• CT chest findings
o Similar to CXR findings; may additionally reveal characteristic patterns
of emphysema
▪ Panacinar emphysema: common in patients with AATD
▪ Centriacinar emphysema: common in patients with COPD
and a history of tobacco use
o May show signs of bronchiectasis, e.g., thickened bronchial walls
Other
• CBC [2]

Secondary polycythemia, ↑ hematocrit

o
o Eosinophil counts influence decisions on whether to use inhaled
corticosteroids.
• ECG/TTE: Right ventricular hypertrophy may be seen in patients with advanced
COPD. [21]

Nonpharmacological management of COPD [1]

Lifestyle modifications
• Counsel on smoking cessation and options for pharmacotherapy, e.g., varenicline.
• Encourage physical activity to reduce the risk of acute exacerbations.
• Recommend maintenance of a healthy nutritional status.
• Educate patients on:
o Indoor air pollution mitigation, e.g., nonpolluting cooking stoves
o Personal protective equipment to prevent work-related lung diseases
Cessation of tobacco use is the single most effective step to slow the decline in lung
function in patients with COPD.

Supportive care
• Recommended immunizations in COPD
o Pneumococcal vaccination: for patients ≥ 19 years of age [22]

o Influenza vaccination (annual)

o COVID-19 vaccination
 o Zoster vaccination: for patients ≥ 50 years of age
o Tdap vaccination: if not administered in adolescence
o See also “ACIP immunization schedule.”
• Pulmonary rehabilitation: especially helpful for patients with moderate to severe
disease

Pharmacological treatment
General principles [1]

• Bronchodilators are the mainstay of pharmacological treatment.

• Inhaled corticosteroids (ICS), e.g., budesonide, fluticasone, or beclomethasone,
should only be used in combination with long-acting bronchodilators.

Initial treatment
If treatment response is inadequate, consider poor inhaler technique and/or poor
adherence as causes.

Follow-up treatment [1]

Follow-up treatment adjustments are based on treatable traits (dyspnea and frequency
of exacerbations) and are made irrespective of the patient's GOLD group (A, B, or, E) at
diagnosis. [1]

Other drugs [1]

• Palliative pharmacotherapy for dyspnea (e.g., opiates): may be considered for all
patients
• Methylxanthines (e.g., theophylline)
o Nonselectively antagonize adenosine receptors and
inhibit phosphodiesterase
o May be trialed if other bronchodilators are not available
o Unproven benefit
• Mucolytics (e.g., N-acetylcysteine, erdosteine)
o Liquefy mucus by reducing the disulfide bonds of mucoproteins
o Can be useful in reducing exacerbations in certain patients
There is insufficient evidence to support treating stable COPD
with antitussives, vasodilators, or leukotriene antagonists. [1]
Management of advanced disease
Respiratory support [1]

• Long-term oxygen therapy (LTOT)

o Indications
▪ PaO2 ≤ 55 mm Hg or SaO2 ≤ 88% at rest despite optimal
medication
▪ OR PaO2 55–60 mm Hg in patients with pulmonary
hypertension, CHF, or polycythemia
o Target oxygen saturation: > 90%
o Recommended duration: continuous oxygen therapy for ≥ 15
hours/day
o Reevaluate after 60–90 days (with ABG or pulse oximetry).
• Ventilatory support
o Continuous positive airway pressure is useful in patients with COPD
and obstructive sleep apnea.
o Long-term noninvasive positive-pressure ventilation may be
considered in select patients with severe chronic hypercapnia.
LTOT increases survival in patients with severe resting hypoxemia.

Invasive treatment
• Surgical bullectomy: indicated in severe emphysema with hyperinflation and
large bullae
• Lung volume reduction
o Indicated for severe emphysema and hyperinflation without
large bullae
o Severely affected emphysematous areas of the lung are removed
either surgically (lung volume reduction surgery) or endoscopically
• Lung transplantation: may be indicated for very severe COPD, patients not
eligible for bullectomy or lung volume reduction, and those with surgical
contraindications
Palliative measures (e.g., low-dose opiates, fans blowing onto the patient's face,
or acupuncture) can be used if distressing breathlessness persists despite optimal
medical therapy. [23][24]