Chronic Obstructive Pulmonary Disease

Introduction

• COPD is a highly prevalent condition globally that is characterized by progressive airway narrowing, resulting in airflow restriction and eventual damage to the lung parenchyma.
• This occurs most commonly due to exposure to noxious substances, such as tobacco smoke, occupational dusts, and environmental pollutants. Some cases are genetically driven by an alpha-1 antitrypsin deficiency.¹
• Disease mediated by activation of the inflammatory cascade, leading to chronic inflammation, airway remodeling, and eventual damage to the lung tissue with continued exposure.
• COPD is the fourth leading cause of death globally and affects approximately 300 million people around the world.²
• Those at highest risk of developing COPD include those over the age of 40 and cigarette smokers.
• Subtypes of COPD include:
  • Emphysema involves the destruction of alveoli and a progressive decrease in the gas-exchange surface area.
  • Chronic bronchitis is characterized by chronic inflammation of the bronchi, resulting in cough and sputum production.
  • Chronic bronchiolitis is characterized by chronic inflammation and narrowing of the bronchioles.

Pathophysiology

• COPD is characterized by persistent airway inflammation, thought to be driven by oxidative stress and a protease-antiprotease imbalance.¹
• Chronic inflammation leads to remodeling and progressive narrowing of the airway, causing obstructive lung disease. This includes increased mucus-producing cells, loss of ciliated epithelial cells, squamous metaplasia of the respiratory tract lining, and airway wall thickening.¹
• Noxious exposures cause oxidant-induced injury that leads to reprogramming of the airway epithelium. Smoking-induced upregulation of epidermal growth factor and amphiregulin stimulates basal cell metaplasia into mucus-producing (goblet) cells. This results in altered defense mechanisms of small airways.³ 
• The new small airway epithelium microenvironment leads to altered immune defense mechanisms, pathological mucus secretion, and worsening of the COPD trajectory.³
• A reduction in forced expiratory volume in 1 second (FEV1) and a decrease in alveolar surface area decrease the lungs’ capacity for gas exchange, leading to air trapping and chronic hypoxemia.
• Air trapping results from increased residual volume and progressive hyperinflation of the lungs, as narrowed airways prevent complete exhalation.
• Chronic hypoxemia is common among individuals with COPD and often causes pulmonary vasculature vasoconstriction in an attempt to compensate for ventilation-perfusion mismatch.
• Moderate to severe exacerbations are more likely to be complicated by co-cultured viruses or bacteria.³
• Persistent vasoconstriction may lead to the development of pulmonary hypertension.
• A less common but important genetic cause of COPD is in those with alpha-1 antitrypsin deficiency.
• This mutation creates nonfunctional antiprotease proteins, creating a protease-dominant landscape that presents with unexplained obstructive lung disease and liver dysfunction.

Clinical Presentation

• The most common symptoms of COPD are dyspnea, chronic cough, and sputum production. Some report chest tightness or expiratory wheezing.
• A thorough history is critical for early recognition and diagnosis of COPD. It should include tobacco smoking status, exposure to secondhand smoke, occupational and environmental exposures, and family history of liver disease or emphysema.
• Physical exam findings can include signs of respiratory distress such as increased work of breathing, accessory muscle use, prolonged expiration, audible wheezing, pursed-lip breathing, and cyanosis.
• Chronic hyperinflation of the lungs and air trapping can contribute to an increased anteroposterior chest diameter.
• Central cyanosis and nail clubbing can indicate worsening disease.
• Lower extremity edema may be present in those who develop pulmonary hypertension and eventual right heart failure.

Diagnosis

• The diagnosis is primarily attained through spirometry and pulmonary function testing (PFT). Laboratory studies and imaging can support the diagnosis.¹
• PFT will demonstrate a pattern consistent with obstructive lung disease, with a postbronchodilation FEV1/FVC (forced vital capacity) of less than 0.70.
• Upon diagnosis, the severity of the disease can be classified according to the Global Initiative for Chronic Lung Disease (GOLD) guidelines, which include:¹
  • GOLD 1 (Mild): FEV₁ ≥ 80% predicted
  • GOLD 2 (Moderate): FEV₁ 50–79% predicted
  • GOLD 3 (Severe): FEV₁ 30–49% predicted
  • GOLD 4 (Very Severe): FEV₁ < 30% predicted
• This classification system, in combination with symptom grading systems such as the COPD Assessment Test (CAT) and the Modified Medical Research Council dyspnea scale (MMRC), determines the symptom burden to suggest proper treatment avenues.¹
• Supporting laboratory investigations, such as a complete blood count with differential and alpha-1 antitrypsin, can narrow the differential diagnosis and suggest eosinophilic or genetically mediated causes. Imaging with chest x-ray or computed tomography may demonstrate lung hyperinflation, diaphragm flattening, and emphysematous changes in support of a COPD diagnosis.
• Together, these modalities including PFTs, guideline classification, and imaging provide a thorough approach to diagnosing and suggesting effective treatment for those suffering from COPD.

Treatment

• Unfortunately, there is no cure for COPD. The goals of treatment are symptom control, improved quality of life, and reduced mortality.
• Pharmacologic treatments for COPD include beta-2 agonists that relax airway smooth muscle, causing bronchodilation; antimuscarinics that prevent bronchoconstriction; and methylxanthines that also relax airway smooth muscle. Inhaled corticosteroids are commonly used to reduce inflammation; however, they can increase the risk of infection with long-term use. Their use should be restricted to acute exacerbations.
• Preventive therapies are highly recommended in the COPD population, including influenza and pneumococcal vaccines, and prophylactic antibiotics such as azithromycin to prevent recurrent exacerbations.
• For those requiring escalation of treatment, inpatient management with supplemental delivery of oxygen and intravenous steroids has been advantageous.
• Nonpharmacologic therapies, such as pulmonary rehabilitation, can benefit patients with COPD by improving functional capacity and health literacy regarding their diagnosis and its management.
• Education of the benefits of smoking cessation, inhaler use technique, and warning signs of exacerbation is also beneficial in the long-term management of this disease process.

Anesthetic Complications

• Risk stratification is essential in the perioperative period. Serum studies, such as a complete blood count and a blood gas, can identify concomitant anemia, efficiency of oxygenation and ventilation, and carboxyhemoglobin levels to rule in tobacco use.⁴
• Additional preoperative assessment includes an electrocardiogram to exclude arrhythmia, an echocardiogram to assess cardiac function in the setting of increased intrathoracic pressure, a chest x-ray to exclude an acute infectious process, and spirometry to assess the current severity of disease.⁵
• On induction, blunting of the sympathetic response with lidocaine or opioid pain medication prevents the risk of developing bronchospasm.
• Intraoperatively, ventilator settings should be adjusted to lower tidal volumes and respiratory rates to prevent positive barotrauma from air trapping. I: E ratio should have an extended exhalation time to account for the limitation of airflow present in COPD patients.⁵
• Volatile anesthetics, such as sevoflurane or isoflurane, are beneficial because they promote bronchodilation, whereas desflurane should be avoided due to the risk of airway irritation.
• Chronic hyperinflation raises intrathoracic pressure, decreasing venous return and preload, increasing the risk of developing right heart strain.
• Applying minimal PEEP facilitates complete exhalation and reduces air trapping.
• Ketamine is an adjunct with bronchodilating effects and sedative and analgesic properties. It should be used with caution, however, due to the tendency to increase airway secretions.²
• Periextubation bronchodilator therapy and complete neuromuscular blockade reversal are critical to promoting uncomplicated extubation, with the use of noninvasive ventilation, such as BiPAP, immediately after extubation.⁵
• Postoperatively, COPD patients are at risk of delayed extubation, prolonged requirement of mechanical ventilation, increased mortality, and extended hospital.