Michael W. Sims

Etiology and Pathophysiology

The most common cause of AECOPD is respiratory infection, with an estimated 50% of cases caused by bacterial infection of the lower respiratory tract. The most commonly isolated organisms are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis, with Pseudomonas aeruginosa (and possibly Enterobacteriaceae such as Escherichia coli and Klebsiella pneumoniae) playing a role in more advanced disease. Knowledge of these commonly isolated organisms guides empiric antibiotic choices for treatment of AECOPD (discussed further later in the chapter).

Respiratory viral infection also plays a major role in AECOPD and may portend a slower recovery than with bacterial infection. Rhinovirus is the most commonly isolated viral pathogen, but influenza, parainfluenza, respiratory syncytial virus, coronavirus, and adenovirus may also precipitate AECOPD, depending on the season of year.

Noninfectious agents contributing to AECOPD may include sedative overdose, aeroallergens, and air pollutants, such as sulfur dioxide, nitrogen dioxide, particulate matter, and ozone. Lastly, comorbid conditions such as congestive heart failure and pulmonary embolism may mimic AECOPD or may directly induce acute respiratory failure by raising ventilatory demands above the level that can be sustained by a patient with underlying COPD (Chapter 1, Figures 1.2 and 1.5, and Appendix B, Figure B2).

AECOPD is an acute inflammatory event, marked by increased numbers of neutrophils, macrophages, and, in the case of viral infection, eosinophils in the sputum. Defects in innate immunity may predispose patients with COPD to infections, which then induce acute airway inflammation. This inflammation increases mucus secretion, airway edema, and airway hyperresponsiveness, thereby narrowing airway luminal diameter and producing the airflow obstruction, dynamic hyperinflation, and ventilation-perfusion mismatch that characterize AECOPD. Increased serum levels of fibrinogen, C-reactive protein, and inflammatory cytokines and chemokines during AECOPD suggest that these episodes may also have systemic manifestations.

Respiratory failure in AECOPD may be multifactorial, with infection and inflammation superimposed upon the loss of alveolar volume (caused by emphysema) and impaired respiratory mechanics (e.g., flattened or inverted diaphragms) characteristic of COPD (in contrast to asthma; see Chapter 75). Infection and inflammation may evoke additional reductions in elastic recoil, further impairing ventilation and oxygenation that is generally compromised even at baseline. Elevated residual volume in patients with COPD compromises inspiratory capacity and breathing reserve. As a consequence, patients compensate for hypoxemia with tachypnea, which promotes air trapping by decreasing expiratory time, further increasing the work of breathing, leading to respiratory muscle fatigue and eventually respiratory failure.

Clinical Evaluation

Because patients admitted to the ICU with a severe AECOPD are at high risk for rapid clinical deterioration, it is important to focus the initial evaluation so as not to delay the initiation of life-saving therapies. A brief, directed medical history should elucidate any significant comorbid illnesses; onset, duration, and severity of any factors indicating an etiology for the AECOPD (e.g., sick contacts with flulike or respiratory illnesses, fever, cough, sputum volume, and purulence); and any features suggesting a possible alternative diagnosis (e.g., chest pain, orthopnea, ankle swelling, calf pain). Initial examination should focus primarily on the cardiopulmonary system, with attention to discovering and rapidly acting on hypoxemia, hemodynamic instability, lethargy or confusion, or signs of an unsustainable pattern of breathing (e.g., rapid shallow breathing > 40 breaths/min, extensive use of accessory muscles, or paradoxical movement of the chest and abdomen). After treating any immediate life-threatening complications, a more comprehensive history and physical examination can then be performed.

Routine laboratory studies, an arterial blood gas (ABG), and an electrocardiogram should be obtained, as well as a chest radiograph and a sputum culture with antibiotic sensitivities if the patient can produce a sample. Although predictive of outcomes during AECOPD, spirometry is generally impractical in the ICU, where respiratory distress and frequent coughing typically prevent valid and reproducible maneuvers.

Interpretation of the ABG in a patient with COPD can be challenging because some patients have abnormal blood gases at baseline. Typical baseline abnormalities in a patient with severe COPD are mild to moderate hypoxemia and variable degrees of chronic respiratory acidosis. The latter is well compensated by renal bicarbonate retention, so that the pH may be near normal despite significant hypercapnia. It is helpful to compare the results of an ABG determination during an AECOPD with those obtained when the patient was in a stable baseline condition, if available. However, a simple rule of thumb can help differentiate acute from chronic respiratory acidosis (see Table 75.1 and Chapter 1, Table 1.2). The presence of acute respiratory acidosis, particularly with a pH < 7.30, is concerning and suggests the need for mechanical ventilatory support (discussed further later in the chapter).

Medical Management

The goals of therapy for severe AECOPD include improving airflow and relieving symptoms of bronchospasm, reducing acute airway inflammation, correcting hypoxemia and acute respiratory acidosis (but not overcorrecting the pH; see Appendix B), managing respiratory secretions, identifying and treating precipitating factors, and avoiding iatrogenic complications such as nosocomial infection or venous thromboembolism. To achieve these many goals, a multimodality approach is generally used that involves medications (see Table 76.1), controlled oxygen administration, nutritional supplementation, respiratory and physical therapy, and mechanical ventilatory support.