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COPD is characterized by persistent expiratory airflow limitation. The underlying pathophysiology involves a complex process of chronic inflammation, remodeling of the small airways with the destruction of alveoli, and an increase in extracellular matrix production. The disease is manifested through a response to noxious particles and gases, including cigarette smoke and environmental pollutants, though genetic factors may also play a role [20, 35, 36]. It has significant social and economic effects and is the fourth leading cause of death in the United States [37–39].

Acute exacerbations are often precipitated by bacterial or viral respiratory tract infections, exposure to pollutants or allergens, or medication noncompliance. The clinical presentation is similar to that of asthma (Box 5.2). Patients typically develop worsening shortness of breath, more frequent and severe cough, and possibly increased sputum production [40]. Clinical examination often reveals wheezing.

Patients with COPD should receive titrated oxygen with a goal to maintain SpO₂ between 88% and 92%, which is associated with reduced mortality [16]. Continuous capnography can aid in the detection of impending respiratory failure. Increasing EtCO₂ levels indicate a deteriorating condition. As with asthma, capnographic waveforms may take the form of a shark fin appearance (Figure 5.2) and can assist with the prehospital diagnosis and assessment of response to treatment [12].

As with asthma, the primary treatments during acute exacerbations are directed toward reversing airway obstruction with SABAs and anticholinergic agents [41]. Corticosteroids are associated with decreased rates of treatment failure and relapse [42]. Antibiotics are also important adjuvant therapy for COPD exacerbations and are associated with a reduction in treatment failure and mortality in selected patients [43]. NIPPV has become established as a lifesaving therapy in the treatment of COPD exacerbations [20, 21, 44]. If it is necessary to intubate a COPD patient, appropriate settings for mechanical ventilation include decreased respiratory rates, lower tidal volumes, and an increased expiratory phase. As with asthma, these patients must be monitored closely for evidence of secondary barotrauma [21, 45].