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Acute exacerbation of chronic obstructive pulmonary disease (COPD) is defined as an increase in dyspnea, cough, or sputum production that requires therapy. The annual rate of exacerbations is 0.5 to 3.5 per patient.1 Hospitalization rates range from 0.1 to 2.4 per patient per year.1 Most exacerbations are caused by viral infections, such as Rhinovirus or influenza species or bacterial infections, such as Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, or Pseudomonas species.2 Occasionally, exacerbations are caused by air pollution and other environmental factors.2 When evaluating a patient suspected of having an exacerbation, concurrent conditions such as pulmonary emboli, pneumothorax, and congestive heart failure should be clinically excluded.2 In about one-third of cases, no underlying etiology is identified.3
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The clinical presentation of exacerbations of COPD is highly variable. Most patients require only an increase of maintenance medications, while others develop frank respiratory failure and require ventilator assistance.4,5 The goals of ventilator assistance are to decrease respiratory distress and dynamic hyperinflation, to improve gas exchange, and to buy time for resolution of the processes that triggered the episode of acute respiratory failure.
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This chapter focuses on the aspects of ventilator management that are unique for patients with COPD. General principles of ventilator management are covered in other chapters—such as ventilator modes, bronchodilator therapy, weaning, and so on—and only the aspects specific to COPD are discussed in the present chapter. More than is the case with any other group of patients, clinical decision making and ventilator management in COPD is predicated on a detailed knowledge of the underlying pathophysiology.
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The basic physiologic abnormalities of patients who experience acute respiratory failure in COPD include deteriorations in respiratory mechanics, respiratory muscle function, and gas exchange.
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Deterioration of Respiratory Mechanics
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Increased Inspiratory Airway Resistance
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In stable patients with COPD, inspiratory flow resistance is approximately 6 cm H2O/L/s above normal.6 During an episode of acute respiratory failure, resistance can increase by an additional 6 cm H2O/L/s or more.7,8 Mechanisms responsible for the increase include bronchospasm, airway inflammation, and mucus production.9 Increases in inspiratory resistance and respiratory motor output lead to increased inspiratory effort (Fig. 31-1).7 In patients with severe COPD, the pressure output of the inspiratory muscles during resting breathing is three times higher than in healthy subjects: average pressure-time products of 259 to 341 versus 94 cm H2O • second per minute.8,10 Values are five times higher when patients are in respiratory distress.8,11
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