A 32-year-old man comes to the emergency department due to worsening shortness of breath. The patient has a 20-year history of asthma. He developed low-grade fever, rhinorrhea, and generalized body aches 4 days ago, followed by increasing dyspnea and cough since yesterday. The patient's as-needed reliever inhaler provided little help. Temperature is 37 C (98.6 F), blood pressure is 155/88 mm Hg, pulse is 120/min, and respirations are 28/min. Pulse oximetry is 84% on room air and 92% on 3 L/min of oxygen. The patient speaks in clipped phrases and uses the accessory muscles of respiration. Examination shows diminished breath sounds bilaterally with scattered expiratory wheezes. Chest x-ray reveals hyperinflated lungs but no infiltrates. Complete blood count shows leukocytes at 11,000/mm³. The patient is started on continuous albuterol and ipratropium nebulizers, as well as intravenous magnesium and methylprednisolone. Repeat examination an hour later is notable for respirations at 36/min, persistently decreased breath sounds, and no wheezing. Results of an arterial blood gas test on 3 L/min of oxygen are as follows: Which of the following is the best next step in management of this patient?

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11ec25c8_d1ed_c4ed_bc81_7d285039064d_MD0003_00 This patient's presentation is consistent with a severe, acute asthma exacerbation and impending respiratory failure. Acute asthma typically causes respiratory alkalosis (↑ pH, ↓ PaCO₂) due to increased respiratory drive. Therefore, elevated or even inappropriately normal PaCO₂ is concerning for respiratory muscle fatigue. Although this patient's PaCO₂ (48 mm Hg) is not significantly elevated, it signals impending failure, given his tachypnea and high work of breathing (ie, extreme effort to maintain relatively normal ventilation). Absence of wheezing ("silent chest") is another alarming sign, signifying poor tidal air movement. Severe asthma can cause significant lower airway obstruction (eg, inflammation, bronchospasm); the full effect of pharmacologic therapy (nebulized bronchodilators, systemic steroids, IV magnesium) will likely be delayed. Therefore, the immediate priority is to stabilize the exacerbation with mechanical ventilation (noninvasive [face mask] or invasive [intubation]) as a bridge to recovery. A time-limited (<2 hr) trial of noninvasive positive pressure ventilation (NIPPV) can be considered in select patients. However, unlike with chronic obstructive pulmonary disease (COPD), data on mortality and intubation rates with NIPPV in asthma exacerbations are scarce and weak. NIPPV instantly improves COPD-related hyperinflation, in which collapsible airways can be stented open by extrinsic pressure. In contrast, severe asthma is marked by concentric smooth muscle hypertrophy, and exacerbations typically involve inflammatory edematous airway closure that is not as readily relieved by positive pressure. Therefore, there is a low threshold to intubate and begin mechanical ventilation. (Choice A) This patient has received appropriate drug therapy for status asthmaticus; however, relief of bronchoconstriction will likely take hours to days. At present, his borderline respiratory acidosis indicates impending respiratory failure. Mechanical ventilation is needed to prevent worsening acidosis and hypercapnia, which can lead to cardiac arrest. (Choice C) Intravenous antibiotics are not recommended for asthma exacerbations because viral infections are the most common trigger; no benefit from antibiotic therapy has been demonstrated. It is not unusual for leukocytes to be elevated, as in this patient, due to acute stress response (demargination) rather than infection. (Choices D and E) Methylxanthines (eg, theophylline) or systemic epinephrine provides no additional benefit over inhaled beta agonists and muscarinic antagonists for acute asthma exacerbations. Systemic (usually intramuscular) epinephrine is reserved for bronchospasm associated with anaphylaxis. Rather than additional pharmacotherapy with little/marginal benefit, this patient requires mechanical support to assist ventilation. Educational objective: In patients with severe, acute asthma, elevated or inappropriately normal PaCO₂ suggests respiratory muscle weakness and impending respiratory failure, which require mechanical ventilatory support. References: Management of acute asthma exacerbations. (http://www.ncbi.nlm.nih.gov/pubmed/21766754) Asthma exacerbations. 5: assessment and management of severe asthma in adults in hospital. (http://www.ncbi.nlm.nih.gov/pubmed/17468458)

A 32-Year-Old Man Comes to the Emergency Department Due to Worsening