A 68-year-old woman with a history of advanced chronic obstructive pulmonary disease comes to the emergency department due to increased shortness of breath and cough for 12 hours. She took 2 extra nebulizer treatments at home with no relief of symptoms. She has no fever, nausea, vomiting, or hemoptysis. The patient has been oxygen dependent for the last 2 years. She has a 45-pack-year smoking history and quit about 6 years ago. Medications include tiotropium daily, fluticasone/salmeterol twice daily, and albuterol by metered-dose inhaler or nebulizer as needed. Temperature is 36.7 C (98.1 F), blood pressure is 110/65 mm Hg, pulse is 110/min, and respirations are 28/min. The patient appears dyspneic and in moderate distress. She is given intravenous antibiotics, methylprednisolone, and 2 treatments of nebulized ipratropium with albuterol. Following these measures, the patient remains dyspneic and uses accessory muscles of respiration but is alert and follows commands. On 4 L/min O₂, her pulse oximetry is 89%, and arterial blood gas shows pH of 7.30, PCO₂ of 63 mm Hg, and PO₂ of 54 mm Hg. Chest x-ray, shown in the image below, demonstrates hyperinflation: Which of the following is the best next step in management of this patient?

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Explanation: 11ec25c8_d1f3_9055_bc81_ab57e3486210_MD0003_00 This patient has an acute exacerbation of chronic obstructive pulmonary disease (AECOPD). During AECOPD, expiratory airway closure causes progressive hyperinflation. As hyperinflation worsens, the alveolar end-expiratory pressure, known as intrinsic PEEP (aka "auto-PEEP"), rises. The diaphragm is pressed flat and has difficulty contracting further. Therefore, it cannot perform its normal function of overcoming intrinsic PEEP, which is necessary to create an inward pressure gradient that allows for inspiration. Diaphragm fatigue leads to compensatory accessory muscle recruitment (eg, sternocleidomastoid). Patients become more tachypneic, shortening the expiratory time even further. This exacerbates gas trapping and perpetuates a vicious cycle of hyperinflation and respiratory muscle exhaustion. Noninvasive positive pressure ventilation (NIPPV) applies extrinsic positive inward pressure (termed extrinsic PEEP), typically via a face mask, helping to break this cycle through the following mechanisms: Noninvasive positive pressure ventilation Deflating the lung: The extrinsic PEEP "stents" open the airways (akin to pursed-lipped breathing) to promote lung emptying, reduce hyperinflation, and restore diaphragm curvature. Decreasing the work of breathing (WOB): The extrinsic PEEP also supplements the diaphragm force to overcome intrinsic PEEP, unloading the muscles of inspiration. The net result is improved ventilation (↑ CO₂ elimination) and reduced WOB (↓ CO₂ production), improving hypercapnia and respiratory acidosis. NIPPV in patients with AECOPD decreases mortality (number needed to treat = 12) and prevents intubation. ₂ ₂ (Choice A) Methylxanthines (eg, aminophylline, theophylline) cause bronchodilation by increasing cyclic adenosine monophosphate. They have no benefit over inhaled bronchodilators and glucocorticoids in the treatment of AECOPD. (Choices B and C) In patients with AECOPD, enough O₂ should be given to compensate for alveolar CO₂ retention and ventilation-perfusion mismatch; however, excessive O₂ can worsen hypercapnia (reversal of adaptive hypoxic pulmonary vasoconstriction, or the Haldane effect). Therefore, the ideal saturation range is 88%-92%. This patient currently meets oxygenation goals (on 4 L/min) but has acute-on-chronic respiratory acidosis with increased WOB. Therefore, NIPPV is needed to improve CO₂ elimination. Oxygen would be added into the NIPPV circuit to achieve the target range. ₂ ₂ ₂ ₂ (Choice D) Invasive mechanical ventilation may be required in hypercapnic patients with poor mental status and an inability to clear secretions, hemodynamic instability, or severe acidosis (pH <7.1). A trial of NIPPV is warranted prior to intubation. If this patient is not improved after a 2-hour trial of NIPPV (eg, worsening respiratory distress, decreased consciousness, and/or acidosis), intubation should be considered. Educational objective: Noninvasive positive pressure ventilation in patients with acute exacerbation of chronic obstructive pulmonary disease helps to unload the work of breathing and decreases mortality and need for intubation. References: Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. (http://www.ncbi.nlm.nih.gov/pubmed/15266518) Contemporary management of acute exacerbations of COPD: a systematic review and metaanalysis. (http://www.ncbi.nlm.nih.gov/pubmed/18321904)

A 68-Year-Old Woman with a History of Advanced Chronic Obstructive