A 73 year-old man, current smoker of 50 pack-years, a history of chronic obstructive pulmonary disease (COPD) on home oxygen, and an ischemic cardiomyopathy presented to the emergency department (ED) with shortness of breath. He noted 1 week of progressive dyspnea on exertion and increasing cough with purulent sputum. He denied fever, chills, hemoptysis, orthopnea, paroxysmal nocturnal dyspnea and leg edema. He has been using inhaled bronchodilators several times daily and had increased the flow rate of his supplemental oxygen to 4 liters per minute without notable improvement. On the morning of admission, he had dyspnea, even at rest, and called EMS. On presentation, he was afebrile, tachycardic to 110 beats per minute and hypertensive to 178/90 mmHg; he had a respiratory rate of 36 breaths per minute and an oxygen saturation of 85% on 4 liters per minute of supplemental oxygen via nasal cannula. An ABG drawn while on oxygen revealed: pH 7.24, pCO 2 60 mmHg, PO 2 55 mmHg. On exam, he was awake, in mild distress, using accessory muscles of inspiration and exhalation. The remainder of his exam was notable for tachycardia, diffuse end-expiratory wheezes bilaterally, and an absence of rales. Chest radiograph demonstrated hyperinflation without focal opacity.
QuestionWhat is the immediate approach to this patient with acute hypercarbic respiratory failure?Answer Non-invasive positive pressure ventilation Non-invasive positive-pressure ventilation (NIPPV) is the preferred method of ventilatory support in patients with acute respiratory failure secondary to an acute exacerbation of COPD (AECOPD). This patient was placed on bilevel NIPPV with an inspiratory pressure of 12 cm of water and an expiratory pressure of 5 cm of water with an inspired fraction of oxygen of 0.5 via an oronasal mask interface. His oxygen saturation was maintained between 88 and 92%. He was given 500 mg of intravenous azithromycin and 60 mg of intravenous methylprednisolone. Within hours, his respiratory rate had decreased to 22 and he appeared comfortable with improvement in his arterial blood gas.The natural history of COPD is punctuated by periods of acute exacerbation, during which patients experience increased symptoms and utilize more healthcare resources. Common symptoms of AECOPD include increased sputum production, cough and dyspnea as a result of increased airway inflammation, mucous plugging and gas trapping [1,2]. Exacerbations of COPD are associated with a mortality of 10% in the hospital, 43% at 1 year and 50% in the subsequent 5 years [3][4][5]. Exacerbations themselves are associated with a step-wise decline in lung function and deteriorating quality of life [6]. The most commonly identified triggers for AECOPD are respiratory viruses, particularly rhinovirus, as well as bacterial pathogens and environmental exposures.
NIPPVNIPPV is indicated in the setting of acute respiratory failure secondary to COPD exacerbation [7,8]. The goal of NIPPV in this setting is to reduce work of breathing, improve ventilation, correct hypercapnia and...