Chronic obstructive pulmonary disease (COPD) is a progressive chronic disease characterized by airflow limitation that is frequently progressive and associated with respiratory impairment. As the fourth leading cause of death in the United States and Europe, COPD results in a substantial and ever increasing economic and social burden [1] . Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are frequently encountered in the intensive care unit (ICU). Although there is no standardized definition, AECOPD are characterized by a significant change in patient symptoms from baseline accompanied by overall increased airway resistance [2] . These exacerbations carry a significant risk to patients, with 10 % in-hospital mortality and 1-year and 2-year all-cause mortality rates of 43 % and 49 %, respectively, in patients with hypercapnic exacerbations [3] . Other studies note in-hospital mortality rates as high as 30 % with worse outcomes associated with older age, severity of respiratory and non-respiratory organ dysfunction, and hospital length of stay [4] . Given that patients transferred to the ICU with AECOPD are at high risk for complications and adverse outcomes, early diagnosis and management are critical to improve patient outcomes and survival in this population. AECOPD are the result of increased airway resistance as a consequence of inflammation and/or increased airway secretions. Data suggests that 50-70 % of AECOPD are due to respiratory infections, with greater than 50 % being due to bacterial pathogens. The most commonly isolated organisms include Haemophilus influenza, Streptococcus pneumonia, Moraxella catarrhalis, and Pseudomonas aeruginosa. Gram-negative rods are isolated less frequently but are more common in patients with advanced disease and more severe exacerbations as well as those with diabetes. Patients may be chronically colonized with bacteria in the respiratory tract, but it is unclear whether asymptomatic colonization leads to exacerbations caused by the same bacterial strains or predisposes to new bacterial growth. Atypical bacteria such as Mycoplasma pneumonia may be responsible for up to 14 % of exacerbations [2, 5] . Viral infections are estimated to cause 20-40 % of exacerbations. However, many patients with documented bacterial infections report a viral prodrome, making the true prevalence of viral illness difficult to estimate. Estimates indicate that rhinovirus (17-25 %), influenza (5-28 %), parainfluenza (5-10 %), and respiratory syncytial virus (5-10 %) are among the most common viral pathogens in AECOPD. Adenovirus, human metapneumovirus, and coronavirus are also potential but less common culprits. In many cases the exact precipitant of an exacerbation may never be identified [2, 5-7]. Acute exacerbations are typically defined by worsening dyspnea, cough with or without increased sputum production, wheezing, and a subjective sense of chest tightness and may be accompanied by pain [1, 7] . It is important to appreciate the severity of underlying airflow limitation, comorbid conditions, duration of worsened symptoms, current outpatient treatment regimen, and previous exacerbations including any 13 S.M. Kassutto, MD Pulmonary, Allergy and Critical Care,
Output: Care of the Surgical ICU Patient with Chronic Obstructive Pulmonary Disease and Pulmonary Hypertension Chronic Obstructive Pulmonary Disease Overview and Epidemiology