supplemental oxygen, bronchodilator therapy, corticosteroids, antibiotics, and sometimes assistance with ventilations. Most of the time, the cause of the exacerbation is unknown, although smoking, air pollution, bacterial infections, and viral infections can all play a role. The uncomplicated patient can be managed as an outpatient. Those with other comorbidities, prior respiratory failure, respiratory acidosis, deteriorating respiratory function, or a new arrhythmia will require an ICU admission. Oxygen should be given, even if it worsens the hypercapnia because it minimizes the ventilation/perfusion mismatch. If hypercapnia is leading to respiratory failure, nasal prongs or a Venturi mask should be considered to better regulate the oxygen intake. Besides oxygen, the first treatment for a COPD exacerbation should be a short-acting beta-agonist, such as albuterol. Anticholinergics, like ipratropium, can also be inhaled. Interestingly, metered dose inhalers with spacers are just as good as nebulizer treatment. All but the mildest of cases should be treated with IV or oral corticosteroids. If there is purulent sputum, antibiotics should be given. The most effective initial antibiotics are trimethoprim/sulfamethoxazole, amoxicillin, and doxycycline, although sicker patients should be treated with a fluroquinolone, second generation cephalosporin, amoxicillin/clavulanate, or extended spectrum macrolides, such as clarithromycin or azithromycin.
RESPIRATORY FAILURE There are two kinds of respiratory failure. The first is acute hypoxemic respiratory failure, which involves severe hypoxemia that does not resolve with supplemental oxygen. The main cause is shunting of blood in areas of the lungs that are not aerating. The main causes of this are left ventricular failure, which fills the alveoli with fluid, increased permeability of the capillaries as in ARDS, or consolidation or blood in the alveoli, which keep them from aerating. In ARDS, there is inflammation of the lungs or systemically along with the release of cytokines that recruit inflammatory molecules and other factors that damage the capillary endothelium, disrupting the respiratory membrane so that the alveoli fill with
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