The acute management of COPD exacerbations is quite analogous to that of asthma exacerbations. A key distinguishing factor is the relative lack of acute reversibility of airflow obstruction, limiting the utility of PEF measurement and reassessments in these patients.

Supplemental oxygen should be administered to maintain saturations of at least 90 %. Additional doses of short-acting β-agonist, combined with an inhaled anticholinergic agent (albuterol/ipratropium) beyond the patient’s baseline regimen, are generally indicated. Oral steroids such as prednisone (or methylprednisolone IV in patients unable to tolerate PO) are also of benefit. A key distinction from acute asthma management is the role of antibiotics. As bacterial infection (particularly Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) is commonly associated with the development of COPD exacerbations, patients with increased sputum production and/or moderate to severe exacerbations should typically be prescribed antibiotics. There is no clear data to support the use of any particular agent. Antimicrobial choice should therefore be guided by local resistance patterns to the above pathogens. Commonly utilized antibiotics include amoxicillin ± clavulanate, doxycycline, azithromycin, and respiratory fluoroquinolones. The optimal duration of antimicrobial treatment is also unclear [8]. Intravenous magnesium can also be considered in severe exacerbations, although evidence supporting its use is lacking. Long-acting inhaled anticholinergics (tiotropium and aclidinium) and inhaled corticosteroids (beclomethasone, budesonide, ciclesonide, fluticasone, and mometasone, often combined with long-acting β-agonists as described in the asthma section), while beneficial in chronic management of COPD, are not of benefit in the setting of an acute exacerbation [9].

Patients with marked worsening from baseline (such as new or increasing oxygen requirements), those who fail to improve (or worsen) despite the above interventions, and those with significant comorbidities or inadequate social support (including poor access to medications or primary care follow-up) should be admitted. If the decision is made to discharge a patient with a COPD exacerbation, ensure adequate supplies of albuterol with or without ipratropium are available to the patient, as well as sufficient amounts of supplemental home oxygen, and any additional medications prescribed for COPD by their primary care physician. A several day course of oral steroids is generally indicated, analogous to asthma management. If indicated, prescribe an appropriate antibiotic regimen. Finally, counsel patients who continue to smoke regarding the role of smoking cessation in the chronic management of COPD, as it is the only intervention shown to favorably alter the course of the disease [9].

Hyperventilation refers to minute ventilation in excess of metabolic needs. Anxiety disorders, including panic disorder, are commonly associated. The diagnosis should be one of exclusion, after careful consideration of the numerous potentially life-threatening etiologies of dyspnea noted above. Patients may report associated feelings of impending doom, palpitations, paresthesias, presyncope, chest pain, diaphoresis, and carpopedal spasm. An inciting distressing event may also be reported. Once emergent diagnoses have been excluded, a small dose of a benzodiazepine, such as lorazepam may be considered for resolution of an acute episode. Rebreathing of CO₂ (such as via a paper bag) was once widely advocated as a remedy for acute hyperventilation. However, due to concerns regarding potential hypoxemia, this treatment modality should be avoided [10]. If episodes are recurrent, treatment of any underlying anxiety disorder should be the focus of therapy as outlined in the Chap. 26 Anxiety.

Inflammation of the larynx and subglottic airway due to viral or bacterial illness resulting in stridor and cough is termed croup. Parainfluenza viruses are the most common culprit, although respiratory syncytial virus and influenza viruses are also implicated. Children between the ages of 6 months and 3 years are most commonly affected, with peak incidence in late fall, early winter, and spring. The course of illness typically begins with several days of URI symptoms such as congestion, rhinorrhea and fever, followed by the onset of the typical barking cough, stridor and hoarseness, which usually abates within 48 h. Young children are much more severely affected due to narrow caliber of the airway in this age group, whereas adults typically only experience the hoarseness attributed to “laryngitis.” Treatment for all pediatric patients presenting with croup includes immediate assessment of the ability to protect their airway, followed by administration of oral steroids. Dexamethasone (0.6 mg/kg, max 10 mg) is the preferred agent given its prolonged half-life. Oral administration is as effective as parenteral and has the advantage of being less alarming to a child than an injection, which could induce further respiratory difficulty. In patients with moderate (stridor at rest, frequent barking cough, chest wall retractions) to severe croup (respiratory distress, marked retraction, inspiratory and expiratory stridor), nebulized epinephrine should be administered. If clinical response is noted, patients should be observed for approximately 4 h as the potential for rebound symptoms exists. Patients with persistent increased work of breathing or stridor at rest, as well as those requiring more than two doses of epinephrine should be admitted.

Pulmonary embolism (PE) is a feared cause of dyspnea with a significant burden of mortality. It has been estimated that up to 100,000 Americans die each year from PE [11], and fear of missing the diagnosis fuels a significant number of evaluations for the condition. The presentation varies from sudden cardiac death to incidentally diagnosed PE in virtually asymptomatic patients. The most common symptoms include dyspnea, pleuritic chest pain, leg pain/swelling, and cough (with or without hemoptysis). The onset of symptoms is often rapid, although significant variation exists. Tachycardia, hypoxemia, tachypnea, and leg tenderness and swelling may be noted on physical exam. Risk factors for PE include the components of Virchow’s triad: venous stasis (prolonged immobilization), thrombophilia (e.g., malignancy, inherited thrombophilias, use of exogenous estrogens), and vascular endothelial injury.

CT pulmonary angiography (CTPA) is the most commonly used imaging study to confirm the diagnosis of PE, although ventilation/perfusion scanning is utilized in some pregnant patients, as well as in patients with contrast allergies and renal insufficiency. The sensitivity and specificity of CTPA are excellent. However, CTPA does expose patients to a significant amount of radiation and nephrotoxic contrast dye. Therefore, appropriate selection of patients for this testing is key. The pulmonary embolism rule-out criteria (PERC rule) identifies patients for whom no further testing is indicated. To fulfill the rule, the clinician must estimate a low pretest probability of PE (<15 %), and the patient must fulfill all of the criteria listed below [12]: