Chapter 34. Asthma and Chronic Obstructive Pulmonary Disease

Although most asthmatic attacks are mild and reversible, severe attacks can be fatal. COPD is the fourth leading cause of death in the world and is the only major cause of death that is increasing in frequency.

Asthma is reversible airway obstruction associated with hyperresponsiveness of the tracheobronchial tree. COPD has 2 dominant forms: (a) pulmonary emphysema, characterized by abnormal, permanent enlargement and destruction of the air spaces distal to the terminal bronchioles; and (b) chronic bronchitis, a condition of excess mucous secretion in the bronchial tree, with a chronic productive cough occurring on most days for at least 3 months in the year for at least 2 consecutive years. Elements of both forms are often present, although one predominates.

Acute exacerbations of asthma and COPD are usually triggered by smoking, exposure to noxious stimuli (eg, pollutants, cold, stress, antigens, or exercise), adverse response to medications (eg, decongestants, β-blockers, nonsteroidal anti-inflammatory drugs), allergic reactions, and noncompliance with prescribed therapies. Triggers and complications of asthma and COPD include respiratory infection, pneumothorax, myocardial infarction, dysrhythmias, pulmonary edema, chest trauma, metabolic disorders, and abdominal processes.

Classically, patients with exacerbations of asthma or COPD present with complaints of dyspnea, chest tightness, wheezing, and cough. Physical examination shows wheezing with prolonged expiration. Wheezing does not correlate with the degree of airflow obstruction; a “quiet chest” may indicate severe airflow restriction. Patients with severe attacks may be sitting upright with forward posturing, with pursed-lip exhalation, accessory muscle use, paradoxical respirations, and diaphoresis. Pulsus paradoxus of 20 mm Hg or higher may be seen. Severe airflow obstruction and ventilation/perfusion imbalance can cause hypoxia and hypercapnia. Hypoxia is characterized by tachypnea, cyanosis, agitation, apprehension, tachycardia, and hypertension. Signs of hypercapnia include confusion, tremor, plethora, stupor, hypopnea, and apnea. Impending respiratory failure may be signaled by alteration in mental status, lethargy, quiet chest, acidosis, worsening hypoxia, and hypercapnia.

Emergency department diagnosis of asthma or COPD usually is made clinically. Severity can be gauged by clinical judgment and more objectively by peak expiratory flow (PEF) rate in cooperative patients. A PEF <40% of predicted in asthmatics or <100 L/min in COPD patients indicates a severe exacerbation. Pulse oximetry is a fast, easy, and noninvasive means for assessing and monitoring oxygen saturation during treatment, but it does not aid in predicting clinical outcomes and cannot predict hypercapnia or acidosis. Arterial blood gas (ABG) serves primarily to evaluate hypercapnia and acidosis in moderate to severe attacks. Compensated hypercapnia and hypoxia is common in COPD patients; comparison with previous ABG values is helpful. Normal Pco2 in the setting of an acute asthmatic attack is an ominous finding (indicating respiratory fatigue) if the patient's clinical appearance is poor. An arterial pH lower than that which is consistent with renal compensation implies acute hypercarbia or metabolic acidosis. Asthma and COPD can coexist or be mistaken for one another, but the larger diagnostic challenge is separating these diagnoses from other serious respiratory emergencies. Congestive heart failure (CHF) commonly coexists or mimics COPD and can also cause wheezing. Chest x-ray, BNP, and signs of fluid overload (jugular venous distention or hepatojugular reflux) help differentiate COPD from CHF. Chest x-ray is used to diagnose complications such as pneumonia and pneumothorax. Electrocardiograms are useful to identify dysrhythmias or suspected ischemic injury. A high index of suspicion is necessary to rule out pulmonary embolism (PE). Sudden onset of symptoms, syncope or near syncope, or classical PE presentation (pleuritic chest pain, dyspnea, tachycardia, hypoxia) warrant further testing.

Although COPD patients often have more comorbidity than do those with asthma, the therapy for acute bronchospasm is similar to that for inflammation. Treatment should precede history-taking in acutely dyspneic patients, because patients may decompensate rapidly. Patients who appear acute should be placed on a cardiac monitor and undergo noninvasive blood pressure and continuous pulse oximetry monitoring. An intravenous line should be started in patients with moderate and severe attacks. The primary goal of therapy is to correct tissue oxygenation.

1. Empiric supplemental oxygen should be administered to correct Sao2 above 90%. Oxygen may exacerbate hypercapnia in the setting of COPD. Perform an ABG measurement if there is concern for symptomatic hypercapnia.

2. β-Adrenergic agonists are first-line agents used to treat acute bronchospasm in COPD and asthma. Aerosolized forms (by nebulizer or metered-dose inhaler with a spacer) minimize systemic toxicity and are preferred. Albuterol sulfate 2.5 to 5 milligrams is the most common agent. Deliver doses every 20 min or as continuous nebulization (10 to 15 milligrams/h), titrating treatment to clinical response and signs of toxicity (tachycardia, hypertension, and palpitations). Levalbuterol can be given at half of the dose of albuterol, but administration by continuous nebulization has not been studied. Terbutaline (0.25 to 0.5 mL) or epinephrine 1:1000 (0.1 to 0.3 mL) SC may be administered to patients not tolerating aerosolized therapy. Epinephrine should be used with caution in the presence of underlying cardiovascular disease.

3. Steroids should be given in the ED, to patients with exacerbations of asthma and COPD. The initial dose is the equivalent of 40 to 60 milligrams of prednisone. Neither the choice of steroid nor the route of administration is critical. If the patient is unable to take oral medication, intravenous methylprednisolone 60 to 125 milligrams may be used. Additional doses may be given every 4 to 6 hours. Inhaled steroids are not indicated for the treatment of acute symptoms. A 5- to 10-day course of oral steroids (prednisone 40 to 60 milligrams/dose) is beneficial for discharged patients with a significant exacerbation of asthma or COPD.

4. Anticholinergics are useful adjuvants when given with other therapies. Nebulized ipratropium (500 milligrams = 2.5 mL) may be administered alone or mixed with albuterol. The effects of ipratropium peak in 1 to 2 hours and last 3 to 4 hours. Dosages may be repeated every 1 to 4 hours.

5. COPD patients with change in sputum color and volume may benefit from antibiotic therapy directed at Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Commonly used agents include doxycycline, the macrolides, cephalosporins, and fluoroquinolones. Antibiotic use in asthma should be reserved for concurrent bacterial infections such as pneumonia.

6. Intravenous magnesium sulfate (1 to 2 grams over 30 min) is used when asthma exacerbations are severe (FEV1 <25% of predicted). However, it is not currently recommended for mild or moderate asthma exacerbations and should not be substituted for standard regimens.

7. Several studies have suggested that an 80%:20% mixture of helium and oxygen (Heliox) can lower airway resistance and aid in drug delivery in the patient with very severe asthma exacerbation. Care must be taken with use of this therapy in the oxygen-dependent patient since Heliox administration necessarily entails an Fio2 less than 1.0.

8. Mechanical ventilation is necessary in patients with respiratory muscle fatigue, respiratory acidosis, altered mental status, or hypoxia refractory to standard therapies. Noninvasive partial pressure ventilation (NPPV) has become a useful alternative to intubation and invasive ventilation. NPPV lowers intubation rates, short-term mortality, and length of hospitalization in COPD. NPPV can be given by continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP). BiPAP has the advantage of reducing the work of breathing. CPAP is titrated up to 15 cm H2O, while BiPAP settings are between 8 and 20 cm H2O for inspiration and 4 and 15 cm H2O for expiration.

9. Patients in whom NPPV is likely to fail include those in whom there is poor mask fit or inability to cooperate with (or tolerate) NPPV, those who are obtunded, cannot clear airway secretions, or are hemodynamically unstable. NPPV is also not viable in extremely obese patients, or those who are status-post recent facial or gastroesophageal surgery or facial burns. When NPPV is not a viable option, oral intubation is indicated. Using rapid inspiratory flow rates at a reduced respiratory frequency (12 to 14 breaths/min), while allowing for an adequate expiratory phase, may help reduce air-trapping and subsequent barotrauma. Therapy should be guided by pulse oximetry and ABG results. Sedation and continued therapy for bronchospasm should continue after the patient has been placed on mechanical ventilation.

10. Admission criteria for patients with asthma include failure of outpatient treatment, persistent and worsening dyspnea, PEF or forced expiratory volume in 1 second (FEV1) less than 40% of predicted, hypoxia, hypercarbia, and altered mental status; presence of comorbidities increases likelihood of need for admission. As compared to asthmatics, patients with acute COPD exacerbations are more likely to require admission. Indications for COPD admission include therapeutic failure, severe dyspnea, significant comorbidities, arrhythmias, older age, insufficient home support, worsening hypoxia and hypercapnia with acidosis, and impaired mental status.

In the absence of intubation, sedatives, hypnotics, and other medications that depress respiratory drive are generally contraindicated. Methylxanthines do not improve lung function in acute asthma or COPD. β-Blockers may exacerbate bronchospasm. Antihistamines and decongestants should be avoided as they diminish clearance of respiratory secretions. Mucolytics should also be withheld; they may exacerbate bronchospasm. Mast cell and leukotriene modifiers have no role in the treatment of acute exacerbations of asthma or COPD. Ketamine and halothane have been reported as therapy for refractory asthma, but controlled studies are lacking.

Close follow-up care must be arranged for discharged patients to ensure resolution of the exacerbation and review the management plan. Despite appropriate therapy, these patients have high relapse rates. Education of the asthma and COPD patients before discharge (ie, review of medications, inhaler techniques, use of PEF measurements, avoidance of noxious stimuli, and need to follow-up) should be an integral part of ED care.