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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.

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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.

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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.

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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.

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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 ...

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