4.3 Obstructive & Inflammatory Airway Disease

Severe Asthma Exacerbation

Acute severe asthma combines bronchospasm, airway inflammation, and mucus plugging, producing progressive airflow obstruction. Classic findings include wheezing, tachypnea, accessory muscle use, and a prolonged expiratory phase. The most dangerous finding is often what you don't hear: a silent chest—airflow is so limited that wheezing disappears—signals impending respiratory arrest, not improvement. Other red flags for impending failure: inability to speak in full sentences, paradoxical (abdominal) breathing, altered mental status, and a PaCO2 that is rising toward normal or above normal. Because severe asthma should drive tachypnea and a low PaCO2, a normalizing or elevated PaCO2 means the patient is tiring and can no longer sustain the work of breathing—an ominous sign requiring immediate escalation.

Management follows a stepwise approach:

• Short-acting beta-agonists (SABA), e.g., albuterol, first line, often continuous nebulized in severe cases
• Ipratropium added to SABA for additional bronchodilation
• Systemic corticosteroids (IV or oral) to reduce airway inflammation—onset takes hours, so give early
• Magnesium sulfate IV for severe exacerbations unresponsive to initial bronchodilators; provides smooth-muscle relaxation
• Epinephrine (IM or IV) and heliox reserved for life-threatening presentations
• NIV may be trialed in an alert patient, but intubation should not be delayed if the patient is fatiguing—asthmatic patients can deteriorate to arrest quickly

COPD Exacerbation

An acute COPD exacerbation presents with worsening dyspnea, increased sputum volume/purulence, and cough beyond the patient's baseline. Two management points are heavily tested:

1. Titrate oxygen carefully. Many chronic COPD patients rely more heavily on a hypoxic (rather than hypercapnic) respiratory drive; delivering excessive oxygen can blunt that drive and worsen hypercapnia. Target SpO2 88–92% (not 95–100%) in known CO2 retainers, using controlled-delivery devices such as a Venturi mask when precision matters.
2. BiPAP is first-line for exacerbations with respiratory acidosis (pH <7.35) in an alert, cooperative patient—it reduces the need for intubation, shortens ICU stay, and improves outcomes compared with delaying to mechanical ventilation.

Bronchodilators (SABA ± ipratropium), systemic corticosteroids, and antibiotics (when signs of bacterial infection are present, such as increased sputum purulence or fever) complete standard therapy.

Sleep Apnea

STOP-BANG is the standard bedside OSA screening tool (Snoring, Tiredness, Observed apnea, blood Pressure, BMI, Age, Neck circumference, Gender). Untreated OSA increases perioperative and sedation risk—patients often desaturate quickly with opioids or benzodiazepines. CPAP is the mainstay treatment for both types in appropriate patients, since a single continuous pressure keeps the airway patent (OSA), while for some CSA patients adaptive servo-ventilation or treating the underlying cause (such as heart failure) is needed instead.

Pulmonary Fibrosis and Sarcoidosis

Pulmonary fibrosis is a chronic, progressive restrictive lung disease characterized by scarring that stiffens lung tissue and impairs gas diffusion. Hallmark findings: progressive exertional dyspnea, a persistent dry cough, fine bibasilar "Velcro" crackles on auscultation, digital clubbing, and reduced diffusing capacity (DLCO) on pulmonary function testing. Unlike obstructive disease, spirometry shows reduced lung volumes (FVC, TLC) with a preserved or increased FEV1/FVC ratio. Management is largely supportive in the acute setting—supplemental oxygen, treating superimposed infection, and avoiding unnecessary intubation when possible since mechanical ventilation carries a poor prognosis in end-stage fibrosis.

Sarcoidosis, a systemic granulomatous disorder, most often involves the lungs, producing bilateral hilar lymphadenopathy and, in advanced disease, pulmonary fibrosis. It can also affect the skin, eyes, heart, and nervous system. Acute pulmonary exacerbations are treated with systemic corticosteroids; progressive care nurses should watch for cardiac sarcoidosis presenting as dysrhythmias or heart block, and for pulmonary hypertension in advanced disease.

Obstructive vs. Restrictive Patterns on Pulmonary Function Testing

Distinguishing an obstructive process (asthma, COPD) from a restrictive process (pulmonary fibrosis, chest wall or neuromuscular disease) helps organize this whole category of disease:

Asthma Exacerbation vs. COPD Exacerbation

Although both are obstructive processes managed with bronchodilators and corticosteroids, they differ in key ways the PCCN expects you to recognize. Asthma exacerbations tend to occur in younger patients, are often triggered by a specific allergen, exercise, or infection, and are frequently fully reversible between episodes. COPD exacerbations occur on top of fixed, progressive airflow limitation from years of damage (chronic bronchitis, emphysema), most often in patients with a significant smoking history, and baseline lung function never fully returns to normal even after the acute episode resolves. This distinction matters for oxygen titration in particular — the hypoxic drive concern applies to chronic CO2-retaining COPD patients, not typically to a young patient in an isolated asthma attack, so blanket "keep everyone's SpO2 low" thinking is a common test-taking error.