4.3 Obstructive & Inflammatory Airway Disease

AACN PCCN Progressive Care Certified Nurse, Adult

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1 Introduction, the Synergy Model & Exam Strategy

1.1 The PCCN Credential & the Progressive Care Nurse 1.2 Exam Blueprint, Format & Scoring 1.3 The AACN Synergy Model & How to Study

2 Cardiovascular Foundations — Hemodynamics, ACS & Catheterization

2.1 Hemodynamic Monitoring in Progressive Care 2.2 Acute Coronary Syndromes: Unstable Angina, NSTEMI & STEMI 2.3 Cardiac Catheterization, PCI & Structural Heart Procedures

3 Cardiovascular — Pump Failure, Rhythm, Vessels & Inflammation

3.1 Heart Failure & Cardiogenic Shock 3.2 Cardiomyopathies & Valvular Heart Disease 3.3 Dysrhythmia Interpretation & Electrical Therapies 3.4 Hypertensive Crisis, Vascular Disease & Aneurysms 3.5 Cardiac Inflammatory Disease, Tamponade & Post-Cardiac-Surgery Care

4 Respiratory — Gas Exchange, Failure & Ventilation

4.1 ABG/VBG Interpretation & Acid-Base Balance 4.2 Respiratory Failure & Oxygenation Support 4.3 Obstructive & Inflammatory Airway Disease 4.4 Acute Lung Injury, Embolism & Pleural Disorders 4.5 Thoracic Surgery & Airway Procedures

5 Endocrine, Renal & Electrolytes

5.1 Glycemic Emergencies: DKA, HHS & Glucose Control 5.2 Fluid-Regulation & Thyroid Disorders 5.3 AKI, CKD/ESRD & Electrolyte Imbalances

6 Neurology, Gastrointestinal, Hematology & Musculoskeletal

6.1 Stroke, TBI & Space-Occupying Lesions 6.2 Seizures, Encephalopathy & Altered Mental Status 6.3 GI Bleeding, Motility & Surgical Conditions 6.4 Hepatic, Pancreatic & Nutritional Disorders 6.5 Hematology, Immunology & Oncology 6.6 Musculoskeletal: Mobility, Falls & Compartment Syndrome

7 Multisystem — Sepsis, Infection, Wounds & End-of-Life

7.1 Sepsis, SIRS & Shock States 7.2 Healthcare-Acquired & Infectious Diseases 7.3 Wounds, Pressure Injuries & Rhabdomyolysis 7.4 Pain, Palliative Care & End-of-Life 7.5 Toxic Ingestion, Overdose & Withdrawal

8 Behavioral/Psychosocial & Professional Caring / Ethical Practice

8.1 Behavioral & Psychosocial Care 8.2 Advocacy, Moral Agency & Ethical Practice 8.3 Caring Practices & Response to Diversity 8.4 Facilitation of Learning & Patient/Family Education 8.5 Collaboration & Systems Thinking 8.6 Clinical Inquiry & Evidence-Based Practice

4.3 Obstructive & Inflammatory Airway Disease

Key Takeaways Explain This Topic AI

A silent chest and a normalizing or rising PaCO2 in severe asthma both signal impending respiratory failure, not improvement.

Target SpO2 88-92% in known chronic CO2 retainers to avoid blunting hypoxic respiratory drive.

BiPAP is first-line for COPD exacerbation with respiratory acidosis in an alert, cooperative patient.

Obstructive sleep apnea shows ongoing chest/abdominal effort against a blocked airway; central sleep apnea shows absent respiratory effort.

Pulmonary fibrosis is a restrictive disease with fine bibasilar 'Velcro' crackles and reduced DLCO, unlike obstructive airway disease.

Last updated: July 2026

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:

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.

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

Type Mechanism Key Distinguishing Feature

Obstructive sleep apnea (OSA) Upper airway collapses despite ongoing respiratory effort Snoring, gasping, visible chest/abdominal effort against a closed airway

Central sleep apnea (CSA) Brainstem fails to signal respiratory effort No chest wall/abdominal movement during apneic episodes

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:

• Feature Obstructive (Asthma, COPD) Restrictive (Pulmonary Fibrosis)
• Primary problem Difficulty exhaling air (airflow limitation) Difficulty expanding the lungs (reduced volume)
• FEV1/FVC ratio Reduced (<70%) Normal or increased
• Lung volumes Normal or increased (air trapping, hyperinflation) Reduced (FVC, TLC)
• Classic exam sound Wheezing, prolonged expiration Fine bibasilar "Velcro" crackles
• Bronchodilator response Often improves obstruction Minimal effect
• 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.