Pathophysiology and Oxygen Safety

COPD encompasses chronic bronchitis and emphysema, both causing airflow limitation from airway inflammation, mucus hypersecretion, and alveolar destruction that traps air and reduces gas exchange surface area. Chronic CO2 retention causes some clients to lose sensitivity to CO2 as a breathing stimulus, relying instead on hypoxia to drive respiration; giving high concentrations of oxygen in this small subset can suppress respiratory drive, causing hypoventilation. The safe approach is titrating oxygen to the lowest flow that achieves an acceptable saturation, typically 88-92% for many COPD clients, rather than the 95-100% target used in other populations, and monitoring for worsening confusion or lethargy suggesting CO2 narcosis.

ABG Interpretation and Assessment

Chronic COPD ABGs typically show compensated respiratory acidosis: low pH-normal range due to compensation, elevated PaCO2, and elevated bicarbonate as the kidneys retain bicarbonate to buffer the chronic acidosis. An acute exacerbation superimposed on this baseline shows further pH drop with even higher PaCO2, indicating decompensation. Physical findings include a barrel chest from air trapping, pursed-lip breathing to prevent airway collapse, clubbing of fingers from chronic hypoxia, and use of accessory muscles. Pursed-lip breathing prolongs exhalation and maintains positive airway pressure, preventing bronchiole collapse and helping clients feel less breathless, a teaching point often tested as a nursing intervention.

Exacerbation Management and Teaching

Acute exacerbations are managed with bronchodilators (short-acting beta agonists like albuterol), corticosteroids to reduce inflammation, and antibiotics if infection is suspected, evidenced by increased sputum purulence or volume. Teach clients diaphragmatic and pursed-lip breathing, energy conservation techniques like pacing activities and resting between tasks, and proper inhaler technique including spacer use for MDIs. Smoking cessation is the single most effective intervention to slow disease progression. Nutrition teaching includes small frequent high-calorie meals since large meals can worsen dyspnea by pushing on the diaphragm, and adequate protein supports respiratory muscle strength.