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Chronic hypoxemia stimulates erythropoietin release, increasing red blood cell mass and hematocrit (secondary polycythemia). This compensatory mechanism improves oxygen-carrying capacity but also increases blood viscosity, potentially raising pulmonary vascular resistance and contributing to cor pulmonale. The oxyhemoglobin curve in chronic hypercapnia/hypoxemia often shifts to the right (facilitating peripheral unloading) due to increased 2,3-BPG and acidosis during exacerbations, not left. The kidneys retain bicarbonate to buffer persistent respiratory acidosis, leading to elevated serum bicarbonate (metabolic compensation), not increased excretion. Pulmonary vascular resistance typically increases with chronic hypoxic vasoconstriction. Prehospital implications include careful oxygen titration to avoid CO₂ retention exacerbation while correcting hypoxemia (often target 88–92%), awareness of polycythemia-related thrombotic risk, and assessment for signs of right heart strain (JVD, edema). Understanding these adaptations helps paramedics anticipate decompensation triggers and tailor oxygen/ventilation strategies during COPD exacerbations.