Oxygen saturation (SpO2 (peripheral capillary oxygen saturation) or SaO2 (arterial oxygen saturation))

Oxygen saturation quantifies the percentage of hemoglobin bound to oxygen in arterial blood, typically 95-100% in healthy individuals at sea level, reflecting the efficiency of pulmonary gas exchange and oxygen delivery to tissues.[3][9] It follows a sigmoidal oxygen-hemoglobin dissociation curve, where saturation remains high until partial pressure of oxygen (PO2) drops below 60 mmHg, enabling stable delivery under varying conditions.[9] Low levels (hypoxemia) trigger compensatory responses like increased ventilation via carotid body sensors involving hydrogen sulfide and nitric oxide, or HIF-mediated erythropoietin production for red blood cell expansion.[1][2][7] Clinically, it is a vital sign for detecting respiratory distress, guiding oxygen therapy in conditions like COPD or pneumonia, and monitoring during anesthesia.[3][9] Abnormalities arise from lung disease, anemia, or circulatory failure, with right-shifts in the curve (e.g., due to acidosis or hyperthermia) facilitating tissue unloading.[7][9] Key regulatory mechanisms include carotid body chemoreceptors that sense low saturation via gasotransmitters like hydrogen sulfide when oxygen falls, increasing breathing and heart rate.[1] Hypoxia-inducible factors (HIFs), stabilized under low oxygen, drive adaptive gene expression for angiogenesis and glycolysis.[2][4][5] Measurement inaccuracies occur with skin pigmentation, nail polish, or low perfusion, emphasizing the need for arterial blood gas confirmation in critical cases.[9]

Other names

Blood oxygen saturationpulse oximetry readingoxyhemoglobin saturationSO2

None (not a druggable target; therapies modulate upstream factors like hemoglobin affinity via 2,3-BPG or pH shifts)