Hypoxemia elicits chemoreflex stimulation, with consequent sympathetic activation and vasoconstriction.18 Sympathetic responses to hypoxemia are attenuated by stretch of thoracic afferents. Hence, apnea, and absence of chest inflation, potentiates the sympathetic vasoconstrictor effects of hypoxemia.18,19 The key role of the chemoreflex in modulating hypoxemia-driven cardiovascular pathophysiology is evidenced by the following considerations. First, chemoreflex responses to hypoxemia are heightened in patients with OSA.20 Second, hypertension is closely linked to OSA, and patients with borderline hypertension manifest markedly potentiated chemoreflex responses to hypoxemia.21 Third, even during normoxic daytime wakefulness, patients with OSA have very high levels of sympathetic activation,22 comparable to that seen in patients with heart failure. Administration of 100% oxygen lowers sympathetic drive, BP, and heart rate, arguing for tonic chemoreflex activation as a contributor to increased daytime sympathetic drive.23 Fourth, apnea-induced nocturnal hypoxemia elicits even further increases in sympathetic activity, with consequent surges in BP to levels as high as 240/130 mm Hg,22 with the patterns of sympathetic activation and inhibition during apnea and subsequent hyperventilation closely following those evident during administration of low inspiratory oxygen combined with voluntary apnea.18,19 Last, the primary response to hypoxemia is bradycardia,24,25 as is seen in the diving reflex.25,26 Varying degrees of bradycardia and bradyarrhythmias are often seen in patients with OSA, and in some patients may manifest as Mobitz II, complete heart block, and sinus arrest. Treatment in these cases should usually consist of treatment of apnea, rather than pacemaker placement.