Kahn and colleagues1 point out that their findings of a decrease in transcutaneous PO2 after episodes of obstructive apnea could be due to a "... redistribution of blood flow away from the skin... ." Their suggestion, however, that the latter is due to a decrease in cardiac output is unlikely. Studies using indwelling arterial catheters during apnea and bradycardia have suggested that, if anything, there is an increase in cardiac output.2,3 Moreover, blood flow measurements3 have shown that there is often a peripheral vasoconstriction during such episodes.