Figure 1.
Top panel: Tracings showing a mild, brief (10 sec) hypopnea produced by decreasing continuous positive airway pressure (CPAP) from 13 cm H2O to 10 cm H2O for three breaths (dial-down). C3/A2 and C4/O1 are two electroencephalogram leads; SpO2, oxyhemoglobin saturation; EKG, electrocardiogram. Time 0 is the time of upper airway opening. Note the increase in flow and in heart rate (numerals above EKG) following the increase in CPAP in the absence of cortical arousal. Bottom panel: Tracings from the same patient showing a long dial- down at 2 cm H2O, producing severe obstruction, which was maintained until the airway opened spontaneously, with intense arousal, at 20 sec. Note that in the brief obstruction (top), peak tachycardia occurred about 10 sec after opening and 18 sec after the onset of the hypopnea (vertical dotted line). At 18 sec following the onset of apnea in the long dial-down (dotted line) there was still no appreciable increase in HR even though the obstruction was much more severe and had lasted longer at this point. Thus, the timing of tachycardia is linked to the end of obstruction and not to the severity of arousal stimuli.