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. Author manuscript; available in PMC: 2013 May 31.
Published in final edited form as: Respir Physiol Neurobiol. 2012 Mar 30;181(3):286–301. doi: 10.1016/j.resp.2012.03.012

Figure 14.

Figure 14

Hypothetical schematic for the transduction of respiratory drive into central respiratory neural output during post-hypoxic periodic breathing. Low respiratory drive (reduced PaCO2 and relatively higher PaO2) causes reduced strength of reciprocal inhibition (dashed lines) resulting in mostly tonic inspiratory and expiratory neural output, subsequently producing hypopnea and apnea (A). High respiratory drive (increased PaCO2 and relatively low PaO2) causes increased strength of reciprocal inhibition (heavy dark lines) resulting in highly phasic inspiratory and expiratory neural output, subsequently producing hyperpnea (B). Eupneic respiratory drive (“normal” PaCO2 and PaO2) causes normal strength of reciprocal inhibition (gray lines) resulting in mostly phasic inspiratory and expiratory neural output, subsequently producing eupnea (C). Note that periods of low and high drive in this Figure correspond to periods of low and high drive in Figure 13.