Key points are not available for this paper at this time.
TWO dominant but apparently conflicting theories explain the regular waxing and waning of tidal volume and respiratory frequency that characterize Cheyne-Stokes breathing. This difference of opinion reflects the two diseases in which Cheyne-Stokes breathing is most often observed: cerebrovascular disease and heart failure.1 , 2 One theory attributes Cheyne-Stokes respiration to a neurologic abnormality; in dispute is whether this neurologic abnormality is an excessively depressed respiratory center or an excessively excitable one. The other theory ascribes Cheyne-Stokes breathing to the prolongation of the circulation time produced by congestive heart failure. Since patients with Cheyne-Stokes respiration frequently have both cardiac and cerebrovascular disease, . . .
Cherniack et al. (Thu,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: