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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. (1973) studied this question.