Ka. Franklin et al., HEMODYNAMICS, CEREBRAL-CIRCULATION, AND OXYGEN-SATURATION IN CHEYNE-STOKES RESPIRATION, Journal of applied physiology, 83(4), 1997, pp. 1184-1191
Because cardiovascular disorders and stroke may induce Cheyne-Stokes r
espiration, our purpose was to study the interaction among cerebral ac
tivity, cerebral circulation, blood pressure, and blood gases during C
heyne-Stokes respiration. Ten patients with heart failure or a previou
s stroke were investigated during Cheyne-Stokes respiration with recor
dings of daytime polysomnography, cerebral blood flow velocity, intra-
arterial blood pressure, and intra-arterial oxygen saturation with and
without oxygen administration. There were simultaneous changes in wak
efulness, cerebral blood flow velocity, and respiration with accompany
ing changes in blood pressure and heart rate similar to 10 s later. Ce
rebral blood flow velocity, blood pressure, and heart rate had a minim
um occurrence in apnea and a maximum occurrence during hyperpnea. The
apnea-induced oxygen desaturations were diminished during oxygen admin
istration, but the hemodynamic alterations persisted. Oxygen desaturat
ions were more severe and occurred earlier according to intraarterial
measurements than with finger oximetry. It is not possible to explain
Cheyne-Stokes respiration by alterations in blood gases and circulator
y time alone. Cheyne-Stokes respiration may be characterized as a stat
e of phase-linked cyclic changes in cerebral, respiratory, and cardiov
ascular functions probably generated by variations in central nervous
activity.