Middle cerebral artery blood flow velocity, end-tidal pCO(2) and blood pressure in patients with obstructive sleep apnea and in healthy subjects during continuous positive airway pressure breathing
Dw. Droste et al., Middle cerebral artery blood flow velocity, end-tidal pCO(2) and blood pressure in patients with obstructive sleep apnea and in healthy subjects during continuous positive airway pressure breathing, NEUROL RES, 21(8), 1999, pp. 737-741
There is conflicting evidence in the literature as to the potential effect
of continuous positive airway pressure (CPAP) an cerebral perfusion. Compro
mising cerebral perfusion could possibly outweigh the benefit of improved o
xygenation. Patients with the obstructive sleep apnea syndrome (OSAS) have
been claimed to have a higher cerebrovascular reactivity to changes in end-
tidal pCO(2). In this study, we investigated 23 patients with OSAS and 16 h
ealthy young adults in the waking state. Both groups performed a series of
10 min of normal breathing, 20 min with 9 cmH(2)O nasal CPAP and then 10 mi
n of normal breathing while wearing a nasal CPAP mask. The following parame
ters were assessed: bilateral transcranial Doppler signal of the middle cer
ebral artery, systolic and diastolic blood pressure assessed manually, and
cerebrovascular reactivity to changes in pCO(2) during hyperventilation and
rebreathing into an airbag. Continuous end-tidal pCO(2) measurements were
performed in 14 subjects. As compared with normal breathing middle cerebral
artery blood flow velocity and pCO(2) remained unchanged during CPAP. Syst
olic and diastolic blood pressure increased slightly by 1.2 mmHg (p = 0.015
) and 1.1 mmHg (p = 0.007), respectively. Cerebrovascular reactivity did no
t differ in the two groups. Nasal CPAP of 9 cmH(2)O is a safe treatment wit
h respect to the maintenance of cerebral blood flow Our study gives further
evidence for the autoregulation's capacity to maintain cerebral blood now
velocity constant during different levels of intrathoracic pressure and dif
ferent cerebral perfusion pressures. We could not demonstrate any differenc
e in cerebrovascular reactivity between patients with OSAS and healthy pers
ons.