Assessment of intracranial hemodynamics in sleep apnea syndrome.

Abstract

Sleep apnea syndrome may lead to changes in cerebral hemodynamics due to altered alveolar ventilation. We investigated the dynamics of CO2- and blood pressure-regulated alterations of cerebral blood flow velocities during apneic episodes and evaluated CO2 reactivity during different sleep stages. A computer-assisted pulsed Doppler system (2 MHz) was used for continuous overnight recordings of middle cerebral artery flow patterns together with simultaneous polysomnography, continuous blood pressure recordings, and measurements of end-expiratory CO2 in six patients with sleep apnea syndrome. Increases in mean flow velocity of 19-219% and in blood pressure of 12.5-83.1% could be observed during the apneic episodes, with maximum increases during rapid eye movement (REM) sleep. CO2 reactivity was in the normal range (4.4 +/- 1.2%) in the waking state and was markedly increased during sleep stages 1 and 2 (p less than 0.005 compared with awake). The greatest increase was found during REM sleep, with a rise of up to three times the waking value (p less than 0.0001 compared with sleep stage 2). The changes of mean flow velocity could be interpreted as reactive adaptation processes because of CO2 and blood pressure increases corresponding to apnea. The increased CO2 reactivity during sleep may indicate a "hypersensitivity" of intracranial vascular CO2 or pH receptors and a disturbance of central catecholaminergic and cholinergic systems. The pronounced velocity changes during apneic episodes and the concomitant alterations of vessel wall tension might lead to microangiopathies and macroangiopathies due to chronic strain on the brain vessels.

Effect of transnasal insufflation on sleep disordered breathing in acute stroke: a preliminary study

“…At the onset of apnea, there is hypotension and progressive bradycardia, followed by abrupt tachycardia on resumption of breathing [37]. These changes are associated with large fluctuations in CBFV [38,39]. The repeated hemodynamic There are several limitations to the current study.…”

Obstructive Sleep Apnea–Hypopnea and Incident Stroke

“…Marked surges in systemic blood pressure occur with each apneic and hypopneic event, followed by abrupt drops in systemic blood pressure. Parallel large fluctuations in cerebral blood flow velocity (21,22) suggest that patients with OSA experience repetitive episodes of cerebrovascular shearing stress, which, in addition to the known oxidative stress associated with intermittent hypoxemia and reoxygenation, likely contributes to cerebral vascular endothelial dysfunction. This is supported by a recent study demonstrating that patients with severe OSA, compared with control subjects, had reduced compensatory cerebrovascular blood flow responses to experimental hypotension (23).…”

“…In a subset of SHHS participants who had undergone brainstem magnetic resonance imaging examinations, we previously reported an inverse association between arousal index and incidence of brainstem white matter disease (34), a subclinical marker of cerebral ischemic injury. Apnea-related increases in cerebral blood flow velocity have been reported to be attenuated by the occurrence of arousals (22), and thus a higher arousal response may protect the cerebral circulation from fluctuating blood pressure changes. Arousals are involved in the termination of apneas/hypopneas and thus may play a role in reducing apnearelated stressors by shortening the duration of respiratory disturbances and reducing the degree of associated desaturation.…”

Obstructive Sleep Apnea and Cardiovascular Disease

“…In addition, cerebral blood flow velocity changes during apneic episodes and concomitant alterations of vessel wall tension associated with alternating obstructive apneas and hyperpneas could lead to changes in vascular shear forces, and acceleration of microangiopathies and macroangiopathies in the brain. [119][120][121][122] The cerebral blood flow response to hypoxia was significantly reduced in patients with OSA and normalized after 4-6 weeks of CPAP therapy. 123 Another study showed that heavy snoring increased the risk of carotid atherosclerosis independently.…”