Cerebral Blood Flow Changes During Acute Apneic Episodes Simulating Obstructive Sleep Apnea

Background: Obstructive sleep apnea (OSA) has not only been linked to hypertension and increased cardiovascular risk, but it can also result in mental status changes such as memory impairment. Under normal conditions, autoregulation in the cerebral vasculature maintains a constant flow rate to the brain. As such, the observed changes in the mental status may result from altered cerebral blood flow in OSA patients. By simulating apneic conditions using Intermittent Hypoxic Training (IHT), we can approximate the effect of OSA on cerebral blood flow using a Transcranial Doppler (TCD) to monitor middle cerebral artery (MCA) flow velocity. Using these techniques, we tested the hypothesis that IHT would cause alterations in cerebral blood flow in healthy individuals. Methods: Nine healthy subjects were recruited for the study. Subjects were between 18-40 years of age and free of any pre-existing OSA or Cardiovascular disease. The IHT protocol consisted of a series of hypoxic apneas in which subjects inhaled 2-3 breaths of nitrogen, followed by a 20-second apnea and 40 seconds of room air breathing recovery every minute for 20 minutes. TCD was used to record MCA velocity throughout the study and, additionally, ECG and cardiopulmonary perimeters were also recorded. Results: The MCA velocity during 5 minutes baseline and 5 minutes post-IHT was compared. The measured TCD flow velocity was not statistically different (p [greater than] 0.05) between baseline and post-IHT including the following TCD variables: systolic, diastolic, mean, pulsatility, MAP coherence, MAP phase, MAP transfer and vascular resistance (all p [greater than] 0.05). Conclusions: Cerebral blood flow measures were not significantly altered following IHT in these healthy individuals. The data demonstrates that a 20 minute period of simulated sleep apnea does not affect steady-state cerebral blood flow. Thus, it is likely that cerebral autoregulation is sufficient to maintain normal blood flow in healthy subjects and is not affected by this period of IHT. Further studies may need to examine chronic OSA subjects to discern whether altered cerebral blood flow plays a pathophysiologic role in the disease.