Archive for the ‘Sleep Apnea’ Category

Intracranial Pressure and Obstructive Sleep Apnea: Conclusion

Intracranial Pressure and Obstructive Sleep Apnea: ConclusionHypercapnia and hypoxia increase ICP, due to a cerebral arterial vasodilation, decreasing cerebral resistance, and increasing CBF. We found a decrease in the CPP during apnea. Loeppky et al found an abnormal cerebrovascular response to carbon dioxide in awake patients with sleep apnea. It is therefore not known whether CBF decreases (due to decreasing stroke volume), increases (due to decreasing cerebral resistance), or remains unchanged during the apneic episode. If CBF is affected during the apnea, then the cerebral autoregulation is overcome.
If CBF ceases during apnea, this might even worsen the cerebral hypoxia developing during the apneic episodes. In our opinion, this is of major importance and should be determined in future studies in order to understand the cerebral consequences of sleep apnea. Read the rest of this entry »

Intracranial Pressure and Obstructive Sleep Apnea: Discussion

The present study has shown (1) that awake values for ICP are pathologically elevated in patients with severe OSA, (2) that the ICP increases further during sleep, especially NREM stages 2 to 3 and REM sleep related to the apneic episodes, and (3) strong correlations between durations of apnea and AP and ICP elevations and between AP variations and ICP elevations.
Elevations in ICP related to respiration, especially Cheyne-Stokes respiration, are well known. Elevations in ICP during OSA have been described by Sugita et al. The CSF pressure was measured via a lumbar cannula in two patients. In this study, significant associations between apnea, hypoxia, and CSF pressure were found; however, AP was not measured. Read the rest of this entry »

Intracranial Pressure and Obstructive Sleep Apnea: Results

Intracranial Pressure and Obstructive Sleep Apnea: ResultsSeveral phases could be described in the AP and ICP variations. In the beginning of the apnea, there was a decrease in AP and ICP. During the apnea, ICP increased, associated with decreasing tcPo2 and increasing tcPo2. At the termination of the apnea, there was a steep pressure increase, both in the AP and in the ICP, while CVP varied associated with the respiratory movements.
In all patients, there was a highly significant correlation between the duration of apnea and systolic AP variations (Fig 2 and Table 2), between the duration of apnea and systolic ICP variations (Fig 3 and Table 3), and between systolic AP and ICP elevations. Read the rest of this entry »

Intracranial Pressure and Obstructive Sleep Apnea: Materials and Methods

A 1.2-mm catheter was placed in the radial artery in the nondominant hand after ensuring sufficient circulation in the ulnar artery. A catheter was placed in the superior central vein via the brachial vein. Correct localization was ensured by a normal pressure curve for CVP. An epidural pressure sensor (Plastimed) was placed in the right frontal region and was connected to a pressure transducer (AE 840).
Parametric statistics were used (linear regression analysis and t-test). A value below 0.05 was considered significant (two-sided test). The statistics were computed on the SPSS-PC+ program (SPSS Inc). Read the rest of this entry »

Intracranial Pressure and Obstructive Sleep Apnea

Intracranial Pressure and Obstructive Sleep ApneaSince its description in 1965 by Gastaut et al, OSA has been widely recognized as a clinical entity consisting of excessive daytime sleepiness, loud irregular snoring, obesity, dementia, and headache, especially morning headache. A central element in the pathogenesis of the condition is the upper-airway closure induced by sleep, giving rise to sleep apnea, increasing inspiratory efforts, hypoxic and hypercapnic episodes, and variations in intrathoracic and arterial pressures. Read the rest of this entry »

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