Interaction of hypocapnia, hypoxia, brain blood flow, and brain electrical activity in voluntary hyperventilation in humans

Burykh, E. A.

doi:10.1007/s11055-008-9029-y

Cited by 12 publications

(4 citation statements)

References 9 publications

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“…On functional neuroimaging studies, HV decreases or even abolishes the occipital cortex response to visual stimulation [12, 13]. The physiological changes induced in the brain culminate just after experimentally induced HV begins [14, 15]. …”

Section: Introductionmentioning

confidence: 99%

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

et al. 2010

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Hyperventilation is often associated with stress, an established trigger factor for migraine. Between attacks, migraine is associated with a deficit in habituation to visual-evoked potentials (VEP) that worsens just before the attack. Hyperventilation slows electroencephalographic (EEG) activity and decreases the functional response in the occipital cortex during visual stimulation. The neural mechanisms underlying deficient-evoked potential habituation in migraineurs remain unclear. To find out whether hyperventilation alters VEP habituation, we recorded VEPs before and after experimentally induced hyperventilation lasting 3 min in 18 healthy subjects and 18 migraine patients between attacks. We measured VEP P100 amplitudes in six sequential blocks of 100 sweeps and habituation as the change in amplitude over the six blocks. In healthy subjects, hyperventilation decreased VEP amplitude in block 1 and abolished the normal VEP habituation. In migraine patients, hyperventilation further decreased the already low block 1 amplitude and worsened the interictal habituation deficit. Hyperventilation worsens the habituation deficit in migraineurs possibly by increasing dysrhythmia in the brainstem-thalamo-cortical network.

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Section: Introductionmentioning

confidence: 99%

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

et al. 2010

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“…In those studies, the altered neurobehavioral performance is more likely due to a mixed effect of hypocapnia and hypoxia. The interaction between hypocapnia, hypoxia, CBF, and brain electrical activity is very complex and not well understood (6,15). We certainly agree that extreme hypoxia by itself may lead to neurocognitive impairment.…”

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confidence: 99%

Hypercapnia is more important than hypoxia in the neuro-outcomes of sleep-disordered breathing

Wang

Thomas

Yee

et al. 2016

Journal of Applied Physiology

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TO THE EDITOR: Obstructive sleep apnea (OSA) results in awake neurocognitive impairment with societal implications (22). However, the relevant pathophysiological mechanism(s) for this impairment are unclear, impacting on disease monitoring and targeted treatment (1, 17). Among a number of candidate factors, hypoxemia and sleep fragmentation are generally recognized as two key underlying mechanisms (1, 4), with hypoxemia having the strongest evidence base (7, 17). However, recent large clinical trials failed to find a strong link between nocturnal hypoxia and neurobehavioral impairment. In the landmark APPLES study, the severity of O 2 desaturation explained only Ͻ2% of the variance of neurocognitive performance improvement in 1,204 OSA patients, and arousal index was not a significant predictor (17). In the recent LATINO study with the largest sample size of 8,059, apnea hypopnea index (AHI) with 3% desaturation was very weakly associated with neurocognitive functions after controlling for confounders (␤ ranged from 0.003 to 0.005) (18). In a multicenter European study, 1,649 OSA patients with excessive daytime sleepiness (EDS) and 1,233 OSA patients without EDS had only 1% of difference in SpO 2 nadir, no difference in mean SpO 2 , and similar arousal index (37/h vs. 33/h) (20). In human experimental studies, neurocognitive function was measured in 11 healthy subjects at ground level and simulated altitude of 13,000 feet. Two weeks of nocturnal continuous hypoxia at altitude did not induce subjective sleepiness or impair objective vigilance and working memory (24). In addition, the effect of 4-wk nocturnal intermittent hypoxia on attention, working memory, Multiple Sleep Latency Test, and the Rey Auditory Verbal Learning Test was measured in 8 healthy subjects and again no effect was detected (29). Moreover, if hypoxemia is the dominant factor for neurocognitive impairment, then EDS should improve with supplemental O 2 therapy. However, studies have not found that supplemental O 2 improves daytime hypersomnolence in OSA patients despite improving oxygenation (13, 16).Interestingly, although OSA usually comes with repetitive episodes of both hypoxia and hypercapnia, only the effect of hypoxia has been more intensively studied. A simple test entering key words of "Sleep Apnea and Hypoxia" in PubMed returns 2,866 publications; In contrast, there are only 867 publications with the key words of "Sleep Apnea and Hypercapnia." It is therefore not surprising that hypercapnia has not been considered as a major factor in OSA-related neurocognitive impairment in any major review in this field (1,5,12).In this context, we conducted a series of clinical and experimental studies to evaluate the effect of hypoxia and hypercapnia on EEG activation and neurobehavioral performance. First, we demonstrated that 97 hypercapnic sleep-disordered breathing (SDB) patients have a significantly high degree of EEG slowing, which was best predicted by increased wake PCO 2 measured by arterial blood gases. Hypoxia-related parameters were not...

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“…Hypocapnia may be associated with decreased systemic vasodilation 8 and may cause tissue ischemia 9 , intestinal ischemia 10 , and cerebral ischemia 11,12 . Animal studies have reported that serotonin levels in the brain, a highly emetogenic substance, increase with intestinal 13,14 and cerebral ischemia 15 .…”

Section: Introductionmentioning

confidence: 99%

Association between Intraoperative End-Tidal Carbon Dioxide and Postoperative Nausea and Vomiting in Gynecologic Laparoscopic Surgery

Dong

Takeda

Yamazaki

et al. 2022

Preprint

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PURPOSE Gynecologic laparoscopic surgery has a high incidence of postoperative nausea and vomiting (PONV). Studies suggest that low intraoperative end-tidal carbon dioxide (EtCO2) is associated with an increased incidence of PONV, but the results have not been consistent among studies. This study investigated the association between intraoperative EtCO2 and PONV in patients undergoing gynecologic laparoscopic surgeries under general anesthesia. METHODS This retrospective cohort study involved patients who underwent gynecologic laparoscopic surgeries under general anesthesia at Kyoto University Hospital. We defined hypocapnia as a mean EtCO2 of <35 mmHg. Multivariable modified Poisson regression analysis examined the association between low EtCO2 and PONV two days after surgery and the postoperative length of hospital stay (PLOS). RESULTS Of the 739 patients, 120 (16%) had low EtCO2, and 430 (58%) developed PONV two days after surgery. There was no substantial association between low EtCO2 and increased incidence of PONV (adjusted risk ratio: 0.96; 95% confidence interval [CI]: 0.80–1.14; p = 0.658). Furthermore, there was no substantial association between low EtCO2 and prolonged PLOS (adjusted difference in PLOS: 0.13; 95% CI, −1.00 to 1.28; p = 0.816). CONCLUSION Intraoperative low EtCO2 was not substantially associated with either increased incidence of PONV or prolonged PLOS.

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Interaction of hypocapnia, hypoxia, brain blood flow, and brain electrical activity in voluntary hyperventilation in humans

Cited by 12 publications

References 9 publications

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

Changes in visual-evoked potential habituation induced by hyperventilation in migraine

Hypercapnia is more important than hypoxia in the neuro-outcomes of sleep-disordered breathing

Association between Intraoperative End-Tidal Carbon Dioxide and Postoperative Nausea and Vomiting in Gynecologic Laparoscopic Surgery

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