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Cortical activity during hypoxic hyperventilation

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This study seeks to determine the pattern of electroencephalogram changes during stimulatory ventilatory responses to acute progressive hypoxia. Electroencephalograms were recorded in the 10-20 electrode system during progressive poikilocapnic hypoxic tests based on the rebreathing routine. Healthy subjects were used for he study. A major finding was that hypoxia decreased the power spectra of the alpha activity. The decrease was surprisingly rapid and greater at mild hypoxic desaturation when pulmonary ventilation was about to pick up than during the maximum hypoxic hyperventilation. The possible relation of hypoxic decline in brain bioactivity to the manifestation of hypoxic hyperventilation remains to be elucidated in further studies.
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Hypoventilation in chronic mountain sickness: a mechanism to preserve energy

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Chronic Mountain Sickness (CMS) patients have repeatedly been found to hypoventilate. Low saturation in CMS is attributed to hypoventilation. Although this observation seems logical, a further understanding of the exact mechanism of hypoxia is mandatory. An exercise study using the Bruce Protocol in CMS (n = 13) compared to normals N (n = 17), measuring ventilation (VE), pulse (P), and saturation by pulse oximetry (SaO2) was performed. Ventilation at rest while standing, prior to exercise in a treadmill was indeed lower in CMS (8.37 l/min compared with 9.54 l/min in N). However, during exercise, stage one through four, ventilation and cardiac frequency both remained higher than in N. In spite of this, SaO2 gradually decreased. Although CMS subjects increased ventilation and heart rate more than N, saturation was not sustained, suggesting respiratory insufficiency. The degree of veno-arterial shunting of blood is obviously higher in the CMS patients both at rest and during exercise as judged from the SaO2 values. The higher shunt fraction is due probably to a larger degree of trapped air in the lungs with uneven ventilation of the CMS patients. One can infer that hypoventilation at rest is an energy saving mechanism of the pneumo-dynamic and hemo-dynamic pumps. Increased ventilation would achieve an unnecessary high SaO2 at rest (low metabolism). This is particularly true during sleep.
The aim of this study was to evaluate the cardiovascular response to the activation of arterial chemoreceptors during voluntary apnea in snoring subjects. Fifty five men were enrolled in the study: 33 snorers and 22 non-snorers (control group). The majority of snorers were overweight and hypertensive. The experimental session consisted of 20 voluntary inspiratory apneas interspersed with 1 min free breathing periods, and 20 min recovery. The following parameters were recorded noninvasively: blood pressure, ECG, and arterial oxygen saturation. Data analysis was based on the Smietanowski procedure, written in the 4-th generation script language of MATLAB environment, which allows assessing the relative contribution of cardiac and vascular components to blood pressure variability. The results indicate that repetitive apneas led to significantly greater increases in blood pressure in the snorers. In this group, the domination of vascular influences during apnea periods reached 67 ±2.0%, which was greater than the 56 ±1.8% in the non-snorers (P<0.01). In contrast, the contribution of the cardiac component in the blood pressure response to apnea was greater in the non-snorers: 33 ±3% vs. 20 ±2% in the snorers (P<0.01). We conclude that activation of carotid chemoreceptors during voluntary apnea evokes a greater cardiovascular response in snorers, related to the reflex increase in total peripheral vascular resistance, and, consequently, a greater increase in blood pressure.
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