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Objective To observe the effects of a fast-acute ascent to high altitude on brain cognitive function and transcranial doppler parameters in order to understand the physiological countermeasures of hypoxia. Methods 17 high-altitude-naïve male subjects (mean age was 26.3 ± 8.1 years) participated in the study. We measured Critical Flicker Fusion Frequency (CFFF), blood oxygen saturation, Psychology Experiment Building (PEBL) including three tests (Modified Math Processing Task, Perceptual Vigilance Task, and Time Estimation Task), as well as Cerebral Blood Flow index (CBFi), mean cerebral artery Systolic and diastolic velocities, Cerebral Pulsatility index (CPi), and heart Rate. All were measured at sea level, at least 1 h after arrival at the hypobaric hypoxia equivalent of 3842 m and 1 h after return to sea level. Results Under acute exposure to hypobaric hypoxic conditions, significant decrease in CFFF [42.1 ± 1 vs. 43.5 ± 1.7 Hz at sea level (asl), p < 0.01], CBFi (611 ± 51 vs. 665 ± 71 asl, p < 0.01) and blood oxygen saturation (83 ± 4% vs. 98 ± 1% asl, p < 0.001) as compared to pre-ascent values were observed. Physiological countermeasures to hypoxia could be involved as there was no significant change in neuropsychometric tests, Systolic and Diastolic velocities and CPi. A significant increase in Heart Rate (81 ± 15 bpm vs. 66 ± 15 bpm asl, p < 0.001) was observed. All parameters returned to their basal values 1 h after regaining sea level. Conclusion Hypoxia results in a decrease in CFFF, CBFi and oxygen saturation and in an increase in heart rate. As it decreased, Cerebral Blood Flow index does not seem to be the physiological measurement of choice to hypoxia explaining the maintenance of cognitive performance after acute exposure to hypobaric hypoxia and requires further investigation. Cerebral oxygen delivery and extraction could be one of the underlying mechanisms.

This case report concerns a 30-year-old man who survived a 4.2 g diltiazem overdose. He sustained vasoplegic shock with a junctional escape rhythm which required high doses of norepinephrine and epinephrine. Among other complications, ileus with paralytic intestinal pseudo-obstruction developed on day three. Cecal distention was demonstrated by abdomen computed tomodensitometry. The ileus resolved on day seven following the poisoning. Diltiazem plasma concentrations were determined during the first three days. The possible role of other medications, activated charcoal and sufentanil, is noted.

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