{'fraction_non_alphanumeric': 0.029329608938547486, 'fraction_numerical': 0.02653631284916201, 'mean_word_length': 4.877049180327869, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Cardiac output during sleep at altitude.

The effects of hypobaric hypoxia and sleep, assessed by EEG, upon cardiac output (Q) were studied by impedance cardiography using two male and two female subjects. Three nights were spent at 746 torr (152 m) followed by two nights at 493 torr (3500 m), all in a hypobaric chamber. Relatively normal sleep was observed except in the presence of Acute Mountain Sickness (AMS). The occurrence of normal levels of synchronized sleep implied that sleep hypoventilation occurred. A nadir of Q was observed at about 0500 hours, implying reduced O2 delivery. It was suggested that hypobaric hypoxia, sleep hypoventilation, and reduced O2 delivery may have interacted to produce AMS.