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Добірка наукової літератури з теми "O2saturation"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 22 червня 2025

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Статті в журналах з теми "O2saturation"

Armstrong, C., KW Burak, and PL Beck. "Benzocaine-Induced Methemoglobinemia: A Condition of which all Endoscopists Should Be Aware." Canadian Journal of Gastroenterology 18, no. 10 (2004): 625–29. http://dx.doi.org/10.1155/2004/620203.

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Methemoglobinemia is a rare complication that can occur with the use of benzocaine-containing compounds. Two cases of methemoglobinemia are reported, and the pathophysiology and treatment of methemoglobinemia are reviewed. Both patients received topical 20% benzocaine spray before endoscopy. Immediately following the procedure, there was a reduction in O2saturation assessed by pulse oximetry that was refractory to O2therapy. Dramatic peripheral and central cyanosis developed. O2saturation measured by pulse oximetry ranged from 83% to 87% on O2by nasal prongs and 100% O2by a nonrebreathing mask. Both patients were mildly confused and one patient complained of a significant headache. The diagnosis of methemoglobinemia was considered and arterial blood gas sampling was performed. In both patients, the arterial blood had a chocolate brown colour. A methemoglobin level of 48% and 18% was noted in patient 1 and patient 2, respectively. Both patients were treated with methylene blue, resulting in a significant improvement with gradual normalization of their O2saturation within 10 min to 30 min. The use of benzocaine spray may not markedly alter the patient's perception of endoscopy and thus, the routine use of these agents should be questioned. If such agents are used, the physician must be aware of this association to prevent a delay in the diagnosis and management of this rare, but potentially lethal, condition.

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SEO, YOOJIN, KAZUYA MATSUMOTO, YOUNG MAN PARK, MOTOHIKO MOHRI, SHIGEAKI MATSUOKA, and KWANG PAK PARK. "Changes in sleep patterns during He-O2saturation dives." Psychiatry and Clinical Neurosciences 52, no. 2 (1998): 141–42. http://dx.doi.org/10.1111/j.1440-1819.1998.tb00995.x.

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Bloos, F., and K. Reinhart. "The value of central venous O2saturation for assessment of tissue oxygenation." DMW - Deutsche Medizinische Wochenschrift 129, no. 48 (2004): 2601–4. http://dx.doi.org/10.1055/s-2004-836082.

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Moszura, Tomasz, Pawel Dryzek, Sebastian Goreczny, et al. "A 10-year single-centre experience in percutaneous interventions for multi-stage treatment of hypoplastic left heart syndrome." Cardiology in the Young 24, no. 1 (2013): 54–63. http://dx.doi.org/10.1017/s104795111200220x.

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AbstractObjectivesThe purpose of this paper is to report our 10 years of experience of interventional treatment of patients with hypoplastic left heart syndrome and to focus on the frequency, type, and results of percutaneous interventions during all the stages of palliation, considering the different techniques, devices, and complications.BackgroundConstant progress in surgical treatment of congenital heart defects in the last decade has significantly improved the prognosis for children with hypoplastic left heart syndrome. However, morbidity and mortality remain relatively high. Modern interventional procedures complement or occasionally replace surgical treatment.MethodsBetween January, 2001 and December, 2010, 161 percutaneous interventions were performed in 88 patients with hypoplastic left heart syndrome. Patients were divided into four groups: (a) before the first surgical treatment including hybrid approach, (b) after first-stage Norwood operation, (c) after second-stage bidirectional Glenn operation, and (d) after third-stage Fontan operation.ResultsPercutaneous interventions resulted in statistically significant changes in pulmonary artery pressures, vessel diameters, and O2saturation. Complications occurred in 4.3% of interventions and were related mainly to stent implantation in stenosed pulmonary arteries.ConclusionsPercutaneous interventions may result in haemodynamic stability and reduction in the number of operations. They may result in significant changes in pulmonary artery pressures, vessel diameters, O2saturation, with a low rate of complications, which are mainly related to stent implantation in the pulmonary arteries.

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Crocker, George H., Balazs Toth, and James H. Jones. "Combined effects of inspired oxygen, carbon dioxide, and carbon monoxide on oxygen transport and aerobic capacity." Journal of Applied Physiology 115, no. 5 (2013): 643–52. http://dx.doi.org/10.1152/japplphysiol.01407.2012.

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We hypothesized that breathing hypoxic, hypercapnic, and CO-containing gases together reduces maximal aerobic capacity (V̇o2max) as the sum of each gas' individual effect on V̇o2max. To test this hypothesis, goats breathed combinations of inspired O2fraction (FiO2) of 0.06–0.21 and inspired CO2fraction of 0.00 or 0.05, with and without inspired CO that elevated carboxyhemoglobin fraction (FHbCO) to 0.02–0.45, while running on a treadmill at speeds eliciting V̇o2max. Individually, hypoxia and elevated FHbCOdecreased fractional V̇o2max(FV̇o2max, fraction of a goat's V̇o2maxbreathing air) in linear, dose-dependent manners; hypercapnia did not change V̇o2max. Concomitant hypoxia and elevated FHbCOdecreased V̇o2maxless than the individual gas effects summed, indicating their combined effects on V̇o2maxare attenuated, fitting the following regression: FV̇o2max= 4.24 FiO2+ 0.519 FHbCO− 8.22 (FiO2× FHbCO) + 0.117, ( R2= 0.965, P < 0.001). The FV̇o2maxcorrelated highly with total cardiopulmonary O2delivery, not peripheral diffusing capacity, and with arterial O2concentration (CaO2), not cardiac output. Hypoxia and elevated FHbCOdecreased CaO2by different mechanisms: hypoxia decreased arterial O2saturation (SaO2), whereas elevated FHbCOdecreased O2capacitance {concentration of hemoglobin (Hb) available to bind O2([Hbavail])}. When breathing hypoxic gas (FiO20.12), CaO2did not change with increasing FHbCOup to 0.30 because higher SaO2of Hbavailoffset decreased [Hbavail] due to the following: 1) hyperventilation with hypoxia and/or elevated FHbCO; 2) increased Hb affinity for O2due to both Bohr and direct carboxyhemoglobin effects; and 3) the sigmoid relationship between O2saturation and partial pressure elevating SaO2more with hypoxia than normoxia.

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Hall, David M., Kirk R. Baumgardner, Terry D. Oberley, and Carl V. Gisolfi. "Splanchnic tissues undergo hypoxic stress during whole body hyperthermia." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (1999): G1195—G1203. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1195.

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Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2saturation, splanchnic arterial-venous O2difference, and venous[Formula: see text], while decreasing venous O2saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ∼20%. Two hours after heat exposure, the splanchnic arterial-venous O2difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.

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Morse, John WI, Sharyle A. Fowler, and Amy L. Morse. "Endoscopist-Administered Propofol: A Retrospective Safety Study." Canadian Journal of Gastroenterology 22, no. 7 (2008): 617–20. http://dx.doi.org/10.1155/2008/265465.

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BACKGROUND: Propofol is an anesthetic agent that is commonly used for conscious sedation. Propofol has advantages as a sedative agent for endoscopic procedures including rapid onset, short half-life and rapid recovery time. However, concerns exist regarding the potential for respiratory depression, hypotension, perforation due to deep sedation and the need for monitoring by an anesthetist. Propofol has been used under endoscopist supervision at the Stanton Territorial Hospital in Yellowknife, Northwest Territories since 1996 (approximately 7000 cases).METHODS: A retrospective chart review of endoscopic procedures conducted at the Stanton Territorial Hospital between January 1996 and May 2007 was performed. A random sample of 680 procedures was reviewed from a total of 6396 procedures.RESULTS: The mean (± SD) baseline systolic blood pressure (SBP) was 122.8±17.0 mmHg. The mean lowest SBP was 101.7±14.5 mmHg. The mean absolute drop in SBP was 21.1±16.7 mmHg, with a mean per cent drop of 16.3%±11.7%. Eighty-eight patients (12.9%) developed transient hypotension (SBP lower than 90 mmHg). All patients regained normal blood pressure spontaneously on repeated measurement. No patients required intravenous fluid resuscitation. The mean O2saturation was 96.4%±2.1%. One patient (0.1%) transiently desaturated (O2saturation 89%), but recovered spontaneously on repeat measurement with no intervention. No procedures were aborted for patient safety. There were no major complications, including perforation or death. There was one mucosal tear during nontherapeutic colonoscopy (0.1%).CONCLUSIONS: Propofol can be safely administered in a community hospital setting under endoscopist supervision, with no additional support or monitoring.

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Kawakami, Michiro, Kazuo Makimoto, Osamu Noi, and Hiroaki Takahashi. "Feasibility of Pulse Oxymetry to Measure Arterial O2Saturation in Studies on Cochlear Blood Circulation." Acta Oto-Laryngologica 111, no. 5 (1991): 908–16. http://dx.doi.org/10.3109/00016489109138429.

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Milingos, D., D. Doumplis, K. Sieunarine, P. Savage, A. D. Lawson, and J. R. Smith. "Uterine arteriovenous malformation: fertility-sparing surgery using unilateral ligation of uterine artery and ovarian ligament." International Journal of Gynecologic Cancer 17, no. 3 (2007): 735–37. http://dx.doi.org/10.1136/ijgc-00009577-200705000-00028.

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Arteriovenous malformations (AVM) are rarely found in the uterus and are usually acquired. The method of treatment is determined by symptoms, desire for future fertility, extent, and location of the malformation. Selective ligation of the vessels supplying the malformation is an effective treatment option when conservative methods have failed and uterine preservation is of primary concern. Measurement of uterine O2saturation and perfusion index has been shown to be effective in the intraoperative assessment of uterine viability, pre- and postligation of pelvic vasculature. We present the case of a 32-year-old woman with a postmolar uterine AVM treated surgically with unilateral uterine artery and ovarian ligament ligation.

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Dufu, Kobina, Ozlem Yalcin, Eilleen S. Y. Ao-ieong, et al. "GBT1118, a potent allosteric modifier of hemoglobin O2affinity, increases tolerance to severe hypoxia in mice." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 2 (2017): H381—H391. http://dx.doi.org/10.1152/ajpheart.00772.2016.

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Adaptation to hypoxia requires compensatory mechanisms that affect O2transport and utilization. Decreased hemoglobin (Hb) O2affinity is considered part of the physiological adaptive process to chronic hypoxia. However, this study explores the hypothesis that increased Hb O2affinity can complement acute physiological responses to hypoxia by increasing O2uptake and delivery compared with normal Hb O2affinity during acute severe hypoxia. To test this hypothesis, Hb O2affinity in mice was increased by oral administration of 2-hydroxy-6-{[(2 S)-1-(pyridine-3-carbonyl)piperidin-2yl] methoxy}benzaldehyde (GBT1118; 70 or 140 mg/kg). Systemic and microcirculatory hemodynamics and oxygenation parameters were studied during hypoxia in awake-instrumented mice. GBT1118 increased Hb O2affinity and decreased the Po2at which 50% of Hb is saturated with O2(P50) from 43 ± 1.1 to 18.3 ± 0.9 mmHg (70 mg/kg) and 7.7 ± 0.2 mmHg (140 mg/kg). In a dose-dependent fashion, GBT1118 increased arterial O2saturation by 16% (70 mg/kg) and 40% (140 mg/kg) relative to the control group during 5% O2hypoxia. In addition, a GBT1118-induced increase in Hb O2affinity reduced hypoxia-induced hypotension compared with the control group. Moreover, microvascular blood flow was higher during hypoxia in GBT1118-treated groups than the control group. The increased O2saturation and improved blood flow in GBT1118-treated groups preserved higher interstitial tissue Po2than in the control group during 5% O2hypoxia. In conclusion, increased Hb O2affinity enhanced physiological tolerance to hypoxia, as evidenced by improved hemodynamics and tissue oxygenation. Therefore, pharmacologically induced increases in Hb O2affinity become a potential therapeutic approach to improve tissue oxygenation in pulmonary diseases characterized by severe hypoxemia.NEW & NOTEWORTHY This study establishes that pharmacological modification of hemoglobin O2affinity can be a promising and novel therapeutic strategy for the treatment of hypoxic hypoxia and paves the way for the clinical development of molecules that prevent hypoxemia.

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