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Toxic and Asphyxiating Hazards in Confined Spaces
Published in Neil McManus, Safety and Health in Confined Spaces, 2018
Hyperventilation refers to alveolar ventilation in excess of that needed to maintain normal arterial partial pressure of oxygen and carbon dioxide (Comroe et al. 1962). Hyperventilation can occur for many reasons: anxiety, injury, disease, hypoxemia (low partial pressure of oxygen in the blood), mechanical overventilation during use of respirators and rebreathers, hypotension (low blood pressure), triggers of pulmonary reflexes, acidosis, hormones, and drugs.
Psychogenic theory
Published in Herman Staudenmayer, Environmental Illness, 2018
Psychiatric symptoms, specifically those of the panic and other anxiety disorders, have been identified in manifestations of both mass psychogenic illness and EI (Brodsky, 1988; Pearson and Rix, 1987). These symptoms are associated with hyperventilation and include: muscle aching, nondescript pains, syncope, light-headedness, shortness of breath, dizziness, heaviness in the chest, weakness, headaches, blurred vision, and paresthesia. With the outbreak of mass psychogenic illness, anxiety can be anticipated as a manifestation of the fear of the unknown. When patients and their doctors do not know the cause of symptoms, it is very alarming. Anxiety is often interpreted to be an understandable consequence of this kind of uncertainty about the future (May, 1979). There are documented cases in which panic attacks are acquired after a toxic exposure (Shusterman and Dager, 1991). Nevertheless, in some cases this kind of reactive anxiety, or “state anxiety” as it is usually called, camouflages pre-morbid, long-term anxiety, or “trait anxiety” as it is called. With every effort made to account for an external explanation, very often the first suggestion is that the patient has been injured by a physical agent, and nonspecific treatment follows.
Emergency First Aid Treatment of Poisoning
Published in Charles R. Foden, Jack L. Weddell, Household Chemicals and Emergency First Aid, 2017
Charles R. Foden, Jack L. Weddell
The first and most dependable sign of poisoning is rapid, deep breathing. This sign is so common that if there is an unexplained increase in rate and depth of breathing, the possibility of asprin poisoning should be borne in mind. Hyperventilation can eventually lead to dangerous or even fatal changes in the body chemistry.
Voluntary hypocapnic hyperventilation lasting 5 min and 20 min similarly reduce aerobic metabolism without affecting power outputs during Wingate anaerobic test
Published in European Journal of Sport Science, 2021
Kohei Dobashi, Naoto Fujii, Masashi Ichinose, Tomomi Fujimoto, Takeshi Nishiyasu
Time-dependent changes in respiratory and metabolic variables and heart rate measured at Baseline and during the Breathing interventions are presented in Table I. At Baseline, none of the variables differed significantly among the three trials. By design, tidal volume, respiratory frequency and minute ventilation were all higher during the Breathing interventions in the two hyperventilation trials than in the control trial (P < 0.05), with no significant difference between the two hyperventilation trials. As a result, the end-tidal CO2 partial pressure was lower in the 5-min and 20-min hyperventilation trials than in the control trial (P < 0.05, Table I). End-tidal O2 partial pressures during the Breathing interventions were higher in both hyperventilation trials than in the control trial, with no significant difference between the two hyperventilation trials. Heart rates measured at Baseline were similar among the three trials, whereas those measured during the Breathing interventions were higher in the 5-min hyperventilation than in the control or 20-min hyperventilation trial (P < 0.05, Table I).
Oxygen: a new look at an old therapy
Published in Journal of the Royal Society of New Zealand, 2019
Richard Beasley, Diane Mackle, Paul Young
Since this report, studies have shown similar physiological responses of an increase in PaCO2 with high flow oxygen therapy across a range of other acute respiratory conditions including asthma (Rodrigo et al. 2003; Perrin et al. 2011) and pneumonia (Wijesinghe et al. 2012) and chronic respiratory conditions such as obesity hyperventilation syndrome (Wijesinghe et al. 2011). In these studies, high flow oxygen increased the PaCO2, compared with breathing room air or titrated oxygen therapy to within a target SpO2 range, suggesting that conservative oxygen administration across all acute and chronic respiratory conditions in which hypoxaemia may be present and oxygen therapy is prescribed may reduce harm. The likely mechanisms for this physiological effect are likely to be worsening ventilation/perfusion mismatch as a result of release of hypoxic pulmonary vasoconstriction, and a reduction in ventilatory drive, both of which will reduce alveolar ventilation, which leads to an increase in PaCO2 (Aubier et al. 1980; Robinson et al. 2000).
Elite versus non-elite cyclist – Stepping up to the international/elite ranks from U23 cycling
Published in Journal of Sports Sciences, 2022
Peter Leo, Dieter Simon, Matthias Hovorka, Justin Lawley, Iñigo Mujika
Laboratory testing was conducted in the first week of March for each respective season. All laboratory tests were completed in the same lab using the same measurement equipment. Open circuit breath by breath spiro-ergometry (ZAN600, nSpire Health GmbH, Germany) was used to record tidal volume, breathing frequency and volume percentages of oxygen (O2) and carbon dioxide (CO2). Volume and gas calibrations were conducted before each measurement according to the manufacturer’s recommendations. Ventilation (STPS) was then derived using the Haldane transformation to calculate oxygen uptake (VO2) and carbon dioxide (VCO2) release (Wilmore & Costill, 1973). All tests were performed on an electromagnetically braked stationary trainer (Cyclus2, RBM elektronik-automation GmbG, Leibzig, Deutschland) with the participants’ own road bikes (Alto Prestige and Revelator, KTM Fahrrad GmbH, Mattighofen, Austria). Laboratory testing involved a standardized warm-up of 3 min at 100 W, followed by a ramp incremental graded exercise test (GXT). The initial workload for the GXT was set at 150 W and was increased by 20 W.min−1 until volitional exhaustion. The measurements included absolute and relative PPO and VO2max. PPO and VO2max were defined as the highest 30s average during the GXT (Scheadler et al., 2017). The ventilatory threshold (VT) and the respiratory compensation point (RCP) were analysed from the GXT according to Beaver et al. (1986). VT was defined as the point where the ventilation rate (VE) increased compared to VO2 (VE/VO2). RCP was defined as the onset of hyperventilation during the GXT, with an increase in VE compared to the volume of carbon dioxide (VCO2) release, known as the VE/VCO2 ratio. Both VT and RCP were independently analysed via visual inspection by two co-authors within an agreement of 10 W, otherwise a third independent expert was involved. Continuous recordings of heart rate (HR) were performed via short range telemetry with a 1 Hz sampling rate (V800, Polar Electro Oy, Kempele, Finland).