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Toxic and Asphyxiating Hazards in Confined Spaces
Published in Neil McManus, Safety and Health in Confined Spaces, 2018
At the end of the respiratory cycle, the alveolar partial pressure of oxygen and carbon dioxide (100 mmHg and 40 mmHg, respectively) approximate those in the pulmonary capillaries. Inspiring gas of the same composition would affect only the volume, not the partial pressures of alveolar gases. Oxygen uptake continues at the end of the breathing cycle. Even without enrichment, alveolar oxygen still has a higher partial pressure than mixed venous blood. However, without enrichment, transfer of oxygen from alveolar air eventually would cease, thus leading to decreasing saturation of hemoglobin and arterial anoxemia. The accompanying decrease in exchange of carbon dioxide into alveolar air would lead to respiratory acidosis (Comroe et al. 1962).
Glossary of scientific and technical terms in bioengineering and biological engineering
Published in Megh R. Goyal, Scientific and Technical Terms in Bioengineering and Biological Engineering, 2018
Winter’s formula evaluates respiratory compensation when analyzing acid-base disorders and a metabolic acidosis are present. It is described by the equation: PCO2= [1.5 x HCO–3] + [8 ± 2], where HCO3- is given in units of mEq/L and PCO2 will be in units of mmHg. Winter’s formula gives an expected value for the patient’s PCO2; the patient’s actual (measured) PCO2 is then compared to this. If the two values correspond, respiratory compensation is considered to be adequate. If the measured PCO2 is higher than the calculated value, there is also a primary respiratory acidosis. If the measured PCO2 is lower than the calculated value, there is also a primary respiratory alkalosis.
Oxygen Delivery and Acute Hypoxia: Physiological and Clinical Considerations
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
A rise in arterial PCO2 leads to increased acidity via the increased production of carbonic acid, which then dissociates to form hydrogen and bicarbonate ions. An increase in hydrogen ions (decreased pH) produced in this way is a ‘respiratory acidosis’. If an increase in hydrogen ion is produced in any other way, by convention the condition is known as a ‘metabolic acidosis’. The terminology is not completely logical as CO2 is a metabolite and many drugs and chemicals, which are not metabolites, are capable of producing a ‘metabolic’ acidosis. Experimentally, increased hydrogen ion stimulates increased ventilation independent of changes in PCO2 and PO2.
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
The first landmark study was a randomised controlled trial of liberal versus titrated oxygen therapy in patients with severe exacerbations of chronic obstructive pulmonary disease (COPD), encompassing emphysema and chronic bronchitis, who were managed by the Ambulance Service in transit to hospital (Austin et al. 2010). The titrated oxygen regimen involved two components: titrated supplementary oxygen if required to achieve an SpO2 of 88% to 92% and the use of bronchodilators delivered by an air-driven nebuliser. The liberal oxygen regimen had two components – high flow oxygen therapy at 8–11 L/min and bronchodilators delivered by nebulisation with oxygen flows of 6–8 L/min. Titrated oxygen reduced mortality by 58% for all patients included in the study (intention to treat analysis) and by 78% for all patients with confirmed COPD. From these data it was calculated that treating 14 patients with liberal oxygen would result in one avoidable death. The high flow oxygen regimen was associated with more severe respiratory acidosis and hypercapnia (raised PaCO2), which likely contributed to the mortality risk as most deaths were due to respiratory failure. A key finding was that just over half of the patients in the titrated oxygen arm received high flow oxygen therapy at some point in their pre-hospital treatment, likely as a result of the entrenched culture that ‘more oxygen is better’ in a breathless distressed patient.
The effect of inspiratory muscle fatigue on acid-base status and performance during race-paced middle-distance swimming
Published in Journal of Sports Sciences, 2019
Mitch Lomax, Jernej Kapus, Samuel Webb, Anton Ušaj
It is known that exercise can increase carbon dioxide storage in the body and this storage capacity is diminished at higher exercise intensities leading to an increase in carbon dioxide excretion (Jones & Jurkowski, 1979). The relatively short duration of the 50-m repeat swims and the fact that they were not maximal effort swims but were instead based on 400-m race pace, could be incompatible with the detection of hypercapnia. Additionally, it took approximately 20–30 s to obtain blood samples for analysis during which time breathing was very intense. If a small swimming-induced increase in PCO2 did occur, it could be reversed during this period resulting in the measured PCO2 failing to change. Lastly, failure to observe hypercapnia does not necessarily mean that ventilation poses no limitation during front crawl swimming, or that hypercapnia does not occur. It may be that a ventilatory limitation was not sufficient to cause respiratory acidosis. In support of this, Ušaj (1999) found ventilation to be less effective at compensating for metabolic acidosis during 400-m race-paced front crawl swimming (pH of 7.09 ± 0.09, PCO2 of 4.0 ± 0.5 kPa) compared to maximal effort kayak paddling (pH of 7.17 ± 0.05, PCO2 of 3.6 ± 0.2 kPa) but this failed to result in hypercapnia in the former. We observed a similar pattern and also found the Δ (increase) in fr between mid- and end- swim (mid-swim being the first time point where IMF was evident in both trials) was correlated with Δ (fall) in PCO2 (r = 0.450), suggesting that the increase in fr, which occurred in both trials, partly contributed to the prevention of hypercapnia. However, the small coefficient of determination (20%) indicates that prevention of hypercapnia was not the primary cause for the increase in fr.
Fluidic and thermal properties of heliox enable the efficient generation and delivery of high concentrations of solid-phase, fine particle aerosols from viscous liquids
Published in Aerosol Science and Technology, 2019
Xin Heng, Jinghai Yi, Donovan B. Yeates
Heliox is a mixture of the inert gas, helium, together with oxygen. Unless otherwise denoted, reference to heliox herein refers to 80% helium and 20% oxygen which is widely used. Other mixtures containing higher percentages of oxygen, i.e., 70% helium and 30% oxygen, are available. Heliox’s physical properties lead to potential physiological and clinical advantages for the delivery of aerosols to the lungs (Corcoran and Gamard 2004). The use of heliox in patients has not been uniformly supportive of its clinical utility, however, there is considerable evidence its use can result in clinical improvements in respiratory function and improved delivery of aerosols to the lungs, especially in children and patients with compromised lung function (Katz et al. 2014). Consistent with the lower Reynolds number of heliox compared to air in conducting airways, the decrease in turbulence enables increased aerosol penetration through these airways with a consequential increase in the deposition of aerosols in the peripheral lung, especially in persons with lung disease (Svartengren et al. 1989; Anderson et al. 1993; Goode et al. 2001; Peterson et al. 2008). Compared to air, heliox shows better penetration into constricted airways to improve gas exchange (Jaber et al. 2000). Due to lower molecular weight and consequent low-density and higher diffusion coefficient of heliox, its use results in decreased CO2 retention and thus a reduction in respiratory acidosis (Gluck, Onorato, and Castriotta 1990). The properties of heliox also increase lung compliance and reduce the work of breathing (Beurskens et al. 2015). The use of heliox also has been shown to be associated with reduced inflammation (Yilmaz et al. 2013; Nawab et al. 2005). Additionally, noninvasive ventilation with heliox has been reported to decrease the incidence of intubation in preterm infants suffering from RDS (Long et al. 2016).