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Physiology of the Airways
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Anthony J. Hickey, David C. Thompson
Alterations in ventilation, therefore, influence blood pH. Impaired ventilation, as may occur during central nervous system depression or airway obstruction, can result in respiratory acidosis. Conversely, respiratory alkalosis can be caused by hyperventilation, as might occur during ascent to high altitude or by fever. In general, renal mechanisms function to compensate for inordinate respiratory alternations in blood pH. In addition, feedback control mechanisms exist in the body that alter respiration in the face of changes in blood pH. For example, changes in blood pH resulting from nonrespiratory (such as may occur in severe diarrhea, altered renal function, and ingestion of acids or bases) or respiratory mechanisms may be returned towards normal (pH = 7.4) by altering the rate and depth of ventilation. Increases in blood hydrogen ion (and carbon dioxide) concentration stimulate carotid chemoreceptors (located in the bifurcation of the common carotid arteries) to elicit a central nervous system reflex in ventilation. A decrease in the blood concentration of hydrogen ions depresses ventilation through the same central nervous system reflex. In addition, ventilation is also regulated by chemoreceptors in the medulla of the brainstem sensitive to changes in hydrogen ion and carbon dioxide concentrations in the cerebrospinal fluid.
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.
Repeated remote ischaemic preconditioning can prevent acute mountain sickness after rapid ascent to a high altitude
Published in European Journal of Sport Science, 2022
Zhen Wang, Bo Lv, Lin Zhang, Ran Gao, Wenbo Zhao, Lin Wang, Zhaojun Min, Zhen Mi, Yang Song, Jing Zhang, Yabin Yu, Xunming Ji, Junjie Li, Liyong Wu
The precise pathogenic mechanisms underlying AMS remain to be elucidated. Hypoxia likely plays a central role in its pathogenesis (Taylor, 2011). Hypoxia at a high altitude can lead to hypoxemia, and the condition is aggravated by a reduced level of carbon dioxide through respiratory alkalosis and inhibition of the hypoxic ventilatory response (HVR) (Taylor, 2011). Hypoxemia induces the upregulation of hypoxia-inducible factor 1 and vascular endothelial growth factor and the formation of free radicals, which, together with hypoxemia, affect cerebrovascular permeability (Wilson, Newman, & Imray, 2009). A series of compensatory mechanisms, including adenosine production, potassium ion accumulation and nitric oxide release, may facilitate vasodilatation and alleviate cerebral hypoxia, although researchers have proposed that the exaggerated activity of these compensatory mechanisms may contribute to altitude maladaptation (Wilson et al., 2009).
Psychophysiological response of different aircrew in normobaric hypoxia training
Published in Ergonomics, 2019
Álvaro Bustamante-Sánchez, Miguel Delgado-Terán, Vicente Javier Clemente-Suárez
The air pressure reduction with increasing altitude leads to hypobaric hypoxia which produces a lower alveolar oxygen partial pressure, reducing oxygen partial pressure in the arterial blood. An acute ventilatory response is the mechanism that works to get back oxygen concentration homeostasis, causing hypocapnia and a respiratory alkalosis (Petrassi et al. 2012), which causes breathing muscles fatigue (Pollard et al. 1997). The individual tolerance of low blood oxygen concentrations defines the symptoms experienced, most of them caused by cerebral oxygen delivery. These symptoms include: psychomotor impairment, impairment of cognitive function, visual impairment, psychological stress and anxiety, shortness of breath, paraesthesia, headache, dizziness, nausea, light-headedness and tachycardia (Neuhaus and Hinkelbein 2014).