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Oxygen Transport
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
P.N. Chatzinikolaou, N.V. Margaritelis, A.N. Chatzinikolaou, V. Paschalis, A.A. Theodorou, I.S. Vrabas, A. Kyparos, M.G. Nikolaidis
The respiratory system per se affects oxygen transport and contributes to fatigue (Dempsey, La Gerche and Hull, 2020). During exercise-induced hypoxemia (a frequent phenomenon in trained athletes), arterial oxygen saturation (SaO2) can reach as low as 88%. For every 1% drop in SaO2, VO2max decreases by 2% (Dempsey, La Gerche and Hull, 2020). Redox-related processes could be involved in this exercise-induced SaO2 drop. Exercise has been reported to induce oxidative stress in the lungs of healthy adults, predominantly by enzymes (e.g., NADPH oxidases) residing at the outer layers of lung cells and in various leukocytes (Araneda, Carbonell and Tuesta, 2016). Moreover, hemoglobin oxidation during exercise decreases its oxygen-carrying capacity. Noteworthy, both these redox responses are amplified under certain environmental conditions frequently faced by athletes (e.g., cold and altitude). Collectively, it becomes reasonable to argue that redox processes (e.g., hemoglobin oxidation, oxidative damage to alveolar cells) are involved in the first step of oxygen pathway, yet it is still unknown to what extent these processes limit oxygen transport.
Pulmonary gas exchange
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
During the Silver Hut Expedition of 1960–61, measurements of arterial oxygen saturation by ear oximetry were made on five subjects who lived for four months at an altitude of 5800 m (PB ∼380 mmHg) in a prefabricated hut. The average arterial oxygen saturation was 67% at rest and fell at work levels of 300 and 900 kg m min−1 to 63% and 56%, respectively (West et al. 1962). The progressive fall in arterial oxygen saturation with increasing work occurred in the face of an increasing alveolar PO2 and was strong evidence for diffusion limitation of oxygen transfer. Alveolar–arterial differences were calculated and nine measurements at the maximal exercise level gave a mean PO2 difference of 26 mmHg with a standard deviation of 4 mmHg. Calculations based on the Bohr integration procedure showed that the results were consistent with a maximum pulmonary diffusing capacity for oxygen of about 60 mL min−1 mmHg−1.
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Thomas Κ. C. King, Robert A. Norum
Clinical observations suggested that control of ventilation may be abnormal in dysautonomia. Infants with this disease learned to manipulate their parents by refusing to breathe until they were frankly blue or got what they wanted. At least one child was killed in an underwater swimming competition from which he did not surface. Experimental demonstrations of abnormal control were first reported by Filler et al. [6]. Six patients with dysautonomia, normal lung volumes, and normal chest x rays were studied for their responses to inhalation of several concentrations of CO2 in air, and to 12% O2 in N2. When 4% CO2 had been inhaled for 12-15 min the response measured as minute ventilation was only about two-thirds that of normal controls. The increase in required to double minute ventilation was 4-6 mmHg compared to 1.7 mmHg in control subjects. Administration of 12% O2 in N2 resulted in an average 60% increase in minute ventilation but no change in , and a fall in arterial oxygen saturation to 55% compared to a fall to 75% saturation in the control subjects. Filler et al. note that in three dysautonomic subjects the experiment with inhalation of 12% CO2 had to be terminated because of one instance each of severe cyanosis, syncope, and grand mal convulsions.
Correlation of refractory hypoxemia with biochemical markers and clinical outcomes of COVID-19 patients in a developing country: A retrospective observational study
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Muhammad Sohaib Asghar, Iftekhar Ahmed, Haris Alvi, Sadia Iqbal, Ismail Khan, Rabia Seher Alvi, Zara Saeed, Saboohi Irfan, Maria Akhtar, Ibraj Fatima
There were a few limitations of our study, we did not utilize the measurement of oxygen saturation of arterial blood gases as a partial oxygen pressure (arterial PaO2) but instead as pulse oximetry. PaO2 should be cautiously interpreted as measured by pulse oximetry [38]. Estimated CO-oximeter oxygen saturation (SpO2) may be roughly ±4% distinct from recorded arterial oxygen saturation. The validation of findings using calculated arterial oxygen saturation may also be a stronger criterion. Furthermore, to be able to accurately determine the lung potential for gas exchange, it is important to know the fraction of inspired oxygen (FiO2), which was not utilized in our study [40]. We solely relied on measurements by pulse oximeter to determine hypoxemia. Lastly, the biomarkers were evaluated in hospitalized patients and thus results cannot be generalizable to patients with milder COVID-19 disease who do not require hospitalization.
Is there a relationship between hematological parameters and duration of respiratory events in severe OSA
Published in The Aging Male, 2020
Dilber Yılmaz Durmaz, Aygül Güneş
PSG in the sleep laboratory included continuous electroencephalographic (EEG) polygraphic recording using EEG leads, the use of right and left electro-oculographic leads, and chin electromyography for sleep staging. Electrocardiography (ECG) monitoring during sleep, airflow measurement at the nose and mouth, and chest and abdominal respiratory movements were measured during sleep. Arterial oxygen saturation was measured with pulse oximetry. All sleep studies were interpreted according to the manual of the AASM for the Scoring of Sleep, by certified sleep physicians. Apnea was identified when the airflow amplitude in the nasal cannula was <10% of baseline and when no flow occurred on the oral airflow sensor (thermistor). Hypopneas were identified when the amplitude of the airflow was reduced by 30%, the event was followed by a 4% desaturation. The AHI was defined as the total number of apnea and hypopnea events per hour of sleep.
Which is more important: the number or duration of respiratory events to determine the severity of obstructive sleep apnea?
Published in The Aging Male, 2020
Dilber Yılmaz Durmaz, Aygül Güneş
Polysomnography in the sleep laboratory included continuous electroencephalographic (EEG) polygraphic recording using EEG leads, the use of right and left electro-oculographic leads, and chin electromyography for sleep staging. Electrocardiography (ECG) monitoring during sleep, airflow measurement at the nose and mouth, and chest and abdominal respiratory movements were measured during sleep. Arterial oxygen saturation was measured with pulse oximetry. All sleep studies were interpreted according to the manual of the AASM for the scoring of sleep, by certified sleep physicians. Apnea was identified when the airflow amplitude in the nasal cannula was <10% of baseline and when no flow occurred on the oral airflow sensor (thermistor). Hypopneas were identified when the amplitude of the airflow was reduced by 30%, the event was followed by 4% desaturation. The AHI was defined as the total number of apnea and hypopnea events per hour of sleep.