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Asthma and COPD
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Balamugesh Thangakunam, Devasahayam J Christopher
In asthma exacerbation, arterial blood gas analysis usually shows hypocapnia. A normal or elevated PaCO2 value suggests an impending respiratory arrest and requirement of intensive care. In contrast, hypercarbia and chronic type II respiratory failure are more common in COPD due to chronic fatigue of respiratory muscles, especially in severe cases (Virchow 2012).
Physiology Related to Special Environments
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Healthy individuals do not demonstrate any adverse effects below an altitude of 2500 m. Rapid exposure to altitudes in the range of 3000–6000 m results in ‘acute mountain sickness’. The symptoms usually appear in the first 24 hours, and they include headache, somnolence, nausea, vomiting, insomnia and muscle fatigue. These symptoms usually decrease after 3–4 days. At altitudes above 4000 m, cerebral hypoxia occurs with psychomotor impairment (diminished sensory acuity, manual skills and judgment and response times). Consciousness is lost within minutes above 6000 m, or within seconds at higher altitudes. These symptoms are the result of hypoxia and hypocapnia or alkalosis or both.
Pulmonary Embolism
Published in Stephen M. Cohn, Peter Rhee, 50 Landmark Papers, 2019
The classic clinical picture of a patient with PE is the sudden onset of pleuritic chest pain, tachypnea, dyspnea, hemoptysis, and in severe cases, cardiovascular collapse. As patients often have a subset of these relatively common symptoms, additional diagnostics beyond clinical acumen are frequently needed. Electrocardiogram and chest radiograph are routinely employed to evaluate for other pathologies with similar presentations. Arterial blood gas analysis is often utilized in the evaluation of these patients, however the classic association of PE with hypoxia and hypocapnia is suggestive at best. While tempting to rule out PE in patients with a normal (A-a)DO2 gradient, a well-designed study from Ottawa Hospital (Rodger et al., 2000) showed that these values were not significantly different in patients with and without PE. These limitations have made imaging the standard (in patients not suffering hemodynamic compromise) for the diagnosis of PE.
An exercise immune fitness test to unravel mechanisms of Post-Acute Sequelae of COVID-19
Published in Expert Review of Clinical Immunology, 2023
The PASC Syndrome is a phenotypically ill-defined and continuously evolving clinical syndrome the characterization of which is considered by some authors to be primarily driven by patient self-reported symptoms [43]. PASC is a debilitating syndrome with onset three months post COVID-19 infection. This sub-population of survivors of acute COVID-19 infection develop, often with a time-lag of >3 months, a highly variable phenotype with >200 described symptoms, of which fatigue, headache, cognitive dysfunction, post-exertional malaise, orthostatic intolerance, and dyspnea are among the most prominent ones. In a population of more than 20 million adults in the U.S. who currently have PASC, more than 80% are so debilitated that they cannot function in their activities of daily living [44]. A related phenotype, hyperventilation-induced hypocapnia, is characterized by a multitude of extremely disabling symptoms such as exertion-induced dyspnea, tachycardia, chest pain, fatigue, dizziness and syncope [45]. A considerable phenotypic overlap exists between PASC and Myalgic-Encephalopathy/Chronic Fatigue Syndrome (ME/CFS). In people with ME/CFS, exercise can cause serious setbacks and deterioration in function [46]. Post-exertional malaise (PEM) appears to be a common and a significant challenge for the majority of this patient group [47].
Is carbonic anhydrase inhibition useful as a complementary therapy of Covid-19 infection?
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Secil Deniz, Tugba Kevser Uysal, Clemente Capasso, Claudiu T. Supuran, Ozen Ozensoy Guler
Generally, under normal physiologic conditions, the value of pCO2 ranges between 35 and 45 mmHg within arterial or venous blood. From Figure 3, it seems that blood pCO2 of Covid-19 and non-Covid-19 patients are rather different (p>.05). Intriguing, in a recent article describing 138 hospitalised cases, the median pCO2 level was 34 mmHg (interquartile range: 30–38; normal range: 35–48)21. Here, we stress that initial exposure to hypoxia at high altitudes leads to an immediate increase in ventilation that blows off large quantities of CO2, producing hypocapnia. Furthermore, blood gases of non-acclimatised mountaineers with severe illness were accompanied by a significant decrease in arterial oxygen due to an increase in alveolar–arterial oxygen difference. However, herein arterial pCO2 did not change significantly21. One of the essential requirements of the body is to eliminate CO2. The large but highly variable amount of CO2 produced within muscle cells has to leave the body finally via ventilation of the alveolar space. To get there, diffusion of CO2 has to occur from the intracellular space of muscles into the convective transport medium blood, and diffusion out of the blood has to take place into the lung gas space across the alveolocapillary barrier22. Covid-19 infection, damaging lung cells, impairs gas transfer provoking severe hypoxia, which is usually the cause of death when it occurs. Besides, in a substantial number of patients, adequate arterial oxygenation cannot be achieved with supplemental oxygen alone23.
Cerebrovascular reactivity after cessation of menopausal hormone treatment
Published in Climacteric, 2019
J. N. Barnes, R. E. Harvey, N. A. Eisenmann, K. B. Miller, M. C. Johnson, S. M. Kruse, B. D. Lahr, M. J. Joyner, V. M. Miller
The cerebrovasculature is highly sensitive to changes in partial pressure of carbon dioxide (CO2), vasodilating in response to hypercapnia while vasoconstricting in response to hypocapnia. Cerebrovascular reactivity to hypercapnia is often used to estimate cerebral vascular responsiveness and has implications for cerebrovascular health1. Cross-sectional studies have shown that women experience an age-related decline in cerebrovascular reactivity after the fifth decade of life; however, this age-associated decline in cerebrovascular reactivity in women was attenuated in postmenopausal women using menopausal hormone therapy (MHT)2. Previous studies that evaluated cerebral blood flow regulation in women in response to MHT used a short-term intervention or included a variety of MHT formulations in the same study. Long-term MHT use could affect the structure of blood vessels reflecting nuclear-directed changes in gene translation, gene transcription, and protein expression as well as activational effects on cerebrovascular endothelial or vascular smooth muscle cells through rapid membrane-associated receptor or enzyme systems3,4. Therefore, these effects might be sustained and influence cerebral blood flow regulation following cessation of long-term MHT use. It is unclear whether MHT alters cerebral blood flow regulation beyond the years of hormonal treatment. Thus, the purpose of this study was to characterize cerebrovascular reactivity and the cerebral pulsatility index (PI) 3 years after cessation of two different formulations of MHT in a well-characterized cohort of women who participated in the Kronos Early Estrogen Prevention Study (KEEPS).