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Anaesthesia in Orthopaedic Surgery
Published in Timothy W R Briggs, Jonathan Miles, William Aston, Heledd Havard, Daud TS Chou, Operative Orthopaedics, 2020
Oxygen therapy should be given to patients with an epidural infusion which contains opiates, or those using a PCA. This supplemental oxygen maintains alveolar oxygen tension longer if respiratory depression and hypoventilation occur. Supplemental oxygen used for the first three days postoperatively can also minimise the risk of perioperative ischaemic events. Any patient with pre-existing respiratory pathology or acquired (respiratory tract infection, atelectasis, thromboembolism) will be relatively hypoxic, and oxygen therapy is essential.
Diagnosis and Treatment of Inhalation Injury in Burn Patients
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Khan Z. Shirani, Joseph A. Moylan, Basil A. Pruitt
The extent of pulmonary damage determines the severity of respiratory failure and the acuteness of need for support of ventilation (Table 4). Pulmonary insufficiency will usually be manifested by reduction in vital capacity below 4 ml/ kg (normal: 12-15 ml/kg), tachypnea (a respiratory rate greater than 40/min), and alveolar hypoventilation (PaCO2 greater than 49 torr). A convenient method of monitoring pulmonary function is frequent analysis of arterial oxygen tension (PaO2). It is generally accepted that patients with a PaO2 of less than 50-60 torr while breathing room air should be provided with ventilatory support. In patients receiving mechanical ventilation, every effort should be made to maintain PaO2 greater than 70 torr while keeping inspired oxygen concentrations (FI02) under 0.5. Ordinarily, the ventilation-perfusion inequality of the lung determines PaO2 values. Under conditions where oxygen delivery lags behind oxygen consumption, such as in patients with hypovolemia, severe anemia, and congestive heart failure, a drastic reduction in the central venous oxygen tension may occur. Under these circumstances, the degree of pulmonary venous unsaturation, not a ventilation-perfusion mismatch, appears to be the prime determinant of PaO2 (Philibin et al., 1970). This implies that hypoxemia in patients with inadequate perfusion responds best to volume expansion or support of a failing myocardium, depending on the underlying pathologic process.
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
Oxygen toxicity can occur if the inspired oxygen tension exceeds 1350 mmHg (180 kPa or 1.8 bar), as at a depth of 8 msw when 100% oxygen is inspired. Symptoms of oxygen toxicity include vertigo, paraesthesia of the arms and legs and muscle twitching around the mouth and eyes, progressing to convulsions. Pulmonary oxygen toxicity can develop at a depth of 16 msw when compressed air is inspired, with an inspired oxygen concentration of 375 mmHg (50 kPa or 0.5 bar). The first sign of pulmonary oxygen toxicity is dyspnoea, and pulmonary oedema and intra-alveolar haemorrhage are seen later. These symptoms usually occur after 30 hours of exposure to high inspired oxygen tensions. The latency of onset decreases with higher inspired oxygen tensions so that symptoms occur after 5 hours if the inspired oxygen tension is 1500 mmHg (200 kPa or 2 bar).
Hb Santa Juana (β 108(G10) Asn > Ser): a low oxygen affinity hemoglobin variant in a family of Bosnian background
Published in Hematology, 2023
N. P. Wildenberg, C. Rossi, A. E. Kulozik, J. B. Kunz
Hemoglobin is a heterotetramer composed of two α- and two β-globin chains, with a total of four heme groups as oxygen binding sites. According to the allosteric two-state-model [2], the heterotetramer can exist in a relaxed R state with high oxygen affinity and a strained T state with low oxygen affinity. Binding of an oxygen molecule to one heme group increases the oxygen affinity of the other subunits. This effect explains the sigmoidal shape of the oxygen binding curve. Hemoglobin variants with decreased oxygen affinity stabilize the T-state and result in increased oxygen delivery to the tissues, while oxygen uptake in the lungs is decreased. The oxygen dissociation curve is right-shifted and characterized by a higher oxygen tension required to reach 50% saturation (p50). However, additional factors contribute to oxygen release into the tissue, such as the concentration of 2,3-bisphosphoglycerate, pH, and CO2 tension. Weak oxygen binding to hemoglobin favors oxygen release into the tissue, suppressing erythropoietin secretion and causing normocytic anemia. Although some patients expressing hemoglobin variants with decreased oxygen affinity present with cyanosis, most are asymptomatic. A low oxygen affinity hemoglobin variant may be suggested by otherwise unexplained reduced pulse oximetry measurements and normocytic anemia.
Plantamajoside inhibits hypoxia-induced migration and invasion of human cervical cancer cells through the NF-κB and PI3K/akt pathways
Published in Journal of Receptors and Signal Transduction, 2021
Hypoxia refers to a condition of low oxygen tension in tissues and has emerged as an adverse factor in cancer development and associated with poor outcome regardless of treatment modality [13,14]. Hypoxic microenvironment changes cellular metabolism and triggers varied molecular responses in cancer cells, which promote tumor progression and confer radiation resistance and chemo resistance to tumors [15]. EMT is a fundamental process of morphogenesis whereby epithelial cells acquire the mesenchymal phenotype with decreased cell adhesion protein E-cadherin and increased mesenchymal proteins such as N-cadherin and vimentin [16]. The process of EMT has been found to be associated with metastasis in cancer. Previous reports have suggested that hypoxia triggers EMT in several types of cancers [17]. Therefore, targeting hypoxia-induced EMT could serve as a good therapeutic strategy for the treatment of cancers.
The Expression and Role of Hypoxia-induced Factor-1α in Human Tenon’s Capsule Fibroblasts under Hypoxia
Published in Current Eye Research, 2021
Xi Qin, Keling Wu, Chengguo Zuo, Mingkai Lin
Wound healing involves a variety of processes including inflammation, angiogenesis, vasculogenesis, fibroplasia, and re-epithelialization.7 Initial tissue injury causes blood vessel damage and thereby an interrupted blood flow that leads to acute tissue hypoxia.8 Moreover, elevated oxygen consumption by infiltrated inflammatory and stromal cells further lowers the tissue oxygen tension leading to prolonged chronic hypoxia.9 Chronic hypoxia in turn induces vascular remodeling ultimately giving rise to progressive liminal narrowing and blockage resulting in progressive exacerbation of the chronic hypoxic state.10 Furthermore, excessive deposition of extracellular matrix (ECM), the hallmark of fibrosis,11 further worsens hypoxia by increasing diffusion distances between blood vessels and tissue cells and increased tissue pressue.12 Extensive microangiopathy, vascular remodeling, and ECM deposition leads to hypoxia that directly contributes to progressive amplification of fibrosis.