China
Africa
Explore chapters and articles related to this topic
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
Malignant forms of acute mountain sickness present as high-altitude pulmonary or cerebral oedema. The symptoms of high-altitude pulmonary oedema are marked dyspnoea and dry cough, followed by productive cough with pink foamy sputum. Alveolar hypoxia leads to hypoxic pulmonary vasoconstriction. The mean pulmonary arterial pressure increases as a result of increased cardiac output and hypoxic pulmonary vasoconstriction. As a result of pulmonary vascular engorgement and pulmonary hypertension, high-altitude pulmonary oedema (containing high-molecular-weight proteins) occurs as a result of increased capillary permeability as well as increased pulmonary capillary pressure. The treatment of this condition is oxygen therapy and descent to a lower altitude.
Applied Physiology and Biochemistry
Published in Elizabeth Combeer, The Final FRCA Short Answer Questions, 2019
Hypoxic pulmonary vasoconstriction works to reduce perfusion to unventilated portions of the lung. However, this results in raised pulmonary vascular resistance and risk of right heart dysfunction and alveolar capillary leak in susceptible patients.
Special environments
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Malignant forms of acute mountain sickness present as high-altitude pulmonary or cerebral oedema. The symptoms of high-altitude pulmonary oedema are marked dyspnoea and dry cough, followed by productive cough with pink foamy sputum. Alveolar hypoxia leads to hypoxic pulmonary vasoconstriction. The mean pulmonary artery pressure increases as a result of increased cardiac output and hypoxic pulmonary vasoconstriction. As a result of pulmonary vascular engorgement and pulmonary hypertension, high-altitude pulmonary oedema (containing high-molecular-weight proteins) occurs as a result of increased capillary permeability as well as increased pulmonary capillary pressure. The treatment of this condition is oxygen therapy and descent to a lower altitude.
Comprehensive viewpoints on heart rate variability at high altitude
Published in Clinical and Experimental Hypertension, 2023
Jun Hou, Keji Lu, Peiwen Chen, Peng Wang, Jing Li, Jiali Yang, Qing Liu, Qiang Xue, Zhaobing Tang, Haifeng Pei
Autonomic nerves are extensively distributed throughout various tissues and organs, playing a crucial role in regulating the physiological functions of the human body. Dysfunctions of autonomic nerves are associated with the development of numerous diseases when the body experiences hypoxia. High altitude pulmonary edema (HAPE) is a severe non-cardiogenic condition characterized by pulmonary edema, which can be life-threatening and is caused by low atmospheric pressure and hypoxia at high altitudes. When individuals rapidly ascend to high altitudes, their lungs face excessive stress within a short period, which can trigger HAPE (95). Exposure to high altitude hypoxia results in increased sensitivity of the pulmonary vascular system to the sympathetic nervous system and endothelin, while the response to vasodilators diminishes, leading to hypoxic pulmonary vasoconstriction. This constriction increases pulmonary artery pressure, potentially exacerbating HAPE (86,96). Furthermore, acute hypoxia and decreased oxygen saturation can cause ventricular diastolic dysfunction, resulting in HAPE. This condition is characterized by a decrease in HRV, an increase in the LF/HF ratio, and other symptoms (97–99).
Kv7 channel inhibition increases hypoxic pulmonary vasoconstriction in endotoxemic mouse lungs
Published in Experimental Lung Research, 2020
Maurizio Turzo, Fabian A. Spöhr, Lasitschka Felix, Markus A. Weigand, Cornelius J. Busch
Hypoxic pulmonary vasoconstriction (HPV) is impaired in patients with pathologies such as pneumonia, sepsis or acute respiratory distress syndrome (ARDS).1 In critically ill patients on intensive care units, prevalence of hypoxia was 54% with a mortality of up to 50% in the group with severe hypoxemia.2 Attenuation of HPV results in increased intrapulmonary shunting and systemic hypoxemia.1,3 A reduced response to alveolar hypoxia with impaired HPV is also observed in several animal models of endotoxemia.4–6 Inflammatory mediators including prostaglandins, thromboxanes, platelet-activating factor, leukotrienes, or nitric oxide (NO) modulate HPV during lung inflammation.4 The observation that unspecific inhibition of voltage gated potassium (Kv) channels augments HPV during endotoxemia in an isolated perfused mouse lung model 7 identifies Kv channels as a key mediator of HPV.8–10
Advances in the available non-biological pharmacotherapy prevention and treatment of acute mountain sickness and high altitude cerebral and pulmonary oedema
Published in Expert Opinion on Pharmacotherapy, 2018
K.E. Joyce, S.J.E. Lucas, C.H.E. Imray, G.M Balanos, A. D. Wright
Pulmonary arterial pressure (PAP) rises with exposure to altitude, being attributed to hypoxic pulmonary vasoconstriction (HPV). An exaggerated elevation in PAP contributes to the development of alveolar capillary leakage and subsequent development of HAPE [26,27]. Potential mechanisms include (1) inflammation, (2) altered alveolar fluid clearance, and/or (3) uneven HPV response [26–28]. Accumulation of lung fluid in response to hypoxia has been attributed to the downregulation of epithelial sodium channels [29,30]. Further, greater endothelin-1 production and reduced exhaled nitic oxide are also apparent in those who develop HAPE [31–34].