Hypoxia

10 Key excerpts on "Hypoxia"

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  Ernsting's Aviation and Space Medicine 5E

  • David Gradwell, David Rainford, David Gradwell, David Rainford(Authors)
  • 2016(Publication Date)
  • CRC Press

    (Publisher)

  49 4 Hypoxia and hyperventilation Revised by DAVID P. GRADWELL INTRODUCTION Living organisms obtain energy for their biological pro-cesses by the oxidation of complex chemical foodstuffs to simpler compounds, usually with the eventual formation of carbon dioxide, water and other waste products. Oxygen, therefore, is essential for the maintenance of continued aerobic respiration and normal function by living mate-rial. Normoxia describes the state in which a physiologi-cally adequate supply of oxygen to the tissues, whether in quantity or molecular concentration, is available. When the level of oxygen available is below that requirement, a state of Hypoxia is said to exist. Humans are extremely sensi-tive and vulnerable to the effects of deprivation of oxygen, and severe Hypoxia nearly always results in a rapid deterio-ration of most bodily functions; eventually, it will lead to death. Hypoxaemia is a general term meaning a deficiency in the oxygenation of the blood, but it is not synonymous with the term tissue Hypoxia , which may arise from one or more causes. Four different types of tissue Hypoxia are recognized and may be classified according to the primary mechanism involved: ● Hypoxic Hypoxia: the result of a reduction in the oxygen tension in the arterial blood and, hence, in the capillary blood. The aetiology includes the low oxygen tension of inspired gas associated with exposure to altitude, i.e. hypobaric Hypoxia. Other causes are hypoventilatory states, e.g. paralysis of respiratory musculature, depres-sion of central control of respiration, airway obstruction and pulmonary atelectasis (including that due to expo-sure to high sustained accelerations); impairment of gas exchange across the alveolar–capillary membrane, e.g. pulmonary oedema, pulmonary fibrosis; impair-ment of the circulation with right-to-left shunts, as may occur with congenital or acquired communications; and ventilation–perfusion mismatches, e.g.

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  Diving and Subaquatic Medicine

  • Carl Edmonds, Michael Bennett, John Lippmann, Simon Mitchell(Authors)
  • 2015(Publication Date)
  • CRC Press

    (Publisher)

  217 16 Hypoxia INTRODUCTION Hypoxia in the context of human physiology means an oxygen (O 2 ) deficiency, or a lower than nor-mal partial pressure of O 2 (PO 2 ; also called the O 2 tension ), in the tissue in question. The term strongly implies inadequate O 2 availability to bodily tissues. The brain, liver and kidney, which extract the great-est amount of O 2 from the blood to supply their energy requirements, are the first affected by falling O 2 levels in the body. Skin, muscle and bone are less vulnerable because of their lower energy require-ments. O 2 does not directly supply the energy but is necessary to liberate the energy required for cellular metabolism from sugar (glucose). Aerobic (‘with O 2 ’) metabolism is much more efficient in the production of biological energy than anaerobic metabolism (‘without O 2 ’) and is the key to complex life on Earth. For example, in the presence of O 2 , 1 molecule of glucose can pro-duce 38 molecules of the energy storage compound adenosine triphosphate (ATP), whereas in the absence of O 2 , 1 molecule of glucose produces only 2 molecules of ATP (via the production of lactic acid). Thus, anaerobic conditions (Hypoxia) drasti-cally reduce the available energy. Dry air, at a barometric pressure of 760 mm Hg, has a PO 2 of 159 mm Hg. When inspired, dry air becomes saturated with water vapour at body temperature. By this dilution the PO 2 drops to 149 mm Hg. Alveolar gas has a lower PO 2 than inspired air because it is further diluted by carbon dioxide (CO 2 ) and contact with de-oxygenated blood, to around 105 mm Hg. O 2 freely diffuses into the capillaries in the lung so that normal arte-rial blood levels are in the region of 100 mm Hg. As the blood moves through the tissue capillaries, O 2 moves by diffusion down partial pressure gradi-ents to the cells, where it is consumed (Figure 16.1). After passage through the tissues the PO 2 falls to approximately 40 mm Hg in mixed venous blood coming back into the lungs.

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  Advanced Environmental Exercise Physiology

  • Stephen S. Cheung, Philip Ainslie(Authors)
  • 2021(Publication Date)
  • Human Kinetics

    (Publisher)

    Use of certain drugs (including alcohol) or poisons: Many pharmacologically active substances have effects similar to those of hypoxic Hypoxia and so mimic or exacerbate the condition. Here, however, factors such as drugs or poisonous compounds (e.g., cyanide, sulfide, or azide) can impair the ability of the tissues or mitochondria to utilize a normal oxygen supply for oxidative processes. Exposure to these compounds is usually accidental due to their production in sewers, in the oil and gas industries, and in the use of insecticides and herbicides. Cyanide has also been used to commit suicides, homicides, and World War II mass killings.

  Summary

  When tissues have inadequate oxygen to conduct normal metabolism, they are described as being in a state of Hypoxia. Although the main form of Hypoxia described in this chapter is hypoxic Hypoxia, other forms of Hypoxia include anemic, circulatory, and histotoxic. The immediate responses to acute Hypoxia involve the respiratory, circulatory, and neurological systems, and together these responses determine the clinical outcomes. The marked individual variability of physiological responses to acute Hypoxia are largely initiated by the respiratory changes that then determine the prevailing oxygen and carbon dioxide tensions. The extent of these latter changes influence both the cardiovascular responses and the impact of Hypoxia on the central nervous system. Understanding the impact of acute Hypoxia has important implications for aviation physiology (e.g., fliers of light aircraft, gliders, and balloons should be aware of the dangers of extreme elevation, and aircrews should be conscious of the dangers of rapid cabin decompression during commercial air flights) and for various occupational (e.g., military and rescue service, mining, astronomy) and recreational (e.g., driving or rail traveling over high-altitude passes) pursuits.

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  Fish Physiology: Hypoxia

  • Jeffrey G. Richards, Anthony Farrell, Colin Brauner, Anthony P. Farrell, Colin J. Brauner(Authors)
  • 2009(Publication Date)
  • Academic Press

    (Publisher)

  Chapter 11 Defining Hypoxia

  An Integrative Synthesis of the Responses of Fish to Hypoxia

  Anthony P. Farrell and Jeffrey G. Richards

  This chapter attempts to synthesize the responses of fish to Hypoxia presented in this Fish Physiology volume. The previous chapters are built on by differentiating between environmental Hypoxia and functional Hypoxia, and by outlining the possible compensatory mechanisms that fish use to counteract these forms of Hypoxia. Environmental Hypoxia is most simply defined as the water PO2 when physiological function is compromised, thus the definition of environmental Hypoxia is dependent upon the physiological system under examination. Hypoxia-induced decrements in maximal oxygen consumption and thus reduced aerobic scope occur at higher water O2 levels than changes in routine oxygen consumption, which when compromised, is quantified as the critical oxygen tension (Pcrit ). At water O2 levels below Pcrit , duration of survival is dependent upon the capacity to reduce metabolic demands to match the limited supply of fermentable fuels. Functional Hypoxia, on the other hand, occurs during situations where tissue O2 demands exceed circulatory O2 supply, which can be evident during exercise, temperature extremes, anemia, acidosis, and changes in gill structure, but the physiological strategies used to survive environmental Hypoxia are not necessarily utilized to endure functional Hypoxia.

  1. Scope of the Chapter

  While a complete picture of the consequences of Hypoxia in fishes will require much work to finalize, several central messages have emerged, which are detailed in the preceding chapters of this volume. The aim here is to synthesize these messages, where possible, and point to where future research might be most valuable.

  2. Defining Hypoxia

  Simply put, Hypoxia is a shortage of O2 . Anoxia is a complete lack of O2 . In its simplest context, regulators define aquatic Hypoxia as dissolved O2 concentrations below 2–3 mg O2 /L in marine and estuarine environments and below 5–6 mg O2 /L in freshwater environments. With these thresholds, regulators are aiming to protect the environment of the most sensitive fish species and for North American and European freshwaters this is often a salmonid. However, as pointed out by Diaz and Breitburg (see Chapter 1 ), this is clearly an oversimplification. Indeed, in a recent meta-analysis of toxicological literature (lethal and sublethal indicators of Hypoxia), fish were found to be generally the most sensitive of marine taxa (Vaquer-Sunyer and Duarte, 2008 ). Furthermore, the current literature range for defining Hypoxia of 0.2 to 4.0 mg O2 /L, with a mean of 2.1 mg O2 /L, fails to adequately protect sensitive species. Instead, Vaquer-Sunyer and Duarte (2008)

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  Textbook of Clinical Neuropsychology

  • Joel E. Morgan, Joseph H. Ricker, Joel E. Morgan, Joseph H. Ricker(Authors)
  • 2017(Publication Date)
  • Taylor & Francis

    (Publisher)

  More than 424,000 deaths due to cardiac and respiratory arrest occur each year in the United States (Kudenchuk et al., 2015). Improvements in emergency and critical care medicine have resulted an increase in successful cardiopulmonary resuscitation, which has led to a fairly stable mortality rate over the last 20 years (Sandroni, Nolan, Cavallaro, & Antonelli, 2007). However, more than half of all survivors experience significant morbidities such as long-term cognitive impairments that include impairments in memory and executive function and they experience depression, anxiety and reduced quality of life (Moulaert, Verbunt, van Heugten, & Wade, 2009). A significant percent of patients with anoxia (up to 90%) are unable to return to their premorbid level of function (Kaplan, 1999). Patient outcomes vary based on the location (in hospital vs. out of hospital) and the cause of cardiac arrest (Kudenchuk et al., 2015). In addition to cardiac or respiratory arrest, a number of other disorders cause a lack of oxygen to the brain. Anoxia, Hypoxia, or ischemia occur in a variety of disorders including asthma, cardiac or respiratory arrest, cardiac disease or surgery, carbon monoxide poisoning, attempted hanging, complications of anesthesia, near downing, obstructive sleep apnea (OSA), chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome. Given that a number of disorders result in an anoxic/ischemic event, a substantial number of individuals will subsequently develop hypoxic brain injury along with its associated morbidities.

  Hypoxic Brain Injury

  The human brain constitutes approximately 2% of the total body mass but utilizes up to 25% of the body’s total oxygen consumption (Haddad & Jiang, 1993). Due to a high metabolic demand, the brain requires a constant supply of oxygen and glucose to produce energy and uses aerobic glucose oxidation to produce 95% of the brain’s adenosine triphosphate (ATP) (Hicks, 1968). It is essential that the neocortical and subcortical areas receive a continuous supply of oxygen, as neurons are not able to store oxygen and glucose for later use (Hicks, 1968). Slight decreases in oxygen delivery to the brain may lead to permanent biochemical and morphological changes. Both Hypoxia and ischemia result in decreased oxygen delivery to the tissues. Ischemia is defined as insufficient blood supply to the brain or other organs (ie.e cardiac arrest) due to interruption or reduction of blood delivery, anoxia is the absence or near complete absence of oxygen in the arterial blood supply to an organ or tissue, Hypoxia is diminished availability of oxygen to the tissues, and hypoxemia is a condition in which there is reduced oxygenation of the blood (Biagas, 1999; Kuroiwa & Okeda, 1994).

  Effects of oxygen deprivation on cognitive function are well known. Early studies found that a decrease in the partial pressure of arterial oxygen (PaO 2 ) in humans such that PaO 2

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  The Neurosciences and the Practice of Aviation Medicine

  • Anthony N. Nicholson(Author)
  • 2017(Publication Date)
  • CRC Press

    (Publisher)

  2 , which partly compensates for the reduced oxygen saturation in chronic Hypoxia. However, polycythaemia increases blood viscosity and the workload of the heart and, when excessive, the disadvantages outweigh the benefits. Oxygen delivery to a tissue = blood flow x arterial oxygen content, so, as well as the factors discussed above, tissue Hypoxia can result from poor perfusion.

  Oxygen Delivery to Tissues

  In the paper ‘On Anoxaemia’ by Barcroft (1920) three mechanisms of tissue Hypoxia were described: reduced arterial PO2 (‘anoxic anoxaemia’), reduced oxygen-carrying capacity, usually due to a reduced haemoglobin concentration (‘anaemic anoxaemia’) and reduced tissue blood flow (‘ischaemic anoxaemia’). The classification remains useful today although the terminology has evolved. ‘Hypoxia’ and ‘hypoxaemia’ have replaced the terms ‘anoxia’ and ‘anoxaemia’ and the terms in brackets, as well as their more modern equivalents (‘hypoxic Hypoxia’, ‘anaemic Hypoxia’ and ‘ischaemic Hypoxia’), are probably best avoided. ‘Hypoxia’ and ‘hypoxic’, when unqualified, are now used to refer to a low arterial PO2 . The statement ‘This patient is hypoxic’ means ‘This patient has a low arterial PO2 ’ and would not be used to describe a patient with anaemia or low cardiac output. The expression ‘anaemic Hypoxia’ is potentially confusing, as anaemia does not lead to a low arterial PO2 . The term ‘anaemic tissue Hypoxia’ would avoid this problem.

  Oxygen is required in the tissues for the production of adenosine triphosphate (ATP), the main energy source of cells. When ATP production fails, many aspects of tissue function will be affected, ultimately leading to cell death. In addition to impairment of oxygen delivery by the three mechanisms cited above, ATP production can be impaired by inadequate utilization of the delivered oxygen. This ‘histotoxic’ form of tissue Hypoxia can be caused by poisoning of the electron transport chain in the mitochondria, for example by cyanide or sepsis.

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  Comparative Physiology, Natural Animal Models And Clinical Medicine: Insights Into Clinical Medicine From Animal Adaptations

  Insights into Clinical Medicine from Animal Adaptations

  • Michael Alan Singer(Author)
  • 2007(Publication Date)
  • ICP

    (Publisher)

  C H AP T E R 6 Hypoxia/Ischemia In higher organisms, respiratory and cardiovascular systems provide and distribute oxygen (O 2 ) to tissues and cells. Oxygen serves as the terminal electron acceptor during mitochondrial oxidative phosphorylation, which is the major biochemical reaction for capturing energy in the form of adenosine triphosphate (ATP). Since the function of the mammalian brain depends on a continuous supply of O 2 and glucose, brain function quickly deteriorates when the supply of these substrates is interrupted (Hansen, 1985). In this chapter, the effects of Hypoxia/ ischemia on mammalian brain structure and function and what is known about the adaptations of Hypoxia tolerant vertebrates such as high altitude birds and certain species of turtle are considered. In humans, a variety of lung diseases impair alveolar gas exchange with the result that the pO 2 of arterial blood is reduced below the range of normal. Perhaps the most common of these lung diseases is tobacco-induced emphysema. In this disorder, destruction of lung tissue with sig-nificant ventilation/perfusion mismatching is the underlying basis for the reduced arterial blood pO 2 . In humans with cerebrovascular disease, ves-sel occlusion results in ischemia of downstream brain tissue with cellular necrosis if the vascular occlusion is not quickly corrected. However, when considering the pathogenesis of brain dysfunction, one must distinguish between hypoxic and ischemic states since the two are quite different. An 190 Hypoxia/Ischemia 191 ischemic state is one in which there is impairment of blood supply result-ing in reduced delivery of substrates (chiefly O 2 and glucose) and reduced removal of waste products, while a hypoxic state is one in which there is reduced delivery of oxygen only (oxygen deprivation) with no interrup-tion of blood flow (Pearigen et al. , 1996; Auer and Sutherland, 2002).

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  The Principles and Practice of Human Physiology

  • O.G. Edholm(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  CHAPTER 5 High Altitudes and Hypoxia D. Denison Introduction 241 Biochemical Properties of the Oxygen Molecule 242 The Distribution of Oxygen in Tissues 246 The Predicted Effects of Hypoxia 258 The Observed Effects of Hypoxia 262 Acute Hypoxia 270 Neurological Effects of Acute Hypoxia 281 Chronic Hypoxia 289 Hyperventilation 291 The Role of Haemoglobin 295 Failures of Adaptation 298 Life-Long Hypoxia 300 Summary 301 Introduction Oxygen lack is one of the most important aspects of human physiology. It is experienced naturally by people living at high altitudes, it is a potential or actual hazard for everyone who flies, and it is the primary consequence of anaemia and many pulmonary and cardiovascular disorders which are common causes of morbidity and mortality in man. The eflfects of oxygen lack are bewildering in number and depend on its severity and rate of onset, 241 242 D. DENISON and on its duration. They range from subtle learning difficulties to loss of consciousness within a few seconds. However, although the subject is vast it is also well understood; few facts are required to make sense of the topic and predict its features with some precision. To do this one needs to know something about the biochemical properties of the oxygen molecule and how it is distributed to the tissues. These points will be discussed before the effects of Hypoxia in man are described. Biochemical Properties of the Oxygen Molecule The oxygen molecule has a paradoxical nature since we bathe in it without apparent harm although it is a powerful poison. With the exception of fluorine, it is the most corrosive of the elements, because it has a very high avidity for electrons and will attract them from any adjacent molecule. This is the essential nature of the process of oxidation. In this respect, all substances can be ranked in order of their tendency to give or receive electrons.

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  Carbon Monoxide in Drug Discovery

  Basics, Pharmacology, and Therapeutic Potential

  • Binghe Wang, Leo E. Otterbein(Authors)
  • 2022(Publication Date)
  • Wiley

    (Publisher)

  Of course, poor lung function or tissue perfusion caused by pathologies such as stenotic vessels or chronic lung disease requires treatment strategies to deliver supplemental oxygen. It is well accepted, however, that elevated levels of oxygen, while life sustaining, promote ROS generation and therein lies the paradox and it is the unavoidable consequence of living in an aerobic environment. Hyperoxia and the Delicate Balance Between Cell Survival and Death The upper limit dose of O 2 that human lungs can tol- erate without injury is not well known, yet hyperoxic gases (defined as oxygen levels greater than 20.9% O 2 ) are routinely delivered to patients as part of sup- portive care and regardless of need. This is of particular importance in instances such as bacterial or viral pneumonia where the lungs become filled with fluid leading to poor oxygen and CO 2 exchange. Of note, COVID-19 patients suffer from pulmonary vascular hyperinflammatory syndrome caused by a cytokine storm where the only treatment that is constant is to increase O 2 . Hyperoxia is defined as any instance where cells, tissues, or organs are exposed to a partial pressure of O 2 (pO 2 ) that is higher than normal atmospheric pO 2 at 40 mmHg (in tissues) or 100 mmHg (in blood; Table 7.1) [9]. Animal studies have clearly shown that exposure to higher than normal oxygen concentrations results in acute lung injury within 3–4 days with significant morbidity and mortality at >95% O 2 [10,11]. High O 2 concentrations injure the epithelial lining of the respiratory tract leading to sterile inflammation, leukocyte infiltration, edema, and ultimately ventilation/perfusion mis- match [12,13]. Persistent exposure to hyperoxia causes irreversible tissue damage [9]. Importantly, other remote organs such as the central nervous system can be affected by the elevated O 2 levels in the blood [14]. Exposure to 50–75% O 2 , while not lethal, does result in chronic lung injury and fibrosis [15].

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  Advances in Structural Biology

  • S.K. Malhotra(Author)
  • 2000(Publication Date)
  • Elsevier Science

    (Publisher)

  Gut Hypoxia not only impairs local function, but breakdown of immune and barrier properties of the mucosa may lead to production or amplification of the multiple organ dysfunc- tion syndrome (Carrico et al., 1985). 72 DAVID R. SCHWARTZ, ATUL MALHOTRA, and MITCHELL P. FINK Ill. CLASSIC VS. CYTOPATHIC Hypoxia A. The Debate If we accept the fact that an 02 extraction defect exists in certain tissues in sepsis despite a hyperdynamic circulation, we must still attempt to explain it. Impaired 0 2 consumption might result from a decreased gradient for diffusion of 0 2 at the mitochondrial level because of a low intracellular pO 2, or from the inability to maintain aerobic respiration despite preserved pO2, i.e., starvation in the midst of abundance. The remark by Astiz et al. in 1988 that the relative importance of systemic hypoperfusion and impaired oxidative metabolism in the development of metabolic failure in sepsis remains controversial is still true 10 years later. Sepsis is believed to represent distributive shock, characterized by a maldistribution of blood flow and volume that results in regional ischemia despite preserved sys- temic cardiac output. Experimental studies have revealed alterations in all aspects of the microcirculation, including capillary dropout (Lam et al., 1994), anatomic obstruction from fibrin, platelets, or leukocytes (Astiz et al., 1995), extrinsic com- pression from tissue edema; impaired vasoreactivity (Bernsten et al., 1992) and altered red blood cell theology (Chung et al., 1991). Although there is some evi- dence that a decreased hemoglobin P50 for oxygen may also be found in sepsis (Lehot et al., 1984), the majority of patients are felt to have relatively normal oxy- hemoglobin dissociation curves (Kalter et al., 1982).

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