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Published: 4 June 2021
Last updated: 31 July 2024

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1

Al-Abdulmunem, M. A. Effects of hypoxia and hypercapnia associated withcontactlenswearon corneal epithelium. Manchester: UMIST, 1994.

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2

Jarsky, Tim M. The effects of hypoxia and hypercapnia on hamster activity rhythms. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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3

Peever, John H. Day-night differences in ventilation, metabolism, and body temperature during normoxia, hypoxia and hypercapnia in the awake adult rat. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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4

Piracha, Kashif. Hypercapnic Respiratory Failure. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-36128-9.

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5

U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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6

United States. National Aeronautics and Space Administration., ed. "CO₂-O₂ interactions in extension of tolerance to acute hypoxia": Final report. [Washington, DC]: National Aeronautics and Space Administration, 1995.

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7

United States. National Aeronautics and Space Administration., ed. "CO₂-O₂ interactions in extension of tolerance to acute hypoxia": Final report. [Washington, DC]: National Aeronautics and Space Administration, 1995.

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8

Laffey, John G., and Brian P. Kavanagh. Hypercapnia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0086.

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Hypercapnia is a central component of current ‘protective’ ventilator management. Hypercapnia, and the associated acidosis, has potentially important biologic effects on immune responses, injury and repair. Arterial carbon dioxide tension PaCO2 is tightly governed under physiological conditions and small elevations rapidly increase spontaneous minute ventilation. In the mechanically-ventilated patient, elevated PaCO2 usually reflects reduced elimination. This can be because tidal volume or respiratory rate delivered by the ventilator are reduced, or because of the diseased lung per se. Hypercapnia has many effects that are clinically obvious, but research over the last decade reveals important consequences on inflammatory and cellular mechanisms that are not apparent at the bedside.
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9

Claudette Marie.* St. Croix. The effect of aging and aerobic fitness level on the ventilatory response to hypercapnia. 1991.

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10

Kreit, John W. Respiratory Failure and the Indications for Mechanical Ventilation. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0007.

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Respiratory failure occurs when a disease process significantly interferes with the respiratory system’s vital functions and causes arterial hypoxemia, hypercapnia, or both. Typically, respiratory failure is divided into three categories based on the underlying pathophysiology: ventilation failure, oxygenation failure, and oxygenation-ventilation failure. With severe disturbances in gas exchange, mechanical ventilation is often needed to assist the respiratory system and restore the PaCO2, PaO2, or both, to normal. Respiratory Failure and the Indications for Mechanical Ventilation defines and describes the three types of respiratory failure and reviews the four indications for intubation and mechanical ventilation—acute or acute-on-chronic hypercapnia, refractory hypoxemia, inability to protect the lower airway, and upper airway obstruction.
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11

Orlikowski, David, and Tarek Sharshar. Epidemiology, diagnosis, and assessment of neuromuscular syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0243.

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Admission to ICU with severe limb weakness, or the occurrence of a respiratory or motor deficit, and failure to wean from mechanical ventilation while in the intensive care unit are common presentations of a neuromuscular disease. Neuromuscular diseases include neuronopathies, neuropathies, myasthenic syndromes, and myopathies. An accurate neurological examination and complementary investigations are necessary for both diagnosis and for evaluating the severity of the disease. Assessment of respiratory muscle function is a key step in deciding the need for mechanical ventilation and subsequently its weaning. Hypercapnia often indicates an impending respiratory arrest, but normocapnia, which can be seen in a patient with severe reduction in vital capacity is not reassuring. Hypoxaemia can be due to hypercapnia, pulmonary injury (atelectasis or pneumonia), or pulmonary embolism. Cardiac evaluation is important as cardiomyopathies are frequent in myopathies.
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12

Wise, Matt, and Simon Barry. Respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0135.

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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnia). Hypoxaemia is defined as an arterial blood partial pressure of oxygen (PaO2) of <8 kPa, and hypercapnia as an arterial blood partial pressure of carbon dioxide (PaCO2) of >6 kPa. Respiratory failure is divided into two different types, conventionally referred to as type 1 and type 2. The distinction between these two is important because it emphasizes not only different their pathophysiological mechanisms and etiologies, but also different treatments. The preferred terminology and definitions are as follows: oxygenation failure (type I respiratory failure), PaO2 of <8 kPa; ventilation failure (type 2 respiratory failure), PaCO2 >6 kPa. Respiratory failure may be acute (onset over hours to days), or chronic (developing over months to years); alternatively, there may be an acute deterioration of a chronic state.
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13

Brimioulle, Serge. Pathophysiology, causes, and management of metabolic alkalosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0257.

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Metabolic alkalosis occurs in up 51% of abnormal acid-base samples in the hospital. It is characterized by a primary increase in bicarbonate concentration and is always associated with chloride depletion. In critically-ill patients, it is most often generated by diuretic administration, digestive losses, alkali administration, or rapid correction of hypercapnia. Even after all causal factor are removed, it can be maintained by blood volume depletion and potassium depletion. Metabolic alkalosis results in hypercapnia, hypoxaemia, cardiac arrhythmias, altered consciousness, and neuromuscular hyperexcitability. It is first treated by removing the causal factors, whenever possible. Maintaining factors must be reversed by sodium chloride and/or potassium chloride administration. Acetazolamide and renal replacement therapy, when given for specific indications, can also correct the alkalosis. Lysine and arginine chloride are no longer used. If metabolic alkalosis is severe or when other treatments are contraindicated or ineffective, hydrochloric acid infusion is useful. Dilute hydrochloric acid can be infused safely, provided adequate precautions are taken to prevent extravascular leakage, vessel damage, and tissue necrosis.
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14

Gheshmy-Bakht, Afshan. The role of central and peripheral influences in the chronic hypercapnia-induced increase in central pH/carbon dioxide chemoreception. 2006.

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15

Rochester, Dudley. Hypercapnic Respiratory Failure. Butterworth-Heinemann, 1997.

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16

Rochester, Dudley F. Hypercapnic Respiratory Failure. Butterworth-Heinemann, 1990.

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17

Devlin, Hugh, and Rebecca Craven. The respiratory system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759782.003.0008.

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The respiratory system in relation to dentistry is the topic of this chapter. Gaseous exchange in the lungs is mainly controlled by central chemoreceptors sensing a change in the pH of the cerebrospinal fluid. These receptors then activate a respiratory response which returns the blood and cerebrospinal fluid pH to normal. Localized airway obstruction, obstructive sleep apnoea, and lung disease can cause hypoxaemia (a low arterial oxygen oncentration) and hypercapnia (a raised carbon dioxide concentration in the blood). We emphasize the specific dental issues in patients with asthma, i.e. the dry mouth when taking β‎‎2-adrenergic agonists and the management of an acute asthmatic attack. Specific points of relevance to the dentist are summarized in sections throughout the chapter.
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18

"CO₂-O₂ interactions in extension of tolerance to acute hypoxia": Final report. [Washington, DC]: National Aeronautics and Space Administration, 1995.

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19

Wecksell, Matthew, and Kenneth Fomberstein. Traumatic Brain Injury and C-Spine Management. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0020.

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Traumatic brain injury encompasses two different types of pathology: that caused at the time of the initial physical insult, called primary injury, and then further, secondary injury caused by either host cellular responses such as oxidative injury and inflammation or by physiological insults such as ischemia, hypoxia, hypo- or hypercapnia, intracranial hypertension, and hypo- or hyperglycemia. While primary injury falls to the realm of public health (e.g., encouraging helmet use for sports, discouraging impaired driving, etc.), many secondary injuries are avoidable with proper medical management. As the stem case for this chapter, an older patient experiences a fall and is incoherent on presentation to the emergency room. This case concerns her initial management, stabilization, diagnosis, and airway management. With progression of her traumatic brain injury, the authors discuss intracranial pressure management, surgical management, and resuscitation as well as likely postoperative sequelae.
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20

Burton, Derek, and Margaret Burton. Gas exchange. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0006.

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Oxygen intake for respiration, also carbon dioxide and, generally, ammonia elimination takes place across gas-exchange surfaces, usually the gills in fish. Water flows across gills, separated by the pharyngeal gill clefts, and supported by gill arches, and which possess highly folded surfaces covered by a very thin epithelium. Blood flow and water flow are separated only by the epithelium with a ‘countercurrent’ gas exchange between the two. A respiratory centre in the hind-brain is a respiratory rhythm pacemaker for the oral and pharyngeal ventilation movements creating water flow across the gills, although ‘ram ventilation’ occurs without such movements. The oxygen and carbon dioxide-carrying capacity of blood is increased considerably by temporary attachment to haemoglobin pigment in the erythrocytes. Some fish are air breathing, using lungs, swim bladder, skin or lips for gaseous exchange. Hypoxia, hypercapnia, supersaturation and high water temperatures present problems for fish respiration, which are discussed.
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21

Wagner, Peter D. Gas exchange principles in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0075.

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Pulmonary gas exchange in the critically-ill patient is almost always impaired. The reasons are usually multiple and complex, with causes both internal and external to the lung. To understand the relative contributions of these many factors in a given patient requires an understanding of the basic principles of gas exchange. This becomes even more important when a patient’s condition changes quickly, which happens commonly in the critically ill. The purpose of this chapter is to lay out those principles and discuss the several causes of arterial hypoxaemia (and hypercapnia) on the basis of those principles. The key principle that governs gas exchange (in the steady state) is conservation of mass, and writing straightforward mass transport equations that express this principle allows gas exchange to be analysed quantitatively. This chapter is intended to serve as a guide to support appropriate application of tests of pulmonary gas exchange, which are laid out in the chapter that immediately follows it.
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22

Junna, Mithri R., Bernardo J. Selim, and Timothy I. Morgenthaler. Central sleep apnea and hypoventilation syndromes. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0018.

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Sleep disordered breathing (SDB) may occur in a variety of ways. While obstructive sleep apnea is the most common of these, this chapter reviews the most common types of SDB that occur independently of upper airway obstruction. In many cases, there is concurrent upper airway obstruction and neurological respiratory dysregulation. Thus, along with attempts to correct the underlying etiologies (when present), stabilization of the upper airway is most often combined with flow generators (noninvasive positive pressure ventilation devices) that modulate the inadequate ventilatory pattern. Among these devices, when continuous positive airway pressure (CPAP) alone does not allow correction of SDB, adaptive servo-ventilation (ASV) is increasingly used for non-hypercapnic types of central sleep apnea (CSA), while bilevel PAP in spontaneous-timed mode (BPAP-ST) is more often reserved for hypercapnic CSA/alveolar hypoventilation syndromes. Coordination of care among neurologists, cardiologists, and sleep specialists will often benefit such patients.
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23

Mitchell, John D., and Marek Brzezinski. Introduction to Pulmonary Urgencies and Emergencies. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0013.

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The lungs exchange gases and also provide for some metabolic functions. Respiratory failure can be grouped into types I-IV. Type I (hypoxemic) and type II (hypercapnic) are the most prominent; type III is perioperative and often considered a subset of type I, while type IV is due to shock. Pulmonary urgencies and emergencies require rapid diagnosis and treatment in order to avoid morbidity and mortality. Identification of risk factors for desaturation and the application of an appropriate management algorithm can facilitate diagnosis and management. The ABCD-A SWIFT CHECK algorithm and its subalgorithms represent a logical approach to rapid diagnosis and management.
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24

Ramsay, Michelle, and Mike Polkey. Non-invasive ventilation and chronic obstructive pulmonary disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0012.

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Non-invasive ventilation is one of the major advances in respiratory medicine over the last century. It can be lifesaving for patients in acute hypercapnic respiratory failure, improving gas exchange and pulmonary mechanics and reducing the need for endotracheal intubation. Adherence to therapy is key to its success, and many patients find this a significant challenge. This case report will examine the pitfalls of initiating non-invasive ventilation, provide a brief overview of the current British Thoracic Society non-invasive ventilation guidelines, and describe common causes of a chronic obstructive pulmonary disease patient ‘failing’ non-invasive ventilation and an approach to the long-term management of the frequently exacerbating chronic obstructive pulmonary disease patient.
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25

Spoletini, Giulia, and Nicholas S. Hill. Non-invasive positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0090.

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Non-invasive ventilation (NIV) has been increasingly used over the past decades to avoid endotracheal intubation (ETI) in critical care settings. In selected patients with acute respiratory failure, NIV improves the overall clinical status more rapidly than standard oxygen therapy, avoids ETI and its complications, reduces length of hospital stay, and improves survival. NIV is primarily indicated in respiratory failure due to acute exacerbations of chronic obstructive pulmonary disease, cardiogenic pulmonary oedema and associated with immunocompromised states. Weaker evidence supports its use in other forms of acute hypercapnic and hypoxaemic respiratory failure. Candidates for NIV should be carefully selected taking into consideration the risk factors for NIV failure. Patients on NIV who are unstable or have risk factors for NIV failure should be monitored in an intensive or intermediate care units by experienced personnel to avoid delay when intubation is needed. Stable NIV patients can be monitored on regular wards.
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26

Mandal, Swapna, and Joerg Steier. Sleep-disordered breathing in the obese. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0018.

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Sleep-disordered breathing in the obese is not a small problem. Obesity-related sleep-disordered breathing is common and may include sleep apnoea or obesity hypoventilation syndrome. Patients present with symptoms of excessive daytime sleepiness, breathlessness, and, in severe cases, hypercapnic respiratory failure. In recent decades, the prevalence of obesity has increased exponentially. Although not exclusively responsible, obesity is directly linked to the development of sleep-disordered breathing due to high resistance in the upper airway, increased work of breathing, and high neural respiratory drive. Obese patients with sleep disorders are complicated with multiple metabolic, cardiovascular, and orthopaedic co-morbidities, frequently presenting at an advanced stage. This chapter reviews a common clinical presentation of an obese patient with a respiratory condition and the difficulties in their management. The chapter explains the complex underlying pathophysiology and the long-term management of these patients, and shows how sleep-disordered breathing may develop as a consequence of obesity.
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27

Wise, Matt, and Paul Frost. ICU treatment of respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0149.

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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnoea). Respiratory failure can develop over years when it is due to conditions such as kyphoscoliosis or motor neuron disease, or minutes in the case of an acute asthma attack or pneumothorax. In this context, respiratory failure is often called acute (e.g. asthma), chronic (e.g. kyphoscoliosis), or acute on chronic (kyphoscoliosis complicated by pneumonia). Chronic respiratory failure is characterized by compensatory mechanisms which aim to adjust the pH of the blood back to the normal physiological range and involve the retention of bicarbonate by the kidney. This topic covers the etiology of respiratory failure as well as signs, symptoms, diagnosis, investigations, prognosis, and treatment.
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28

Fullerton, James N., and Mervyn Singer. Oxygen in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0032.

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Oxygen therapy is primarily administered to alleviate arterial hypoxaemia and tissue hypoxia, and to facilitate aerobic cellular respiration. Hypoxaemia (PaO2 < 8 kPa [60 mmHg], SaO2 <92%) is associated with end-organ damage and adverse clinical outcomes, serving as a proxy measure for reduced intracellular PO2. Increasing the fraction of inspired oxygen should form part of an overall strategy to maximize tissue oxygen delivery. Permissive hypoxaemia represents a valid treatment strategy in a selected patient cohort. Oxygen is a drug and oxygen therapy is not benign, and oxygen administration at high, sustained doses (FiO2 >0.5, >12 hours) may cause oxygen toxicity. Observational studies in both mechanically-ventilated patients and survivors of non-traumatic cardiac arrest indicate an independent association between increasing hyperoxaemia and mortality. Oxygen therapy may additionally precipitate hypercapnic ventilatory failure in those at risk and oxygen should be administered to achieve a prescribed target SaO2 or PaO2 range, via adjustment of dose and delivery device. If no monitoring is available, hypoxaemia should be avoided by giving high-flow oxygen to achieve a FiO2 of near 1.0 with subsequent titration once oxygenation status is established.
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29

Sampson, Brett G., and Andrew D. Bersten. Therapeutic approach to bronchospasm and asthma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0111.

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The optimal management of bronchospasm and acute asthma is reliant upon confirmation of the diagnosis of asthma, detection of life-threatening complications, recognition of β‎2 agonist toxicity, and exclusion of important asthma mimics (such as vocal cord dysfunction and left ventricular failure). β‎2 agonists, anticholinergics, and corticosteroids are the mainstay of treatment. β‎2 agonists should be preferentially administered by metered dose inhaler via a spacer, and corticosteroids by the oral route, reserving nebulized (and intravenous) salbutamol, as well as intravenous hydrocortisone, for situations when these routes are not possible. A single intravenous dose of magnesium may be of benefit in severe asthma, but repeat dosing is likely to cause serious side effects. Parenteral administration of adrenaline may prevent the need for intubation in the patient in extremis. Aminophylline has an unfavourable side effect profile and has not been shown to offer additional benefit in adults. However, it does have a role in paediatric asthma. Unproven medical therapies with potential benefit include ketamine, heliox, inhalational anaesthetics, and leukotriene antagonists. The need for ventilatory support is usually preceded by worsening dynamic hyperinflation, exhaustion, hypoxia, reduced conscious state, or a combination of these. While non-invasive ventilation may have a temporizing role to allow time for response to medical therapy, there is insufficient evidence for its use, and should not delay invasive ventilation. If invasive ventilation is indicated, a strategy of hypoventilation and permissive hypercapnoea, minimizes barotrauma and dynamic hyperinflation. Extracorporeal support may have a role as a rescue therapy.
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