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Published: 9 March 2023
Last updated: 10 March 2023

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1

Oakes, Dana F. Oakes' ABG instructional guide. Orono, Me: RespiratoryBooks, 2009.

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2

Shapiro, Barry A. Clinical application of blood gases. 5th ed. Chicago, IL: Mosby-Year Book, 1993.

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3

Shapiro, Barry A. Clinical application of blood gases. 5th ed. St. Louis: Mosby, 1994.

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4

F, Walker Jerome, ed. Clinical arterial blood gas analysis. St. Louis: Mosby, 1987.

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5

J, Malley William. Clinical blood gases: Assessment and intervention. 2nd ed. St. Louis, Mo: Elsevier Saunders, 2005.

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6

J, Malley William. Clinical blood gases: Assessment and intervention. 2nd ed. St. Louis, Mo: Elsevier Saunders, 2005.

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7

J, Malley William. Clinical blood gases: Application and noninvasive alternatives. Philadelphia: Saunders, 1990.

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8

Wincek, Jenifer. Introduction to pediatric blood gas interpretation. 2nd ed. Milwaukee, WI: Maxishare, 1990.

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9

1937-, Shapiro Barry A., and Shapiro Barry A. 1937-, eds. Clinical application of blood gases. 4th ed. Chicago: Year Book Medical Publishers, 1989.

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10

J, Malley William. Clinical blood gases: Invasive and noninvasive techniques and applications. Philadelphia: Saunders, 1990.

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11

Hennessey, Iain. Arterial blood gases made easy. Edinburgh: Elsevier Churchill Livingstone, 2008.

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12

Toffaletti, John G. Blood gases and electrolytes. 2nd ed. Washington, DC: American Association for Clinical Chemistry, 2009.

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13

service), SpringerLink (Online, ed. Handbook of Blood Gas/Acid–Base Interpretation. London: Springer London, 2009.

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14

Lawrence, Martin. All you really need to know to interpret arterial blood gases. Philadelphia: Lea & Febiger, 1992.

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15

All you really need to know to interpret arterial blood gases. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 1999.

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16

Paul, Berghuis, ed. Respiration. Redmond, Wash: SpaceLabs, Inc., 1992.

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17

D, Wimberley Peter, Scandinavian Society for Clinical Chemistry., and Scandinavian Workshop on Future Perspectives for Comprehensive Blood Gas Analysis (1st : 1987 : Copenhagen, Denmark), eds. Future perspectives for comprehensive blood gas analysis: First Scandinavian workshop, Copenhagen 1987. Oxford: Published for Medisinsk Fysiologisk Forenings Forlag, Oslo by Blackwell Scientific Publications, 1988.

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18

Oakes, Dana F. Oakes' ABG pocket guide. Orono, Me: RespiratoryBooks, 2009.

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19

1943-, Chatterjee Molly S., ed. Biochemical monitoring of the fetus. New York: Springer-Verlag, 1993.

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20

Insight, LLC Medtech. U.S. markets for blood gas/electrolyte monitoring, pulmonary function assessment, and sleep apnea management products. Newport Beach, CA: Medtech Insight, 2005.

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21

Blood gases and acid-base physiology. 2nd ed. New York: Thieme, 1987.

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22

L, Jones Norman. Blood gases and acid-base physiology. London: Verlag, 1987.

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23

N, Kourteli Elena, and Winter, Robert J. D. (Robert James David), eds. Maîtriser les épreuves fonctionnelles respiratoires: De la théorie à la clinique. Issy-les-Moulineaux: Elsevier Masson, 2007.

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24

VandenBoer, Trevor. Development of an analysis for ketamine in wistar rat femoral bone, bone marrow and blood following a single acute administration by enzyme-linked immunosorbent assay and gas chromatography electron capture detection methods. Sudbury, Ont: Laurentian University, 2007.

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25

International, Bioanalytical Forum (7th 1987 Guildford England). Bioanalysis of drugs and metabolites, especially anti-inflammatory and cardiovascular. New York: Plenum Press, 1988.

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26

1922-, Reid Eric, Robinson J. D, Wilson Ian D, and International Bioanalytical Forum, (7th : 1987 : Guildford, England), eds. Bioananlysis of drugs and metabolytes: Especially anti-inflammatory and cardiovascular. New York: Plenum Press, 1988.

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27

Paul, Richard, and Paul Grant. Blood gas analysis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0018_update_001.

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Acid-base homeostasis is vital for the maintenance of normal tissue and organ function, as both acidosis and alkalosis can have harmful and potentially life-threatening effects. Arterial blood gas analysis, combined with routine clinical history and examination, can provide useful information for the management of the critically ill cardiac patient. Most acid-base derangements are reversed by treatment of the underlying disease process, rather than simple correction of the abnormal pH, and prognosis is determined by the nature of the underlying disease, rather than the extent of pH value deviation. Within this chapter, a six-step approach is presented for prompt and accurate acid-base interpretation. Water and electrolyte disorders are common in the intensive cardiac care unit, particularly in patients with cardiac failure. Prompt recognition and treatment is required to prevent cardiovascular and neurological compromise. Therapeutic strategies range from simple electrolyte substitution and fluid management to extracorporeal filtration of excess fluid and electrolytes. These are discussed within this chapter.
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28

Arterial Blood Gas Analysis. Anup Research & Multimedia Lp, 2009.

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29

Simple Guide to Blood Gas Analysis. Wiley-Blackwell, 1997.

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30

Richards, John. Analysis of Arterial Blood Gas: Solving Arterial Blood Gas Problems. Independently Published, 2020.

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31

Workbook to Accompany Clinical Application of Blood Gases. 5th ed. Mosby-Year Book, 1994.

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32

Arterial Blood Gas Analysis Made Easy. A B Anup, 1996.

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33

Arterial Blood Gases Made Easy. Churchill Livingstone, 2007.

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34

Joynt, Gavin M., and Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.

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Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.
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35

Garby, Lars. Respiratory Functions of Blood. Springer, 2012.

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36

Garby, Lars. The Respiratory Functions of Blood. Springer, 2012.

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37

Paul, Richard, Pavlos Myrianthefs, George Baltopoulos, and Shaun McMaster. Blood gas analysis: acid–base, fluid, and electrolyte disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0018.

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Acid-base homeostasis is vital for the maintenance of normal tissue and organ function, as both acidosis and alkalosis can have harmful and potentially life-threatening effects. Arterial blood gas analysis, combined with routine clinical history and examination, can provide useful information for the management of the critically ill cardiac patient. Most acid-base derangements are reversed by treatment of the underlying disease process, rather than simple correction of the abnormal pH, and prognosis is determined by the nature of the underlying disease, rather than the extent of pH value deviation. Within this chapter, a six-step approach is presented for prompt and accurate acid-base interpretation. Water and electrolyte disorders are common in the intensive cardiac care unit, particularly in patients with cardiac failure. Prompt recognition and treatment is required to prevent cardiovascular and neurological compromise. Therapeutic strategies range from simple electrolyte substitution and fluid management to extracorporeal filtration of excess fluid and electrolytes. These are discussed within this chapter.
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38

Arterial Blood Gases Made Easy. Elsevier - Health Sciences Division, 2015.

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39

Stacey, Victoria. Respiratory. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199592777.003.0010.

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Asthma - Chronic obstructive pulmonary disease (COPD) - Non-invasive ventilation - Venous thromboembolism - Pneumonia - Spontaneous pneumothorax - Respiratory failure and oxygen therapy - Arterial blood gas analysis - SAQs
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40

Intrapartum biochemical monitoring of the fetus: Proceedings of the first international symposium, Atlantic City, USA, June 1987. Berlin: De Gruyter, 1988.

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41

THE HISTORY OF BLOOD GASES, ACIDS AND BASES. Munksgaard, 1986.

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42

Chatterjee, Molly S. Biochemical Monitoring of the Fetus. Springer London, Limited, 2013.

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43

Toffaletti, John G. Blood Gases And Electrolytes: Special Topics in Diagnostic Testing. AACC Press, 2001.

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44

Magee, Patrick, and Mark Tooley. Intraoperative monitoring. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0043.

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Chapter 25 introduced some basic generic principles applicable to many measurement and monitoring techniques. Chapter 43 introduces those principles not covered in Chapter 25 and discusses in detail the clinical applications and limitations of the many monitoring techniques available to the modern clinical anaesthetist. It starts with non-invasive blood pressure measurement, including clinical and automated techniques. This is followed by techniques of direct blood pressure measurement, noting that transducers and calibration have been discussed in Chapter 25. This is followed by electrocardiography. There then follows a section on the different methods of measuring cardiac output, including the pulmonary artery catheter, the application of ultrasound in echocardiography, pulse contour analysis (LiDCO™ and PiCCO™), and transthoracic electrical impedance. Pulse oximetry is then discussed in some detail. Depth of anaesthesia monitoring is then described, starting with the electroencephalogram and its application in BIS™ monitors, the use of evoked potentials, and entropy. There then follow sections on gas pressure measurement in cylinders and in breathing systems, followed by gas volume and flow measurement, including the rotameter, spirometry, and the pneumotachograph, and the measurement of lung dead space and functional residual capacity using body plethysmography and dilution techniques. The final section is on respiratory gas analysis, starting with light refractometry as the standard against which other techniques are compared, infrared spectroscopy, mass spectrometry, and Raman spectroscopy (the principles of these techniques having been introduced in Chapter 25), piezoelectric and paramagnetic analysers, polarography and fuel cells, and blood gas analysis.
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45

Determination of the lactate threshold by respiratory gas exchange measures and blood lactate levels during incremental-load work. 1989.

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46

Determination of the lactate threshold by respiratory gas exchange measures and blood lactate levels during incremental-load work. 1987.

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47

Determination of the lactate threshold by respiratory gas exchange measures and blood lactate levels during incremental-load work. 1989.

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48

Simbiosys. ABG Bloodgas Interpretation: An Interactive Tutorial for Blood Gas & Acid-Base Analysis (CD-ROM for Windows). Critical Concepts, Incorporated, 1997.

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49

Wagner, Peter D. Gas exchange assessment in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0076.

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Chapter 75 laid out the basic principles that govern pulmonary gas exchange, a step necessary for the appropriate application and interpretation of common clinical tests of gas exchange. The present chapter discusses the several common tests and indices used to analyse and quantify gas exchange abnormalities in critically-ill patients. There is special emphasis on inherent limitations of each technique, as well as on ways to minimize technical and experimental errors when the necessary measurements are made. Limitations and errors are considered to be of major clinical importance because, while the measurements and indices themselves are easy to obtain, and have been in routine use for many years, serious errors of interpretation can occur if the limitations and common errors are not appreciated and allowed for. In particular, it is pointed out that factors external to the lungs can dramatically change arterial oxygenation in the critically-ill patient. This means that not all changes in gas exchange reflect changes in lung pathology. It is not uncommon for arterial PO2 to change without change in lung disease severity when external factors such as metabolic rate, cardiac output, and blood temperature change.
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50

Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.

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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.
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