Oxygen

From Ganfyd

Jump to: navigation, search
Symbol: O Atomic No: 8Oxygen
NitrogenFluorine Sulphur Data
Molecular weight 32.00

Density 1.335kg/m3 (at 15°C)

Boiling point -183.1°C (at 1 bar)

Importance in Man of Oxygen
Essential to aerobic metabolism & human life. Critical evolutionary interactions
Web Resources for Oxygen
Relevant Clinical Literature
UK Guidance

Element. Present in the atmosphere (21%) as the molecule O2 and higher up as O3 - Ozone. Odourless, colourless gas (at 15°C and 1 bar), pale blue as a liquid. Essential for survival as required for aerobic metabolism. The oxygenation of organic compounds is an essential feature of many biochemical processes.

Contents

Oxygen in Metabolism

  • Aerobic respiration, mitochondria
  • Basal oxygen consumption about 250ml/min for a body surface of 1.8m2.
    • Natural sleep reduces this by about 10%
    • Each 1°C fall in core body temperature will reduce by about 5%

Oxygen Delivery

Oxygen delivery = DO2 = CaO2 x CO

  • Where CaO2 is total oxygen content of arterial blood and CO is cardiac output.
CaO2 = (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2% x 0.01) + (0.023 x PaO2)
  • SO2 = percentage saturation of haemoglobin with oxygen
  • Hb = haemoglobin concentration in grams per 100 ml blood (g/dl)
  • PO2 = partial pressure of oxygen (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg)

Although not tightly regulated it is actually one of the most important physiological variables in determining physiological organ viability. Oxygen content of the blood is determined predominantly by the concentration of haemoglobin and the oxygen saturation - and to a much lesser extent by the partial pressure. Accordingly as demonstrated in infective shock it is mixed venous oxygen saturation (SvO2) that correlates better with outcome than the more usually determined arterial oxygen saturation (SaO2).

See also:

LogoKeyPointsBox.pngVenous oxygen saturation is a better indicator of cardiac output than is arterial saturation. For a given oxygen uptake by the peripheral tissues the lower the cardiac output is, the less oxygen will remain in the venous blood returning from those tissues.

Peripheral oxygen saturation (SpO2) is even easier to determine with pulse oximetry but may not reflect oxygen delivery to more central organs. Supra-physiological oxygen delivery to the tissues does not show benefit in critical illness no doubt due to oxygen toxicity, with for example myocardial infarction where treatment with oxygen is associated with worse prognosis[1] fully fitting the known cardiovascular effects of hyperoxaemia. Patients with COPD have a higher mortality if given more oxygen than required[2] reinforcing recommendations to maintain pO2 at no more than 88-92%[3].

Normal adult male values at sea level (on Earth)

  • Oxygen content of arterial blood = CaO2 = 20.4 ml/100 ml
  • Oxygen content of mixed venous blood (for oxygen saturation (SvO2) = 75% and venous partial pressure of oxygen (PvO2) = 6 kPa ) = CvO2 = 15.2 ml/100 ml
  • The in vitro maximum oxygen carrying capacity is 1.39 ml O2/g Hb
  • The in vivo maximum oxygen carrying capacity is 1.34 ml O2/g Hb (Hüfner’s constant).

Neonatal oxygen delivery

The evidence base suggests no role for high inspired oxygen values in initial resuscitation of babies born at or after term as room air is associated with at least a 30% lower mortality than 100% oxygen[4]. Matters are more complex with pre-term children where a target range of oxygen saturation of (91 to 95%) is associated with lower mortality but more retinopathy of prematurity than a target of 85 to 89%[5]. The present international guidelines recommend initial resuscitation with blended oxygen and air to reach target oxygen saturations. However room air is an alternative, although it will risk hypoxaemia in some pre-term infants. 100% oxygen is not recommended for initial premature infant resusciation[4]. The variability of practice world wide reflect that oxygen therapy was established in neonates by 1780 and that it took some time after the 1998 WHO guidelines for evidence base reinforcement to change practice in cultures where oxygen supplementation availability was rarely an issue at birth. This started to happen in a major way in 2006.

LogoKeyPointsBox.png

Oxygen in Clinical Practice

"Pink" gas. Often useful for blue patients. This use in systemic hypoxia does not extend to localised tissue hypoxia. Accordingly in suspected acute myocardial infarction without hypoxia it does not benefit mortality[6], consistent with the clinical trial evidence of net increase in myocardial damage[7][8]. Use in stroke is unclear as it may be initially beneficial[9], perhaps for first 72 hours[10] but then reverse the cell adaptions in chronic hypoxia that prevent ischaemic perumbra cell death caused by mitochondrial dysfunction[11]. There is as yet no convincing evidence of long term improvement in clinical outcome in stroke[12] but trials are underway.

LogoWarningBox4.pngOxygen supports combustion but does not, of course, explode. Folk stories that smoking near oxygen equipment "may cause an explosion" abound, and are wrong. The one exception is if you have another inflammable vapour in the air so setting up a still next to your oxygen concentrator would be interesting. Smoking in an atmosphere even slightly enriched with oxygen may kill the smoker and has burnt their bed partner, due to secondary consequences of the enhanced burning of the cigarette causing a conflagration.

Any compressed gas cylinder can explode in a fire, but Oxygen is less frightening than Nitrous Oxide or Acetylene in this respect.

Oxygen Toxicity

Oxygen is a very important toxin, indeed of such importance that complex mechanisms exist in most life forms to mitigate its toxicity. There are two main mechanisms for this toxicity, the well characterised one of reactive oxygen species and physiological consequences of the body having means to sense and react to oxygen concentrations. While hyperbaric oxygen has distinct toxicity even normobaric concentrations of oxygen can be toxic in some common presentations. However hyperoxia is very appropriate treatment in many trauma and infective presentations and can considerably reduce mortality. Accordingly it can and should be used in the acute emergency situation until accurate diagnosis indicates that it is not indicated. Generally acutely unwell patients should be optimised for a capillary oxygen saturation of between 94 to 98% (with potential hypercapnia aim for 88-92% until arterial blood gas gives better guidance). In those with acute respiratory distress syndrome 85% is the proven target[13]. Oxygen has all the characteristics of any therapy, too little can be harmful or useless, to much can be harmful or useless.

LogoKeyPointsBox.pngAdverse physiological effects of normobaric oxygen hyperoxia

Acute toxicity

  • Pulmonary oedema - moderate level hyperbaric oxygen
  • Seizures - at higher hyperbaric oxygen neurological manifestations may occur before the pulmonary oedema

Chronic toxicity

  • There is now strong evidence that excessive medical oxygen is harmful to most patients(increased 30 day and long term mortality), however randomised trials have only been done in stroke, cardiac, intensive care and emergency surgery patients. Hospital acquired pneumonia in surgical patients may be an exception[19] but problematically the same group have had multiple studies retracted due to statistical issues[20][21].
  • Retrolental fibroplasia

Neonatal studies with 100% normobaric exposure have demonstrated:

  • Retinopathy of prematurity
  • Bronchopulmonary dysplasia
  • Injury to the developing brain
  • Childhood malignancy
  • Premature senescence is likely from a large number of experimental models

Physiology

Acute pulmonary toxicity classically has a significant inflammatory component although actually the inflammatory component is less at higher inspired oxygen concentrations (2 atmospheres) and the aveolar cells just become leaky[22]. Vasoconstriction in critical organs such as the CNS and heart might well be important in explaining the poor outcomes when oxygen is given in the absence of definite systemic hypoxia.

Biochemistry

Toxicity is mediated through oxidative products such as superoxides, peroxides and peroxynitrites. These produce secondary and tertiary products. Some enzyme systems such as the xanthine oxidase system or common intermediate chemicals such as nitric oxide are likely to play a role through their reactivity[23]. For example xanthine oxidase converts hypoxanthine to xanthine in the presence of molecular oxygen, producing superoxide that will not be salvageable if too much is produced. Peroxide reacts with transition metals to produce the highly reactive hydroxyl radical leading to lipid peroxidation (cell membrane lipids such as phosphatidylethanolamine get converted to phosphatidylethanolamine hydroperoxide) and much else. In another example peroxynitrite produced by the interaction of nitric oxide and oxygen damages via:

  1. Lipid peroxidation, protein oxidation, and DNA damage.
  2. Induction of several transcription factors leading to cytokine-induced chronic inflammation.

Oxygen radical scavengers such as the superoxide dismutases, glutathione peroxidases and catalases (peroxidase) provide protection at normal inspired oxygen concentrations, but so too probably do compounds as diverse as haemoglobin and melatonin. Lung toxicity may be mediated through particular nitric oxide synthase isoforms[23] depending upon the inspired oxygen concentration.


Oxygen in evolution

Its key role is accepted, not only because its presence allows a much more complex and diverse biochemistry and fauna[24], but because it has driven organ structure[25] and has still active postulated selective roles[26].

References

  1. Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart (British Cardiac Society). 2009 Mar; 95(3):198-202.(Link to article – subscription may be required.)
  2. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. l A Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. BMJ 341:doi:10.1136/bmj.c5462
  3. O'Driscoll BR, Howard LS, Davison AG. BTS guideline for emergency oxygen use in adult patients. Thorax. 2008 Oct; 63 Suppl 6:vi1-68.(Link to article – subscription may be required.)
  4. a b Perlman JM, Wyllie J, Kattwinkel J, Atkins DL, Chameides L, Goldsmith JP, Guinsburg R, Hazinski MF, Morley C, Richmond S, Simon WM, Singhal N, Szyld E, Tamura M, Velaphi S. Part 11: neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010 Oct 19; 122(16 Suppl 2):S516-38.(Link to article – subscription may be required.)
  5. Carlo WA, Finer NN, Walsh MC, Rich W, Gantz MG, Laptook AR, Yoder BA, Faix RG, Das A, Poole WK, Schibler K, Newman NS, Ambalavanan N, Frantz ID, Piazza AJ, Sánchez PJ, Morris BH, Laroia N, Phelps DL, Poindexter BB, Cotten CM, Van Meurs KP, Duara S, Narendran V, Sood BG, O'Shea TM, Bell EF, Ehrenkranz RA, Watterberg KL, Higgins RD. Target ranges of oxygen saturation in extremely preterm infants. The New England journal of medicine. 2010 May 27; 362(21):1959-69.(Link to article – subscription may be required.)
  6. Hofmann R, James SK, Jernberg T, Lindahl B, Erlinge D, Witt N, Arefalk G, Frick M, Alfredsson J, Nilsson L, Ravn-Fischer A, Omerovic E, Kellerth T, Sparv D, Ekelund U, Linder R, Ekström M, Lauermann J, Haaga U, Pernow J, Östlund O, Herlitz J, Svensson L. Oxygen Therapy in Suspected Acute Myocardial Infarction. The New England journal of medicine. 2017 Aug.(Print-Electronic) (Link to article – subscription may be required.)
  7. Nehme Z, Stub D, Bernard S, Stephenson M, Bray JE, Cameron P, Meredith IT, Barger B, Ellims AH, Taylor AJ, Kaye DM, Smith K. Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction. Heart (British Cardiac Society). 2016 Mar; 102(6):444-451.(Print-Electronic) (Link to article – subscription may be required.)
  8. Stub D, Smith K, Bernard S, Nehme Z, Stephenson M, Bray JE, Cameron P, Barger B, Ellims AH, Taylor AJ, Meredith IT, Kaye DM. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 2015 Jun; 131(24):2143-2150.(Print-Electronic) (Link to article – subscription may be required.)
  9. Liu WC, Jin XC. Oxygen or cooling, to make a decision after acute ischemia stroke. Medical gas research. 2016 Oct-Dec; 6(4):206-211.(Electronic-eCollection) (Link to article – subscription may be required.)
  10. Roffe C, Ali K, Warusevitane A, Sills S, Pountain S, Allen M, Hodsoll J, Lally F, Jones P, Crome P. The SOS pilot study: a RCT of routine oxygen supplementation early after acute stroke--effect on recovery of neurological function at one week. PloS one. 2011 ; 6(5):e19113.(Print-Electronic) (Link to article – subscription may be required.)
  11. Huang JL, Zhao BL, Manaenko A, Liu F, Sun XJ, Hu Q. Medical gases for stroke therapy: summary of progress 2015-2016. Medical gas research. 2017 Apr-Jun; 7(2):107-112.(Electronic-eCollection) (Link to article – subscription may be required.)
  12. Ejaz S, Emmrich JV, Sitnikov SL, Hong YT, Sawiak SJ, Fryer TD, Aigbirhio FI, Williamson DJ, Baron JC. Normobaric hyperoxia markedly reduces brain damage and sensorimotor deficits following brief focal ischaemia. Brain : a journal of neurology. 2016 Mar; 139(Pt 3):751-764.(Print-Electronic) (Link to article – subscription may be required.)
  13. Aggarwal NR, Brower RG, Hager DN, Thompson BT, Netzer G, Shanholtz C, Lagakos A, Checkley W; National Institutes of Health Acute Respiratory Distress Syndrome Network Investigators. Oxygen Exposure Resulting in Arterial Oxygen Tensions Above the Protocol Goal Was Associated With Worse Clinical Outcomes in Acute Respiratory Distress Syndrome. Crit Care Med. 2018 Apr;46(4):517-524.doi: 10.1097/CCM.0000000000002886
  14. Tan A, Schulze A, O'Donnell CP, Davis PG. Air versus oxygen for resuscitation of infants at birth. Cochrane database of systematic reviews (Online). 2005; (2):CD002273.(Epub) (Link to article – subscription may be required.)
  15. Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart (British Cardiac Society). 2009 Mar; 95(3):198-202.(Link to article – subscription may be required.)
  16. Rønning OM, Guldvog B. Should stroke victims routinely receive supplemental oxygen? A quasi-randomized controlled trial. Stroke; a journal of cerebral circulation. 1999 Oct; 30(10):2033-7.
  17. Bulte DP, Chiarelli PA, Wise RG, Jezzard P. Cerebral perfusion response to hyperoxia. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. 2007 Jan; 27(1):69-75.(Link to article – subscription may be required.)
  18. Kuisma M, Boyd J, Voipio V, Alaspää A, Roine RO, Rosenberg P. Comparison of 30 and the 100% inspired oxygen concentrations during early post-resuscitation period: a randomised controlled pilot study. Resuscitation. 2006 May; 69(2):199-206.(Link to article – subscription may be required.)
  19. Schietroma M, Cecilia EM, De Santis G, Carlei F, Pessia B, Amicucci G. Supplemental Peri-Operative Oxygen and Incision Site Infection after Surgery for Perforated Peptic Ulcer: A Randomized, Double-Blind Monocentric Trial. Surg Infect (Larchmt). 2016 Feb;17(1):106-13. doi: 10.1089/sur.2013.132. Epub 2015 Nov 10
  20. Retraction notice to "High-concentration supplemental perioperative oxygen and surgical site infection following elective colorectal surgery for rectal cancer: A prospective, randomized, double-blind, controlled, single-site trial" (Schietroma M, Cecilia EM, Sista F, Carlei F, Pessia B, Amicucci G. Am J Surg 208 (2014) 719-726).Am J Surg. 2018 Mar;215(3):534.doi: 10.1016/j.amjsurg.2018.01.069.
  21. Retraction notice.(Schietroma M, Piccione F, Cecilia EM, Carlei F, De Santis G, Sista F, Amicucci G. How does high-concentration supplemental perioperative oxygen influence surgical outcomes after thyroid surgery? A prospective, randomized, double-blind, controlled, monocentric trial. J Am Coll Surg. 2015 May;220(5):921-33.) J Am Coll Surg. 2017 Aug;225(2):359.doi: 10.1016/j.jamcollsurg.2017.05.007
  22. Demchenko IT, Welty-Wolf KE, Allen BW, Piantadosi CA. Similar but not the same: normobaric and hyperbaric pulmonary oxygen toxicity, the role of nitric oxide. American journal of physiology. Lung cellular and molecular physiology. 2007 Jul; 293(1):L229-38.(Link to article – subscription may be required.)
  23. a b Demchenko IT, Atochin DN, Gutsaeva DR, Godfrey RR, Huang PL, Piantadosi CA, Allen BW. Contributions of nitric oxide synthase isoforms to pulmonary oxygen toxicity, local vs. mediated effects. American journal of physiology. Lung cellular and molecular physiology. 2008 May; 294(5):L984-90.(Link to article – subscription may be required.)
  24. Jiang YY, Kong DX, Qin T, Zhang HY. How does oxygen rise drive evolution? Clues from oxygen-dependent biosynthesis of nuclear receptor ligands. Biochemical and biophysical research communications. 2010 Jan 8; 391(2):1158-60.(Link to article – subscription may be required.)
  25. Mess AM, Ferner KJ. Evolution and development of gas exchange structures in Mammalia: The placenta and the lung. Respiratory physiology & neurobiology. 2010 Jan 18.(Epub ahead of print) (Link to article – subscription may be required.)
  26. Bigham AW, Mao X, Mei R, Brutsaert T, Wilson MJ, Julian CG, Parra EJ, Akey JM, Moore LG, Shriver MD. Identifying positive selection candidate loci for high-altitude adaptation in Andean populations. Human genomics. 2009 Dec; 4(2):79-90.
Personal tools