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Effect of Inspiration of 12%O2 (Balance N2) on Cardiac Output, Respiration, Oxygen Saturation, and Oxygen Delivery

Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 701)

Abstract

Low arterial oxygen saturation (SaO2) will result in a reduced rate of arterial oxygen delivery to the tissues (DO2), unless there is a compensatory increase in cardiac output (CO) or haemoglobin concentration (Hb). An adequate DO2 can therefore be maintained by increasing ventilation, CO, or both. Sustaining a tissue specific oxygen extraction is thought to play an important part in overall compensation. The present study has examined responses to acute hypoxic exposure in 8 volunteers (breathing 12% oxygen, balance nitrogen) and describes changes in CO, ventilation and the SaO2. Aims included: examination of the extent of intersubject variations and seeing whether DO2 was maintained. SaO2, PCO2, respiration (via stethograph) and Finapress (non-invasive) arterial blood pressure (BP) were recorded, firstly on air and then on 12% oxygen. CO was derived, off-line, from the BP record. CO was increased in 5 subjects (22%-45%) but was virtually unchanged in 3, and yet comparison for all 8 subjects showed that DO2 on 12% oxygen was not significantly different from DO2 on air (mean on air 1017 ml. min–1; hypoxia 1080 ml. min–1, p = 0.27). SaO2 on 12% oxygen ranged between 85% and 93%. In conclusion, exposure to the same hypoxic gas mixture resulted in differing individual ventilatory and CO responses. However, DO2 was well maintained.

Keywords

Cardiac Output Oxygen Delivery Ventilatory Response Acute Mountain Sickness Hypoxic Ventilatory Response 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.DoncasterUK
  2. 2.Faculty of Health and Life SciencesCoventry UniversityCoventryUK
  3. 3.William Harvey Research Institute, Anaesthetics LaboratoryLondon UniversityLondonUK

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