Systematic review of studies of the effect of hyperoxia on coronary blood flow.
BACKGROUND
International guidelines recommend the routine use of oxygen in the initial treatment of myocardial infarction, yet it is uncertain what effect this might have on physiologic and clinical outcomes.


METHODS
We undertook a systematic search of Medline, Cochrane Database of Systematic Reviews, EMBASE, and CINHAL using the key words "oxygen," "coronary blood flow," "hyperoxia," and "coronary circulation" to identify human studies involving a measure of coronary blood flow while breathing oxygen and room air. The primary outcome measure was coronary blood flow; secondary outcomes included coronary vascular resistance and myocardial oxygen consumption.


RESULTS
From 2,072 potential publications, there were 6 studies from 4 publications that met the inclusion criteria, with 6 healthy subjects and 61 subjects with cardiac disease. It was not possible to undertake a meta-analysis due to methodological limitations. In the 6 studies, high-concentration oxygen therapy resulted in hyperoxia, with a range in mean Pao(2) of 273 to 425 mm Hg. Hyperoxia caused a significant reduction in coronary blood flow (mean change -7.9% to -28.9%, n = 6 studies). Hyperoxia caused a significant increase in coronary vascular resistance (mean change 21.5% to 40.9%, n = 4 studies) and a significant reduction in myocardial oxygen consumption (mean change -15.3% to -26.9%, n = 3 studies).


CONCLUSIONS
Hyperoxia from high-concentration oxygen therapy causes a marked reduction in coronary blood flow and myocardial oxygen consumption. These physiologic effects may have the potential to cause harm and are relevant to the use of high-concentration oxygen therapy in the treatment of cardiac and other disorders.
Farquhar
Hamish
H
Medical Research Institute of New Zealand, Wellington, New Zealand.
Weatherall
Mark
M
Wijesinghe
Meme
M
Perrin
Kyle
K
Ranchord
Anil
A
Simmonds
Mark
M
Beasley
Richard
R
D003326:Coronary Circulation / Q000502:physiology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D018496:Hyperoxia / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D010102:Oxygen Inhalation Therapy / Q000009:adverse effects*; D014655:Vascular Resistance / Q000502:physiology