Why shouldn't we put Oxygen on chest pain patients

WHY  NO  OXYGEN  ON  MY  CHEST  PAIN  PATIENT???

I've received an email from a follower to cover the oxygen on a chest pain issue from a Why we don't use oxygen any more on AMI patients.

I'll start by saying... Do what your policies /protocols say, and if they are wrong, lobby to have them changed.

Second what I'm summarising here is a distillation of literature that spans papers back to 1964.

Cabello, J. et.al. (2010). Oxygen therapy for acute myocardial infarction (Review). The Cochrane Library
http://www.thecochranelibrary.com/details/file/742697/CD007160.html


Burls et al 2011
Emergency med Journal did a meta analysis.
http://www.medscape.com/viewarticle/752314

Beazley et al 2007 who looked at
Historical perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809170/

And the article that probably started the debate early in 1900, yes 113 years ago...
Steele's article in the BMJ claiming oxygen relieved Angina.

And it does.  No one is disputing this. It is like saying Crack makes you High, but does it mean that it is the right thing to use??

Oxygen in the blood of a MI / chest pain patient is (more often than not) in sufficient saturations (94-99%).

Pain is caused by a narrowing, vasospasm or clot blockage to a coronary vessel feeding oxygenated blood to a chunk of heart muscle.

When cardiac blood flow reduces, the cells suffer Ischaemia (hypoxia) not due to lack of oxygen in the blood, but lack of flow to tissue (perfusion).

The thought originally was improve O2 in blood, and we prove O2 cell delivery in what little perfusion we have. But it doesn't work.

It doesn't work.!!

When you increase O2 concentration in blood it dissolves more oxygen in plasma (Pa02). It doesn't carry more on haemoglobin. And high plasma concentrations (pressures) of oxygen exert a vasoconstrictor effect on coronary arteries.  

Doesn't  that seem dumb to you?  In Angina, or AMI, aren't we trying to improve blood flow?!!

Effect 2
Oxygen molecules when released to previously ischaemic cardiac tissue cause physical damage to the cardiac cell membranes.  This Oxidative burst results in the overproduction of oxygen free radicals.  Hydrogen Peroxide, superoxide dismutase, singlet oxygen, to name a few.  These substances are the route cause of the cell damage that occurs when we dissolve the clot or give GTN restoring blood flow.  This lipid peroxidation of the cell membranes is called Reperfusion Injury.  It destabilises action potentials in the cardiac mass , which leads to reperfusion arrhythmias.

So in a nut shell organisations are scrambling to change policies to ensure clinicians only use oxygen on patients in shock or those with desaturation. If sats are <94% Use oxygen, but if not, they don't need it, and it is probably doing damage.

ILCOR  and our own Australian Resuscitation Council are on it with guideline changes in 2010 as a result of Cabello's work.

The giants of the cardiac world Am Heart Assn , Australian Heart Foundation has given it the tick!

 Queensland Health is on it with policy written categorically stating to only oxygenate to maintain O2 above 93%. (PCCM 2011 page 80)

For more than 45 years we have known that oxygen delivery on chest pain patients is potentially damaging.  Use it judiciously.