In 2010 most of the resuscitation councils in the universe made interesting changes to the use of oxygen for ischaemic chest pain and MI. It was a final straw in the oxygen coffin culmination from 50 years of its use being complete dogma. While the cardiology world and its protocols are largely on board with this global reluctance to apply oxygen to chest pain /MI patients, there exists a sense in nurses that we just go with the flow and just do what we are told without understanding the reasons for change.
So let's explore the three reasons oxygen is no longer "routinely" used, and I emphasise "routinely used", because we all know that there are clear indications eg hypoxaemia (Sats <94%).
1. They are not Hypoxaemic.
Haemoglobin, that oxygen carrying protein in your red blood cells holds 4 molecules of oxygen. When it does it is full, and can't hold more, it is what we call "100% Saturated". In patients with cardiac chest pain their sats are normal (SpO2 94-100%), so their haemoglobin can't carry any more than it already has loaded. Ischaemic chest pain is ... Wait for it ... Ischaemic. The hypoxia of cardiac tissue is caused by ischaemia which means poor perfusion or blood flow. The ischaemia is due to vessel spasm (angina) or a physical blockage of a coronary arteriole from a clot. The blood dammed up behind the blockage is well oxygenated, it just can't get through. If the Sats are fine, then oxygen is unnecessary, they already have all they need.
2. Vessel size.
In chest pain management, the focus of interventions is placed on improving blood flow to the oxygen starved muscle (perfusion). The GTN you give, the rest, the morphine and even the Aspirin all aims to relax the blood vessel walls that are restricting blood flow. On the other hand, we have previously administered oxygen routinely, thinking that this is what they need, when we missed an important property of oxygen; it is vasoconstrictive. During gas exchange in the lungs, oxygen saturates available haemoglobin sites, while dissolving into the plasma, exerting oxygen tensions higher that the 80-100mmHg normal. In fact breathing oxygen from a simple face mask at 6-8 lpm is 3 x as concentrated than room air. This high concentration of breathed oxygen increases plasma oxygen tension vasoconstrictive heights. Doesn't it seem a bit dumb to give all these vasodilation, vessel relaxation, perfusion improving drugs, and at the same time, give oxygen which is profoundly vasoconstrictive? Yep... Dumb.
Counter productive in fact.
3. Oxygen destroys cells
Big call I know, but in normal physiology, some oxygen we consume becomes radicalised. Oxygen is stable in its O2 configuration. During metabolism some splits in to radically reactive single atoms which bind to other substances in your body to form damaging and corrosive molecules called "oxygen free radicals". An example is hydrogen peroxide formed when a single oxygen (O) binds to water (H2O). The resulting H2O2 causes damage to cell membranes, especially previously hypoxic ones like heart and brain tissue. Your cell membranes are made of fat (lipids). Cell membranes are called a phospholipid bilayer, and if there is one thing H2O2 loves to attack, or "oxidise" it is cell membranes. The more oxygen you breathe, the more free radicals you make. In chest pain management, this oxidisation of cell membranes targets ischaemic cardiac cells, and destroys them (necrosis). It is called lipid peroxidation.
Filling up a patient with oxygen while waiting for the clot to be dissolved, allows for the formation of these reactive oxygen species (free radicals). Now the blockage is dissolved, and a flush of highly concentrated oxygen free radical blood floods the ischaemic tissue, causing a wave of destruction. This is called an oxidative burst or more commonly, reperfusion injury.
There it is. Three reason to be weary of oxygen in chest pain.
1 they don't need it
2 it narrows and reduces flow
3 it damages cardiac tissue
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