To recap the last blog post about the importance of counting respiratory rate:
- Ventilation is the physical movement of air in and out of the lungs
- In a normal person, it is an elevated carbon dioxide level in our bodies that causes the respiratory centre in our brain to initiate a breath
- When we experience a failure to ventilate, we have a problem with our carbon dioxide
- A decrease in oxygen saturations only occurs at the point of decompensation when the patient can no longer keep up the ventilation effort/work of breathing to clear their carbon dioxide
- A failure to ventilate is known as type 2 respiratory failure, defined as elevated carbon dioxide levels and low oxygen levels
- Low oxygen levels in a patient failing to ventilate is a late sign and deterioration should be picked up earlier by monitoring the trend of the respiratory rate and work of breathing
In this blog post, we are going to discuss respiration and the relationship between oxygen saturations and the partial pressure of oxygen (PaO2) in our bodies when we are experiencing a failure to oxygenate (type 1 respiratory failure). Respiration is defined as the process of gas exchange, namely carbon dioxide and oxygen. It occurs at the end point of our lungs known as the alveoli. When we ventilate air from the atmosphere into our alveoli, there is more oxygen in the air in our alveoli than there is in blood that is passing our alveoli. Therefore, oxygen moves via diffusion from an area of high concentration (alveoli) to an area of low concentration (blood). The oxygenated blood carries the oxygen around the body to be used up by the various cells in our bodies.
There is one important thing you must understand about oxygen; it is a terrible swimmer! What do I mean by that? I mean that it struggles to move around efficiently when it is sitting in fluid of any kind. So when it enters the bloodstream, it needs something that will help carry it around otherwise it will float around the blood inefficiently. Oxygen therefore attaches itself to the haemoglobin in our body and uses the haemoglobin as a transport device to help move it around the body to the cells that require oxygen to function. The important thing to note here is that in order for our cells to be able to use the oxygen, oxygen needs to de-attach itself from the haemoglobin and be freely floating around the blood once again.
Think of our alveoli as country A, our cells as country B, oxygen as the people and the haemoglobin as the cruise ship that gets the people from country A to country B. If the people don’t get on the cruise ship when they step off the dock at country A, they will float around in the water and never get to country B. If they get on the cruise ship and make it to country B, they need to get off the cruise ship if they want to step onto the dock of country B. If they don’t get off the cruise ship, they make the return trip to country A. With this analogy in mind, consider that oxygen moves from our alveoli into our blood stream. It attaches to haemoglobin that moves it around the body to the cells that require oxygen. The oxygen de-attaches from the haemoglobin and is taken up by the cells that required it. If the oxygen does not de-attach from the haemoglobin, it will be carried back to the lungs again without being used.
So what is the relationship between oxygen saturations and PaO2? The amount of haemoglobin in the body that has oxygen attached is our oxygen saturations. The normal range for oxygen saturations are between 95 – 100%. The amount of oxygen floating around in the bloodstream without being attached to any haemoglobin is our PaO2. The normal range for PaO2 is between 80 – 100 mmHg. As cells use up the floating oxygen, the PaO2 begins to fall. To maintain an equilibrium, the oxygen on the haemoglobin de-attaches (dissociates) to float in the bloodstream ready to be used by the cells. For this reason, oxygen saturations and PaO2 have a predictable relationship which is often denoted by the oxy-haemoglobin dissociation curve.
There are a couple of things that can be immediately identified on this curve:
- Respectively, oxygen saturations of 95% and 100% match with a PaO2 of 80 and 100, which is where the normal range for PaO2 is derived from
- The red line can never go vertically higher than 100% because haemoglobin cannot be more than 100% saturated
- The red line can extend horizontally well beyond the constraints of this graph because there is plenty of room for oxygen to float around in the blood, often up to a PaO2 of 600mmHg when normal lungs are exposed to high enough levels of oxygen for long enough periods of time
- The red line experiences a steep drop when oxygen saturations fall below 90%, which is very technically known as the “slippery slope” – the further down the slope you go, the more easily oxygen dissociates from the haemoglobin and the quicker your oxygen saturations are going to drop
- Notice how a 20 mmHg drop in PaO2 from 100 mmHg to 80 mmHg only causes a 5% reduction in oxygen saturations
- Now notice how a 20 mmHg drop in PaO2 from 40 mmHg to 20 mmHg causes a massive 40% reduction in oxygen saturations
Unlike ventilation problems, oxygenation problems are easy to identify simply by the oxygen saturations trending down. Remembering that oxygen is not a very good swimmer, oxygen is not going to get very far if there is any fluid in the alveoli. As a result, the capacity for the body to get oxygen from the alveoli into the bloodstream to the cells diminishes. Imagine Mr Wilson has lungs that are partially filled with water; how well is oxygen going to be able to swim through the water in order to get to the edge of the alveoli and facilitate gas exchange into the bloodstream?
Mr Wilson has no issues ventilating and getting air into his lungs, his body has an issue with the ability to move the oxygen in the air from his alveoli into the bloodstream. It is only when Mr Wilson’s oxygen saturations drop below 90% that we start seeing an increase in respiratory rate. This is a backup feature the body has to attempt to get more air into Mr Wilson’s lungs in order to help optimise gas exchange. If this doesn’t work, Mr Wilson’s oxygen saturations and PaO2 will continue to fall to the point where his cells can no longer function effectively, if at all. Failure to oxygenate is also known as type 1 respiratory failure and is defined as a decreased PaO2 with a normal carbon dioxide level. The reason for why oxygenation problems do not result in a high carbon dioxide level is because unlike oxygen, carbon dioxide is a fantastic swimmer that will make it’s way through the bloodstream and into the alveoli, even if there is fluid in the alveoli. Then the carbon dioxide in the lungs are simply ventilated away.
Remember the following:
A failure to oxygenate causes a decrease in oxygen saturations and PaO2
Oxygen is 1 word
Therefore, a failure to oxygenate is type 1 respiratory failure
When you consider what you have read in this blog post and in the previous blog post, consider this very important notion. A failure to ventilate will eventually cause issues with oxygenation and likewise, a failure to oxygenate will eventually cause issues with ventilation. Despite having independent reasons that can cause a patient to deteriorate, ventilation and oxygenation are also co-dependent. It is always easier to fix a problem when there is only one problem, a bit more difficult when another problem is introduced. So aim to pick up the deterioration early and avoid having to deal with the age old question: which came first, the ventilation problem or the oxygenation problem?
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