CO2 retention

#KYJ - CO2 retention

In our #Pirate seminar and #RespNursing we touch on CO2 retention.   It’s a commonly used term, and most nurses will recall hearing it, and associating it with end stage COPD.

That said, do you know what it means to be a carbon dioxide retainer?  Where is the CO2? Where does it come from? And; given that the patient is still breathing, why are they not just blowing it off?

Ok.   Take a deep breath...

Physiology refresh: cells burn glucose with oxygen to make energy (ATP).

Like all engines that burn carbon, (wood on a furnace, petrol in a car, diesel in a truck) so too, glucose in a cell produces   Carbon dioxide (CO2) as a waste gas.

Now stay with me ...

As cells produce CO2, this diffuses into the extra cellular fluid around the cells.   Now capillary blood in close proximity to those cells absorbs this CO2 and two things happen.

The capillary plasma pH drops (CO2 is acidic) so blood becomes acidic.  This also causes micro-vessel dilation.

Entrapped acidic blood in engorged dilated vessels now slows and saturates with CO2, red blood cells off load their oxygen, now freeing up space to absorb the CO2 and transport it to lungs to be blown off (expelled).

So a couple of things here.  

Oxygen binds to haemoglobin;

but so does CO2.  

As the blood cell carrying oxygen starts to off load the oxygen in these peripheral tissues, CO2 hops on because there is space in the RBC.

Think of a bus full of footballers arriving at the field, they get off the bus, and now there is space for the cheerleaders to get on the bus.  

Ok- enter the world of lung disease.  Chronic bronchitis, asthma and alveolar destruction called emphysema.  

Now slowly and insidiously over years, the person with lung disease reduces their oxygen carriage, and subsequently increases CO2 carriage.  They start accumulating more carbon dioxide in blood.  Now this blood should normally just release it’s CO2 in the lungs, but remember, these are the same chronically diseased lungs that had reduced oxygen exchange, so they also have diminished CO2 diffusion and off-gassing.

They start becoming slowly hypoxaemic (lower sats), and slightly CO2 retentive. Slightly more acidic-slightly more vasodilated.  As lower oxygen levels reach the tissues, cells now starving for oxygen (hypoxia), start burning more glucose (carbon) to attempt to make energy anaerobically (lacking oxygen).  

As more glucose is burned, then more carbon dioxide is produced.  This is the cause of increasing levels of carbon dioxide in tissues.  As tissue CO2  levels increase, then blood CO2 levels also increased.

Diseased lungs can’t off gas it, so it becomes retained in tissues and in blood. Now- acidic blood has another interesting property... it won’t carry oxygen.  So this is a downward spiral where the diseased lungs won’t in-gas oxygen, and acidic blood is reluctant to transport it.  Acidosis leads to hypoxia leads to CO2 retention leads to acidosis; and around it goes.

So we think that oxygenating these guys should help, but remember the bus?  If you fill it with footy players, there is no room to transport the cheerleaders.

CO2 retention is worsened by unnecessarily oxygenating end-stage COPD patients.  Allow SpO2 levels of 88-92% in these patients if not distressed. And if you must oxygenate them, just enough (1-2lpm via Nasal prongs) to get their sats into the 88-92% range.

For years we’ve taught the dogma of “Hypoxic Drive” in CO2 retainers; and cautioned clinicians against giving oxygen for fear the patient would stop breathing.  Well we had it wrong.  By all means withhold oxygen as a routine, but it is for worsening of CO2 retention, not loss of drive to breathe.

CO2 retention like the COPD disease pathophysiology is complex, and slow to develop, but one thing is certain, unnecessary oxygen exacerbates it.

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