We’ve all heard it at some point or another: “Don’t give that COAD patient too much oxygen”. It has led us to believe that oxygen is a REALLY bad thing in patients with chronic obstructive airways disease (COAD). This has caused nurses to be afraid to put oxygen on a COAD patient with low oxygen saturations; yes, even with the REALLY low oxygen saturations! Why? Because of a little something known as the hypoxic drive…
Let’s Start With Respiratory Physiology
Central chemoreceptors are found in the cerebrospinal fluid (CSF) and are sensitive to changes in pH. Changes in pH can occur as a result of changes in the level of carbon dioxide (CO2) within the body. When there is an increased level of CO2 in the body, CO2 will bind with water (H2O) within the CSF to convert into carbonic acid (H2CO3 ) which in turn releases hydrogen ions (H+) that lower the pH. When there is a decreased level of CO2 in the body, hydrogen ions will bind with bicarbonate ions (HCO3–) and convert into carbonic acid and then convert into CO2. This equilibrium is maintained by the respiratory centre establishing a respiratory rate that maintains CO2 within the normal range of 35 – 45 mmHg and pH within the normal range of 7.35 – 7.45.
As the respiratory centre becomes aware of a decreasing pH from the central chemoreceptors, it will innervate the diaphragm causing the person to take a breath. In people with chronically high levels of CO2, such as COAD patients that are CO2 retainers, the normal breathing mechanics involving central chemoreceptors would result in an unwanted high respiratory rate. The body gradually starts to develop a progressive ventilatory desensitisation to CO2, as bicarbonate ions increase to bind with hydrogen ions in order to achieve a pH level that is within the normal range. This is known as metabolic compensation. As a result, the body switches over to what is known as the “hypoxic drive” and utilises the peripheral chemoreceptors found in the aortic arch and bifurcation of the carotid arteries instead. Peripheral chemoreceptors are sensitive to low oxygenation levels. As the respiratory centre becomes aware of a PaO2 falling below 60 mmHg which approximately correlates with an oxygen saturation of 90%, it will innervate the the diaphragm in order to make the person take a breath.
The Hypoxic Drive Theory
So the hypoxic drive theory is as follows: if you give a CO2 retainer too much oxygen, their PaO2 will increase and you will knock out their hypoxic drive to breathe therefore causing apnoea. However, their central chemoreceptors are still working enough to signal the brain to breathe to bring their CO2 levels back into a range that is normal for them. Therefore, the hypoxic drive theory is debunked! And even if you are unconvinced that this is the case, the hypoxic drive only starts to theoretically be affected when the patient’s oxygen saturations are more than 90%. So if your COAD patient has low oxygen saturations, put oxygen on them until they have an oxygen saturation at least 90%. There have been many a MET call that I have arrived to with a COAD patient that has oxygen saturations of 75% with 2 L/min of oxygen via nasal prongs because “they are a CO2 retainer and I didn’t want to give them too much oxygen”. Want to know the first thing I do when I arrive? I put on a hudson mask on this COAD patient with oxygen saturations of 75% and I turn the oxygen flow up, up and up. If there is only one thing that you remember after reading this article, let it be this:
Your patient will die of HYPOXIA before they die of APNOEA!
The current evidence for managing an acute COAD exacerbation is to titrate oxygen therapy to an oxygen saturation between 88 – 92%. This is most likely due to our long time belief in the hypoxic drive and a small study of 405 patients in 2010 that demonstrated a lower mortality rate in patients titrating oxygen to oxygen saturations of 88 – 92% compared to the patients receiving high flow non-titrated oxygen. This has further cemented the view that giving oxygen to a COAD patient is bad. However, giving high flow non-titrated oxygen to ANY patient is bad! The increased mortality rate with the high flow non-titrated oxygen COAD group could therefore be attributed to the deleterious effects observed with oxygen toxicity. Oxygen toxicity has been associated with various clinical consequences including diminished lung volumes, hypoxemia due to absorptive atelectasis, accentuation of hypercapnia, and damage to airways and pulmonary parenchyma. Until we have further evidence that may demonstrate that higher saturation levels in the COAD patient are non-detrimental, aim for 88 – 92%.
Bottom line: if your patient is hypoxic, turn up the oxygen! Get them to this acceptable range of 88 – 92% and then wean back your oxygen to the lowest possible flow rate to maintain this range. The only time you are going to see a CO2 retainer lose their drive to breath due to an increase in oxygen is when you have someone who is struggling to breathe, is worn out, and has fatigued their respiratory muscles to the point where they have no further capacity to blow off the excess CO2. But guess what? This is called type 2 respiratory failure and a “normal” patient will also have a similar outcome in the same situation!
Consider the scenario of a COAD patient that arrived to the emergency department with a respiratory rate of 45 bpm and oxygen saturations of 70% on room air. An arterial blood gas was done and showed a PaO2 of 44 mmHg, PaCO2 of 66 mmHg and pH of 7.35. The nurse on the shift put 10 L/min of oxygen via a face mask on the patient and after a few minutes, the patient’s respiratory rate was 26 bpm with a much less laboured respiratory effort. Another arterial blood gas revealed a PaO2 of 90 mmHg, PaCO2 of 80 mmHg and pH of 7.25. Did we knock out the patient’s drive to breathe? Or did we relieve the hypoxia sufficiently that it allowed the patient to return to a normal breathing pattern for them? But what about the rise in CO2? This is actually attributed to a ventilation/perfusion (V/Q) mismatch and something known as the Haldane effect.
V/Q Mismatch in the COAD Patient
The body is very clever at trying to keep us alive! So in the chronic COAD patient with some alveoli that may not ventilate as well, the body overcomes this through hypoxic vasoconstriction of the pulmonary vasculature to direct blood to the alveoli that are functioning well. Therefore, the V/Q match is enhanced and gas exchange is optimised. Giving these patients oxygen overcomes the hypoxic vasoconstriction observed, and there is an increased blood flow to the poorly ventilated alveoli that results in a V/Q mismatch for the patient. As a result, gas exchange is compromised affecting both PaO2 and carbon dioxide.
The Haldane Effect in the COAD Patient
Deoxygenated haemoglobin tends to hold on to carbon dioxide with a greater affinity than oxygenated haemoglobin. So when our patient arrived in the emergency department with oxygen saturations of 70% and a PaCO2 of 66 mmHg, the deoxygenated haemoglobin could have been holding on to a fair amount of carbon dioxide that wouldn’t show up on the arterial blood gas. The Haldane effect occurs when the oxygenated haemoglobin release the carbon dioxide that they were holding in their deoxygenated state, causing a rise in the PaCO2. If the patient has not fatigued their respiratory muscles at this point, hypoxic drive or not, their central chemoreceptors will sense the carbon dioxide level rise outside the normal parameters for the patient, and will increase their respiratory rate to clear the additional carbon dioxide. If the Haldane effect causes the carbon dioxide to be persistently high with a low pH, we need to be on the look out for impending type 2 respiratory failure and have our non-invasive or intubation equipment ready.
What Does That Mean For Your Practice?
It is possible to survive a severe respiratory acidosis with no adverse outcomes provided that oxygenation and circulation are maintained. The issue with a patient that is not breathing, is that they are not oxygenating. Remember: your patient will die of HYPOXIA before they die of APNOEA! So when in doubt, oxygen is the good guy! But as with everything in life, all in moderation! Let’s not leave our poor COAD patient’s in a hypoxic state any longer; the hypoxic theory has been debunked!
- Austin, M. A., Willis, K. E., Blizzard, L., Walters, E. H., & Wood-Baker, R. (2010). Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomised controlled trial. The British Medical Journal, 341(c5462), 1-8. doi: 10.1136/bmj.c5462
- Abdo, W. F., & Heunks, L. M. (2012). Oxygen-induced hypercapnia in COPD: Myths and facts. The Journal of Critical Care, 16(5), 323 – 327. doi: 10.1186/cc11475
- Feller-Kopman, D. J., & Schwartzstein, R. M. (2015). Mechanism, causes and effects of hypercapnia. Retrieved from: https://www.uptodate.com/contents/mechanisms-causes-and-effects-of-hypercapnia
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- Life in the Fast Lane. (2014). Oxygen and CO2 retention in COPD. Retrieved from: http://lifeinthefastlane.com/ccc/oxygen-and-co2-retention-in-copd/
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- Stoller, J. K., Barnes, P. J., & Hollingsworth, H. (2016). Management of exacerbations of chronic obstructive pulmonary disease. Retrieved from: https://www.uptodate.com/contents/management-of-exacerbations-of-chronic-obstructive-pulmonary-disease
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