Now I get it

COPD and oxygen administration for emergency paramedics

COPD and oxygen administration for emergency paramedics

For many years, the management of COPD patients was governed by the hypoxic drive theory. Patients who were administered high flow supplemental oxygen therapy during acute illness frequently deteriorated by becoming increasingly acidotic and the complications that went with that. The hypoxic drive is a very old school understanding and typical of so many things that were long thought to be for one reason when in fact they were quite another. Hypoxic drive is not a discredited element but it is not the main factor with only a few people being reliant on this entirely10.

COPD, itself a combination of the somewhat different diseases of emphysema and chronic bronchitis, has as its common core limitation of airflow through the lungs that is not well, if at all, reversible. Though it is easily associated with airway tissue of bronchi, bronchioles and alveoli, it can also involve considerable surrounding connective tissue destruction and inflammatory changes in the pulmonary vasculature. Inflammation, including due to smoking or infection, can produce changes in vascular endothelium. This in turn can lead to vascular responses such as vasoconstriction and vasodilation. Where this occurs in the longer term, as in COPD, it can also lead to changes in vascular structure8.

Hyperoxia normally causes vasoconstriction to reduce blood flow through the circulation and hypoxia to vasodilate3.  This is because the body does not really want either state. With hyperoxia it attempts to reduce oxygen delivery and hypoxia, the opposite. Hence supplemental oxygen can actually reduce blood flow through the brain circulation and coronary arteries by causing vasoconstriction.

It is well recognised now that oxygen should be delivered only where there is a genuine state of hypoxemia as guided by pulse oximetry. This is particularly so for patients with signs of acute coronary syndrome and stroke. It is even possible for 100% oxygen administration for ten minutes to increase vascular resistance in the left anterior descending artery by 23%10. That is, the ‘good gas’ itself reduced blood flow through a main coronary artery by one quarter, hardly a helpful feature in the setting of arterial occlusion and ischemia.

The pulmonary circulation is slightly different in that the pulmonary arteries, right through the pulmonary tree, have the means to regulate supply of blood flowing past the alveoli, likely through calcium regulation of smooth muscle. Hence they can constrict blood vessels and reduce blood flow where hypoxic alveoli are detected, the opposite of what usually happens6,9,11.  Normally attempts would be made to increase blood flow where hypoxia was detected. This difference though turns out to be a good defence point as it means that when some alveoli are under-ventilating, blood can be directed away from them to maximise blood flow past better working alveoli.  This helps to avoid shunting of blood past alveoli that will not oxygenate it on the way through. It is an effective way to maintain the normal balance between ventilation and perfusion11.

The reverse actions within the pulmonary circulation are thought to have derived from the in utero need to keep blood away from non-inflating lungs but then increase blood flow to the lungs with oxygen appears in the alveoli3.

That is good of course except if you now administer supplemental oxygen and fool the body into thinking things aren’t so bad after all. Now blood flow can be restored to those poorly ventilating parts of the lungs. The effect is that blood goes back to passing alveoli that are not effectively ventilating.  In essence blood is being shunted past, creating a ventilation perfusion mismatch. In this case more perfusion without a corresponding increase in ventilation. That is, increased oxygen might diffuse in, but there may not be much increase in removal of carbon dioxide back out through these under-ventilating alveoli. The fuel for respiratory acidosis remains in circulation.

It is understood that high flow oxygen therapy during acute COPD exacerbation is associated with increased mortality, duration of hospital stay and high dependency and ventilation needs. Where this high flow is reduced to titrated lower flows, all of these measures improve. In particular, increased respiratory acidosis is produced with higher flows that can often be reduced with lower amounts of oygen1. Titrating pulse oximetry between 88 and 92% could reduce risk of death by as much as 78% in known COPD patients1. At the other end, as many as one in fourteen patients would die if administered uncontrolled high flow oxygen therapy1. That should satisfy the statisticians.

In short, patients managed in pre-hospital time frames, typically less than an hour, are more likely to develop respiratory acidosis and respiratory failure if administered supplemental oxygen therapy not supported by a reduced pulse oximetry target range.

Then you add to this what is known as the Haldane effect.  Keep in mind that the extra fuel for respiratory acidosis is still present because there has not been a corresponding increase in ventilation. When haemoglobin is not holding oxygen, it can bind with more carbon dioxide.  The hypoxia helps reduce acidosis. In COPD you have lots of CO2.  In sick COPD you have even more.  Additional oxygen therapy without altering ventilation means that more oxygen can combine with more haemoglobin. That in itself might sound good, but the price is it displaces the carried CO2.  That’s the bad bit.  It cannot be easily ventilated away hence it now contributes to the respiratory acidosis worsening10,11,13.

That all said, it must be absolutely stated that all of this is very poorly understood and even these explanations do not reliably cover every observation of the acidotic deterioration in COPD patients following high flow oxygen administration9,12,13.

That is not to say that there is no role for oxygen therapy for COPD patients. Clearly, in the acute exacerbation stage, titrating to pulse oximetry levels of 88 – 92% is associated with improved outcomes. Further, patients who have severe demonstrable hypoxemia when at rest will benefit in quality of life measures when administered low flow long term oxygen therapy. This does not translate to patients who have less severe signs of the disease so recipients must be carefully chosen2.

These pulmonary responses to acute hypoxia and supplemental oxygen therapy produce long term consequences where chronic illness exists including COPD in particular.  Prolonged vasoconstriction in the pulmonary circulation on a large scale leads to pulmonary hypertension.  The initial endothelium induced inflammatory vascular response is eventually followed by thickening of the vascular smooth muscle intima7.  This so called ‘remodelling’ of the arteries changes blood flow through them that is more problematic and difficult to manage.  Current therapies include long term low flow oxygen therapy to try to avoid the problem happening with research evaluating the role of vasodilators such as calcium channel blockers and others4,5.

Though alveolar hypoxia alone can contribute to the pulmonary arterial intima thickening, the addition of smoking related inflammation with the vasculature worsens the overall effect considerably, at least in guinea pigs anyway7.  Apparently smoking is bad for guinea pigs also.

Jeff Kenneally www.prehemt.com

  1. Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. Bmj. 2010 Oct 18;341:c5462
  2. Stoller JK, Panos RJ, Krachman S, Doherty DE, Make B. Oxygen therapy for patients with COPD: current evidence and the long-term oxygen treatment trial. CHEST Journal. 2010 Jul 1;138(1):179-187
  3. Weissmann N, Sommer N, Schermuly RT, Ghofrani HA, Seeger W, Grimminger F. Oxygen sensors in hypoxic pulmonary vasoconstriction. Cardiovascular research. 2006 Sep 1;71(4):620-629
  4. Zakynthinos E, Daniil Z, Papanikolaou J, Makris D. Pulmonary hypertension in COPD: pathophysiology and therapeutic targets. Current drug targets. 2011 Apr 1;12(4):501-513
  5. Rowan SC, Keane MP, Gaine S, McLoughlin P. Hypoxic pulmonary hypertension in chronic lung diseases: novel vasoconstrictor pathways. The Lancet Respiratory Medicine. 2016 Mar 31;4(3):225-236
  6. Sajkov D, Mupunga B, Bowden JJ, Petrovsky N. Pulmonary Hypertension in Chronic Lung Diseases and/or Hypoxia.2013. Chapter 2
  7. Blanco I, Piccari L, Barberà JA. Pulmonary vasculature in COPD: The silent component. Respirology. 2016 Jan 1
  8. Gassama A, Turner A, Egginton S, Kumar P. Effects of hypoxia & inflammation on vascular reactivity in rats: a model of co-morbidities in chronic obstructive pulmonary disease?. In Proceedings of The Physiological Society 2013. The Physiological Society.
  9. Ariyaratnam P, Loubani M, Morice AH. Hypoxic pulmonary vasoconstriction in humans. BioMed research international. 2013 Aug 20;2013.
  10. Cornet AD, Kooter AJ, Peters MJ, Smulders YM. The potential harm of oxygen therapy in medical emergencies. Critical Care. 2013 Apr 18;17(2):1
  11. Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Critical Care. 2012 Oct 29;16(5):1
  12. Littleton SW. Hypercapnia From Hyperoxia in COPD: Another Piece of the Puzzle or Another Puzzle Entirely?. Respiratory care. 2015 Mar 1;60(3):473-475
  13. Brill SE, Wedzicha JA. Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2014 Jan 1;9:1241-1252

3 thoughts on “COPD and oxygen administration for emergency paramedics

  1. ayrat / Reply August 23, 2016 at 7:36 pm

    Paramedics transported all patients to a single receiving facility. The researchers instructed the ED staff to refrain from altering the prehospital oxygen administration rates until after obtaining arterial blood gas samples.

  2. telgen / Reply August 25, 2016 at 7:58 pm

    During the 1950s and 60s, it was postulated that administration of high concentration oxygen to patients dependant on hypoxia to stimulate their breathing might lead to a progressive decline in this

  3. Alfie / Reply August 25, 2018 at 10:48 pm

    Thanks for the terrific guide

Leave a Reply

Your email address will not be published. Required fields are marked *