Pulmonary diseases and oxygen therapy

Question

The team first aid guidelines in France say that for an adult victim, a saturation (SpO2) below 94 triggers the administration of 9L/min of oxygen using a non-rebreather mask. We first aid guys are not doctors, so we strictly apply this rule before reporting to the medical control.

However, I noticed that when the victim is known or suspected¹ to have certain pulmonary diseases², we are instructed to reduce the oxygen flow to 2L/minute or so, even if the SpO2 is still low³. This happens either when we contact the medical control or when a doctor arrives on the scene by request.

I find this interesting, so the following questions:

• Is there a precise pulmonary diseases list that require oxygen therapy to be handled that way ?
• Why could a high O2 flow be deleterious for these particular diseases and not others?

This is just curiosity. I mean by this that I won't try to anticipate should such a case occur again in the future: it's only up to the doctor to order an oxygen flow that doesn't appear in the first-aid guidelines.

---

Footnotes:

¹ We don't determine that by ourselves, a doctor does.

² Not completely sure of what kind. Thanks to @anongoodnurse's heads-up I could determine that some of them were diagnosed or suspected COPDs, and some of them unknown to us (we were just not told what was precisely diagnosed or suspected).

³ The doctor can instruct us to do this, even if not according to the first-aid guidelines, as he/she has a higher competence.

Answer 1

The basic idea is that people with pulmonary diseases that involve chronic hypoventilation rely on mild hypoxia to stimulate respiration.

To understand this, consider a basic homeostatic feedback loop that controls respiratory drive. During a breath hold, carbon dioxide levels rise and oxygen levels fall. Carbon dioxide diffuses across the blood-brain barrier and causes a decrease in CSF pH sensed at central chemoreceptors in the brainstem. The peripheral serum pH may also be depressed, stimulating peripheral chemoreceptors in the carotid and aortic bodies. In normally ventilating people, these "hypercarbic indicators" are the primary mediators of the drive to breath.

In patients with chronic hypoventilation, PaCO₂ is chronically elevated. Common hypo-ventilatory diseases include:

• COPD (chronic obstructive pulmonary disease)
• obesity-hypoventilation syndrome
• neuro-muscular weakness syndromes (generally only in later phases when the diaphragm is affected: Becker/Duchenne muscular dystrophy, amyotrophic lateral sclerosis, etc.)

The old theory goes that because these folks have chronically elevated PaCO₂*, the hypercarbic respiratory feedback loop described above “acclimates” and is no longer the primary driver of breathing. Instead, they rely on the hypoxic respiratory drive, which is secondary in normal people. These individuals may have a usual SpO₂ ~88-90%. When a non-rebreather mask is applied and suddenly drives their SpO₂ up to 100%, their respiratory drive decreases because their blunted hypercarbic response mechanisms do not respond normally to the progressive rise in PaCO₂.

There are data in support of this theory. One study in COPD patients administered 100% oxygen to patients with COPD and observed a 18% decrease in ventilation after 15 minutes that returned to baseline when oxygen was removed (Aubier). However, these authors also showed that two other factors were at play explaining the observed rise in PaCO₂:

1. About 30% of the increase in PaCO₂ associated with high-flow oxygen administration was attributable to the Haldane effect, which is basically an offloading of CO2 by hemoglobin (due to a rightward shift of the carboxyhemoglobin dissociation curve), increasing the CO₂ dissolved in blood but not reflecting a true change in ventilation.

2. An additional 48% of the increase in hypercapnia was due to dead space ventilation. The simplified idea is that the vessels in the lung compensate for hypoxia by vaso-constricting areas with low oxygen tension, so-called ventilation-perfusing matching. When high-flow oxygen is administered, the vaso-constriction is released so perfusion of poorly ventilated areas increases. Now a higher percentage of the blood is not being cleared of CO₂. This is called ventilation-perfusion ​mis​matching.

Something similar has been demonstrated in patients with obesity-hypoventilation (Wijesinghe). In light of this, a recent study investigated the best strategy for oxygen administration in patients with chronic hypoventilation (Kim). They found that a strategy titrating oxygen administration to achieve SpO₂ 88% to 92% minimized the risk of worsening hypoventilation while achieving adequate relief of shortness of breath and adequate oxygenation.

A helpful review of these topics provides a bit more detail for those interested (Abdo).

---

_{Abdo WF and Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.}

_{Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, Derenne JP. Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis. 1980 Nov;122(5):747-54.}

_{Kim V, Benditt JO, Wise RA, Sharafkhaneh A.Oxygen therapy in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2008 May 1;5(4):513-8.}

_{Wijesinghe M, Williams M, Perrin K, Weatherall M, Beasley R. The effect of supplemental oxygen on hypercapnia in subjects with obesity-associated hypoventilation: a randomized, crossover, clinical study. Chest. 2011 May;139(5):1018-24. .}

---

_{*normal PaCO2 = 40 mmHg; may be 50-80 mmHg in chronic retention, possibly higher}