The Hypoxic Drive Theory: completely debunked

(This is part five of a six post series. To go to part one click here.)

I hope my readers understand by now that there is a hypoxic drive, but the hypoxic drive theory is not true. This is a distinction that is very important when providing adequate care for our COPD patients.

I mentioned this before on my blog, that only a small percentage of COPD patients are real chronic CO2 retainers. Thus, 70% of COPD patients can and should be given oxygen as they need it. And even the remaining 30% should get oxygen as they need it regardless of the hypoxic drive.

Read on I'll explain.

Here's one recent example. The COPD patient was in the emergency room for 8 hours on a 75% non-rebreather. His PO2 was only 70 on the mask. His CO2 was 45 (no big deal), and his HCO3 was 27. Usually, chronic retainers have a chronically elevated HCO3 level. So, upon the initial ABGs, I surmised the patient was not a retainer.

The patient was awake, alert and was still slightly labored, but his gases were improving. He was moved upstairs. The admitting doctor wrote this order: "Oxygen at 2.5 lpm and never higher."

I talked to the doctor and told him that the patient had been in the ER for eight hours and did not have any complications to the high oxygen level, but he said he didn't care. "We have to take care of our CO2 retainers," he said, and hung up.

This is what we call taking the hypoxic drive theory overboard.

Another patient who was an end stage COPD patient came into the hospital by ambulance with a 75% nonrebreather on. He had this mask on for about 45 minutes. The patient never showed any complications to the high oxygen.

If the hypoxic drive theory is true, then why didn't this patient stop breathing? Wasn't this oxygen supposed to knock out his drive to breathe.

One doctor even went as far as to tell this man was going to die with in the next two weeks, and more than likely because in order to maintain a PO2 of 50, he needed an FiO2 of 100%. According to the doctor, this man was going to die of hypoxemia (low blood oxygen) or we will simply knock out his drive to breath. This man was given a 10% chance of living.

Well, guess what? This man survived four days on 100% oxygen.

Ironically, he was eventually discharged to home on 2lpm, and the next time he came in with a similar problem, the doctor refused to allow us RTs to put his oxygen on anything higher than a 40% ventimask because "he's a chronic retainer. We don't want to knock out his drive to breathe."

Needless to say, I cringed.

Now, According Jeff Whitnack, RRT/RPFT in an online article he wrote called "The Death of the Hypoxic Drive Theory," the hypoxic drive accounts for approximately 10-15% of a person's drive to breathe. So that's a little lower than the 30% I estimated earlier. Some have it even lower.

"We all have it," he writes, "unless perhaps we've had bilateral carotid surgery. It becomes obliterated at a PaO2 about 170, and becomes a greater stimulus as the PaO2 drops below 70, and especially below 50."

But this is not what causes CO2 retainer's CO2 to go up when he or she is given high amounts of oxygen. There are other factors at play here, and they are called the Haldane Effect and V/Q mismatching. (I covered these in yesterday's post)

Let me sum this us: Yes, there is such a thing as the hypoxic drive. If you give a CO2 retainer too much oxygen, you will knock out his hypoxic drive. But the central chemoreceptors will still work enough to signal the brain to breathe. Thus, the hypoxic drive theory is debunked.

As you increase the oxygen of 90% of COPD patients their CO2 will go up. That's just common knowledge. But the CO2 does not go up because you knocked out their hypoxic drive. Their CO2 goes up due to V/Q mismatching about 70% of the time, and the haldane effect the other 30% of the time.

Likewise, COPD patients who are not labored and not fatigued will blow off that extra CO2 just like a normal person would. Thus, that extra oxygen will not knock out this stable COPD patient's drive to breath.

And, even if they don't blow off that CO2, it will not be a big deal. All COPD patients have their CO2 levels rise from time to time. It does not kill them. What kills them is lack of oxygen.

When you have a chronic CO2 retainer in the emergency room of whom is struggling to breathe, already has a high CO2 level, and has worn out, fatigued, respiratory muscles and no further capacity to blow off the excess CO2, then these patients are the ones you have to worry about knocking out their drive to breath when you increase their FiO2.

Thus, yes, a high level of oxygen given to a COPD patient can still knock out his drive to breath, can cause them to become lethargic, and can cause them to go into cardiopulmonary arrest, but only when the patient is already compromised, and still only to about 30% of Chronic retainers.

So, if a COPD patient comes into the hospital, is in respiratory distress, and requires more than a 40% FiO2 to maintain an appropriate SpO2, it is acceptable to give them the oxygen they need. It is mandatory to give them the oxygen they need.

However, Whitnack writes, if their CO2 goes up over 90, and they become lethargic, "one should not fear apnea and cardiopulmonary arrest when giving oxygen to a patient with an exacerbated obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation."

Back when Whitnack wrote his article (I believe it was in 2000), I'm not sure if BiPAP was used regularly on COPD patients, but it is now. I find that as the CO2 rises and PO2 falls on COPD patients, a trial of BiPAP usually works well, if they can tolerate it. Most of the time when a patient is sick enough they tolerate it just fine. If not, a small dose of a sedative or xanax work well in this situation.

If the patient is not a DNR (Do Not Resuscitate) patient, and they do not tolerate the BiPAP, mechanical ventilation is always an option.

At the same time, however, whether we resort to BiPAP or mechanical ventilation or not, the patient should definitely get adequate oxygenation, even if that means 100% FiO2. (However, this should be titrated down as fast as possible while maintaining an appropriate SpO2).

Historically, according to Egan, an appropriate, acceptable, SpO2 is anything between 80-90%, or a PO2 of 50-60. However, if the patient does not show signs of oxygen toxicity, an SpO2 of 92% should be maintained.

In light of recent evidence, and understanding now that the hypoxic drive theory is not true, and that V/Q mismatching cause CO2 to rise in most of these situations, medical staff should feel comfortable adequately oxygenating a majority of COPD patients without worrying about their respiratory drive.

Whitnack quotes Dr. John Hoyt, "Debunking Myths of Chronic Obstructive Lung Disease," Critical Care Medicine, editorial Sept. 1997:

"The human body, particularly key organs such as the heart and brain, are not
all that forgiving of insufficient supplies of oxygen. Thus, medical decision-making—based on the mythology that oxygen causes apnea and cardiorespiratory arrest in patients with chronic obstructive pulmonary disease by turning off the oxygen respiratory drive—might take the path of with-holding or delivering inadequate doses of oxygen to meet the metabolic needs of the patient in respiratory failure. This mistake is generally fatal for the patient, and a treatment tragedy for the misinformed physician."

Thus, if a patient needs oxygen, he should be provided oxygen. If his drive to breathe diminishes, appropriate means to ventilate the patient should be sought.

And, as a final reminder, this issue pertains to the patient who is in respiratory distress, and not the CO2 retainer who is stabilized in his room, and "not the CO2 retainer whom is home and stable while eating and watching a ball game on TV."

Of course this is obvious, but I will state it again and again: "At all costs, we must first relieve the hypoximia. Ideally, we will do so without increasing hypercarbia needlessly. But it is bound to happen to a degree anyway. If the level of PaCO2 becomes a clinical problem, you local RCP should be there to assist ventilation, either in a non-invasive fashion or with a secure airway."

Or, in other words, "In the midst of this dilemma, we must remember that hypoxia kills, hypercarbia by itself does not."

(To view part six click here to advance to part one click here.)