The crux of the theory is that the main drive to breath comes from neurons in the medulla oblongata at the base of the brain. These neurons receive signals from central chemoreceptors on the medulla and peripheral chemoreceptors located in the bifurcations of the aortic arteries and the aortic arch.
Respiratory rate is adjusted to maintain a normal acid base balance (pH) throughout the body. The majority of the times, the central chemo receptors send signals to the brain that control breathing. They monitor carbon dioxide (CO2) levels. When CO2 levels are high a signal is sent to speed up the drive to breathe to blow off the excess CO2. In this way, CO2 is our main drive to breathe.
The peripheral chemo receptors send a signal to breathe when the partial pressure of oxygen in the arteries (PaO2) is less than 60. This is referred to as the hypoxic drive. This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing.
In COPD patients, chronic airway obstruction due to bronchospasm and increased mucus secretion blocks air passages, and as a result many alveoli become ineffective at ventilating (CO2 cannot get out and oxygen cannot get in). For these patients, this results in a chronically elevated CO2 (greater than 50), and lowered oxygen levels (SpO2 less than 90 and Po2 less than 60). (2)
As CO2 rises, bicarbonate (HCO3) falls in order to compensate and prevent acidosis (a drop in pH, or a pH less than 7.35). The result here is that many of these patients normally live with something like a PaCO2 of 50, a PaO2 of 50, and a Bicarb of 30. These patients are aptly referred to as CO2 retainers, or simply retainers.
In many instances students are incorrectly taught that all COPD patients are retainers who breathe under influence of the hypoxic drive. The truth is that less than 25 percent of chronic CO2 retainers use the hypoxic drive to breathe, (4) and it's not as significant as once believed.
In fact, of patients who present to hospitals in respiratory distress, half will have reversible CO2 retention, and half will be chronic CO2 retainers. (5)
The hypoxic drive theory has it that the high CO2 may make the chemoreceptors tolerant of the high CO2, and thus CO2 ceases to be that person's drive to breath. These patients are your prototypical CO2 retainers. The hypoxic drive theory, thus, states that many of them are hypoxic drive breathers.
Those who believe in the theory believe if you give these patients too much oxygen, enough to drive their PO2 above 70, then you will blunt their hypoxic drive and knock out their drive to breathe. Their respiratory rare will slow, their CO2 will therefore rise even more, acidosis will occur, the patient will become lethargic (very sleepy or somnolent), and ultimately they will stop breathing.
It is for this reason that most medical experts champion for never over-oxygenating patients who are CO2 retainers. The experts recommend using a nasal cannula set at 2-4lpm, and never higher. Or, if their respiratory rate is sporadic, to use a venturi mask set no higher than 40% FiO2.
These experts say that if the CO2 rises, that the FiO2 should be lowered. This has resulted in many physicians accepting PO2s in the lower 80s and even the upper 70s in certain patients.
Yet this often results in the ire of caregivers taking care of these patients, because they are the ones who have to watch them suffer from dyspnea, or air hunger, or the feeling they can't catch their breath.
It has also resulted in ire because many of these patients are placed on 100% oxygen with no ill effect. Many of these patents have been given breathing treatments using oxygen, estimated to be about 60%, and have never seen any patient drop dead during a breathing treatment.
It was evidence like this that made clinicians second guess the hypoxic drive theory. It was from here that various studies were done to show, once and for all, whether the hypoxic drive theory is a fact, or whether it's nothing more than a medical myth.
What in turn happened was that, even though most studies proved the theory was in fact a myth, the subject became even more controversial.
- Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath: Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53
- Wilkins, Robert L, James K. Stoller, ed. "Egan's Fundamentals of Respiratory Care," 2009, pages 309-310
- Caruana-Montaldo, Brendan, et al, "The Control of Breathing in Clinical Practice," Chest, 2000, 117, pages 205-225 (This article also provides a good review of the central and peripheral chemoreceptors and the drive to breathe)
- Wojciechowski, William V., "Entry Level Exam Review for Respiratory Care: Guidelines for success," 3rd edition, 2011, U.S., page 487?
- Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
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