Hypoxic drive is often cited for its limiting oxygen saturations in COPD patients. The risks associated with elevated oxygen saturations are passed down from educators and clinicians to students, but the actual literature supporting the hypoxic drive theory is limited, with the vast majority existing prior to 1985.
Assumptions Behind the Hypoxic Drive
The premise for hypoxic drive is that elevated oxygen levels depress the peripheral chemo receptors located in the aortic arch and carotid bodies. High oxygen saturations in a patient who has a diminished respiratory drive could pose a further deterioration of the drive.
Patients identified as most at risk are those who are chronically hypoxic with moderate to severe hypercarbia.
OPINION POLL: Hypoxic Drive Theory: Myth or Reality?
As a patient retains CO2, they buffer the increasing acidosis by retaining more bicarbonate, which in turn reduces the H-ion stimulation of the respiratory center. With a decreased stimulus, the need to maintain an elevated minute ventilation is reduced. This results in mild hypoventilation, which in turn results in mild hypoxia. The body then attempts to strike a balance between overventilation (alkalosis) and hypoventilation (acidosis).
Depending upon the physical ability of the patient, this balance is established using small, incremental corrections over a long period of time (chronic adaptation). At that point, the hypoxic drive is a minor but integral part of the overall respiratory drive for the patient.
The Reality
In actuality, the hypoxic drive is a very small part of the overall stimulus driving the patient’s respiratory system – it exists in everyone.
The hypoxic drive offers a fairly rapid response to changes in oxygen levels, but it is not in isolation. Often, there are other factors affecting the respiratory drive such as acidosis/alkalosis, metabolic demands, the physical condition of the patient, neurologic status/level of consciousness and pharmacologic agents.
In order for the peripheral chemo receptors to have any substantial effect on the patient’s respiratory drive, the other factors driving the respiratory center have to be diminished.
Clinical Example:
A COPD patient contracts an acute respiratory infection, which increases the metabolic demands on the respiratory system beyond the patient’s physical ability to meet those demands. Physical exhaustion, muscle fatigue, lactic acid accumulation, elevated carbon dioxide production and high oxygen demands pose a very real risk of complete ventilatory failure.
By sacrificing the established “normal,” achieved by chronic compensation, the patient is able to sustain his respiratory work of breathing.
At this point, the new compensation activities succeed or the patient continues to deteriorate- the hypoxic drive is exerting its full respiratory stimulus (although only a small portion of the overall drive stimulus) as part of the compensation stimuli. If unsuccessful, the patient is now at the point of undergoing progressive respiratory and ventilatory failure and medical assistance is required.
Once in the hospital, the degree of infection is established by chest X-ray and lab testing. High exertion of breathing and low oxygen are identified as the immediate issues, and antibiotics, fluids and oxygen are initiated. As the blood oxygen increases and passes through the optimal hypoxic drive range of an SpO2 of 88-92% (PaO2 55-60 mm Hg), the level of drive reduces and the peripheral chemoreceptors provide a decreased level of stimulus.
As the patient exhausts his ability to increase his work of breathing and is physiologically attempting to recover from that work, the loss of this minimal part of the overall drive “tips the balance” and the rate of failure begins to increase. The patient begins to become hypercarbic and acidotic and enters progressive ventilatory failure. Without medical intervention, the failure will lead to respiratory arrest.
Did supplementary oxygen contribute to the failure? Yes! Was it solely responsible for the progressive failure? No! But it has a direct effect on the rate of failure and is easily under the clinician’s control.
Conclusion
Hypoxic drive is real, but its role in in ventilatory failure is often overstated. It is only in combination with other factors that it has a significant role in interfering with the respiratory drive.
The clinician needs to be aware of actions or factors that add to sources of failure– respiratory depressive drugs (narcotics, sedatives), neurologic impairment, acute infection, bronchospasm/increased work of breathing, nutritional deficiency issues, increased metabolic demands secondary to exertion, and fluid and electrolyte issues. Each of these issues, in isolation, is not a significant factor in ventilatory failure, but as they combine, the effects are synergistic. Into this clinical mix of factors comes the hypoxic drive and, like many other factors, it is under clinician control.
Awareness of these factors is the key to ensuring a balanced approach in the treatment of the patient. In isolation, supplementary oxygen would not interfere with this patient’s respiratory drive but in combination with other factors leading to failure, it has a definitive effect. The key feature is that hypoxia kills, oxygen is used to treat hypoxia and like all drugs, it has definitive side effects that the clinician needs to be aware of in the treatment of the patient’s disease pathology.
Many of the risks of oxygen toxicity are known and taught to students early on in their careers. However, there is a growing body of evidence suggesting that oxygen has a definitive role in the worsening of CHF and other diseases. The more we know, the more there is to learn about the risks associated with supplemental oxygen.
Dave Swift, RRT, is campus coordinator, professional practice respiratory therapy, at Ottawa Hospital – Civic Campus, Ottawa, Ontario, Canada. He is also respiratory therapy lead/subject matter expert, for the National Office of the Healthcare Emergency Response Team, Public Health Canada.
