What is: Hypoxic drive?
You've heard of it in COPD, so let's explain what it really is:
As mentioned previously, the respiratory control center responds to altered levels of CO2 and O2 by changing the respiratory rate and pattern. Interestingly, the response to hypoxia differs from the response to hypercapnia. Hypoxia induces a breathing pattern of rapid and shallow breaths with a relatively higher increase in respiratory rate than tidal volume. The aim is to decrease the cost of breathing by avoiding the need to overcome the lungs' higher elastance at high volumes.
In simple terms, breathing with high tidal volumes requires more negative pressure generation in the intra-pleural space and, thus, more oxygen utilization by respiratory muscles, especially in an already hypoxic patient. In contrast, hypercapnia triggers a breathing pattern of deep and slow breaths with a relatively more significant increase in tidal volume than respiratory rate. This pattern aims to limit dead space ventilation and optimize carbon dioxide elimination.
So what does this mean in COPD?
COPD is another chronic obstructive airway disease that shares many similarities with asthma. However, COPD is an irreversible process that gradually progresses over time, leading to chronic air-trapping and persistent hypercapnia. At first, central chemoreceptors sense hypercapnia as it would in a healthy individual and signal the respiratory center to increase breathing depth. As a result, a respiratory pattern of deep and slow breaths ensues. Studies have shown that supplemental oxygen during acute COPD exacerbation causes an increase in PaCO2 and a transient decrease in minute ventilation.
Previously, it was hypothesized that central chemoreceptors gradually become resistant to carbon dioxide levels in the blood such that the medullary sensors no longer respond to changes in pH as they would in a healthy counterpart. This led to the belief that hypercapnia no longer acts as the primary drive for respiration, and these patients become dependent on hypoxia for respiratory drive, causing generalized reluctance to administer supplemental oxygen during acute COPD exacerbation in the healthcare setting. This theory is no longer widely accepted as studies have shown that the transient decrease in minute ventilation in these patients is not sustained and does not consistently correlate proportionally with the degree of PaCO2 increase. Instead, administration of supplemental oxygen counteracts the reflex hypoxic pulmonary vasoconstriction that would otherwise shunt perfusion away from the damaged alveoli with poor ventilation to maximize perfusion to the "good" alveoli. The resulting dead space ventilation and ventilation-perfusion (V/Q) mismatch is likely a better explanation for the oxygen-induced increase in PaCO2. Another proposed mechanism is that supplemental oxygen causes a right shift in the hemoglobin-CO2 dissociation curve, increasing PaCO2, referred to as the Haldane effect.
Taken from: https://www.statpearls.com/ArticleLibrary/viewarticle/28414