Commentaries on Viewpoint: Why do some patients stop breathing after taking narcotics? Ventilatory chemosensitivity as a predictor of opioid-induced respiratory depression VIEWPOINT COMMENT ON VENTILATOR CHEMOSENSITIVITY AS A PREDICTOR OF OPIOID-INDUCED RESPIRATORY DEPRESSION

TO THE EDITOR: Patients who are to undergo opioid-induced ventilatory chemoreceptor depression respond variably to narcotics. This is illustrated in Potter and Moon’s (2) Fig. 1 in which great variability is shown of the hypercapnic ventilatory response (HCVR) test. In patients not undergoing pharmacological alterations (3, 4), there is great uniformity in hydrogen ion (H ) regulation. This might be explained by chemical stimulus being H and not carbon dioxide (CO2). Having tested their patients under partial anesthesia, increasing CO2, Potter and Moon (2) have a mix of stimuli but only an insensitive CO2 stimulus. Above the anaerobic threshold, H only drives ventilation. Patients may seriously underventilate and it does serious harm to patients when putting them under anesthesia. The reason for the variability is that the HCVR and the hypoxic ventilatory response (HVR) test of chemosensitivity may be insensitive and atypical when tested in nonphysiological ranges. This would be especially problematic if the patient has a background of heart or lung disease (4). Normal patients are extremely sensitive to H ventilatory regulation. However, they are insensitive to CO2 regulation over the entire range of chemical receptor control (3, 4). When arterial CO2 competes with hypoxemia or as the stimulus provided by CO2 gas, the CO2 loses its power and arterial [H ] wins. We conclude that the arterial [H ] is the chemical controller rather than CO2. See Fig. 4 in Ref. 3. This concept was in agreement with findings from other groups (1).