The Hazards of Measuring the Drive to Breathe

Abstract

Accessible online at: www.karger.com/journals/res In this issue of Respiration, Moura et al. [1] report on the effects of consecutive nights of nasal continuous positive air pressure on the occlusion pressure and ventilatory response to CO2 in 12 patients with obstructive sleep apnea in an attempt to determine changes in ventilation drive, i.e. chemoreceptor responses. Theoretically, in hypercapnic patients, nasal continuous positive air pressure might improve sensitivity to CO2 by reducing resting levels of PCO2, which in turn would lead to a fall in bicarbonate levels. In normocapnic patients, such as those studied by Moura et al. [1], relief of sleepiness might improve CO2 responses [2]. The results of Moura et al. [1] were inconclusive; the occlusion pressure increase with CO2 was greater but the ventilatory response was not. Moura et al. [1] state that the occlusion pressure response (the pressure generated at the mouth during inspiration in the first 100 ms after airway occlusion) is a more sensitive measure of drive than ventilation. However, there is little or no evidence to support this. The occlusion pressure response was conceived as a way to measure chemosensitivity in the face of impaired lung mechanics, since poor mechanics could depress the response to ventilation even when the sensitivity of the chemoreceptors was normal [3–5]. The occlusion pressure was assumed to reflect the ‘net respiratory pressure’ generated by the respiratory muscles under isometric conditions, and this is less affected by increased airway resistance than ventilation. However, in the study of Moura et al. [1], lung function is reported to be normal. Occlusion pressure does depend on the ability of the respiratory muscles to generate force and this in turn depends on their length. A decrease in functional residual capacity with the treatment of sleep apnea could give rise to an increase in occlusion pressure, but there is no reason why this should have occurred, and in fact, resting occlusion pressure was unchanged. The real problem in measuring chemosensitivity, I believe, is the difficulty in measuring the drive to breathe by any technique and particularly by the technique used in this study. Great care is needed to obtain reliable measurements. In this study, 8% CO2 in 42% O2 was breathed and measurements were made before and between the 4th and 5th minute of CO2 breathing. To be valid, both before and after measurements have to be made in the steady state. There is no evidence that this is true for either one [6]. Initial measurements were made with the subjects apparently breathing room air and not with 42% O2. The enriched O2 mixture breathed might have affected breathing, albeit slightly. More importantly, it has been known for some time that a steady state is not achieved during CO2 breathing for well over 20 min, particularly with the high concentration of 8% used in this study. Also, the rate of equilibration will vary not just with the dynamics of the ventilatory response but will also depend on the magnitude and dynamics of the systemic circulatory and cerebral blood flow response. More accurate and reproducible