Factors in the interpretation of mouth occlusion pressure during measurements of chemosensitivity.

T he ventilatory responses to hypoxia and to hyper-capnia can be depressed, and resting levels of PaCO, and PaO, may be significantly abnormal in the presence of minimal lung disease.' It has been suggested that the chemical drive to respiration has adapted, but using the ventilatory response to measure chemosensitivity or the "chemical drive" is complicated by the negative effect on ventilation of the stretch receptors and by lung and chest wall mechanics. Recently, Whitelaw et a12 have developed a prmis-ing new technique which attempts to measure more immediately the neural output of the medullary respiratory centers during a chemical challenge. The authors feel that by measuring the mouth pressure 0.1 sec after the initiation of an occluded breath (Po,,), they omit any significant interference from the Hering-Breuer inflation reflex or the negative influences of abnormal compliance or resistance. In their study using the re-breathing technique, normal subjects began with a mix-N2. We were interested in applying the Po,, technique to both hypoxia and hypercapnia-stimulated ventilation in the same subject. Specifically, we have been trying to determine if these two nonpharmacologic stimuli, hyper-capnia and hypoxia, stimulate the respiratory muscula-ture similarly when the increases in ' ?E are the same. Hence, our question was: when the increase in VE due to hypoxia equals that due to hypercapnia, are both Po,, values the same? However, before we began to match VE values, some of our experimental results suggested that one should equate the Po,, with medullary respiratory drive only with great caution, if at all. Two factors would seem to compromise that interpretation: changes in FRC (ie, respiratory muscle length) provoked by the gases, and changes in the status of the contractile mechanism of the respiratory muscles generated by changes in the gases. Occlusion pressure is developed by muscular force; and though the force of an isometric contraction is indeed directly proportional to the amount of neural traffic to the muscle, the force is also influenced by the length of the muscle and the normal functioning of the contractile mechanism. Hence, if a certain Po,, were established for a population of "normal" subjects at a given PaCO,, a depressed Po,, in a patient may be due to a depressed respiratory center, but it may also be due to a perfectly normal respiratory center acting on a shortened muscle, or on a muscle with a compromised contractile mechanism. With respect to changes in …