Acid-base regulation and control of ventilation in human pregnancy

The purposes of this review were twofold: to apply modern physicochemical p rinciples to explain changes in acid-base regulation and the control of ven tilation in human pregnancy; and to demonstrate the value of pregnancy as a model for the study of endocrine effects on physiological control systems. Application of P.A. Stewart's approach (P.A. Stewart. Can. J. Physiol. Pha rmacol. 61: 1444-1461, 1983) shows that lower values of plasma hydrogen ion concentration ([H+]) observed at rest and in association with exercise in pregnancy are the result of lower values for carbon dioxide tension (PCO2) and total weak acid ([A(tot)]). This effect is partly offset by a lower str ong ion difference ([SIDI]). The ability to predict plasma [H+] at rest and following strenuous exercise in pregnancy (J.G. Kemp, EA. Greer, and L.A. Wolfe. J. Appl. Physiol. 83: 644-651, 1997) supports the validity of Stewar t's approach. Jennings and associates (D.B. Jennings. Can. J. Physiol. Phar macol. 72: 1499-1512, 1994) have further demonstrated in animal models the involvement of plasma osmolality and circulating levels of angiotensin II ( ANG II) and arginine vasopressin (AVP) in the chemical control of ventilati on. We hypothesize that pregnancy-induced increases in respiratory sensitiv ity to carbon dioxide are the combined result of reduced plasma osmolality, reduced cerebrospinal fluid [SID], and augmented circulating levels of pro gesterone, ANG II, and AVP.