Nasal versus oronasal raised volume forced expirations in infants--a real physiologic challenge.

Raised volume rapid thoracoabdominal compression (RTC) generates forced expiration (FE) in infants typically from an airway opening pressure of 30 cm H(2)O (V(30)). We hypothesized that the higher nasal than pulmonary airway resistance limits forced expiratory flows (FEF(%)) during (nasal) FE(n), which an opened mouth, (oronasal) FE(o), would resolve. Measurements were performed during a brief post-hyperventilation apnea on 12 healthy infants aged 6.9-104 weeks. In two infants, forced expiratory (FEFV) flow volume (FV) curves were generated using a facemask that covered the nose and a closed mouth, then again with a larger mask with the mouth opened. In other infants (n = 10), the mouth closed spontaneously during FE. Oronasal passive expiration from V(30) generated either the inspiratory capacity (IC) or by activating RTC before end-expiration, the slow vital capacity ((j) SVC). Peak flow (PF), FEF(25), FEF(50), FEF(25-75), FEV(0.4), and FEV(0.5) were lower via FE(n) than FE(o) (P < 0.05), but the ratio of expired volume at PF and forced vital capacity (FVC) as percent was higher (P < 0.05). FEF(75), FEF(85), FEF(90), FVC as well as the applied jacket pressures were not different (P > 0.05). FEFV curves generated via FE(o) exhibited higher PF than FV curves of IC (P < 0.05); PF of those produced via FE(n) were not different from FV curves of IC (P > 0.05) but lower than those of (j) SVC (P < 0.05). In conclusion, the higher nasal than pulmonary airways resistance unequivocally affects the FEFV curves by consistently reducing PF and decreases mid-expiratory flows. A monitored slightly opened mouth and a gentle anterior jaw thrust are physiologically integral for raised volume RTC in order to maximize the oral and minimize nasal airways contribution to FE so that flow limitation would be in the pulmonary not nasal airways.