Neck and body position effects on pulmonary mechanics in infants.

Pulmonary mechanics and ventilatory parameters were measured in 30 former preterm infants at a postterm age of 8 to 10 months. All subjects had required assisted ventilation in the neonatal period and 16 had a history of bronchopulmonary dysplasia. Each infant was studied in both supine and semisitting positions, and in each body position the infants were studied with neutral, flexed, and extended neck positions. Baseline measurements (body supine, neck neutral) and the response to postural changes did not differ between infants who had had bronchopulmonary dysplasia and those who had not. Change in body position from supine to semisitting decreased total pulmonary resistance (P less than .05) and increased specific lung compliance (P less than .01). Neck flexion increased resistance (P less than .001) in both body positions but did not influence compliance. These postural effects are consistent with an increase in functional residual capacity in the semisitting position and a decrease in pharyngeal area during neck flexion. Thus, posture needs to be precisely controlled during pulmonary function testing in infants. Furthermore, optimal neck and body position may improve their clinical status.

Increasing arterial carbon dioxide tension: influence on transcutaneous carbon dioxide tension measurements.

Despite widespread use of transcutaneous PCO2 (TcPCO2) monitoring, the precise relationship between TcPCO2 and PaCO2 remains unclear. It has been widely assumed that theoretical correction of TcPCO2 (combining temperature correction with a constant metabolic factor of 4 mm Hg) accounts for the elevation of TcPCO2 over PaCO2. To test this assumption, TcPCO2 was measured with a 44 degrees C electrode and compared to PaCO2 in 60 normotensive infants with cardiorespiratory disease during the first four +/- six days of life (mean +/- SD) (range one to 36 days). During hypocapnea, from PaCO2. In contrast, during normocapnea, theoretically corrected TcPCO2 exceeded PaCO2 by 5 +/- 4 mm Hg (P less than .001), and similarly during hypercapnea, theoretically corrected TcPCO2 exceeded PaCO2 by 9 +/- 6 mm Hg (P less than .001). These data suggest that, as PaCO2 increases, there may be an imbalance between tissue CO2 production and removal, resulting in a progressively increasing gradient between TcPCO2 and PaCO2. Clarification of the relationship between TcPCO2 and PaCO2 should enhance the interpretation of TcPCO2 measurements in infants.

Current correction factors inadequately predict the relationship between transcutaneous (tc) and arterial PCO2 in sick neonates.

Despite widespread tcPCO2 monitoring the relationship between tcPCO2 and PaCO2 remains unclear. It has been assumed that after standard temperature correction, a constant metabolic factor can explain the elevation of tcPCO2 over PaCO2. Our data demonstrate a progressive increase in the difference between temperature corrected tcPCO2 and PaCO2 as PaCO2 increases. Thus a constant metabolic factor cannot account for the elevation of temperature corrected tcPCO2 over PaCO2. We speculate that as PaCO2 rises, CO2 production exceeds removal resulting in a progressive gradient between temperature corrected tcPCO2 and PaCO2.

High-frequency jet ventilation in neonatal pulmonary hypertension.

To determine if high-frequency jet ventilation is beneficial in neonates with persistent pulmonary hypertension, we compared the ventilator settings, blood gas concentrations, and outcome of infants who met established criteria for a high predictive mortality. During a six-year period, 14 neonates who had severe respiratory failure and hypoxemia while receiving conventional ventilation were treated with high-frequency jet ventilation. Twenty-three comparable infants meeting the same criteria were treated exclusively with conventional ventilation. After initiation of high-frequency jet ventilation there was a significant reduction in mean airway pressure and partial pressure of arterial carbon dioxide (PaCO2). In contrast, neonates treated exclusively with conventional ventilation continued to have higher airway pressures and PaCO2. However, there was no difference in the alveolar-to-arterial oxygen gradient, air leakage, incidence of bronchopulmonary dysplasia, or duration of assisted ventilation or oxygen supplementation. Furthermore, mortality was comparable in both groups of infants. These preliminary observations suggest that high-frequency jet ventilation can reduce airway pressure and PaCO2 in neonates with persistent pulmonary hypertension but does not appear to improve outcome.