Physiological dead space and alveolar ventilation in ventilated infants

Abstract

Background Dead space is the volume not taking part in gas exchange and, if increased, could affect alveolar ventilation if there is too low a delivered volume. We determined if there were differences in dead space and alveolar ventilation in ventilated infants with pulmonary disease or no respiratory morbidity. Methods A prospective study of mechanically ventilated infants was undertaken. Expiratory tidal volume and carbon dioxide levels were measured. Volumetric capnograms were constructed to calculate the dead space using the modified Bohr–Enghoff equation. Alveolar ventilation (VA) was also calculated. Results Eighty-one infants with a median (range) gestational age of 28.7 (22.4–41.9) weeks were recruited. The dead space [median (IQR)] was higher in 35 infants with respiratory distress syndrome (RDS) [5.7 (5.1–7.0) ml/kg] and in 26 infants with bronchopulmonary dysplasia (BPD) [6.4 (5.1–7.5) ml/kg] than in 20 term controls with no respiratory disease [3.5 (2.8–4.2) ml/kg, p < 0.001]. Minute ventilation was higher in both infants with RDS or BPD compared to the controls. VA in infants with RDS or BPD was similar to that of the controls [p = 0.54]. Conclusion Prematurely born infants with pulmonary disease have a higher dead space than term controls, which may influence the optimum level during volume-targeted ventilation. Impact Measurement of the dead space was feasible in ventilated newborn infants. The physiological dead space was a significant proportion of the delivered volume in ventilated infants. The dead space (per kilogram) was higher in ventilated infants with respiratory distress syndrome or evolving bronchopulmonary dysplasia compared to term controls without respiratory disease. The dead space volume should be considered when calculating the most appropriate volume during volume-targeted ventilation.

Pathophysiology of gas exchange impairment in extreme prematurity: Insights from combining volumetric capnography and measurements of ventilation/perfusion ratio

“…These technical characteristics could account for some of the observed differences. We have previously used a flow sensor with a low dead space of 0.8 ml to measure a dead space of approximately 5 ml/kg in preterm infants with respiratory distress syndrome and bronchopulmonary dysplasia and reported that the dead space was large but the tidal volume was higher than the dead space with a median dead space to tidal volume ratio of approximately 0.75 ( 14 ). In the same paper we described that in response to this inefficient ratio, ventilated preterm infants possibly increase their spontaneous respiratory rate to maintain alveolar ventilation ( 33 ).…”

“…We have previously used a novel methodology to non-invasively calculate indices of gas exchange impairment such as the ventilation to perfusion ratio (V A /Q) and right-to-left shunt in premature infants with BPD ( 10 ), in ventilated infants with pulmonary interstitial emphysema ( 11 ) and healthy term infants without respiratory disease ( 12 , 13 ). We have also used latest generation, low-dead space, mainstream volumetric capnography to measure the anatomical and alveolar dead space in ventilated premature infants with respiratory distress syndrome or bronchopulmonary dysplasia ( 14 ). Volumetric capnography can differentiate the phases of gas emptying from the lungs: emptying of mixed gas from the conducting airways and alveoli (phase II) or purely from the alveoli (phase III) with steeper phases representing more severe ventilation inhomogeneity ( 15 , 16 ).…”

Functional morphometry: non-invasive estimation of the alveolar surface area in extremely preterm infants

“…41 We performed a comprehensive physiological assessment in a vulnerable cohort of infants. Previously described methods of calculating the V A /Q, respiratory dead space and focused echocardiography 13,20,26 were combined with a recently validated animal model. 13,20,26 We should acknowledge that the current cohort included only infants born extremely prematurely and all infants developed BPD; hence, the adjusted S A index was unable to differentiate between those preterm infants who did and did not develop BPD.…”

Adjusting ventilator settings to avoid air trapping in extremely premature infants reduces the need for tracheostomy and length of stay

“…As lung architecture changes under the influence of prematurity, oxygen exposure, and inflammatory mediators that could be incited by sepsis, necrotizing enterocolitis, or ventilator induced lung injury, lung mechanics change significantly. While initial tidal volume targets of 4.5-6 ml/kg (14) are used by many Neonatal Intensive Care Units (NICU), it is known that anatomical dead space increases significantly with prolonged ventilation, this is likely contributed to by the development of tracheomegaly (15)(16)(17)(18). This increase in dead space is often accompanied by rising lung compliance as the alveoli lose elastic recoil from alveolar simplification, and increasing airway resistance as the airways develop epithelial lesions and bronchomalacia.…”