Fellow King's College London London, England, United Kingdom
Background: In persistent pulmonary hypertension of the newborn (PPHN) there is extrapulmonary right-to-left shunting of deoxygenated blood, leading to hypoxaemia and re-circulation of blood rich in carbon dioxide. Re-direction of blood from the pulmonary to systemic circulation causes pulmonary oligaemia and ventilation-perfusion mismatch with increased alveolar dead space. The presence and magnitude of alveolar dead space can be estimated by the difference in the arterial and end-tidal carbon dioxide pressures (PaCO2 – EtCO2 gradient). Objective: (i) To describe the PaCO2 – EtCO2 gradient in term born infants with PPHN and compare it to those without. (ii) To determine if the gradient would reduce in PPHN infants as their condition improved. Design/Methods: A prospective, observational study of term born, ventilated infants in a level three NICU was undertaken. Infants with echocardiographically confirmed PPHN were included and infants ventilated for non-respiratory reasons acted as controls. Ethical approval was granted and the study registered with the local clinical governance department. The PaCO2 – EtCO2 gradient was calculated from arterial blood gases from indwelling catheters and continuous microstream sidestream capnography. Infants with PPHN were assessed during the acute illness and prior to extubation when the PPHN had clinically resolved. Non-parametric tests used included the Mann Whitney U test and linear regression analysis. Results: Twenty infants were studied with a median (IQR) gestational age of 39.5 (38.7 – 40.4) weeks and birthweight of 3.56 (3.15 – 3.93) kg. The PaCO2 – EtCO2 gradient was larger in the infants with PPHN compared to those without [80.3 (6.8 – 36.0) mmHg versus 27.8 (62.3 – 126.0) mmHg, p< 0.001], and related to both mean airway pressure (MAP) (r = 0.62, p = 0.04) and fraction of inspired oxygen (FiO2) (r = 0.71, p< 0.01). Linear regression analysis demonstrated that the PaCO2 – EtCO2 gradient was predicted by a diagnosis of PPHN (p = 0.037, 95% CI 0.7 – 18.0) after adjusting for differences in MAP and FiO2. In infants with PPHN the PaCO2 – EtCO2 gradient decreased significantly during acute illness to pre-extubation compared to those without PPHN (p = 0.02).
Conclusion(s): The arterial to end-tidal carbon dioxide gradient was larger in infants with PPHN compared to those without. Furthermore, the PaCO2 – EtCO2 gradient decreased over the first week in infants with PPHN. This gradient might have potential in monitoring the evolution and resolution of PPHN.
