ABSTRACT
OBJECTIVE: Accurate and reliable noninvasive methods to estimate gas exchange are necessary to guide clinical decisions to avoid frequent blood samples in children with pediatric acute respiratory distress syndrome (PARDS). We aimed to investigate the correlation and agreement between end-tidal P CO 2 ${P}_{{\mathrm{CO}}_{2}}$ measured immediately after a 3-s inspiratory-hold (PLAT CO2 ) by capnometry and P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ measured by arterial blood gases (ABG) in PARDS. DESIGN: Prospective cohort study. SETTING: Seven-bed Pediatric Intensive Care Unit, Hospital El Carmen de Maipú, Chile. PATIENTS: Thirteen mechanically ventilated patients aged ≤15 years old undergoing neuromuscular blockade as part of management for PARDS. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: All patients were in volume-controlled ventilation mode. The regular end-tidal P CO 2 ( P ETCO 2 ) ${P}_{{\mathrm{CO}}_{2}}({P}_{{\mathrm{ETCO}}_{2}})$ (without the inspiratory hold) was registered immediately after the ABG sample. An inspiratory-hold of 3 s was performed for lung mechanics measurements, recording P ETCO 2 ${P}_{{\mathrm{ETCO}}_{2}}$ in the breath following the inspiratory-hold. (PLAT CO2 ). End-tidal alveolar dead space fraction (AVDSf) was calculated as [ ( P aCO 2 - P ETCO 2 ) / P aCO 2 ] $[({P}_{{\mathrm{aCO}}_{2}}\mbox{--}{P}_{{\mathrm{ETCO}}_{2}})/{P}_{{\mathrm{aCO}}_{2}}]$ and its surrogate (S)AVDSf as [ ( PLAT CO 2 - P ETCO 2 ) / PLAT CO 2 ] $[{(}_{\mathrm{PLAT}}{\mathrm{CO}}_{2}\mbox{--}{P}_{{\mathrm{ETCO}}_{2}}){/}_{\mathrm{PLAT}}{\mathrm{CO}}_{2}]$ . Measurements of P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ were considered the gold standard. We performed concordance correlation coefficient (ρc), Spearman's correlation (rho), and Bland-Altmann's analysis (mean difference ± SD [limits of agreement, LoA]). Eleven patients were included, with a median (interquartile range) age of 5 (2-11) months. Tidal volume was 5.8 (5.7-6.3) mL/kg, PEEP 8 (6-8), driving pressure 10 (8-11), and plateau pressure 17 (17-19) cm H2 O. Forty-one paired measurements were analyzed. P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ was higher than P ETCO 2 ${P}_{{\mathrm{ETCO}}_{2}}$ (52 mmHg [48-54] vs. 42 mmHg [38-45], p < 0.01), and there were no significant differences with PLAT CO2 (50 mmHg [46-55], p > 0.99). The concordance correlation coefficient and Spearman's correlation between P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ and PLAT CO2 were robust (ρc = 0.80 [95% confidence interval [CI]: 0.67-0.90]; and rho = 0.80, p < 0.001.), and for P ETCO 2 ${P}_{{\mathrm{ETCO}}_{2}}$ were weak and strong (ρc = 0.27 [95% CI: 0.15-0.38]; and rho = 0.63, p < 0.01). The bias between PLAT CO2 and P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ was -0.4 ± 3.5 mmHg (LoA -7.2 to 6.4), and between P ETCO 2 ${P}_{{\mathrm{ETCO}}_{2}}$ and P aCO 2 ${P}_{{\mathrm{aCO}}_{2}}$ was -8.5 ± 4.1 mmHg (LoA -16.6 to -0.5). The correlation between AVDSf and (S)AVDSf was moderate (rho = 0.55, p < 0.01), and the mean difference was -0.5 ± 5.6% (LoA -11.5 to 10.5). CONCLUSION: This pilot study showed the feasibility of measuring end-tidal CO2 after a 3-s end-inspiratory breath hole in pediatric patients undergoing controlled ventilation for ARDS. Encouraging preliminary results warrant further study of this technique.
ABSTRACT
The Acute Respiratory Distress Syndrome (ARDS) is a life-threatening disease with a high mortality rate. In children it represents a diagnostic and therapeutic challenge. The primary feature in the development of ARDS is the non-cardiogenic pulmonary edema resulting from a disproportionate inflammatory response that increases the blood-gas barrier permeability. There is strong evidence that aninappropriate ventilatory support may induce lung injury, organ dysfunction and increasing mortality.The aim of this article is to review current concepts related to the diagnostic of pediatric ARDS, its pathophysiologic mechanisms, ventilator induced lung injury and a brief description of rescue therapies.
El Síndrome de Distrés Respiratorio Agudo (SDRA) es una entidad grave de elevada mortalidad, siendo en pediatría un desafío diagnóstico y terapéutico. La característica primaria del SDRA es el desarrollo de edema pulmonar no cardiogénico debido a una respuesta inflamatoria excesiva que aumenta la permeabilidad de la barrera sangre-gas. Existe una fuerte evidencia de que una estrategia inadecuada de soporte ventilatorio puede aumentar el daño pulmonar, inducir disfunciones de َrganos a distancia y aumentar la mortalidad.El presente artيculo pretende revisar conceptos actuales relacionados al diagnóstico de SDRA pediátrico, mecanismos fisiopatológicos, daño pulmonar inducido por la ventilación mecánica y una breve revisión de las terapias de rescate.
