Effects of Arterial Carbon Dioxide Tension on Cerebral and Somatic Regional Tissue Oxygenation and Blood Flow in Neonates After the Norwood Procedure With Deep Hypothermic Cardiopulmonary Bypass.

George M Hoffman,Eckehard A Stuth,John P Scott

doi:10.3389/fped.2022.762739

George M Hoffman, Eckehard A Stuth + Show 1 more

Open Access

https://doi.org/10.3389/fped.2022.762739

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Abstract

Neonates undergoing the Norwood procedure for hypoplastic left heart syndrome are at higher risk of impaired systemic oxygen delivery with resultant brain, kidney, and intestinal ischemic injury, shock, and death. Complex developmental, anatomic, and treatment-related influences on cerebral and renal-somatic circulations make individualized treatment strategies physiologically attractive. Monitoring cerebral and renal circulations with near infrared spectroscopy can help drive rational therapeutic interventions. The primary aim of this study was to describe the differential effects of carbon dioxide tension on cerebral and renal circulations in neonates after the Norwood procedure. Using a prospectively-maintained database of postoperative physiologic and hemodynamic parameters, we analyzed the relationship between postoperative arterial carbon dioxide tension and tissue oxygen saturation and arteriovenous saturation difference in cerebral and renal regions, applying univariate and multivariate multilevel mixed regression techniques. Results were available from 7,644 h of data in 178 patients. Increases in arterial carbon dioxide tension were associated with increased cerebral and decreased renal oxygen saturation. Differential changes in arteriovenous saturation difference explained these effects. The cerebral circulation showed more carbon dioxide sensitivity in the early postoperative period, while sensitivity in the renal circulation increased over time. Multivariate models supported the univariate findings and defined complex time-dependent interactions presented graphically. The cerebral and renal circulations may compete for blood flow with critical limitations of cardiac output. The cerebral and renal-somatic beds have different circulatory control mechanisms that can be manipulated to change the distribution of cardiac output by altering the arterial carbon dioxide tension. Monitoring cerebral and renal circulations with near infrared spectroscopy can provide rational physiologic targets for individualized treatment.

Highlights

The neonate undergoes profound changes in pulmonary and systemic circulations over the first week of life, with overlying developmental influences on circulatory controls of cerebral and renal-mesenteric systemic beds [1,2,3,4]
This study used near-infrared spectroscopy (NIRS) to measure cerebral and renal/somatic oxygenation and blood flow following the Norwood procedure in nearly 200 neonates
The major finding was the differential effect of changes in PaCO2 on cerebral and renal/somatic oxygenation and blood flow

Summary

Introduction

The neonate undergoes profound changes in pulmonary and systemic circulations over the first week of life, with overlying developmental influences on circulatory controls of cerebral and renal-mesenteric systemic beds [1,2,3,4]. In addition to vulnerabilities related to the transitional circulation and the neonatal myocardium, neonates with univentricular heart disease have vulnerabilities related to decreased ventricular mass, obligate mixing with arterial desaturation, and the pulmonarysystemic tradeoff inherent in parallel circulation [5,6,7,8] Such circulatory limitations increase the risk for hypoxic-ischemic injury in both cerebral and renal/somatic circulations [3, 9]. Monitoring cerebral and renal/somatic circulations with near-infrared spectroscopy (NIRS) in neonates before, during, and after surgical palliation of hypoplastic left heart syndrome (HLHS) with the Norwood procedure, has helped uncover circulatory vulnerabilities, describe relationships between monitored parameters and outcomes, and determine targets for intervention [3, 8, 10,11,12,13,14] Both cerebral and renal-somatic organ beds are at risk for hypoxic injury following Norwood palliation of HLHS [9, 11, 15,16,17,18,19,20,21]. The combination of arterial blood pressure and renal oxygenation by NIRS can define a low cardiac output condition associated with increased mortality [13]

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