Edouard Marques, Etienne J Couture, Jean S Bussières, Stephan Langevin, Paul Poirier, Pierre Voisine, Manon Caouette, Patrice Brassard
{"title":"Effects of noradrenaline and phenylephrine on cerebral oxygen saturation during cardiopulmonary bypass in cardiac surgery.","authors":"Edouard Marques, Etienne J Couture, Jean S Bussières, Stephan Langevin, Paul Poirier, Pierre Voisine, Manon Caouette, Patrice Brassard","doi":"10.1113/EP092387","DOIUrl":null,"url":null,"abstract":"<p><p>Cardiopulmonary bypass (CPB) in cardiac surgery is associated with a high risk of postoperative neurological complications. Perioperative use of vasopressors is common to counteract arterial hypotension in this setting. However, use of α-agonist vasopressors has been associated with cerebral desaturations. Given that reductions in cerebral oxygen saturation ( <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> ) can increase postoperative neurological dysfunction, we aimed to investigate the impact of noradrenaline (NA) and phenylephrine (PE) on <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> during the CPB period of a cardiac surgery in 36 patients scheduled for an elective cardiac surgery. Patients were randomized to the intra-operative use of either NA or PE. During CPB, mean arterial pressure (MAP) was elevated pharmacologically to predefined thresholds of 60 and 80 mmHg, while CPB flow was kept constant. The <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> values were recorded for 5 min per MAP threshold. The MAP increased adequately between thresholds of 60 and 80 mmHg (NA, 59 ± 3 vs. 81 ± 3 mmHg and PE, 61 ± 4 vs. 81 ± 3 mmHg; P ˂ 0.01). The <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> decreased between pressure thresholds of 60 and 80 mmHg (NA, 70 ± 11 vs. 69 ± 11 mmHg and PE, 64 ± 11 vs. 63 ± 11 mmHg; P ˂ 0.01). Reduction in <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> did not differ between vasopressors. The mean relative decrease in <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> across groups was 2.0% (95% confidence interval: 0.6 to 2.1). Elevation in MAP mediated solely by vasopressors induces significant decreases in <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> during cardiac surgery under CPB. However, their impact on <math> <semantics><msub><mi>S</mi> <mrow><mi>c</mi> <msub><mi>O</mi> <mn>2</mn></msub> </mrow> </msub> <annotation>${S_{{\\mathrm{c}}{{\\mathrm{O}}_2}}}$</annotation></semantics> </math> remains clinically non-significant according to current guidelines.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6000,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP092387","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Cardiopulmonary bypass (CPB) in cardiac surgery is associated with a high risk of postoperative neurological complications. Perioperative use of vasopressors is common to counteract arterial hypotension in this setting. However, use of α-agonist vasopressors has been associated with cerebral desaturations. Given that reductions in cerebral oxygen saturation ( ) can increase postoperative neurological dysfunction, we aimed to investigate the impact of noradrenaline (NA) and phenylephrine (PE) on during the CPB period of a cardiac surgery in 36 patients scheduled for an elective cardiac surgery. Patients were randomized to the intra-operative use of either NA or PE. During CPB, mean arterial pressure (MAP) was elevated pharmacologically to predefined thresholds of 60 and 80 mmHg, while CPB flow was kept constant. The values were recorded for 5 min per MAP threshold. The MAP increased adequately between thresholds of 60 and 80 mmHg (NA, 59 ± 3 vs. 81 ± 3 mmHg and PE, 61 ± 4 vs. 81 ± 3 mmHg; P ˂ 0.01). The decreased between pressure thresholds of 60 and 80 mmHg (NA, 70 ± 11 vs. 69 ± 11 mmHg and PE, 64 ± 11 vs. 63 ± 11 mmHg; P ˂ 0.01). Reduction in did not differ between vasopressors. The mean relative decrease in across groups was 2.0% (95% confidence interval: 0.6 to 2.1). Elevation in MAP mediated solely by vasopressors induces significant decreases in during cardiac surgery under CPB. However, their impact on remains clinically non-significant according to current guidelines.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.