{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T04:31:03Z","timestamp":1772253063612,"version":"3.50.1"},"reference-count":16,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,3,18]],"date-time":"2013-03-18T00:00:00Z","timestamp":1363564800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatric Anesthesia"],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Dexmedetomidine is an alpha2\u2010adrenergic agonist used for sedation and analgesia in children. We previously showed that dexmedetomidine depresses sinus and <jats:styled-content style=\"fixed-case\">AV<\/jats:styled-content> nodal function resulting in adverse hemodynamic effects such as bradycardia and increased blood pressure. We hypothesized that these effects of dexmedetomidine might be antagonized by co\u2010administration of ketamine, which has sympathomimetic properties.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Twenty\u2010two children (ages 5\u201317\u00a0years) undergoing electrophysiologic (<jats:styled-content style=\"fixed-case\">EP<\/jats:styled-content>) study and ablation for supraventricular tachycardia were enrolled. Patients were kept sedated with continuous infusion of propofol at a fixed rate. Hemodynamic and <jats:styled-content style=\"fixed-case\">EP<\/jats:styled-content> parameters were measured before and after a loading dose of dexmedetomidine (1\u00a0\u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>). A continuous infusion of dexmedetomidine (0.7\u00a0\u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>) was initiated and a ketamine loading dose (1\u00a0mg\u00b7kg<jats:sup>\u22121<\/jats:sup>), followed by continuous infusion (1\u00a0mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>), was given. A repeat set of hemodynamic and <jats:styled-content style=\"fixed-case\">EP<\/jats:styled-content> parameters were then measured at the time of projected peak tissue concentration for both drugs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A significant increase in mean arterial pressure (<jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content>) was seen compared with baseline after loading of dexmedetomidine. This returned to baseline after co\u2010administration of ketamine (mean difference between baseline and after ketamine 1.8\u00a0mmHg; 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>, \u22127.8 to 4.3; <jats:italic>P<\/jats:italic>\u00a0=\u00a0&lt;0.001). A decrease in heart rate was seen after dexmedetomidine followed by a return to baseline after co\u2010administration of ketamine (mean difference between baseline and after ketamine \u22126.5\u00a0bpm; 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>, \u221211.2 to \u22121.8; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.005). Sinus node recovery time was lengthened after dexmedetomidine but returned to baseline after ketamine (mean difference between baseline and after ketamine \u221216.2\u00a0ms; 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>, \u221263 to 30; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.014). <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content> was prolonged after dexmedetomidine and returned to baseline after ketamine (mean difference between baseline and after ketamine \u221234.2\u00a0ms; 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>, \u221248.4 to \u221220.2; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.004). <jats:styled-content style=\"fixed-case\">AV<\/jats:styled-content> nodal effective refractory period was also impaired after dexmedetomidine and showed weak evidence for return to baseline function after ketamine (mean difference between baseline and after ketamine \u221222.8\u00a0ms; 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>, \u221240.2 to \u22125.2; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.069).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The concurrent use of ketamine may mitigate the negative chronotropic effects of dexmedetomidine.<\/jats:p><\/jats:sec>","DOI":"10.1111\/pan.12143","type":"journal-article","created":{"date-parts":[[2013,3,18]],"date-time":"2013-03-18T16:48:25Z","timestamp":1363625305000},"page":"898-905","source":"Crossref","is-referenced-by-count":44,"title":["The effects of ketamine on dexmedetomidine\u2010induced electrophysiologic changes in children"],"prefix":"10.1111","volume":"23","author":[{"given":"Danton","family":"Char","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David R.","family":"Drover","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kara S.","family":"Motonaga","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sanjiv","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christina Y.","family":"Miyake","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne M.","family":"Dubin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory B.","family":"Hammer","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Stanford University School of Medicine Stanford CA USA"},{"name":"Department of Pediatrics Stanford University School of Medicine Stanford CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,3,18]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2044.1999.01114.x"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/00007611-200405000-00007"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.PCC.0000200967.76996.07"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9592.2006.01857.x"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1213\/01.ane.0000217204.92904.76"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1213\/01.ane.0000297421.92857.4e"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1097\/00000542-200008000-00016"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(95)00417-J"},{"key":"e_1_2_8_10_1","doi-asserted-by":"crossref","unstructured":"RamamoorthyC HammerGB GalinkinJet\u00a0al.The pharmacokinetics of ketamine in pediatric cardiac patients. 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