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Effects of phenylephrine on systemic and cerebral circulations in humans: a systematic review with mechanistic explanations.
Meng, L; Sun, Y; Zhao, X; Meng, D M; Liu, Z; Adams, D C; McDonagh, D L; Rasmussen, M.
Affiliation
  • Meng L; Department of Anesthesia, Indiana University School of Medicine, IA, Indianapolis, USA.
  • Sun Y; Department of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
  • Zhao X; Department of Anesthesiology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
  • Meng DM; Choate Rosemary Hall School, CT, Wallingford, USA.
  • Liu Z; Department of Biostatistics and Health Data Science, Indiana University School of Medicine, IA, Indianapolis, USA.
  • Adams DC; Department of Anesthesia, Indiana University School of Medicine, IA, Indianapolis, USA.
  • McDonagh DL; Departments of Anesthesiology and Pain Management, Neurological Surgery, Neurology and Neurotherapeutics, UT Southwestern Medical Center, TX, Dallas, USA.
  • Rasmussen M; Department of Anesthesiology, Section of Neuroanesthesia, Aarhus University Hospital, Aarhus, Denmark.
Anaesthesia ; 79(1): 71-85, 2024 Jan.
Article in En | MEDLINE | ID: mdl-37948131
ABSTRACT
We conducted a systematic review of the literature reporting phenylephrine-induced changes in blood pressure, cardiac output, cerebral blood flow and cerebral tissue oxygen saturation as measured by near-infrared spectroscopy in humans. We used the proportion change of the group mean values reported by the original studies in our analysis. Phenylephrine elevates blood pressure whilst concurrently inducing a reduction in cardiac output. Furthermore, despite increasing cerebral blood flow, it decreases cerebral tissue oxygen saturation. The extent of phenylephrine's influence on cardiac output (r = -0.54 and p = 0.09 in awake humans; r = -0.55 and p = 0.007 in anaesthetised humans), cerebral blood flow (r = 0.65 and p = 0.002 in awake humans; r = 0.80 and p = 0.003 in anaesthetised humans) and cerebral tissue oxygen saturation (r = -0.72 and p = 0.03 in awake humans; r = -0.24 and p = 0.48 in anaesthetised humans) appears closely linked to the magnitude of phenylephrine-induced blood pressure changes. When comparing the effects of phenylephrine in awake and anaesthetised humans, we found no evidence of a significant difference in cardiac output, cerebral blood flow or cerebral tissue oxygen saturation. There was also no evidence of a significant difference in effect on systemic and cerebral circulations whether phenylephrine was given by bolus or infusion. We explore the underlying mechanisms driving the phenylephrine-induced cardiac output reduction, cerebral blood flow increase and cerebral tissue oxygen saturation decrease. Individualised treatment approaches, close monitoring and consideration of potential risks and benefits remain vital to the safe and effective use of phenylephrine in acute care.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oxygen / Vasoconstrictor Agents Type of study: Systematic_reviews Limits: Humans Language: En Journal: Anaesthesia Year: 2024 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oxygen / Vasoconstrictor Agents Type of study: Systematic_reviews Limits: Humans Language: En Journal: Anaesthesia Year: 2024 Document type: Article Affiliation country: