Effect of Dexmedetomidine on Pulmonary Artery Pressure: A Systematic Review

Afsaneh Hashemidoust; Mahmoudreza Moharreri; Pouria Namaee; Alireza Sharifian Attar; Ali Moradi

doi:10.18502/aacc.v12i1.20547

Afsaneh Hashemidoust Department of Anesthesiology, Mashhad University of Medical Sciences, Mashhad, Iran.
Mahmoudreza Moharreri Clinical Research Development Unit, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.
Pouria Namaee Department of Anesthesiology, Mashhad University of Medical Sciences, Mashhad, Iran.
Alireza Sharifian Attar Department of Anesthesiology, Mashhad University of Medical Sciences, Mashhad, Iran.
Ali Moradi Clinical Research Development Unit, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.

DOI: https://doi.org/10.18502/aacc.v12i1.20547

Keywords: Dexmedetomidine; Pulmonary artery pressure; Pulmonary function

Abstract

Background: Dexmedetomidine, a selective α2-adrenergic receptor agonist, is widely used for sedation and analgesia in critically ill pediatric patients. Its dose-dependent modulation of pre- and postsynaptic receptors induces sympatholysis and vascular effects. While systemic hemodynamic impacts are well-documented, its influence on pulmonary artery pressure (PAP) remains underexplored. This systematic review evaluates dexmedetomidine’s effects on PAP.

Methods: This systematic review analyzes studies from databases including SID, IranMedex, Magiran, Google Scholar, Cochrane, Scopus, and Web of Science (2005–2024). Keywords such as “dexmedetomidine,” “pulmonary artery pressure,” and “pulmonary effects” identified cross-sectional studies assessing PAP changes. Fifteen high-quality articles met inclusion criteria.

Results: Dexmedetomidine’s effects on PAP seem inconsistent. Animal studies have reported both increased PAP with intravenous administration and no significant changes. Paradoxically, some models demonstrated PAP reduction in hypertensive states via suppressed vascular contraction. Human studies have observed transient PAP elevation after bolus dosing, though loading doses have shown no sustained pulmonary vascular effects. Preoperative administration reduced pulmonary vascular resistance and mean arterial pressure. Secondary pulmonary outcomes included improved oxygenation and lung mechanics in restrictive lung disease, though benefits were not universal.

Conclusion: Dexmedetomidine exhibits variable PAP modulation, with evidence suggesting transient pressure spikes after bolus doses but neutral or beneficial effects in controlled administrations. Animal-human discrepancies highlight physiological differences, necessitating further clinical research. Beyond hemodynamics, dexmedetomidine may enhance oxygenation and ventilation-perfusion matching while mitigating pulmonary inflammation, though inconsistent oxygenation outcomes underscore context-dependent variability. These findings emphasize cautious dosing in pulmonary hypertension and identify gaps for future human trials to clarify its role in cardiopulmonary management.