The Hemodynamic Response to Dexmedetomidine Loading Dose in Children With and Without Pulmonary Hypertension

Abstract

BACKGROUND Dexmedetomidine, an α-2 receptor agonist, is widely used in children with cardiac disease. Significant hemodynamic responses, including systemic and pulmonary vasoconstriction, have been reported after dexmedetomidine administration. Our primary goal of this prospective, observational study was to quantify the effects of dexmedetomidine initial loading doses on mean pulmonary artery pressure (PAP) in children with and without pulmonary hypertension. METHODS Subjects were children undergoing cardiac catheterization for either routine surveillance after cardiac transplantation (n = 21) or pulmonary hypertension studies (n = 21). After anesthetic induction with sevoflurane and tracheal intubation, sevoflurane was discontinued and anesthesia was maintained with midazolam 0.1 mg/kg IV (or 0.5 mg/kg orally preoperatively) and remifentanil IV infusion 0.5 to 0.8 μg/kg/min. Ventilation was mechanically controlled to maintain Pco2 35 to 40 mm Hg. When end-tidal sevoflurane was 0% and fraction of inspired oxygen (Fio2) was 0.21, baseline heart rate, mean arterial blood pressure, PAP, right atrial pressure, pulmonary artery occlusion pressure, right ventricular end-diastolic pressure, cardiac output, and arterial blood gases were measured, and indexed systemic vascular resistance, indexed pulmonary vascular resistance, and cardiac index were calculated. Each subject then received a 10-minute infusion of dexmedetomidine of 1 μg/kg, 0.75 μg/kg, or 0.5 μg/kg. Measurements and calculations were repeated at the conclusion of the infusion. RESULTS Most hemodynamic responses were similar in children with and without pulmonary hypertension. Heart rate decreased significantly, and mean arterial blood pressure and indexed systemic vascular resistance increased significantly. Cardiac index did not change. A small, statistically significant increase in PAP was observed in transplant patients but not in subjects with pulmonary hypertension. Changes in indexed pulmonary vascular resistance were not significant. CONCLUSION Dexmedetomidine initial loading doses were associated with significant systemic vasoconstriction and hypertension, but a similar response was not observed in the pulmonary vasculature, even in children with pulmonary hypertension. Dexmedetomidine does not appear to be contraindicated in children with pulmonary hypertension.

Beneficial aspect of dexmedetomidine as a postoperative sedative for cardiac surgery

“…A loading dose according to the recommended administration method of dexmedetomidine may cause systemic vasoconstriction, hypertension [14], excessive sedation and airway obstruction [15], and a high maintenance dose (> 0.7 mg/kg/h) may cause bradycardia [16]. In the present study, the loading dose of dexmedetomidine was omitted and titration was continued with less than 0.7 mg/kg/h.…”

Hemodynamic response to ketamine in children with pulmonary hypertension

“…Yet hemodynamic reactivity to circulating catecholamines was preserved during fentanyl anesthesia , suggesting that reactivity in response to catecholamines increased by ketamine (centrally mediated release and inhibition of reuptake) would remain intact. The anesthetic combination used for baseline conditions in our subjects was also described in a previous study , and we believe it to be appropriate for investigations of pulmonary hemodynamics in children.…”

Dexmedetomidine-Induced Contraction Involves CPI-17 Phosphorylation in Isolated Rat Aortas

“…An initial loading dose or bolus administration of dexmedetomidine produces transient hypertension and increased systemic vascular resistance [31,32]. In addition, high doses or high concentrations of dexmedetomidine cause hypertension in humans [9,10,11,12].…”