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The hemodynamic response to dexmedetomidine loading dose in children with and without pulmonary hypertension
Robert H Friesen1, Christopher S Nichols, Mark D Twite
1From the Department of Anesthesiology, Department of Pediatrics, The Research Institute, and Department of Pediatrics (Cardiology), Children's Hospital Colorado, University of Colorado, Denver, Colorado.
Insights
Dexmedetomidine loading doses caused systemic vasoconstriction and hypertension in children, but did not significantly affect pulmonary artery pressure (PAP), even in those with pulmonary hypertension. This suggests dexmedetomidine is safe for pediatric cardiac patients with pulmonary hypertension.
Area of Science:
- Pediatric Cardiology
- Anesthesiology
- Pharmacology
Background:
- Dexmedetomidine, an alpha-2 receptor agonist, is frequently used in pediatric cardiac patients.
- Concerns exist regarding its potential to cause systemic and pulmonary vasoconstriction.
- Quantifying its hemodynamic effects, particularly on pulmonary artery pressure (PAP), is crucial.
Purpose of the Study:
- To prospectively evaluate the impact of dexmedetomidine initial loading doses on mean PAP in pediatric cardiac patients.
- To compare these effects in children with and without pulmonary hypertension.
Main Methods:
- Observational study involving children undergoing cardiac catheterization.
- Anesthesia maintained with midazolam and remifentanil infusion after sevoflurane induction.
- Hemodynamic parameters, including PAP, were measured before and after dexmedetomidine infusion (0.5-1 μg/kg over 10 minutes).
Main Results:
- Dexmedetomidine administration led to significant decreases in heart rate and increases in mean arterial blood pressure and indexed systemic vascular resistance.
- Cardiac index remained unchanged.
- A minor, statistically significant increase in PAP was noted in transplant patients, but not in those with pulmonary hypertension. Indexed pulmonary vascular resistance did not change significantly.
Conclusions:
- Dexmedetomidine loading doses induce systemic vasoconstriction and hypertension in children.
- Pulmonary vascular responses to dexmedetomidine were not significant, even in children with pulmonary hypertension.
- Dexmedetomidine is likely not contraindicated in pediatric cardiac patients with pulmonary hypertension.
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 i.v. (or 0.5 mg/kg orally preoperatively) and remifentanil i.v. 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.
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