Dexmedetomidine bolus resulted in minimal affects on pulmonary hemodynamics.  (Image source: Thinkstock)

Dexmedetomidine bolus resulted in minimal affects on pulmonary hemodynamics. (Image source: Thinkstock)

Dexmedetomidine is now commonly used for sedation of patients undergoing diagnostic and therapeutic procedures.  Given that the procedures include patients undergoing cardiac catheterization, it is important to know how dexmedetomidine affects pulmonary hemodynamics.  To that end, Dr. Robert H. Friesen, Department of Anesthesiology, Children’s Hospital Colorado, University of Colorado, Aurora, CO and coauthors documented pulmonary vascular hemodynamics of dexmedetomidine in children undergoing cardiac catheterization for routine surveillance after cardiac transplantation, or children with pulmonary hypertension.  Their findings are published in this month’s edition of Anesthesia & Analgesia, in the article, “The Hemodynamic Response to Dexmedetomidine Loading Dose in Children With and Without Pulmonary Hypertension.”

The authors studied 42 patients total (21 transplant patients and 21 pulmonary hypertensive patients).  Anesthesia was induced with sevoflurane, which was maintained throughout the procedure. After IV insertion, patients received an infusion of remifentanil, a bolus of rocuronium. Midazolam was given orally before the procedure, or intravenously after IV insertion.

Dexmedetomidine was given in doses of 1, 0.75 or 0.5 µg/kg, given over 10 minutes. Seven pulmonary hypertension subjects and 7 transplant subjects received each of the three doses. Following the initial doses dexmedetomidine was continued as a 0.7 µg/kg/h infusion.

Dexmedetomidine was followed by a statistically significant but clinically modest increase in pulmonary artery pressure in heart transplant patients. This was not observed in patients with pulmonary hypertension. Indexed pulmonary artery pressures were not different between the two groups. Both groups also had clinically insignificant decreases in heart rate and mean arterial pressure, and clinically insignificant increases in systemic vascular resistance and right arterial pressure.

The patients with pulmonary hypertension also received chronic pulmonary vasodilator medications (i.e., phosphodiesterase inhibitors, endothelin receptor antagonists, prostacyclin analogues, and calcium channel blockers). These medications independently reduce anesthesia-related complications in patients with pulmonary hypertension and thus may have reduced any changes seen with dexmedetomidine.

While dexmedetomidine appears to be well tolerated in children with pulmonary hypertension, the study does not address whether older anesthesia regimens might be just as safe.