The hemodynamic response to dexmedetomidine loading dose in children with and without pulmonary hypertension. (Kamat)

Friesen RH, Nichols CS, Twite MD, Cardwell KA, Pan Z, Pietra B, Miyamoto SD, Auerbach SR, Darst JR, Ivy DD. The hemodynamic response to dexmedetomidine loading dose in children with and without pulmonary hypertension. Anesth Analg. 2013 Oct;117(4):953-9.

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.

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Predictors of mortality in pediatric patients on venous-arterial extracorporeal membrane oxygenation. (from Journal of the American College of Cardiology, March 2013 – Stockwell)

Journal of the American College of Cardiology, 61 (10), Supplement, 12 March 2013, E436.

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BACKGROUND:  Currently, there are no established echocardiographic (echo) or hemodynamic predictors of mortality after venous-arterial extracorporeal membrane oxygenation (ECMO) wean in children. We attempted to determine which echo and hemodynamic measurement predicts mortality.

METHODS:  Over 2 years, we prospectively assessed 6 echo and 6 hemodynamic variables at 3-5 ECMO flow rates during flow wean. Hemodynamic measurements were: heart rate, inotropic score, arterio-venous oxygenation difference (AV-02), pulse pressure, oxygenation index (OI) and serum lactate. Echo variables included: shortening and ejection fraction, outflow tract Doppler-derived stroke distance (VTI), amount of atrioventricular valve regurgitation, global longitudinal strain (GLS) and global circumferential strain (GCS). Patients were stratified into those who died or needed a transplant (Gr1) and those that did not (Gr2). For each patient, we compared the change within each of these variables between full versus minimum flow for Gr1 versus Gr2 using a paired t-test.

RESULTS:  Twenty-one patients were enrolled in the study with an age range of 0.05-15 years. Five had dilated cardiomyopathy while the remaining 16 had structural heart disease with cardiomyopathy. Twelve patients comprised Gr1 with only one heart transplant while 9 who lived constituted Gr2. In Gr1, subjects had a significantly greater increase in AVO2 (31% mean increase, p<0.01) and Ol (43% mean increase, p<0.01) off ECMO compared to full flow but no change in VTI with flow wean. In Gr2, VTI increased significantly (30% mean increase p<0.01) with no change in AVO2 or Ol. GLS was nearly significantly increased off ECMO in Gr2 (p=0.09). Pulse pressure increased significantly in both groups and was not discriminatory (p<0.01).

CONCLUSIONS:  Failure to augment VTI during ECMO flow wean or an increase in OI and AVO2 portend poor outcomes in pediatric patients. These measurements should be a part of practice standards for patients weaning from ECMO and may discern who will require alternative methods of support. Future studies appear indicated to confirm these findings with a larger sample size.