Dexmedetomidine use in patients undergoing electrophysiological study for supraventricular tachyarrhythmias.

BACKGROUND: Dexmedetomidine is a selective alpha-2 adrenergic agonist with sedative, analgesic, and anxiolytic properties. Dexmedetomidine has not been approved for use in pediatrics. Dexmedetomidine has been reported to depress sinus node and atrioventricular nodal function in pediatric patients; it has been suggested that the use of dexmedetomidine may not be desirable during electrophysiological studies. AIM: We hypothesize that the use of dexmedetomidine does not inhibit the induction of supraventricular tachyarrhythmias (SVT) during electrophysiological studies and does not inhibit the ablation of such arrhythmias. METHODS: In this retrospective, observational cohort study, we reviewed all cases presenting to the cardiac catheterization laboratory for diagnosis or treatment of SVT since 2007. All cases were performed by the same electrophysiologist. The anesthesia was provided by one of the three cardiac anesthesiologists. One cardiac anesthesiologist did not use dexmedetomidine during electrophysiological studies. A second used dexmedetomidine, but only with an infusion. The third used dexmedetomidine with a primary bolus and an infusion. Thus, the patients were stratified into three different groups: Group 1 patients did not receive any dexmedetomidine. Group 2 patients received a dexmedetomidine infusion of 0.5-1 µg·kg-1 ·h-1 . Group 3 patients received a dexmedetomidine infusion of 0.5-1 µg·kg-1 ·h-1 and a dexmedetomidine bolus prior to the infusion of 0.5-1 µg·kg-1 . We then compared those patients for the following variables: demographic data including age, sex, height, weight; anesthetic data such as, mask vs intravenous induction, identity of induction agent, amount of sevoflurane and propofol used; amount of dexmedetomidine used; presence of congenital heart disease and other comorbidities; the need for isoproterenol and dose, the need for adenosine and dose, and the need for any other medications to affect rhythm both before and after radiofrequency ablation; the ability to induce the arrhythmia, the type of arrhythmia, the presence of Wolff-Parkinson-White syndrome, the presence of an accessory pathway, the ablation rate, and the recurrence rate. RESULTS: There was no difference in the anesthetic agents, except there was a lesser amount of propofol used in the dexmedetomidine groups (χ2(2) = 48.2, P < 0.001). There was no difference in the electrophysiological parameters among groups, except the Group 1 patients did require the use of isoproterenol in the preablation period less often compared to the dexmedetomidine groups (χ2(2) = 15.2, P < 0.01). However, with the greater use of isoproterenol, there was no difference in the ability to induce the arrhythmia. Moreover, the percentage of patients ablated, and the recurrence rate among groups was the same. CONCLUSIONS: We conclude that dexmedetomidine does not interfere with the conduct of electrophysiological studies for SVT and the successful ablation of such arrhythmias. However, dexmedetomidine use did result in a greater need for isoproterenol.

Initial experience with dexmedetomidine for diagnostic and interventional cardiac catheterization in children.

BACKGROUND: Children undergoing diagnostic and interventional cardiac catheterization require deep sedation or general anesthesia (GA). Dexmedetomidine, a selective alpha-2 adrenergic agonist, has sedative, analgesic and anxiolytic properties without respiratory depression. These characteristics make it potentially suitable as a sedative agent during diagnostic procedures in children. We report our experience using dexmedetomidine in 20 children aged 3 months to 10 years undergoing cardiac catheterization. METHODS: Following a midazolam premedication, intravenous access was secured facilitated by the inhalation of sevoflurane in oxygen. A loading dose of 1 microg x kg(-1) dexmedetomidine was administered over 10 min followed by an initial infusion rate of 1 microg x kg(-1) x h(-1). Nasal cannulae were applied, allowing endtidal CO2 monitoring with the patients breathing spontaneously. Hemodynamic parameters, Bispectral Index Score (BIS) and sedation score were measured every 5 min. Patient movement or evidence of inadequate sedation were treated with propofol (1 mg x kg(-1)). The dexmedetomidine infusion rate was titrated to the level of sedation to a maximum of 2 microg x kg(-1) x h(-1) to maintain a sedation score of 4-5 and a BIS value <80. RESULTS: Five patients (25%) had some movement on local infiltration or groin vessel access. This did not necessitate restraint or result in difficulty securing vascular access. No patients failed sedation that required the addition of another sedative agent or conversion to GA; eight patients were sedated with dexmedetomidine alone; however, 12 (60%) patients did receive a propofol bolus at some time during the procedure due to movement, increasing BIS value or in anticipation of stimulation. There were no incidences of airway obstruction or respiratory depression. In all cases the heart rate and blood pressure remained within 20% of baseline. No patient required treatment for profound bradycardia or hypotension. The average infusion rate for dexmedetomidine following the loading dose was 1.15 (+/-0.29)microg x kg(-1) x h(-1) (range 0.6-2.0 microg x kg(-1) x h(-1)). CONCLUSIONS: This initial experience showed dexmedetomidine, with or without the addition of propofol, may be a suitable alternative for sedation in spontaneously breathing patients undergoing cardiac catheterization.

Anesthetic management of the neonate with congenital complete heart block: a 16-year review.

BACKGROUND: Anesthesia for patients with complete heart block can be associated with significant hemodynamic instability. The aim of this study is to review our anesthetic experience of neonates with congenital complete heart block (CCHB) who underwent placement of either a temporary epicardial pacing system or a permanent epicardial pacemaker. METHODS: The anesthetic management of neonates with CCHB who underwent pacemaker placement at a single institution over a 16-year period was reviewed. RESULTS: Twenty-four neonates were identified, 17 with a structurally normal heart (NL) and seven with associated congenital heart defects (CHD). Median (range) gestational age was 36.9 (26-41) weeks, birth weight 2.9 (1.0-4.1) kg, and baseline heart rate 47 (38-80) b.min(-1). A temporary epicardial pacing system was placed in six patients (four CHD, two NL; P = 0.003) following institution of mechanical ventilation and inotropic support for a low cardiac output state, and a permanent epicardial pacemaker was placed in 18 patients. Atropine 0.02 mg.kg(-1) IV prior to induction (n = 5) increased heart rate less than 20%. Intraoperative hypotension was documented in nine neonates, five of seven with CHD and four of 17 with NL (P = 0.02). In four patients (44%) hypotension occurred despite concurrent inotropic support. Intraoperative cardiac arrest occurred in one neonate, necessitating institution of extracorporeal membrane oxygenation. Two patients (8.3%) died in hospital from complex CHD and complications of prematurity. CONCLUSIONS: Early institution of mechanical ventilation, inotropic support and pacing are necessary in the neonate with CCHB and poor hemodynamic function, particularly with coexisting CHD or prematurity.