Dexmedetomidine controls junctional ectopic tachycardia during Tetralogy of Fallot repair in an infant.

Dexmedetomidine is a highly selective α2 -adrenergic agonist approved for short-term sedation and monitored anesthesia care in adults. Although not approved for use in the pediatric population, an increasing number of reports describe its use in pediatric patients during the intraoperative period and in the intensive care unit. Dexmedetomidine can potentially have an adverse impact on the cardiovascular system secondary to its negative chronotropic and dromotropic effects. However, it is these cardiac effects that are currently being explored as a therapeutic option for the treatment of perioperative tachyarrhythmias in pediatric patients with congenital heart disease (CHD). We report the use of dexmedetomidine to treat junctional ectopic tachycardia (JET), which developed following cardiopulmonary bypass for surgical correction of Tetralogy of Fallot in a 6-week-old infant. Within 15 min of increasing the dexmedetomidine infusion from 0.5 to 3 μg/kg/h, JET converted to normal sinus rhythm. This case report provides additional anecdotal evidence that dexmedetomidine may have a therapeutic role in the treatment of perioperative tachyarrhythmias in pediatric patients with CHD. The specific effects of dexmedetomidine on the cardiac conduction system are reviewed followed by a summary of previous reports describing its use as a therapeutic agent to treat perioperative arrhythmias.

Sudden cardiac death under anesthesia in pediatric patient with williams syndrome: A case report and review of literature.

Williams syndrome is a complex syndrome characterized by developmental abnormalities, craniofacial dysmorphic features, and cardiac anomalies. Sudden death has been described as a very common complication associated with anesthesia, surgery, and procedures in this population. Anatomical abnormalities associated with the heart pre-dispose these individuals to sudden death. In addition to a sudden and rapid downhill course, lack of response to resuscitation is another significant feature seen in these patients. The authors report a five-year-old male with Williams syndrome, hypothyroidism, and attention deficit hyperactivity disorder. He suffered an anaphylactic reaction during CT imaging with contrast. Resuscitation was unsuccessful. Previous reports regarding the anesthetic management of patients with Williams are reviewed and the potential for sudden death or peri-procedure related cardiac arrest discussed in this report. The authors also review reasons for refractoriness to defined resuscitation guidelines in this patient population.

Changes in near infrared spectroscopy during deep hypothermic circulatory arrest.

Monitoring cerebral oxygenation with near infrared spectroscopy may identify periods of cerebral desaturation and thereby the patients at risk for perioperative neurocognitive issues. Data regarding the performance of near infrared spectroscopy monitoring during deep hypothermic circulatory arrest are limited. The current study presents data regarding use of a commercially available near infrared spectroscopy monitor during deep hypothermic circulatory arrest in paediatric patients undergoing surgery for congenital heart disease. The cohort included 8 patients, 2 weeks to 6 months of age, who required deep hypothermic circulatory arrest for repair of congenital heart disease. The baseline cerebral oxygenation was 63 +/- 11% and increased to 88 +/- 7% after 15 min of cooling to a nasopharyngeal temperature of 17-18 degrees C on cardiopulmonary bypass. In 5 of 8 patients, the cerebral oxygenation value had achieved its peak value (either >or=90% or no change during the last 2-3 min of cooling on cardiopulmonary bypass). In the remaining 3 patients, additional time on cardiopulmonary bypass was required to achieve a maximum cerebral oxygenation value. The duration of deep hypothermic circulatory arrest varied from 36 to 61 min (43.4 +/- 8 min). After the onset of deep hypothermic circulatory arrest, there was an incremental decrease in cerebral oxygenation to a low value of 53 +/- 11%. The greatest decrease occurred during the initial 5 min of deep hypothermic circulatory arrest (9 +/- 3%). Over the entire period of deep hypothermic circulatory arrest, there was an average decrease in the cerebral oxygenation value of 0.9% per min (range of 0.5 to 1.6% decline per minute). During cardiopulmonary bypass, cooling and deep hypothermic circulatory arrest, near infrared spectroscopy monitoring followed the clinically expected parameters. Such monitoring may be useful to identify patients who have not achieved the highest possible cerebral oxygenation value despite 15 min of cooling on cardiopulmonary bypass. Future studies are needed to define the cerebral oxygenation value at which neurological damage occurs and if interventions to correct the decreased cerebral oxygenation will improve perioperative outcomes.