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Table of Contents
EDITORIAL  
Year : 2012  |  Volume : 15  |  Issue : 3  |  Page : 177-179
Dexmedetomidine in pediatric cardiac anesthesia


Additional Professor Anaesthesiology, SCTIMST, Trivandrum, India

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Date of Web Publication4-Jul-2012
 

How to cite this article:
Neema PK. Dexmedetomidine in pediatric cardiac anesthesia. Ann Card Anaesth 2012;15:177-9

How to cite this URL:
Neema PK. Dexmedetomidine in pediatric cardiac anesthesia. Ann Card Anaesth [serial online] 2012 [cited 2019 Jul 19];15:177-9. Available from: http://www.annals.in/text.asp?2012/15/3/177/97972


Dexmedetomidine is a highly selective α2-adrenoceptor agonist with sedative, anxiolytic and analgesic properties and has minimal effects on respiratory drive. [1],[2],[3] It was approved by the United States Food and Drug Administration (FDA) on December 24, 1999, for the sedation of adults receiving mechanical ventilation in an intensive care unit (ICU) setting. On October 17, 2008, it received an additional indication for sedation of non-intubated patients prior to or during surgery or other medical procedures. [4] Recently, dexmedetomidine was approved in Europe for sedation of adult ICU patients requiring a sedation level not deeper than arousal in response to verbal stimulation. [5] It should be noted that dexmedetomidine is yet not approved by FDA for use in pediatric patients. However, several papers describe its use in pediatric patients in operating room, in catheterization laboratory, in MRI suits and in ICU. The indications in these situations were as a part of anesthesia technique, sedation, analgesia, reduction of narcotic use, control of agitation in ICU, etc.

The central pharmacologic effects of dexmedetomidine are mediated via α2A and imidazoline type 1 receptors which results in a reduction in the sympathetic outflow from the locus ceruleus of the brainstem resulting in decreases in heart rate (HR) and systemic vascular resistance (SVR). [4] The analgesic effects of dexmedetomidine are thought to result from activation of α2B-adrenoceptors at the level of the dorsal horn of the spinal cord and the inhibition of substance P release. [6],[7] The peripheral vascular effects of dexmedetomidine results from stimulation of α2B-adrenoceptors in the peripheral vasculature and cause an initial increase in SVR. [8],[9] No adverse effects on the pulmonary vasculature have been reported including patients with preexisting pulmonary hypertension. [10] It is structurally related to clonidine, but has a much greater affinity for α2-adrenoceptor over α1-adrenoceptors with a ratio of 1,600:1. Dexmedetomidine is initially administered as a bolus in the doses of 0.5 to 1 μg/kg over 10 min followed by its infusion at the rate of 0.3 to 0.7 μg/kg/h. However, because of the possibility of bradycardia and hypotension, several authors, particularly, in cardiac anesthesia practice avoid the loading dose and administer it as continuous infusion at the rate of 0.3 to 0.7 μg/kg/h. Indeed, Ingersoll-Weng et al.[11] reported severe bradycardia and cardiac arrest in a woman who underwent thymectomy for myasthenia gravis, the patient was treated with pyridostigmine and had received loading dose of dexmedetomidine (1 μg/kg over 10 min), fentanyl 250 μg, midazolam 10 mg, and propofol 200 mg for anesthetic induction. Presumably, the bradycardic response observed with dexmedetomidine was augmented by the concurrent use of other medications with negative chronotropic and/or vagal effects. Arguably, one should be cautious while simultaneously administering multiple drugs with negative chronotropic effects.

In this issue of Annals of Cardiac Anaesthesia, LeRiger et al, [12] describes successful conversion of junctional ectopic tachycardia (JET) to sinus rhythm (SR) with dexmedetomidine in an infant undergoing intracardiac repair of Tetralogy of Fallot (TOF). Conversion to SR occurred within 15 min of increasing the dexmedetomidine infusion from 0.5 μg/kg/h to 3 μg/kg/h. Several authors have described successful management of arrhythmias by dexmedetomidine. [13],[14] In a few anecdotal reports dexmedetomidine was successful in restoring SR in situations where routine antiarrhythmic agents had failed. [15],[16],[17] These reports clearly indicate that dexmedetomidine has antiarrhythmic actions. Hammer et al, [18] in a clinical study in pediatric patients undergoing electrophysiological study, evaluated effect of dexmedetomidine on sinus node, atrioventricular node and conduction pathways and found a decrease in HR with significant depression of sinus and atrioventricular nodal function. Chrysostomou et al[19]

reported changes in various electrophysiological parameters, including the PR interval, PRc, PR index and the QRS interval; however, they determined that the changes were related to changes in HR and not related to a direct effect of dexmedetomidine on cardiac conduction tissues. The important cardiovascular effects of dexmedetomidine are a decrease in HR, SVR, and antiarrhythmic effects. These pharmacologic actions of dexmedetomidine are highly desirable in the post-bypass period and intensive care management of pediatric cardiac surgical patients.

The hemodynamic goals during management of pediatric cardiac surgical patients varies from patient to patient; the patients with right to left shunt lesions such as TOF generally require sustained or increased SVR to limit right to left shunt and to sustain pulmonary blood flow. The patients with obstructive lesions and hypertrophied myocardium such as pulmonary stenosis or aortic stenosis require increased SVR to maintain myocardial perfusion. In neonates, infants and small children the cardiac output is HR dependent. Although, a decrease in SVR appears undesirable in pediatric cardiac surgical patients having right to left shunt or obstructive lesions of major vessels; the attenuation of sympathetic responses, a decrease in HR and systemic vasodilation, become desirable in presence of surgical stimulation during surgical repair of cardiac defects of these patients. In majority of pediatric cardiac surgical patients, drugs with cardiovascular effects are used at the time of separation from cardiopulmonary bypass (CPB) and in the postoperative period for augmenting the myocardial functions and for reducing the afterload. Dobutamine, because of its ino-dilatory action is preferred in many pediatric cardiac surgery units. Logically, simultaneous infusion of dexmedetomidine would add to vasodilator action of dobutamine, decrease its required dose and counter tachycardia by its HR decreasing action. Finally, the well appreciated actions of dexmedetomidine such as anesthetic and opioid sparing effect, sedation and smooth emergence, and minimal interference with respiratory system paves way for early weaning from ventilatory support and extubation. Used judiciously, dexmedetomidine has salutary cardiovascular actions; however, one should be careful with its use in the prebypass period in patients undergoing repair of complex congenital defects and obstructive lesions; however, its cardiovascular actions in the post bypass period and intensive care of these patients are desirable.

Neurological injury is a major cause of morbidity in pediatric cardiac surgical patients undergoing correction of congenital cardiac defects. Magnetic resonance imaging (MRI) identified abnormalities are present preoperatively in 33% of cardiac neonates, and in as many as 93% postoperatively. [20] Early in life, the brain undergoes an intensive period of neuronal development and axonal growth. The immature brain's fragile vasculature, high metabolic activity, and immature cerebral autoregulation, make it particularly susceptible during CPB to hypoperfusion as well as hyperperfusion, increased permeability, edema formation and ischemia-reperfusion injury. Presently, in neonates, the post-CPB neurologic injury is estimated to range from 2% to 30%. [21],[22] The evidences strongly indicate necessity to provide neuroprotection to pediatric patients undergoing cardiac surgery with CPB. There is an increasing body of both in vitro and in vivo evidences which indicates that dexmedetomidine exerts a cell-protective effect on nervous tissue under ischemic conditions. [23],[24],[25],[26] Recent evidence suggest that this effect is mediated by dexmedetomidine's α2A-agonistic properties and also by imidazoline type 1-recepors. [27] Sato et al[26] in an experimental study compared the combination of dexmedetomidine and hypothermia with the controls and found improved short-term neurologic outcome with combination therapy. In a review Afonso and Reis [28] observed that dexmedetomidine seems to have promising future applications in neuroprotection, cardioprotection and renoprotection. It is apparent that dexmedetomidine have several beneficial cardiovascular and neuroprotective properties; therefore, there is an urgent need to confirm these beneficial effects in well-designed studies to establish its place in pediatric cardiac anesthesia.

 
   References Top

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2.Virtanen R, Savola JM, Saano V, Nyman L. Characterization of the selectivity, specificity and potency of dexmedetomidine as an alpha 2-adrenoceptor agonist. Eur J Pharmacol 1988;150:9-14.   Back to cited text no. 2
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3.McDonald T, Hoffman WE, Berkowitz R, Cunningham F, Cooke B. Heart rate variability and plasma catecholamines in patients during opioid detoxification. J Neurosurg Anesthesiol 1999;11:195-9.  Back to cited text no. 3
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4.Buck ML. Dexmedetomidine use in pediatric intensive care and procedural sedation. J Pediatr Pharmacol Ther 2010;15:17-29  Back to cited text no. 4
    
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6.Munoz R, Berry D. Dexmedetomidine: promising drug for pediatric sedation? Pediatr Crit Care Med 2005;6:493-4.  Back to cited text no. 6
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7.Precedex [package insert]. Lake Forest, IL: Hospira, Inc; October 2008. Available from: http://www.precedex.com. [Last accessed on 2009 Sept 25].   Back to cited text no. 7
    
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9.Philipp M, Brede M, Hein L. Physiological significance of alpha(2)-adrenergic receptor subtype diversity: one receptor is not enough. Am J Physiol Regul Integr Comp Physiol 2002;283:R287-95.   Back to cited text no. 9
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10.Tobias JD, Gupta P, Naguib A, Yates AR. Dexmedetomidine: Applications for the pediatric patient with congenital heart disease. Pediatr Cardiol 2011 Dec; 32:1075-87.  Back to cited text no. 10
    
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12.LeRiger M, Naguib A, Gallantowicz M, Tobias JD. Dexmedetomidine controls junctional ectopic tachycardia during Tetralogy of Fallot repair in an infant. Ann Card Anaesth 2012;15:224-28.   Back to cited text no. 12
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14.Chrysostomou C, Sanchez-de-Toledo J, Wearden P, Jooste EH, Lichtenstein SE, Callahan PM, et al. Perioperative use of dexmedetomidine is associated with decreased incidence of ventricular and supraventricular tachyarrhythmias after congenital cardiac operations. Ann Thorac Surg 2011; 92:964-72; discussion 972.  Back to cited text no. 14
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23.Hoffman WE, Kochs E, Werner C, Thomas C, Albrecht RF. Dexmedetomidine improves neurologic outcome from incomplete ischemia in the rat. Reversal by the alpha 2-adrenergic antagonist atipamezole. Anesthesiology 1991;75:328-32.  Back to cited text no. 23
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25.Engelhard K, Werner C, Eberspacher E, Bachl M, Blobner M, Hildt E, et al. The effect of the alpha 2-agonist dexmedetomidine and the N-methyl-D-aspartate antagonist S(+)-ketamine on the expression of apoptosis-regulating proteins after incomplete cerebral ischemia and reperfusion in rats. Anesth Analg 2003;96:524-31.  Back to cited text no. 25
    
26.Sato K, Kimura T, Nishikawa T, Tobe Y, Masaki Y. Neuroprotective effects of a combination of dexmedetomidine and hypothermia after incomplete cerebral ischemia in rats. Acta Anaesthesiol Scand 2010;54:377-82.  Back to cited text no. 26
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27.Dahmani S, Paris A, Jannier V, Hein L, Rouelle D, Scholz J, et al. Dexmedetomidine increases hippocampal phosphorylated extracellular signal-regulated protein kinase 1 and 2 content by an alpha 2-adrenoceptor-independent mechanism: evidence for the involvement of imidazoline I1 receptors. Anesthesiology 2008;108:457-66.  Back to cited text no. 27
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Correspondence Address:
Praveen Kumar Neema
B-9, NFH, Sree Chitra Quarters, Kumarapuram, Trivandrum
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.97972

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