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      Sustained Ventricular Arrhythmias in an Asymptomatic Child Posted for Laparoscopic Rectopexy: An Anesthetist's Dilemma?

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          Abstract

          The Editor, Sustained ventricular premature complexes (VPCs) are rare in the pediatric population, especially with structurally normal heart. We would like to describe a case where we observed sustained ventricular arrhythmias in an asymptomatic child posted for surgery. A 14-year-old boy weighing 56 kg (body mass index-24.49) with a history of rectal prolapse was posted for laparoscopic rectopexy under general anesthesia. Preanesthetic evaluation was unremarkable. He was premedicated in the preoperative area with 1 mg of intravenous (IV) midazolam. Anesthetic induction was done with 250 mg of IV thiopentone sodium, 100 μg of IV fentanyl, and 25 mg of IV atracurium. After securing the airway with a 7.0 mm uncuffed endotracheal tube, anesthesia was maintained with oxygen, air, isoflurane, and intermittent positive pressure ventilation. Ventricular ectopics with a heart rate of 70/min were observed on the monitor. There was no response to IV glycopyrrolate 0.2 μg, IV atropine 0.6 mg, or 50 mg of IV xylocard. Instead, it soon progressed to ventricular bigeminy with a blood pressure of 88/60 mmHg. The case was cancelled due to sustained arrhythmias. Postoperatively, the patient was hemodynamically stable with normal sinus rhythm. On further cardiac evaluation, he was found to have resting VPCs which disappeared on exercise. Echocardiography revealed a structurally normal heart. The child was started on oral metoprolol 25 mg twice daily as advised by the cardiologist. He was posted for the same surgery after a week. Preinduction, electrocardiography (ECG) showed ventricular ectopics with hemodynamic values in the normal range. Two large bore IV cannulas and arterial line were secured. He was induced with IV ketamine 100 mg, 100 μg of IV fentanyl, 0.6 mg IV atropine, and 25 mg IV atracurium. Anesthetic plane was deepened with isoflurane and IV xylocard 60 mg was given before laryngoscopy. Postinduction, the patient developed ventricular bigeminy with a heart rate of 60–80 beats/min and blood pressure of 80–90/50–55 mmHg [Figure 1a]. Figure 1 (a) Postinduction, electrocardiography showing ventricular bigeminy figure. (b) Postextubation, electrocardiography patient did not have ectopics Some of the common causes for ventricular arrhythmias such as lighter planes of anesthesia, hypoxia, hypercarbia, acidosis, and dyselectronemias were ruled out. There was no response to treatment with IV calcium gluconate 1000 mg and IV xylocard 60 mg. Isoprenaline infusion was started at 0.1 μg/kg/min for its nonselective beta agonistic action to increase the heart rate and also to reduce QT prolongation. There was only transient response to isoprenaline infusion. Hence, surgeons were persuaded to abandon laparoscopic rectopexy and sclerosant was injected. Postextubation, his heart rate was 103 with a blood pressure of 131/61 mmHg with no ectopics [Figure 1b]. He was advised to undergo a complete workup with the cardiologist and endocrinologist. Although most VPCs are benign in pediatrics, they can be due to various causes such as congenital heart disease, cardiomyopathies, prolonged QT syndrome, electrolyte abnormalities, and Brugada syndrome.[1] A reference to cardiologist is necessary when the diagnosis is new or ECG abnormalities are seen. On the first occasion, our patient was incidentally detected to have ventricular bigeminy on induction of anesthesia. Cardiologist opined it to be of benign origin as it disappeared on exercise.[2 3] Hence, he was taken up for surgery the second time, but ventricular bigeminy was still observed with hemodynamic values in lower limit of normal with no response to treatment. The natural history of VPCs in children with an anatomically normal heart differs depending on the origin of the VPCs. They are classified as VPCs with right bundle branch block (RBBB), VPCs with left bundle branch block, catecholamine-induced ventricular tachycardia, and accelerated idioventricular rhythm (AIVR). VPCs originating from the left ventricle (VPC with RBBB) usually disappear during childhood. In contrast, VPCs originating from the right ventricle and AIVR are reported to be significant and should be regularly followed by a cardiologist.[4 5] With regard to our patient, he suffered from obesity which may lead to ECG abnormalities and left ventricular hypertrophy. However, postoperative echocardiogram revealed a structurally normal heart. Perioperative adrenergic stimulation causing ventricular ectopic activity was offset with IV midazolam, adequate depth of anesthesia, and analgesia. It is noteworthy that many anesthetic and antidysrhythmic agents have prodysrhythmic effects and prolonged QT interval. In fact, the prolongation of QT interval can itself precipitate progression of VPCs to dysrhythmias.[6] Atropine should be contemplated in such cases as it can prolong QT interval and may be the cause for worsening of ECG rhythm.[7 8] In conclusion, we consider the progression of ventricular ectopic to bigeminal rhythm to be an atropine-induced ventricular bigeminy, emphasizing the fact that routine use of antiarrhythmic agents is not indicated in asymptomatic patients. Thus, it is a concern for the anesthesiologist to differentiate children with benign arrhythmias in whom anesthesia can be safely induced and those cases at risk which need to be postponed for further follow-up. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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          Impact of anaesthetic drugs and adjuvants on ECG markers of torsadogenicity.

          Drug-induced prolongation of cardiac repolarization may trigger malignant ventricular arrhythmias, such as torsade de pointes. The duration of QT interval, QT corrected for heart rate (QTc), JT interval, QT dispersion (QTd), QT variability index, and transmular dispersion of repolarization (TDR) are ECG markers of torsadogenicity. All volatiles, especially isoflurane and desflurane, have been found to prolong QTc and QTcd, while sevoflurane has probably no effects on TDR. Among i.v. anaesthetics, propofol seems superior due to its minimal effects on QTc and TDR; moreover, a decrease in QTc and QTcd has been demonstrated in many studies. Regarding opioids, fentanyl, alfentanil, and remifentanil produce no effects on QTc, while sufentanil, at high doses, may induce QT prolongation. Succinylcholine, but not the non-depolarizing neuromuscular blockers, produces QTc prolongation which can be attenuated by opioids and β-blockers. Reversal of neuromuscular block with anticholinesterase-anticholinergic combinations has been associated with significant QTc prolongation, while such an effect has not been demonstrated for sugammadex, even at high doses. Local anaesthetics have probably no intrinsic action on duration of repolarization; nevertheless, an extensive subarachnoid sympathetic block may increase the duration of QTc. On the contrary, thoracic epidural anaesthesia has been associated with a decrease in both QTc and TDR. Among adjuvants, midazolam seems to have no effect on QTc and TDR, while commonly used antiemetics, such as droperidol, domperidone, and most 5-HT3 antagonists, produce significant QT prolongation. The effects of anaesthetic drugs and techniques on electrocardiographic torsadogenic markers should be considered in the perioperative management of patients with preexisting repolarization abnormalities.
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            Natural history of ventricular premature contractions in children with a structurally normal heart: does origin matter?

            Premature ventricular contractions (PVCs) are thought to be innocent in children with normal hearts, especially if they disappear during exercise. The aim of our study was to study the natural history of PVCs in childhood and whether there is a difference between PVCs originating from the right [premature ventricular contraction with left bundle branch block (PVC-LBBB)] or the left ventricle [premature ventricular contraction with right bundle branch block (PVC-RBBB)]. We evaluated children with frequent PVCs and anatomically normal hearts (n= 59; 35M/24F) by 12-lead ECG, echocardiography, Holter recording, and an exercise test. Age at the first visit was 7.1 +/- 4.3 years (mean +/- SD), and follow-up was 3.1 +/- 3.1 years. We could evaluate each child for 2.5 +/- 1.5 times. Premature ventricular contraction with left bundle branch block was seen in 41% of the children; PVC-RBBB in 36%; and undetermined in 23%. Mean percentage PVCs in the Holter recording decreased (14.3 +/- 13.7% in the age group 1-3 years to 4.8 +/- 7.2% in the age group >OR=16 years; P= 0.08). Mean percentage PVC-LBBB did not change (12.3 +/- 21.4 vs. 11.7 +/- 5.5%), whereas PVC-RBBB decreased (16.3 +/- 4.2 to 0.6 +/- 1.4%; P < 0.02). We conclude that there is a difference in the natural history between PVC-LBBB and PVC-RBBB in children with an anatomically normal heart. Premature ventricular contraction with right bundle branch block disappears during childhood. Follow-up of these children seems not necessary. Premature ventricular contraction with left bundle branch block does not disappear and, therefore, it may be necessary to follow these children even during adulthood.
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              Premature ventricular contractions in normal children

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                Author and article information

                Journal
                Ann Card Anaesth
                Ann Card Anaesth
                ACA
                Annals of Cardiac Anaesthesia
                Medknow Publications & Media Pvt Ltd (India )
                0971-9784
                0974-5181
                Jul-Sep 2018
                : 21
                : 3
                : 343-344
                Affiliations
                [1] Department of Paediatric Anaesthesia, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India
                Author notes
                Address for correspondence: Dr. Kavya R Upadhya, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India. E-mail: kavya.upadhya@ 123456gmail.com
                Article
                ACA-21-343
                10.4103/aca.ACA_223_17
                6078037
                30052234
                8a8502f0-99d0-4efc-bc52-cbaccc05ceb9
                Copyright: © 2018 Annals of Cardiac Anaesthesia

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

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