Congenital Cardiac Anesthesia Society
A Section of the the Society for Pediatric Anesthesia

{“questions”:{“mlbh2”:{“id”:”mlbh2″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Anuradha Dev, MD and Marc Atwell MD – Georgetown Public Health Corporation (GPHC), Georgetown, Guyana AND Destiny F. Chau, MD – Arkansas Children\u2019s Hospital\/University of Arkansas for Medical Sciences, Little Rock, AR, USA \r\nA 10-year-old boy presents with shortness of breath and declining exercise capacity. Transthoracic echocardiography demonstrates a double chamber right ventricle. Which of the following percentages reflects the approximate number of patients with double chamber right ventricle with a concurrent ventricular septal defect? \r\n\r\n”,”desc”:”EXPLANATION \r\nDouble chamber right ventricle (DCRV) is a rare cardiac diagnosis reported in up to 2.6% of patients with congenital heart disease. It typically presents in childhood with few cases reported in adults. DCRV is described by a sub-infundibular tissue substrate within the body of the right ventricle (RV) that leads to progressive RV outflow obstruction. The obstructing tissue has been identified as hypertrophied trabecular muscle bands and\/or atypical moderator bands that divide the RV into a proximal high-pressure inlet chamber located close to the apical region of the RV and a distal low-pressure outlet chamber located near the infundibular region. There is typically an increased pressure gradient greater than 20 mmHg across the two chambers (see Figure below). \r\n\r\nIt is hypothesized that the anatomical substrate for DCRV is often present at birth. For example, congenital cardiac defects that create flow turbulence may trigger tissue hypertrophy leading to obstruction within the RV cavity. Although over 75% of DCRVs are associated with ventricular septal defect (VSD), it is also associated with tetralogy of Fallot (TOF), double outlet right ventricle, and Ebstein anomaly. The VSD of DCRV is usually small and perimembranous. Although it may be located in any location along the interventricular septum, the VSD usually connects with the proximal high-pressure inlet chamber. The resulting pathophysiology is due to shunt flow characteristics as determined by the location of the VSD in relation to the obstruction within the RV. When the VSD is distal to the obstructing muscle bundle, the resulting physiology is akin to an isolated VSD, but when the VSD connects to the RV proximal to the muscle bundle, the physiology is akin to tetralogy of Fallot. \r\n\t\r\n\r\n\r\n \r\n\r\nFigure: Two-dimensional TTE with color-flow Doppler. Parasternal short-axis view at the aortic valve level in end systole demonstrates muscular septation of the RV into a high-pressure proximal chamber and low-pressure distal subvalvular chamber. Arrows indicate RV muscular bundles causing subvalvular obstruction. AV= aortic valve, PV=pulmonic valve, TV=tricuspid valve, RA=right atrium, pRV=proximal RV, dRV=distal RV. \r\nFrom Malone RJ, Henderson ER, Wilson ZR, et al. Double-chambered right ventricle in adulthood: a case series. CASE (Phila). 2024;8(3Part A):202-209. doi:10.1016\/j.case.2023.12.012. Creative Commons Licensing 4.0. \r\n\r\nPatients with severe RVOT obstruction typically present with dyspnea on exertion and limited exercise capacity. Echocardiography is a good first-line screening tool for many cardiac defects, but the identification of DCRV may often be overlooked unless there is a high index of suspicion. Other imaging modalities such as magnetic resonance imaging or cardiac catheterization can confirm the diagnosis of DCRV. Surgery involves transatrial or transventricular resection of the obstructing muscle bundles and a VSD closure. Survival rates in the current era are excellent. However, there is the potential for a right bundle branch block or complete heart block. \r\n\r\nThe correct answer is C, over 75% of patients with DCRV also have an associated VSD.\r\n\r\n\r\n \r\nREFERENCES \r\nLoukas M, Housman B, Blaak C, Kralovic S, Tubbs RS, Anderson RH. Double-chambered right ventricle: a review. Cardiovasc Pathol<\/em>. 2013;22(6):417-423. doi:10.1016\/j.carpath.2013.03.004\r\n\r\nStout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA\/ACC guideline for the management of adults with congenital heart disease: Executive summary: A report of the American College of Cardiology\/American Heart Association task force on clinical practice guidelines [published correction appears in J Am Coll Cardiol. 2019.14;73(18):2361]. J Am Coll Cardiol<\/em>. 2019;73(12):1494-1563. doi:10.1016\/j.jacc.2018.08.1028\r\n\r\nSaid SM, Burkhart HM, Dearani JA, O’Leary PW, Ammash NM, Schaff HV. Outcomes of surgical repair of double-chambered right ventricle. Ann Thorac Surg<\/em>. 2012;93(1):197-200. doi:10.1016\/j.athoracsur.2011.08.043\r\n\r\nKahr PC, Alonso-Gonzalez R, Kempny A, et al. Long-term natural history and postoperative outcome of double-chambered right ventricle–experience from two tertiary adult congenital heart centres and review of the literature. Int J Cardiol<\/em>. 2014;174(3):662-668. doi:10.1016\/j.ijcard.2014.04.177\r\n\r\nHubail ZJ, Ramaciotti C. Spatial relationship between the ventricular septal defect and the anomalous muscle bundle in a double-chambered right ventricle. Congenit Heart Dis<\/em>. 2007; 2:421-423. \r\n\r\n\r\n\r\n”,”hint”:””,”answers”:{“842tz”:{“id”:”842tz”,”image”:””,”imageId”:””,”title”:”A.\t25%”},”c3amd”:{“id”:”c3amd”,”image”:””,”imageId”:””,”title”:”B.\t50%”},”qjgeb”:{“id”:”qjgeb”,”image”:””,”imageId”:””,”title”:”C.\t75%”,”isCorrect”:”1″}}}}}

{“questions”:{“cl5v4”:{“id”:”cl5v4″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Philicia Findlay-Hardyal, MD and Arturo Marrero, MD- Georgetown Public Health Corporation – Georgetown, Guyana AND Destiny F. Chau, MD – Arkansas Children\u2019s Hospital\/University of Arkansas for Medical Sciences, Little Rock, AR, USA \r\n\r\nA 3-month-old infant with a suspected vascular ring is undergoing rigid bronchoscopy, which demonstrates the presence of complete tracheal rings. Which of the following types of vascular rings is MOST likely present in this patient? “,”desc”:”EXPLANATION \r\nVascular rings describe congenital anomalies whereby the aortic arch and its primary branches form a circle around the trachea, the esophagus, or both, potentially resulting in tracheal and\/or esophageal obstruction and obstructive symptoms. The incidence of isolated vascular rings has been reported as seven in 10,000 live births (0.07%). As vascular rings are rare, diagnosis requires a high index of clinical suspicion. Patients may be misdiagnosed with refractory asthma and\/or gastrointestinal pathology, thus deferring further workup until the vascular ring is finally diagnosed. \r\n\r\n\r\nThe embryologic mechanism for vascular rings originates from the interruption at different stages of the normal regression of the six pharyngeal arches that are connected to the dorsal aortae during the embryologic development of the aortic arch and its main branches. This results in the persistence of vascular structures or ligamentous remnants that may compress the trachea or esophagus.\r\n\r\n\r\nThe majority of vascular ring malformations can be classified into the following grouping system described by Backer and Mavroudis: \r\n\r\n\r\nA.\tDouble aortic arch: the left and right aortic arches encircle the trachea and esophagus. \r\nB.\tRight aortic arch with left ligamentum: the aortic arch is to the right of the trachea, with the ligamentum connecting the main pulmonary artery to the descending aorta. \r\nC.\tInnominate artery compression syndrome: the innominate artery compresses the anterior trachea by over 80%. \r\nD.\tPulmonary artery sling: the left pulmonary artery originates from the right pulmonary artery traveling posteriorly, between the trachea and esophagus.\r\n\r\n\r\nThe figure below illustrates reconstructed computed tomography of the different types of vascular rings.\r\n\r\n\r\n\r\n \r\n\r\nFigure: Vascular rings reconstructed from cardiac computed tomography. A: double aortic arch; two aortic arches (white bold arrows) comprise the complete ring in this patient. B: right aortic arch with persistent left ligamentum arteriosum; Kommerell’s diverticulum (arrowhead) and fibrotic band (white dotted arrows) comprise the complete ring in this patient. C: right aortic arch with aberrant left subclavian artery (red bold arrow). D: pulmonary sling; left pulmonary artery originates from the right pulmonary artery (red dotted arrow), compressing the bronchus. \r\nSource: Suh YJ, Kim GB, Kwon BS, et al. The clinical course of vascular rings and risk factors associated with mortality. Korean Circ J. 2012;42(4):252-258. doi:10.4070\/kcj.2012.42.4.252- Creative Commons License\r\n\r\n\r\n\r\nOnce clinical suspicion arises, confirmatory diagnosis is usually made by cardiac computed tomography or magnetic resonance imaging. Echocardiography is unreliable for definitive diagnosis but does aid in the detection of associated cardiac anomalies occurring in approximately 12% of patients. Bronchoscopy allows for the delineation of tracheal abnormalities, such as tracheobronchomalacia, and for the detection of complete tracheal rings.\r\n\r\n\r\nExcept for pulmonary artery slings, vascular ring repair is usually performed through a thoracotomy for surgical division of the ring. Surgical repair of a pulmonary artery sling is performed through a median sternotomy approach and under cardiopulmonary bypass, as the left pulmonary artery needs to be translocated. Additionally, 60-80% of patients with pulmonary artery slings also have tracheal stenosis secondary to complete cartilaginous tracheal rings, which are repaired during the same procedure. Tracheal reconstruction is usually recommended after the vascular ring repair to avoid contamination of the surgical field from secretions within the trachea. The most common repair for complete tracheal rings is a slide tracheoplasty for long-segment stenosis. Resection of a short, narrowed segment of complete tracheal rings may be repaired with an end-to-end anastomosis. Although survival rates are excellent, patients often require repeat airway evaluation and intervention for persistent tracheomalacia, granuloma formation, or balloon dilation. Patients also require regular follow-up to evaluate for the development of left pulmonary artery stenosis.\r\n\r\n\r\nIn this infant, the presence of the complete tracheal rings indicates a moderate to high probability of a pulmonary artery sling. Although double aortic arch and right aortic arch\/left ligamentum are much more common than pulmonary artery slings, they are not typically associated with complete tracheal rings. \r\n\r\n\r\n \r\nREFERENCES \r\n\r\nWadle M, Joffe D, Backer C, Ross F. Perioperative and anesthetic considerations in vascular rings and slings. Semin Cardiothorac Vasc Anesth<\/em>. 2024;28(3):152-164. doi:10.1177\/10892532241234404\r\n\r\n\r\nWorhunsky DJ, Levy BE, Stephens EH, Backer CL. Vascular rings. Semin Pediatr Surg<\/em>. 2021;30(6):151128. doi:10.1016\/j.sempedsurg.2021.151128\r\n\r\n\r\nMcKenzie I, Markakis Zestos M, Stayer S, Kaminski E, Davies P, Andropoulos D. Anesthesia for miscellaneous lesions. In: Andropoulos D, Mossad E, Gottlieb E, eds. Anesthesia for Congenital Heart Disease<\/em>. 4th Edition. New Jersey: John Wiley & Sons, Inc.; 2023: 816-820.\r\n\r\n\r\nSuh YJ, Kim GB, Kwon BS, et al. Clinical course of vascular rings and risk factors associated with mortality. Korean Circ J. 2012;42(4):252-258. doi:10.4070\/kcj.2012.42.4.252\r\n”,”hint”:””,”answers”:{“etcn7”:{“id”:”etcn7″,”image”:””,”imageId”:””,”title”:”A.\tDouble aortic arch”},”keig0″:{“id”:”keig0″,”image”:””,”imageId”:””,”title”:”B.\tPulmonary artery sling”,”isCorrect”:”1″},”tfkzq”:{“id”:”tfkzq”,”image”:””,”imageId”:””,”title”:”C.\tRight aortic arch with left ligamentum\r\n\r\n”}}}}}

{“questions”:{“nm19a”:{“id”:”nm19a”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Childrens Hospital Colorado\r\nA 7-year-old boy with a history of acute lymphoblastic leukemia treated with doxorubicin presents with symptoms of heart failure. Which of the following morphological subtypes of cardiomyopathy is MOST likely to be found in this patient? \r\n\r\n”,”desc”:”EXPLANATION \r\nAnthracyclines are a class of cytotoxic drugs extracted from the Streptomyces<\/em> bacterium. They are utilized as chemotherapeutic agents and include doxorubicin (the most commonly used), daunorubicin, and epirubicin. First used in the 1960s, anthracyclines remain one of the most commonly used and effective chemotherapeutics for solid and hematological cancers. Anthracyclines are inhibitors of the DNA topoisomerase II enzyme, leading to DNA double-strand breaks and subsequent upregulation of p53, which results in programmed cell death (apoptosis). \r\n\r\nAnthracyclines are thought to be the primary drugs related to chemotherapy-induced cardiotoxicity. The risk of cardiotoxicity increases as the total cumulative dose of doxorubicin (Dox) increases, with a 3-5% risk at 400 mg\/m^{2<\/sup> and 18-48% at 700 mg\/m2<\/sup>. Apoptosis-mediated loss of cardiomyocytes and oxidative stress are the main culprits of Dox-induced cardiomyopathy. Extremes of age (less than 5 years of age or greater than 65 of age), preexisting cardiac disease or cardiovascular risk factors, and radiation therapy are additional risk factors for Dox-induced cardiomyopathy. \r\n\r\nAnthracycline-induced cardiotoxicity can develop at various time points after the initiation of doxorubicin treatment, leading to a dated classification. Acute cardiotoxicity occurs after a single dose or course with the onset of symptoms within 2 weeks. Early-onset chronic occurs within 1 year and presents as a dilated-hypokinetic cardiomyopathy, with progressive development of heart failure. Late-onset chronic occurs years to decades after completion of doxorubicin therapy. Anthracycline-induced cardiotoxicity is defined as a decrease in left ventricular ejection fraction greater than 10% with a final value less than 53% after exposure. It is typically detected via cardiac imaging such as echocardiography and magnetic resonance imaging, along with monitoring of cardiac biomarkers. \r\n\r\nMost guidelines recommend serial monitoring after anthracycline use. While historically, doxorubicin-induced cardiotoxicity has been thought of as irreversible and associated with high mortality, more recent studies are suggesting that there may be some effectiveness of heart failure therapy. Primary prevention includes lifestyle modification of cardiovascular risk factors, limitations on total dosage, and the use of less cardiotoxic analogs such as epirubicin. Additionally, dexrazoxane, an iron-chelating agent that prevents the accumulation of oxygen-free radicals, is often included in chemotherapy regimens to protect against the cardiotoxic effects of anthracyclines. The mainstays of heart failure therapy for anthracycline-mediated dilated cardiomyopathy are angiotensin-converting enzyme inhibitors and beta blockers. \r\n\r\nAnthracyclines, and specifically doxorubicin-induced cardiotoxicity, are most commonly associated with a dilated hypokinetic cardiomyopathy (answer B). Hypertrophic cardiomyopathy (answer C) is typically associated with genetic disorders. While restrictive cardiomyopathy (answer A) can develop as a result of anthracycline use, it is much less common and presents years or decades after exposure. Restrictive cardiomyopathy is more commonly associated with deposition disorders such as amyloidosis and hemochromatosis. \r\n\r\n\r\n \r\nREFERENCES \r\nCardinale D, Iacopo F, Cipolla CM. Cardiotoxicity of Anthracyclines. Front Cardiovasc Med<\/em>. 2020;7:26. doi: 10.3389\/fcvm.2020.00026. \r\n\r\nRawat PS, Jaiswal A, Khurana A, Bhatti JS, Navik U. Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management. Biomed Pharmacother<\/em>.2021;139:111708. doi: 10.1016\/j.biopha.2021.111708. \r\n\r\nMancilla TR, Iskra B, Aune GJ. Doxorubicin-Induced Cardiomyopathy in Children. Compr Physiol<\/em>. 2019:12;9(3):905-931. doi: 10.1002\/cphy.c180017. \r\n\r\n”,”hint”:””,”answers”:{“kenij”:{“id”:”kenij”,”image”:””,”imageId”:””,”title”:”A.\tRestrictive cardiomyopathy”},”ggit0″:{“id”:”ggit0″,”image”:””,”imageId”:””,”title”:”B.\tDilated cardiomyopathy”,”isCorrect”:”1″},”huyfa”:{“id”:”huyfa”,”image”:””,”imageId”:””,”title”:”C.\tHypertrophic cardiomyopathy\r\n\r\n”}}}}}}

{“questions”:{“gc68c”:{“id”:”gc68c”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Children\u2019s Hospital Colorado \r\n\r\nA six-day-old boy with a prenatal diagnosis of D-transposition of the great arteries and ventricular septal defect presents for arterial switch operation and ventricular septal defect repair. Which of the following Society of Thoracic Surgeons and the European Association for Cardio-thoracic Surgery Congenital Heart Surgery Mortality Categories characterize this surgical procedure?\r\n”,”desc”:”EXPLANATION \r\nGiven the complexity and heterogeneity of congenital heart disease and surgical repair, comparison of procedures proves challenging when analyzing outcomes and data. Historically, procedure risk and complexity were categorized using methodologies based on expert opinion such as the Aristotle Basic Complexity Score (ABC Score) and ABC Level (ABC Level), in addition to the Risk Adjustment for Congenital Heart Surgery-1 (RACHS-1) methodology. With the creation of large databases of surgical outcomes, it became apparent that a more quantitative and validated scoring system was needed in recent decades. \r\n\r\nIn 2009 O\u2019Brien et al. analyzed the mortality risk of 148 types of operations that had been conducted on more than 77,000 patients who were entered into the European Association for Cardiothoracic Surgery (EACTS) Congenital Heart Surgery database and the Society of Thoracic Surgeons (STS) Congenital Heart Surgery database. Procedure-specific mortality rate estimates were calculated, and each procedure was assigned a numeric score, ranging from 0.1 to 5.0 based on the estimated mortality rate. This score was termed the STS-EACTS Congenital Heart Surgery Mortality Score or STS-EACTS score, more commonly referred to as STAT mortality categories. These surgical procedures were then grouped into five categories, referred to as the STS-EACTS Congenital Heart Surgery Mortality Categories (STS-EACTS categories). This scoring system categorizes procedures based on complexity and mortality, with category 1 being the lowest mortality risk and category 5 being the highest mortality risk. This model was then independently validated and compared with the ABC Score and the RACHS-1 score. The STS-EACTS scores and categories have demonstrated high discrimination (C-index) for predicting mortality as compared to the prior models. Although there are numerous congenital cardiac diagnoses for specific surgical procedures, representative examples of procedures and mortality categories are shown in Table 1 below.\r\n\r\n\r\n\r\nTable 1: Common examples of procedures in each STS-EACTS mortality category.\r\n\r\nThe STS-EACTS mortality categories have been increasingly utilized for both research and outcomes reporting. They are utilized in the STS Congenital Heart Surgery Database public reporting of mortality risk for participating hospitals. Given the expanded availability of this data, patients and parents are increasingly aware of and utilize this information when choosing a hospital for surgical care of congenital heart disease. \r\n\r\n \r\nREFERENCES \r\nO’Brien SM, Clarke DR, Jacobs JP et al. An empirically based tool for analyzing mortality associated with congenital heart surgery. J Thorac Cardiovasc Surg<\/em>. 2009;138(5):1139-53. doi: 10.1016\/j.jtcvs.2009.03.071. PMID: 19837218.\r\n\r\nJacobs JP, Jacobs ML, Maruszewski B et al. Initial application in the EACTS and STS Congenital Heart Surgery Databases of an empirically derived methodology of complexity adjustment to evaluate surgical case mix and results. Eur J Cardiothorac Surg<\/em>. 2012;42(5):775-779 i: 10.1093\/ejcts\/ezs026. \r\n\r\nJacobs JP, Jacobs ML, Lacour-Gayet FG et al. Stratification of complexity improves the utility and accuracy of outcomes analysis in a Multi-Institutional Congenital Heart Surgery Database: Application of the Risk Adjustment in Congenital Heart Surgery (RACHS-1) and Aristotle Systems in the Society of Thoracic Surgeons (STS) Congenital Heart Surgery Database. Pediatr Cardiol<\/em>. 2009;30(8):1117-1130. doi: 10.1007\/s00246-009-9496-0. PMID: 19771463.\r\n\r\nThe Society for Thoracic Surgeons Public Reporting. https:\/\/publicreporting.sts.org\/chsd. Accessed November 13, 2024.\r\n\r\n”,”hint”:””,”answers”:{“ft11c”:{“id”:”ft11c”,”image”:””,”imageId”:””,”title”:”A. 3″},”bedlj”:{“id”:”bedlj”,”image”:””,”imageId”:””,”title”:”B. 4″,”isCorrect”:”1″},”jctpe”:{“id”:”jctpe”,”image”:””,”imageId”:””,”title”:”C. 5″}}}}}

{“questions”:{“3ajp7”:{“id”:”3ajp7″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Fernando F. Cuadrado, MD and Matthew Monteleone, MD – Cincinnati Children\u2019s Hospital Medical Center \r\n\r\nA seven-year-old boy with a history of orthotopic heart transplantation is undergoing cardiac catheterization and biopsy under general endotracheal anesthesia. He is erroneously administered a 15 mcg\/kg bolus dose of dexmedetomidine due to an infusion pump programming error. The heart rate immediately decreases to 67 bpm with a blood pressure of 72\/43. Which of the following side effects is MOST likely to be observed in this patient? “,”desc”:”EXPLANATION \r\nDexmedetomidine is a highly selective alpha_{2<\/sub> adrenergic receptor agonist that induces sedation, anxiolysis, and analgesia by inhibiting norepinephrine release, thereby reducing sympathetic tone and promoting sedation without respiratory depression. In pediatric anesthesia, it is frequently used for postoperative sedation, particularly following cardiac catheterization. Dexmedetomidine is preferred in this setting because it provides sedation with stable hemodynamics and minimal to no respiratory depression, making it an ideal choice for children with cardiac conditions.\r\n\r\nThe most common side effects include hypotension, bradycardia, and, less frequently, hypertension, which typically occurs shortly after rapid bolus administration. The hypotensive effects are mediated via stimulation of central alpha2A<\/sub> receptors, resulting in decreased catecholamine release and sympathetic outflow from the locus ceruleus of the brainstem. In heart transplant patients, the bradycardic effects may be diminished due to cardiac denervation, though hypotension and hypertension can still occur. While these side effects are well-documented, less common adverse events such as hypoglycemia and miosis may arise, particularly with high doses or prolonged high-dose infusions. In a 2009 case report, a 20 month-old, 11kg patient was accidentally administered 36 mcg\/kg of dexmedetomidine over 36 minutes. A blood glucose check prompted by several shaking episodes in the recovery unit was 26 mg\/dL. The authors speculate that the hypoglycemia was due to the drug\u2019s sympatholytic effects of reducing circulating norepinephrine levels with a reduction in gluconeogenesis and glycogenolysis. Additionally, a decrease in serum cortisol levels may blunt the stress response induced by surgery, further affecting glucose homeostasis. In another case report, a 3-year-old, 11 kg child was accidentally given 100 mcg of dexmedetomidine as a bolus. The child presented with significant bradycardia, hypotension, bradypnea, deep hypnosis, and miosis, requiring treatment with an epinephrine infusion. Although this patient\u2019s glucose remained normal, the authors speculate that this may have been due to the epinephrine counteracting the sympatholytic effects of dexmedetomidine. In summary, when there is concern about oversedation, blood glucose levels should be closely monitored because of the increased risk of hypoglycemia with the administration of high-dose dexmedetomidine.\r\n\r\nThe correct answer is B, hypoglycemia. Dexmedetomidine offers effective sedation with a favorable safety profile in pediatric patients, particularly after cardiac procedures. However, there is a potential for hypoglycemia with higher-than-usual clinical doses. Notably, dexmedetomidine does not cause hyperglycemia. Additionally, xerostomia, rather than sialorrhea, is a common side effect due to reduced salivary gland activity. Finally, dexmedetomidine produces pupillary constriction in awake volunteers, possibly due to absent inhibition of the pupilloconstrictor nucleus and reduced sympathetic tone of the iris muscles. \r\n\r\n\r\n \r\nREFERENCES \r\nBernard PA, Makin CE, Werner HA. Hypoglycemia associated with dexmedetomidine overdose in a child? J Clin Anesth<\/em>. 2009; 21:50\u201353.\r\n\r\nG\u00f6rges M, Poznikoff AK, West NC, Brodie SM, Brant RF, Whyte SD. Effects of Dexmedetomidine on Blood Glucose and Serum Potassium Levels in Children Undergoing General Anesthesia: A Secondary Analysis of Safety Endpoints During a Randomized Controlled Trial. Anesth Analg<\/em>. 2019;129:1093-1099\r\n\r\nNath SS, Singh S, Pawar ST. Dexmedetomidine overdosage: An unusual presentation. Indian J Anaesth<\/em> 2013; 57(3):289-291.\r\n\r\nJooste EH, Muhley WT, Ibinson JW, et al. Acute hemodynamic changes after rapid intravenous bolus dosing of dexmedetomidine in pediatric heart transplant patients undergoing routine cardiac catheterization. Anesth Analg<\/em>. 2010;111(6):1490-1496.\r\n\r\n”,”hint”:””,”answers”:{“fbw95”:{“id”:”fbw95″,”image”:””,”imageId”:””,”title”:”A.\tSialorrhea “},”whv28”:{“id”:”whv28″,”image”:””,”imageId”:””,”title”:”B.\tHypoglycemia”,”isCorrect”:”1″},”fgzhl”:{“id”:”fgzhl”,”image”:””,”imageId”:””,”title”:”C.\tMydriasis”}}}}}}