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

{“questions”:{“pe13n”:{“id”:”pe13n”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: David Fitzgerald, MD and Destiny F. Chau MD – Arkansas Children\u2019s Hospital \/University of Arkansas for Medical Sciences – Little Rock, AR \r\n\r\nAn 18-year-old woman with a history of exertional dyspnea and frequent lower respiratory tract infections undergoes bronchoscopy that demonstrates abnormal right lower lobe bronchial architecture. A chest x-ray demonstrates a nonspecific irregularity over the right lower lung field with dextroposition of the heart, and an echocardiogram reveals right heart dilation. Which of the following congenital heart defects is the MOST likely diagnosis?\r\n”,”desc”:”EXPLANATION \r\nScimitar syndrome is a subtype of partial anomalous pulmonary venous return (PAPVR) in which the right pulmonary vein drains abnormally to the inferior vena cava (IVC), typically near the level of the diaphragm. It is associated with varying degrees of right lung hypoplasia and cardiac dextroposition. The name, Scimitar syndrome, is owed to the crescent shape of the anomalous right pulmonary vein resembling the curved blade of a scimitar sword. The incidence is approximately one to three per 100,000 live births, and accounts for 0.5 to 1% of all congenital heart disease. \r\n\r\n\r\nScimitar syndrome can present in infancy or early adulthood. In infants, the median age at diagnosis is estimated to be seven months old. Among neonates diagnosed with Scimitar syndrome, up to 75% have associated anomalies, which include right lung hypoplasia, dextrocardia, right pulmonary artery hypoplasia, collateral blood vessels from infra-diaphragmatic aorta to the right lower lobe of the lung, secundum atrial septal defect (ASD), and diaphragmatic hernia. More severe cases are typically diagnosed within the first two months of life due to the presence of pulmonary hypertension, heart failure, and recurrent pulmonary infections. The adult form is typically milder in clinical presentation with the Scimitar vein often found incidentally in otherwise healthy patients. Symptomatic young adults usually present with recurrent pulmonary infections and exertional dyspnea from pulmonary sequestration. The characteristic Scimitar vein is often demonstrated on chest x-ray (CXR) (see Figure 1). \r\n\r\n\r\n\r\n\r\n\r\n\r\nFigure 1. Chest radiograph demonstrating Scimitar vein. https:\/\/commons.wikimedia.org\/wiki\/File:Scimitar_syndrome_chest_xray.jpg, licensed under the Creative Commons Attribution-Share Alike 4.0 International license.\r\n\r\nThe Scimitar vein produces a left to right shunt leading to excessive pulmonary blood flow and right heart dilation. Medical management centers on reducing excessive pulmonary blood flow to slow the progression to pulmonary hypertension and heart failure. Patients with the infantile form who exhibit signs of pulmonary hypertension require surgical correction. Other indications for surgical correction include a Q_{p<\/sub>:Qs<\/sub> greater than 1.5 in an asymptomatic patient, recurrent pneumonia, and heart failure. \r\n\r\n\r\nAny preoperative anesthetic evaluation should include a review of cardiac imaging and functional studies given the high association of Scimitar syndrome with other congenital cardiac defects. Evaluation should also include the presence and severity of pulmonary hypertension, quantification of left to right shunt, baseline cardiopulmonary status, and degree of pulmonary hypoplasia. While the adolescent and adult forms tend to be milder in clinical presentation, the presence of recurrent infections, lung hypoplasia and longstanding pulmonary circulatory overload should be closely evaluated prior to anesthetic administration. \r\n\r\n\r\nThis patient\u2019s history, clinical presentation, CXR, echocardiography and bronchoscopy strongly suggest a diagnosis of Scimitar syndrome. Though both sinus venosus atrial septal defect and Ebstein\u2019s anomaly lead to right heart dilation, neither defect is typically associated with right lung hypoplasia. \r\n\r\n\r\n\r\n \r\nREFERENCES \r\n\r\nMidyat L, Demir E, A\u015fkin M, et al. Eponym. Scimitar syndrome. Eur J Pediatr<\/em>. 2010;169(10): 1171-1177. doi:10.1007\/s00431-010-1152-4. \r\n\r\nBrown D, Geva T. Anomalies of the Pulmonary Veins. In: Shaddy R, Penny D, Feltes T, Cetta F and Mital S, eds. Moss and Adams\u2019 Heart Disease in Infants, Children and Adolescents including the Fetus and Young Adult. 10th Edition. Philadelphia: Wolters Kluwer; 2022: 854-856.\r\n\r\n\r\nChowdhury UK, Anderson RH, Sankhyan LK, et al. Surgical management of the scimitar syndrome. J Card Surg<\/em>. 2021; 36(10):3770-3795. doi:10.1111\/jocs.15857\r\n\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<\/em>. 2019 May 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\n\r\n\r\n”,”hint”:””,”answers”:{“x73aq”:{“id”:”x73aq”,”image”:””,”imageId”:””,”title”:”A.\tEbstein\u2019s anomaly”},”62p0m”:{“id”:”62p0m”,”image”:””,”imageId”:””,”title”:”B.\tSinus venosus atrial septal defect”},”5iyl3″:{“id”:”5iyl3″,”image”:””,”imageId”:””,”title”:”C.\tScimitar syndrome\r\n\r\n”,”isCorrect”:”1″}}}}}}

{“questions”:{“1ld82”:{“id”:”1ld82″,”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\nAn 11-year-old boy with a family history of desmoplakin cardiomyopathy presents for cardiac magnetic resonance imaging. He was recently found to be a carrier for a DSP gene mutation. Which of the following features is MOST likely to be present in desmoplakin cardiomyopathy as compared to other types arrhythmogenic cardiomyopathy?”,”desc”:”EXPLANATION \r\nDesmoplakin (DSP)<\/em> is a desmosomal protein encoded by the DSP<\/em> gene located on chromosome 6. It is expressed in both cardiomyocytes and skin and plays an important role in linking the cardiac desmosome to intermediate filaments. It is essential for normal force transmission in myocardial tissue. Mutations in the DSP<\/em> gene have been identified in arrhythmogenic right ventricular cardiomyopathy (ARVC) and in familial dilated cardiomyopathy (DCM). However, more recently, mutations in the DSP<\/em> gene have been associated with a distinct form of cardiomyopathy with a high prevalence of left ventricular fibrosis and systolic dysfunction, which differs from ARVC and DCM. Termed desmoplakin (DSP)<\/em> cardiomyopathy, this disease has distinct features as compared to other forms of arrhythmogenic cardiomyopathy. Recently, the Padua criteria has categorized arrhythmogenic cardiomyopathy (ACM) into three phenotypes including arrhythmogenic right ventricular cardiomyopathy (ARVC), arrhythmogenic left ventricular cardiomyopathy (ALVC), and biventricular arrhythmogenic cardiomyopathy. \r\n\r\nThe pathophysiology of DSP<\/em> cardiomyopathy includes episodic inflammatory myocardial injury that leads to progressive ventricular fibrosis and myocardial scarring, left ventricular systolic dysfunction, and ventricular arrythmias. This clinically manifests as episodic chest pain, heart failure, and ventricular arrythmias. Patients will often exhibit ST segment changes and troponin elevations but will have normal coronary angiography. There is heterogeneity in phenotype regarding single or biventricular systolic dysfunction and arrhythmogenic burden. Ventricular arrythmias may be life-threatening and the initial presentation may include syncope or cardiac arrest. Varying criteria have been established for diagnosis, but typically include left ventricular (LV) or biventricular systolic dysfunction, ECG abnormalities, cardiac magnetic resonance imaging (CMRI) demonstrating late LV gadolinium enhancement due to scar, ventricular arrhythmias, and personal or familial DSP<\/em> mutation. CMRI is the most sensitive test for phenotype in DSP<\/em> cardiomyopathy as extensive fibrosis may be detected prior to echocardiographic or ECG changes. Due to the expression of DSP<\/em> in skin, more than 50% of patients also exhibit palmoplantar keratoderma (callused skin on hands and soles of the feet). \r\n\r\nTherapy includes management of underlying heart failure and arrythmias with prevention of sudden cardiac death (SCD). Recommendations for risk stratification and management specific to DSP<\/em> cardiomyopathy continue to evolve. Studies by Wang and Smith have differed on the prognostic markers, such as male gender and ejection fraction (EF), which predispose patients to an increased risk of arrhythmia and SCD. An EF below 35% has consistently been associated with high risk for malignant ventricular arrhythmias, though some events may also be associated with an EF of 35% to 55%. Without specific guidelines for DSM<\/em> cardiomyopathy, the current recommendations for primary prevention of SCD with an implantable cardioverter-defibrillator (ICD) are to follow guidelines for other ventricular arrhythmias and heart failure. \r\n\r\nIn contrast to other types of arrhythmogenic and dilated cardiomyopathy, DSP<\/em> cardiomyopathy predominantly involves the left ventricle, often without any RV involvement, and has a unique pathophysiology, clinical presentation, and outcome. Episodes of myocardial injury and epicardial fibrosis occur and precede overt systolic dysfunction in DSP<\/em> cardiomyopathy. Ventricular arrhythmias are common to all forms of arrhythmogenic cardiomyopathy. Left ventricular systolic dysfunction rather than biventricular systolic dysfunction is more common in DSP<\/em> cardiomyopathy. Right ventricular dysfunction is more typical of ARVC. \r\n\r\n \r\nREFERENCES \r\nBrand\u00e3o M, Bariani R, Rigato I, Bauce B. Desmoplakin Cardiomyopathy: Comprehensive Review of an Increasingly Recognized Entity. J Clin Med<\/em>. 2023;12(7):2660. doi: 10.3390\/jcm12072660. \r\n\r\nSmith ED, Lakdawala NK, Papoutsidakis N et al. Desmoplakin Cardiomyopathy, a Fibrotic and Inflammatory Form of Cardiomyopathy Distinct From Typical Dilated or Arrhythmogenic Right Ventricular Cardiomyopathy. Circulation<\/em>. 2020;141(23):1872-1884. doi: 10.1161\/CIRCULATIONAHA.119.044934. \r\n\r\nWang W, Murray B, Tichnell C et al. Clinical characteristics and risk stratification of desmoplakin cardiomyopathy.Europace<\/em>. 2022;24(2):268-277. doi: 10.1093\/europace\/euab183.\r\n\r\nDi Lorenzo F, Marchionni E, Ferradini V et al. DSP-Related Cardiomyopathy as a Distinct Clinical Entity? Emerging Evidence from an Italian Cohort.Int J Mol Sci<\/em>. 2023;24(3):2490. doi: 10.3390\/ijms24032490.\r\n\r\nGraziano F, Zorzi A, Cipriani A et al. The 2020 \”Padua Criteria\” for Diagnosis and Phenotype Characterization of Arrhythmogenic Cardiomyopathy in Clinical Practice. J Clin Med<\/em>. 2022;11(1):279. doi: 10.3390\/jcm11010279. \r\n”,”hint”:””,”answers”:{“tqyx6”:{“id”:”tqyx6″,”image”:””,”imageId”:””,”title”:”A. Left ventricular epicardial fibrosis”,”isCorrect”:”1″},”zso0c”:{“id”:”zso0c”,”image”:””,”imageId”:””,”title”:”B. Ventricular arrhythmias”},”yjc44″:{“id”:”yjc44″,”image”:””,”imageId”:””,”title”:”C. Biventricular systolic dysfunction “}}}}}

{“questions”:{“sl1zl”:{“id”:”sl1zl”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Gibbs Yim, MD and Nicholas Houska, DO – University of Colorado and Children\u2019s Hospital Colorado \r\n\r\nA 13-year-old boy with dilated cardiomyopathy is prescribed dapagliflozin as part of a regimen for decompensated heart failure. Which of the following adverse events is MOST likely associated with dapagliflozin? \r\n”,”desc”:”EXPLANATION \r\nDapagliflozin is an oral sodium-glucose co-transporter (SGLTS) inhibitor used in the treatment of heart failure, diabetes, and chronic kidney disease. SGLT2 is a sodium-glucose co-transporter located in the renal proximal tubules responsible for the reabsorption of glucose. Inhibition of this receptor reduces serum glucose and decreases the renal reabsorption of sodium, inducing natriuresis and diuresis. This medication has been shown to have cardioprotective and renal protective effects in adults and is recommended as a component of medical therapy for heart failure with reduced ejection fraction. More recently dapagliflozin has been trialed in children with heart failure and reduced ejection fraction.\r\n\r\n\r\nIn a single-center, prospective observational study by Newland et al, of 38 nondiabetic pediatric patients with heart failure, dapagliflozin was added to their standard multi-drug heart failure regimen. Sixty-eight percent of patients had dilated cardiomyopathy and 65.8% had a reduced left ventricular ejection fraction of 40% or less. Dapagliflozin was shown to decrease serum B-type natriuretic peptide at 130 days and to improve ejection fraction in the subset of patients with heart failure due to dilated cardiomyopathy. However, the authors point out that this improvement in ejection fraction may not be attributed to dapagliflozin alone, as many of these patients were on a multi-drug regimen therapy for heart failure. \r\n\r\n\r\nAdverse events associated with dapagliflozin use include increased rates of urinary tract infections, which was demonstrated in 16% of patients in the study by Newland. This is likely due to the increased urine glucose concentration because of inhibited renal glucose reuptake. Dapagliflozin is not associated with significant changes in serum electrolytes, hypoglycemia, or hypovolemia. When used in diabetic patients, dapagliflozin has the potential for reducing the degree of hyperglycemia exhibited in diabetic ketoacidosis (DKA). In adult patients on SGLT2 inhibitors, euglycemic DKA has been reported. \r\n\r\n \r\nREFERENCES \r\n\r\nNewland DM, Law YM, Albers EL, Friedland-Little JM, Ahmed H, Kemna MS, Hong BJ. Early Clinical Experience with Dapagliflozin in Children with Heart Failure. Pediatr Cardiol<\/em>. 2023; 44(1):146-152. doi: 10.1007\/s00246-022-02983-0. \r\n\r\n\r\nGrube PM, Beckett RD. Clinical studies of dapagliflozin in pediatric patients: a rapid review. Ann Pediatr Endocrinol Metab<\/em>. 2022; 27(4):265-272. doi: 10.6065\/apem.2244166.083. \r\n\r\n\r\nLoss KL, Shaddy RE, Kantor PF. Recent and Upcoming Drug Therapies for Pediatric Heart Failure. Front Pediatr<\/em>. 2021;9:681224. doi: 10.3389\/fped.2021.681224. \r\n”,”hint”:””,”answers”:{“8t78h”:{“id”:”8t78h”,”image”:””,”imageId”:””,”title”:”A.\tHypoglycemia”},”x2znb”:{“id”:”x2znb”,”image”:””,”imageId”:””,”title”:”B.\tUrinary Tract Infection”,”isCorrect”:”1″},”263me”:{“id”:”263me”,”image”:””,”imageId”:””,”title”:”C.\tHyperkalemia”}}}}}

{“questions”:{“sb62h”:{“id”:”sb62h”,”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\nAn 8-day-old boy born with skeletal abnormalities, congenital heart disease, hypotonia, and facial dysmorphisms presents for cardiac surgery. Genetic testing reveals a pathogenic variant in the KMT2D gene consistent with a diagnosis of Kabuki syndrome. Which of the following types of congenital heart disease is MOST likely to be present?\r\n\r\n”,”desc”:”EXPLANATION \r\nFirst described in 1981, Kabuki syndrome is a heterogeneous disorder associated with multiple congenital defects including heart disease, developmental delay, hypotonia, renal malformations, skeletal anomalies, and distinct facial anomalies (laterally sparse and arched eyebrows, long palpebral fissures, large and everted ears, eversion of the lateral eyebrows, and pillowed lower lip). \r\n\r\n\r\nPrior to 2010, the diagnosis of Kabuki syndrome was based on the phenotypic manifestations above. However, in 2010, the first and most common causative (55-80%) gene, KMT2D<\/em>, was identified. Since then, three additional genes have been identified as pathogenic variants in a minority of Kubuki patients. \r\n\r\n\r\nRetrospective studies describe the presence of congenital heart disease (CHD) in 58-70% of patients with Kabuki syndrome. In patients with Kabuki syndrome and CHD, the most common diagnoses are left-sided obstructive lesions (35-47%). The most common left-sided lesions include coarctation of the aorta (17.1%) and hypoplastic left heart syndrome (10.5%). Other left sided-obstructive lesions include aortic stenosis, mitral stenosis, and Shone\u2019s complex. Septal defects are the next most common heart defects, either as a primary diagnosis or in conjunction with the above obstructive lesions. The remainder of children with Kabuki syndrome and CHD exhibit a heterogenous spectrum of cardiac lesions including conotruncal defects, atrioventricular canal defects, and right sided obstructive lesions. Of the identified genetic mutations associated with Kabuki syndrome, the KMT2D (MLL2) gene has been found to be most frequently associated with CHD. \r\n\r\n\r\nAs indicated above, left-sided obstructive lesions, such as coarctation of the aorta and Hypoplastic Left Heart Syndrome, are most commonly observed in patients with Kabuki syndrome versus Tetralogy of Fallot or Transposition of the Great Arteries. \r\n\r\n\r\n\r\n \r\nREFERENCES \r\n\r\nYuan SM. Congenital heart defects in Kabuki syndrome. Cardiol J<\/em>. 2013;20(2):121-4. doi: 10.5603\/CJ.2013.0023. PMID: 23558868.\r\n\r\n\r\nDigilio MC, Marino B, Toscano A, Giannotti A, Dallapiccola B. Congenital heart defects in Kabuki syndrome. Am J Med Genet<\/em>. 2001 May 15;100(4):269-74. doi: 10.1002\/ajmg.1265. PMID: 11343317.\r\n\r\n\r\nDigilio MC, Gnazzo M, Lepri F et al.Congenital heart defects in molecularly proven Kabuki syndrome patients. Am J Med Genet A<\/em>. 2017 Nov;173(11):2912-2922. doi: 10.1002\/ajmg.a.38417. Epub 2017 Sep 8. PMID: 28884922.\r\n”,”hint”:””,”answers”:{“q7e8o”:{“id”:”q7e8o”,”image”:””,”imageId”:””,”title”:”A.\tTetralogy of Fallot”},”9bkq9″:{“id”:”9bkq9″,”image”:””,”imageId”:””,”title”:”B.\tHypoplastic left heart syndrome (HLHS)”,”isCorrect”:”1″},”gxlic”:{“id”:”gxlic”,”image”:””,”imageId”:””,”title”:”C.\tTransposition of the great arteries”}}}}}

{“questions”:{“phvb5”:{“id”:”phvb5″,”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-week-old infant with a history of congenital central hypoventilation syndrome (CCHS) presents for an exam under anesthesia and rectal biopsy for suspected Hirschsprung\u2019s disease. Which of the following cardiac arrhythmias is MOST likely to be coexistent in this patient?\r\n”,”desc”:”EXPLANATION \r\nCongenital central hypoventilation syndrome (CCHS), or \u201cOndines curse\u201d, is an abnormality in the autonomic regulation of ventilation by the central nervous system not explained by any pulmonary, neurological, or muscular disorders. This results in a reduced or absent ventilatory response to hypercapnia and hypoxia, as well as other autonomic disorders.\r\n\r\n\r\nThe main presenting symptom of CCHS is acute or chronic hypoventilation. Depending on the phenotype, this may present as a neonate, infant, or less commonly later in life. Other conditions associated with CCHS include: Hirschsprung disease, neural crest tumors, esophageal dysmotility, and cardiac arrythmias. \r\n\r\n\r\nIn 2003, mutations in the PHOX2B gene were identified as the major genetic cause of CCHS. These mutations have further been classified as polyalanine repeat mutations (PARMs), or less commonly, non-PARMs. These genotypes have been found to exhibit different phenotypes of CCHS, each with varying onset, degrees of hypoventilation, and other autonomic disorders as mentioned in the previous paragraph. Transmission of the PHOX2B mutation is autosomal dominant, with a 50% risk of transmission to offspring. \r\n\r\n\r\nDiagnosis is based on clinical signs and symptoms, exclusion of other causes of hypoventilation, and polysomnography which typically shows hypoventilation, worse while sleeping than awake, and most severe during non-rapid eye movement sleep. Concern for signs, symptoms, and other known manifestations of CCHS should prompt genetic testing for mutations of the PHOXB gene. \r\n\r\n\r\nThere is no pharmacologic management for the ventilatory symptoms of CCHS, and lifelong ventilatory support will be required for these patients. Depending on phenotype, this ventilatory support may be required only while asleep or 24 hours a day. Ventilation strategies may be non-invasive or invasive ventilation via tracheostomy, particularly in children. Support options include positive pressure ventilation, mask ventilation, and diaphragm pacing via phrenic nerve stimulation. The anesthesiologist caring for these children should be aware that even patients requiring nighttime ventilatory support only will often exhibit increased hypoventilation due to the effects of anesthesia. Preparation should be made for extended monitoring and ventilatory support in the perioperative period. \r\n\r\n\r\nPatients with CCHS often exhibit cardiac arrythmias, typically sinus node dysfunction, sinus pauses, bradycardia, and prolonged R-R intervals. Manifestations of this autonomic dysfunction include syncope, postural hypotension, nocturnal hypertension, and increased risk of sudden death. Patients should be monitored with an annual ECG Holter monitor. Syncope should warrant extended Holter monitoring and\/or consideration of pacemaker implantation. The current recommendation for CCHS patients is to follow the ACC\/AHA guidelines for pacemaker placement. These guidelines recommend pacemaker placement for patients with R-R interval >3 seconds and recurrent syncopal episodes. Typically, a single chamber atrial pacemaker is sufficient. However, a dual-chamber device may be preferable due to the subsequent possibility of developing atrioventricular block. Patients with phrenic nerve pacers require special attention during pacemaker implantation to not cause cross interference between devices. In these patients, the cardiac pacemaker lead should be bipolar to avoid interference with the phenic nerve pacer.\r\n\r\n\r\nFor the patient in the stem, the most likely arrhythmia is sick sinus syndrome due to a known association of CCHS with sinus node dysfunction. Supraventricular tachycardias and ectopic atrial tachycardia are not commonly associated with CCHS.\r\n\r\n \r\nREFERENCES \r\n\r\nTrang H, Samuels M, Ceccherini I, et al. Guidelines for diagnosis and management of congenital central hypoventilation syndrome.Orphanet J Rare Dis<\/em>. 2020;15(1):252.\r\n\r\n\r\nGronli JO, Santucci BA, Leurgans SE, Berry-Kravis EM, Weese-Mayer DE. Congenital central hypoventilation syndrome: PHOX2B<\/em> genotype determines risk for sudden death. Pediatr Pulmonol<\/em>. 2008; 43(1): 77-86. \r\n\r\n\r\nWeese-Mayer DE, Rand CM, Khaytin I, et al. Congenital Central Hypoventilation Syndrome. 2004 Jan 28 [Updated 2021 Jan 28]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews\u00ae [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2024. Available from: https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK1427\/\r\n”,”hint”:””,”answers”:{“dbbdo”:{“id”:”dbbdo”,”image”:””,”imageId”:””,”title”:”A. Supraventricular tachycardia “},”53kdl”:{“id”:”53kdl”,”image”:””,”imageId”:””,”title”:”B. Sick sinus syndrome”,”isCorrect”:”1″},”ujv5y”:{“id”:”ujv5y”,”image”:””,”imageId”:””,”title”:”C. Ectopic atrial tachycardia”}}}}}