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

{“questions”:{“n0imx”:{“id”:”n0imx”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:”https:\/\/ccasociety.org\/wp-content\/uploads\/2023\/03\/CCAS-Graphic-JPEG.jpg”,”imageId”:”6384″,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Sana Ullah, MB, ChB, FRCA – Children\u2019s Medical Center, Dallas \r\nA 3-year-old female toddler with a large atrial septal defect (ASD) in addition to dysplastic mitral and tricuspid valves (both with severe regurgitation) presents for repair of both valves and ASD closure. After intubation, vital signs are as follows: HR 120, BP 90\/50, SpO2 92%. During the pre-bypass transesophageal echo (TEE), agitated saline contrast is injected into a left arm peripheral IV with two of the TEE images demonstrated below. What is the MOST likely diagnosis? \r\n\r\n”,”desc”:”EXPLANATION \r\nIn the TEE images above, contrast is clearly seen entering the left atrium initially and then into the left ventricle, confirming the presence of a left superior vena cava (LSVC) draining into an unroofed coronary sinus. A persistent LSVC is found in approximately 4% of patients with congenital heart disease compared with 0.5% in the general population. In 80-90% of cases, it drains into the right atrium via the coronary sinus. In 10-20% of cases, the LSVC drains into the left atrium due to partial or complete absence of the \u201croof\u201d of the coronary sinus. It can be diagnosed with echocardiography by injecting agitated saline contrast into an IV placed in the left arm. \r\n\r\nAn unroofed coronary sinus has several important clinical implications including: (1) It is a source of right to left shunting (often called a coronary sinus ASD) leading to mild cyanosis; (2) It can lead to systemic thromboembolism, potentially resulting in an ischemic stroke or cerebral abscess; (3) It can impact repair of an ostium primum ASD and usually requires baffling into the right atrium. \r\n\r\n\r\nA persistent LSVC also has important clinical implications: (1) It may require additional venous drainage cannulation during cardiopulmonary bypass cases, depending on the presence of a bridging vein; (2) An unrecognized LSVC can be a source of systemic desaturation in a bidirectional cavopulmonary anastomosis or a Fontan; (3) A heart transplant recipient with a LSVC will require modification to the venous drainage anastomoses; (3) It may render retrograde cardioplegia ineffective; (4) It can complicate procedures such as central venous cannulation or pacemaker implantation. \r\n\r\n\r\nPulmonary arteriovenous fistulas are congenital or acquired intrapulmonary right-to-left shunts. The diagnosis can be confirmed with echocardiography by showing a shortened transpulmonary transit time from the right heart to the left atrium during injection of contrast into a peripheral IV. \r\n\r\n\r\nA sinus venosus defect will show contrast entering the right atrium first, and therefore, answer C is incorrect. \r\n\r\nREFERENCES \r\n \r\n\r\n1.\tAzizova A, Onder O, Arslan S, Ardali S, Hazirolan T. Persistent left superior vena cava: clinical importance and differential diagnoses. Insights into Imaging. <\/em>2020. 11:110. https:\/\/doi.org\/10.1186\/s13244-020-00906-2 \r\n2.\tOotaki Y, Yamaguchi M, Yoshimura N et al. Unroofed coronary sinus syndrome: diagnosis, classification, and surgical treatment. J Thorac Cardiovasc Surg. <\/em> 2003; 126:1655-6. doi:10.1067\/S0022-5223(03)01019-5\r\n\r\n”,”hint”:””,”answers”:{“e61zy”:{“id”:”e61zy”,”image”:””,”imageId”:””,”title”:”A.\tLeft superior vena cava (LSVC) with an unroofed coronary sinus”,”isCorrect”:”1″},”vcajs”:{“id”:”vcajs”,”image”:””,”imageId”:””,”title”:”B.\tPulmonary arteriovenous fistula”},”0hy3h”:{“id”:”0hy3h”,”image”:””,”imageId”:””,”title”:”C.\tSinus venosus atrial septal defect”}}}}}

{“questions”:{“h0uon”:{“id”:”h0uon”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Sana Ullah, MB ChB, FRCA. Children\u2019s Medical Center, Dallas \r\n\r\nA 17-year-old male with a history of hypertrophic cardiomyopathy presents to cardiology clinic for routine follow-up. During transthoracic echocardiography, which of the following maneuvers is MOST likely to reveal a latent gradient across the left ventricular outflow tract?”,”desc”:”EXPLANATION \r\nHypertrophic cardiomyopathy (HCM) is the most common cause of sudden death in competitive athletes. The most common etiology is ventricular arrhythmia secondary to myocardial fibrosis, microvascular coronary disease, and structural disarray of cardiomyocytes. A comprehensive evaluation for HCM includes a detailed family history as well as a thorough clinical history and physical exam with the following diagnostic work up: (1) 12-lead and Holter ECG; (2) transthoracic echocardiography (TTE) to assess wall thickness, left ventricular outflow tract (LVOT) gradient, and degree of mitral regurgitation; (3) cardiac MRI to detect late gadolinium enhancement (LGE) as a marker for fibrosis; and (4) genetic testing. \r\n\r\nAn LVOT gradient of > 50 mmHg is a hemodynamically significant gradient. If less than 50 mmHg, provocative measures may be used to assess the dynamic component of the LVOT gradient. Maneuvers that increase LV afterload, such as isometric hand grip, squatting, and phenylephrine infusion, will reduce the gradient. Factors that decrease afterload and\/or increase contractility will increase the gradient and can be useful in detecting a latent gradient. TTE after stress with exercise is the preferred method to detect LVOT gradient versus pharmacologic stress. The effect of various maneuvers on the LVOT gradient are summarized in the table. \r\n\r\nAssessment of risk for sudden cardiac death (SCD) is a key component to managing patients with HCM. Any HCM patient surviving cardiac arrest is a candidate for secondary prevention with an implantable cardioverter-defibrillator (ICD) device. Guidelines for primary prevention have recently been published by the American Heart Association and the American College of Cardiology (1,2). Accurate risk stratification for primary prevention is important as ICDs are associated with significant morbidity. This includes inappropriate defibrillation in approximately 30% of patients as well as negative psychological repercussions and the imposition of limitations on participation in certain sports. Major factors under recommendation for risk stratification include: (1) Family history of sudden death; (2) extreme LV hypertrophy; (3) unexplained syncope; (4) non-sustained ventricular tachycardia; (5) LGE on cardiac MRI; (6) end-stage HCM, and (7) LV apical aneurysm. Family history of sudden death, extreme LV hypertrophy, and unexplained syncope are the most important factors for risk stratification of children and adolescents. Patients with one or more of these factors are candidates for an ICD device. \r\n\r\nREFERENCES \r\n1.\tOmmen SR, Mital S, Burke MA et al. 2020 AHA\/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy. J Am Coll Cardiol <\/em>. 2020;76:e159-e240. https:\/\/doi.org\/10.1016\/j.jacc.2020.08.045 \r\n\r\n2.\tMaron BJ, Desai MY, Nishimura RA et al. Management of hypertrophic cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol <\/em>.2022; 79:390-414. https:\/\/doi.org\/10.1016\/j.jacc.2021.11.021\r\n\r\n3.\tMaron BJ, Desai MY, Nishimura RA et al. Diagnosis and evaluation of hypertrophic cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol <\/em>. 2022; 372-389. https:\/\/doi.org\/10.1016\/j.jacc.2021.12.002\r\n\r\n”,”hint”:””,”answers”:{“kc7q5”:{“id”:”kc7q5″,”image”:””,”imageId”:””,”title”:”A.\tIsometric hand grip”},”lq4f2″:{“id”:”lq4f2″,”image”:””,”imageId”:””,”title”:”B.\tExercise”,”isCorrect”:”1″},”nydnn”:{“id”:”nydnn”,”image”:””,”imageId”:””,”title”:”C.\tPhenylephrine infusion”},”2b5ro”:{“id”:”2b5ro”,”image”:””,”imageId”:””,”title”:”D.\tSquatting”}}}}}

{“questions”:{“h2cqv”:{“id”:”h2cqv”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Sana Ullah, MB ChB, FRCA – Children\u2019s Medical Center, Dallas TX \r\n\r\nA dysmorphic, 3-week-old neonate is referred to pediatric cardiology due to a systolic murmur. Genetic testing revels a karyotype of 45 XO. What is the MOST likely congenital cardiac defect in this patient?”,”desc”:”EXPLANATION \r\nThe karyotype 45 XO is consistent with a diagnosis of Turner Syndrome (TS), which occurs in approximately 1 in 2500 live born females. Characteristic clinical features include a webbed neck, short stature, and lymphedema of the hands and feet. Cardiovascular disease is the major cause of death in TS. Congenital heart defects are found in about 50% of individuals with TS, consisting mostly of left-sided lesions. The most common cardiac abnormality is a bicuspid aortic valve (15% – 30% of cases), followed by coarctation of the aorta (7% – 18%). A recent American Heart Association Scientific Statement (1) has recommended that the presence of a bicuspid aortic valve or a left-sided obstructive lesion in a female patient should prompt a genetic evaluation of TS. Other less common but well recognized congenital cardiac defects associated with TS include partial anomalous pulmonary venous connection and hypoplastic left heart syndrome (HLHS). Coronary abnormalities are also common, particularly absent left main coronary. These are important to identify as they may have surgical implications. \r\n\r\n\r\nTurner Syndrome patients are at increased risk of aortic dissection at six times the rate as compared to the general population. Therefore, they require regular follow-up and serial imaging of the aorta, in addition to monitoring and treatment of hypertension. \r\n\r\n\r\nThe most common cardiac surgical procedures performed in TS patients are coarctation repair and aortic arch reconstruction. Due to lymphatic dysfunction, TS patients have a higher incidence of chylothorax and increased length of stay in the intensive care unit. \r\n\r\n\r\nTS patients with HLHS have a higher incidence of poor outcomes, though they have improved in the most recent era. Due to the increased mortality after the Stage I\/Norwood procedure, some centers are more likely to refer TS patients for primary cardiac transplantation as there is evidence of better clinical outcomes. \r\n\r\n\r\nTruncus arteriosus and other cono-truncal abnormalities are frequently associated with chromosome 22q11 deletion syndrome. \r\n\r\n\r\nSupravalvar aortic stenosis is a feature of Williams syndrome. \r\n\r\n\r\n\r\n \r\nREFERENCES \r\n1.\tSilberbach M, Roos-Hesselink JW, Andersen NH et al. Cardiovascular Health in Turner Syndrome. A scientific statement from the American Heart Association. Circ Genom Precis Med <\/em>. 2018; 11(10): e000048. https:\/\/doi.org\/10.1161\/HCG.0000000000000048 \r\n\r\n2.\tChew JD, Hill KD, Jacobs ML, et al. Congenital heart surgery outcomes in Turner Syndrome: The Society of Thoracic Surgeons Database Analysis. Ann Thorac Surg <\/em>.2019;108:1430-1438. \r\n3.\tPhilip J, Gupta D, Bleiweis MS, Pietra BA, Vyas HV. Hypoplastic left heart in Turner\u2019s syndrome: a primary indication for transplant. Card Young <\/em>. 2018; 28:458-460 \r\n4.\tChew JD, Soslow JH, Hall M, et al. Heart transplantation in children with Turner syndrome: Analysis of a linked dataset. Ped Cardiol . 2018; 39:610-616.\r\n”,”hint”:””,”answers”:{“984q5”:{“id”:”984q5″,”image”:””,”imageId”:””,”title”:”A.\tTruncus arteriosus”},”l2mhk”:{“id”:”l2mhk”,”image”:””,”imageId”:””,”title”:”B.\tBicuspid aortic valve”,”isCorrect”:”1″},”y7c6r”:{“id”:”y7c6r”,”image”:””,”imageId”:””,”title”:”C.\tSupravalvar aortic stenosis”},”5tu8y”:{“id”:”5tu8y”,”image”:””,”imageId”:””,”title”:”D.\tCoarctation of the aorta”}}}}}

{“questions”:{“ioram”:{“id”:”ioram”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Sana Ullah, MB ChB, FRCA \u2013 Children\u2019s Medical Center, Dallas TX \r\n\r\nA 4-year-old previously healthy girl is admitted with fever, shortness of breath and abdominal pain. A chest x-ray demonstrates cardiomegaly and a transthoracic echocardiogram (TTE) reveals a large pericardial effusion. Vital signs are as follows: HR 150, BP 65\/45, RR 35. Which of the following echocardiographic findings is MOST diagnostic for cardiac tamponade?”,”desc”:”EXPLANATION \r\nCardiac tamponade is both a clinical diagnosis based on hypotension, tachycardia, and jugular venous distension and one based on echocardiographic findings. The decision to perform a pericardiocentesis may be assisted with echocardiography in determining the severity of tamponade and the potential for cardiovascular compromise during pericardiocentesis. Due to the fixed volume of the pericardial space, changes in intrapericardial pressure are transmitted to the cardiac chambers and the major systemic veins leading to core findings on echocardiogram including a pericardial effusion, diastolic right ventricle (RV) collapse, systolic right atrium (RA) collapse, plethoric IVC with minimal respiratory variation, and exaggerated respiratory changes in mitral valve (MV) and tricuspid valve (TV) inflow velocities. \r\n\r\nCollapse of the RA is seen at early ventricular systole when the RA is relaxed with low blood volume. Brief RA collapse can be seen without tamponade, but the presence of this sign for more than one third of the cardiac cycle is more specific for tamponade. The sensitivity of RA collapse during ventricular systole is higher ranging from 50% in early tamponade to 100% with worsening tamponade physiology. \r\n\r\nCollapse of the right ventricle (RV) is seen during early diastole when RV pressure is at its lowest. Diastolic collapse of the RV is highly specific with lower sensitivity for cardiac tamponade. It indicates very high intrapericardial pressures impeding RV filling. Longer duration of RV collapse correlates with increasing severity of tamponade. \r\n\r\nIncreased intrapericardial pressure impedes systemic venous return and this can be assessed by imaging the inferior vena cava (IVC) at its entrance into the RA. During normal spontaneous inspiration, the IVC diameter decreases by 50% or more. In tamponade physiology, the IVC remains distended (plethoric), and its diameter decreases by less than 50% during inspiration. However, even if there is minimal respiratory variation of IVC diameter with respiration, tamponade is very unlikely in the absence of chamber collapse. \r\n\r\nPulsus paradoxus is a normal physiologic phenomenon whereby the systolic blood pressure decreases by 10% or less during inspiration. Increased venous return to the RV during normal spontaneous inspiration occurs due to increasing negative intrathoracic pressure. This briefly shifts the ventricular septum into the left ventricle resulting in lower LV output and blood pressure. This phenomenon is exaggerated in tamponade physiology. These changes in systemic and pulmonary venous return can be characterized by measuring tricuspid and mitral inflow velocities and their changes with respiration. Under normal circumstances, these variations of inflow velocities during respiration do not exceed 20%-25%. However, during tamponade physiology, mitral inflow decreases<\/em> by 25% or more and tricuspid inflow velocity increases<\/em> by 40% or more. In the absence of any chamber collapse, these changes are not sensitive or specific for tamponade. \r\n\r\nREFERENCES \r\n1.\tAlerhand S, Carter JM. What echocardiographic findings suggest a pericardial effusion is causing tamponade?Am J Emerg Med <\/em>. 2019; 37:321-326. https:\/\/doi.org\/10.1016\/j.ajem.2018.11.004 \r\n2.\tHoit BD. Cardiac tamponade. In Uptodate; 2023. Accessed 1\/22\/2023. https:\/\/www.uptodate.com\/contents\/cardiac-tamponade#H22 \r\n3.\tKlein AL, Abbara S, Agler DA et al. American Society of Echocardiography Clinical Recommendations for Multimodality Cardiovascular Imaging of Patients with Pericardial Disease.J Am Soc Echocardiogr<\/em>. 2013; 26:96501012. http:\/\/dx.doi.org\/10.1016\/j.echo.2013.06.023 \r\n4.\tGuntheroth WG. Sensitivity and specificity of echocardiographic evidence of tamponade: implications for ventricular interdependence and pulsus paradoxus.Pediatr Cardiol <\/em>2007;28(5):358\u201362.\r\n\r\n”,”hint”:””,”answers”:{“rg6si”:{“id”:”rg6si”,”image”:””,”imageId”:””,”title”:”A.\tCollapse of the right atrium during ventricular diastole”},”p4rzx”:{“id”:”p4rzx”,”image”:””,”imageId”:””,”title”:”B.\tCollapse of the right ventricle during ventricular diastole”,”isCorrect”:”1″},”dt4rk”:{“id”:”dt4rk”,”image”:””,”imageId”:””,”title”:”C.\tDilated IVC with 50% reduction in diameter during inspiration”},”f3s41″:{“id”:”f3s41″,”image”:””,”imageId”:””,”title”:”D.\t15% decrease in mitral valve inflow velocity during inspiration”}}}}}

{“questions”:{“tmpk8”:{“id”:”tmpk8″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Daniela Perez-Velasco, DO; Chinwe Unegbu, MD; and Christopher Busack, MD \u2013 Children\u2019s National Hospital \r\n\r\nThe proposed renaming of the Blalock-Taussig (BT) shunt represents an attempt to acknowledge the tremendous contributions of which researcher, surgical assistant, and instructor?\r\n”,”desc”:”EXPLANATION \r\nVivien Theodore Thomas was born in New Iberia, Louisiana on August 29, 1910. He and his family later moved to Nashville, Tennessee where his father worked as a master carpenter. In 1929, after working to raise money for college and with plans to study medicine, he enrolled at Tennessee Agricultural and Industrial College. While Thomas dreamed of becoming a doctor, circumstances led to a different fate. His college savings were depleted during the Great Depression, forcing him to withdraw from college. \r\nOn February 10, 1930, Thomas walked into the animal lab of a young doctor named Dr. Alfred Blalock to interview for the job of laboratory assistant. In a matter of days, Thomas was administering anesthesia and performing arterial punctures on laboratory dogs. Over the many years at Vanderbilt, Blalock and Thomas worked to compile a massive amount of data pertaining to hemorrhagic and traumatic shock. \r\nAfter four years as a laboratory assistant, Thomas was promoted to the role of a senior research fellow. Unfortunately, Vanderbilt University classified him only as a janitor which was reflected in his salary. In 1937, Blalock then received an offer for the chairmanship and surgeon-in-chief at Henry Ford Hospital in Detroit. However, the hospital\u2019s policy against hiring blacks would result in rejection of the offer. In 1940, Blalock was offered the surgeon-in-chief position at his alma mater, Johns Hopkins Hospital. Blalock ensured that Thomas was also offered a position. They arrived in Baltimore in 1941, a time when the hospital had segregated restrooms and entrances to the hospital. \r\nDr. Helen Taussig soon approached Dr. Blalock, inquiring about a surgical remedy for the \u201cblue babies\u201d under her care. She wondered if there was a way to \u201cchange the pipes around\u201d and deliver more blood to the lungs. Blalock and Thomas had already done previous work to reroute arterial blood to the lungs. Thomas worked diligently to first reproduce the physiology of Tetralogy of Fallot (TOF) in the canine heart. Once Thomas had created the dog model of hypoxic circulation, he contributed to the concept and methodology of diverting blood from the subclavian artery to the pulmonary artery. Thomas single-handedly performed this procedure on nearly 200 dogs and taught Blalock the delicate vascular procedure. During a time that pre-dated vascular and microvascular surgery, many of the instruments and sutures were designed by Thomas. As Dr. Denton Cooley, who was trained by Thomas stated, \u201cThere wasn\u2019t a false move, not a wasted motion, when he operated.\u201d Dr. Blalock and Mr. Thomas were a remarkable combination. Thomas translated Blalock\u2019s concepts into reality, creating entire surgical procedures where none had existed previously. On November 29, 1944, the first blue baby operation was performed by Blalock. Vivien Thomas, high school graduate, son of a carpenter, and grandson of enslaved ancestors, guided one of the greatest surgeons of the 20th century, Dr. Alfred Blalock, through the revolutionary surgical procedure referred to at the time as the Blalock-Taussig shunt (BT shunt). Blalock insisted that Thomas stand by him on a step stool in order that he could guide Blalock through the surgery for he had only performed the procedure once as Thomas\u2019 assistant. It became widely known that while Blalock was operating, the space behind his right shoulder was reserved for Thomas. In 1946, Thomas went on to conceptualize and perform the atrial septectomy to improve circulation in patients with transposed great vessels. \r\nThe BT shunt ushered in a new era of pediatric cardiovascular surgery. It was the first pediatric cardiac surgical procedure performed in the United States. The Blalock-Taussig shunt was hailed as a miracle operation and established Johns Hopkins Hospital as the hospital to treat \u201cblue babies\u201d with TOF. When the work was reported in the press and published in the 1945 JAMA article entitled \u201cThe Surgical Treatment of the Malformations of the Heart: In Which There is Pulmonary Stenosis or Pulmonary Atresia\u201d by Blalock and Taussig, the name Vivien Thomas was not mentioned anywhere. Thomas\u2019 work was not recognized for the following 30 years. After 37 years at Johns Hopkins, Thomas was finally recognized as a Clinical Instructor and Faculty of the School of Medicine in 1976. Since an Honorary Doctorate of Medicine was not permitted at that time, he was presented with an Honorary Doctorate of Law. \r\nThe alliance between Thomas and Blalock was dramatized in the 2004 movie \u201cSomething the Lord Made\u201d, which was based on the autobiography of Thomas entitled \u201cPartners of the Heart\u201d. Thomas made a place for himself as a teacher to surgeons at a time when he could not become one himself. He was a surgical pioneer before Johns Hopkins opened its doors to the first African American surgical resident 30 years later, Dr. Levi Watkins. Thomas retired in 1979, battled pancreatic cancer, and was put to rest in 1985. \r\nIn operating rooms all over the world, a modified version of the BT shunt is still performed today. While Thomas\u2019 portrait hangs alongside other titans of medicine at Johns Hopkins Hospital, there has been a growing campaign to solidify his contributions with an official name change. In 2003, a proposal to rename the Blalock-Taussig shunt to the Blalock-Thomas-Taussig shunt was published in the journal Pediatric Critical Care Medicine and in 2009, a similar proposal was published in the journal Cardiology in the Young. The idea was again revisited in 2020 at the Society of Thoracic Surgeons Inaugural Vivien T. Thomas Lecture and in a 2022 opinion article published in the JAMA Surgery. \r\nChoice C is the correct answer because Vivien Thomas helped create the Blalock-Taussig shunt. Choice A is not correct. Dr. Daniel Hale Williams was one of the first African American physicians in the Chicago area and one of the first physicians to perform open heart surgery. Choice B is not correct. John Beauregard Johnson was an African American cardiologist and head of the Department of Medicine at Howard University. He pioneered the use of angiography and cardiac catheterization as diagnostic tools. Choice D is not correct as Dr. Levi Watkins Jr. was the first African American cardiac surgery resident at Johns Hopkins Hospital and performed the first implantation of an automatic implantable cardioverter defibrillator. \r\n\r\nREFERENCES \r\n \r\n\r\nThe Remarkable Story of Vivien Thomas, the Black Man Who Helped Invent Heart Surgery. Washingtonian<\/em>. 2020. https:\/\/www.washingtonian.com\/2020\/06\/19\/the-remarkable-story-of-vivien-thomas-the-black-man-who-helped-invent-heart-surgery. Accessed November 11, 2022. \r\nBlake K, Yancy CW. Change the Name of the Blalock-Taussig Shunt to Blalock-Thomas-Taussig Shunt. JAMA Surg.<\/em> 2022;157(4):287\u2013288. doi:10.1001\/jamasurg.2021.5611\r\nBlalock A., Taussig HB. The Surgical Treatment of Malformations of the Heart: In which There is Pulmonary Stenosis or Pulmonary Atresia. JAMA. <\/em> 1945;128(3):189-202. doi:10.100\/jama.1945.02860200029009\r\nKiran U, Aggarwal S, Choudhary A, Uma B, Kapoor PM. The Blalock and Taussig Shunt Revisited. Ann Card Anaesth<\/em>. 2017;20(3):323-330. doi:10.4103\/aca.ACA_80_17\r\nThomas VT. Partners of the Heart : Vivien Thomas and His Work with Alfred Blalock : An Autobiography<\/em>. Univ. Of Pennsylvania Press; 1998. \r\n\r\nJust One More-Vivien Thomas: Remembering a Pioneering Legend. Cardiology Magazine<\/em>. 2021. https:\/\/www.acc.org\/latest-in-cardiology\/articles\/2021\/02\/01\/01\/42\/just-one-more-vivien-thomas-remembering-a-pioneering-legend. Accessed September 20, 2022. \r\n\r\nBrogan TV, Alfieris GM. Has the Time Come to Rename the Blalock-Taussig Shunt? Pediatr Crit Care Med<\/em>. 2003;4(4):450-453. doi:10.1097\/01.PCC.0000090014.95775. \r\nEvans WN. The Blalock-Taussig shunt: The Social History of an Eponym. Cardiol Young<\/em>. 2009;19(2):119-128. doi:10.1017\/S1047951109003631.”,”hint”:””,”answers”:{“qf6f3”:{“id”:”qf6f3″,”image”:””,”imageId”:””,”title”:”A. Daniel Hale Williams”},”caeez”:{“id”:”caeez”,”image”:””,”imageId”:””,”title”:”B. John Beauregard Johnson”},”3pc0o”:{“id”:”3pc0o”,”image”:””,”imageId”:””,”title”:”C. Vivien Thomas”,”isCorrect”:”1″},”omq6n”:{“id”:”omq6n”,”image”:””,”imageId”:””,”title”:”D. Levi Watkins Jr.”}}}}}