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

{“questions”:{“ckp55”:{“id”:”ckp55″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Anila B. Elliott, MD – University of Michigan, C.S. Mott Children\u2019s Hospital \r\nA 3-day-old male with total anomalous pulmonary venous return (TAPVR) is transferred from an outside hospital. He is hemodynamically stable on no vasoactive medications and supported on nasal cannula at 2L\/min with an FiO2 of 0.21. Transthoracic echocardiography shows unobstructed flow of pulmonary venous blood to systemic venous circulation with right to left shunting through a moderate-sized secundum atrial septal defect. Which of the following is a risk factor for increased morbidity and mortality?\r\n\r\n”,”desc”:”EXPLANATION \r\nTotal anomalous pulmonary venous return (TAPVR) is a rare congenital cardiac lesion, occurring in 1-3% of the congenital heart disease population^{1<\/sup>. There are four main types of TAPVR: supracardiac (most common), cardiac, infracardiac and mixed. Mixed TAPVR is the least common and the most challenging to surgically repair as there is often no pulmonary confluence and multiple pulmonary venous connections both above and below the diaphragm2<\/sup>. \r\n\r\n\r\nSince the introduction of prostaglandins to maintain ductal patency in many congenital cardiac lesions, obstructed TAPVR remains one of the few true congenital cardiac surgical emergencies. \r\nTAPVR can be associated with other anomalies, including heterotaxy, hypoplasia of left-sided structures, or other lesions requiring palliation down the single-ventricle pathway2<\/sup>. \r\n\r\n\r\nA pure right-to-left shunt across the atrial septum on echocardiogram is usually indicative of TAPVR1<\/sup>. A key factor in peri-operative management is whether there is obstruction to pulmonary venous flow. On echocardiography, flow acceleration in pulmonary veins of \u2265 2.0 m\/sec indicates significant obstruction2<\/sup>. Clinical presentation of obstructed TAPVR includes severe pulmonary edema, pulmonary hypertension, cyanosis, metabolic acidosis and cardiogenic shock3<\/sup>. Management involves maintaining forward flow and avoiding pulmonary vasodilation, which can lead to increased flow in the already congested pulmonary circulation. In those with unobstructed pulmonary veins, as long as there is adequate mixing, they may present with mild cyanosis, signs of pulmonary over circulation, and potentially right-sided dilation\/hypertrophy depending on age1<\/sup>.\r\n\r\n\r\nSupracardiac TAPVR is usually unobstructed but may become obstructed if the vertical vein passes between the bronchus and the left pulmonary artery2<\/sup>. Infracardiac TAPVR usually presents as (or is considered to be) obstructed due to the long course of the vasculature to return to the atrium, with the potential for narrowing and obstruction at several points, especially in the intra-hepatic region3<\/sup>. Cardiac TAPVR is less likely to be obstructed1<\/sup>. \r\n\r\n\r\nThe most common post-operative complication includes recurrence of pulmonary venous obstruction and has been reported to occur in 8-54% of cases2<\/sup>. Other risk factors for increased morbidity and mortality include single ventricle multidistributive circulation, obstructed veins pre-operatively, pre-operative invasive ventilation, and pulmonary hypertension1,3<\/sup>. \r\n\r\n\r\nThe correct answer is choice C: perioperative complications (including mortality) are increased2,3<\/sup> in patients with persistent pulmonary hypertension. Pulmonary veins draining into the coronary sinus describe cardiac TAPVR, which is less likely to be obstructed1<\/sup> and a patient with a vertical vein and unobstructed flow is less likely to present in extremis with pulmonary hypertension or end-organ dysfunction3<\/sup>. \r\n\r\n\r\n \r\nREFERENCES \r\n\r\n1.\tHancock Friesen, CL,, Zurakowski, D., Thiagarajan, RR., et al. Total anomalous pulmonary venous connection: an analysis of current management strategies in a single institution. Ann Thorac Surg<\/em>. 2005; 79(2): 596-606 \r\n2.\tKaramlou, T., Gurofsky, R., Al Sukhni, E., et al. Factors associated with mortality and reoperation in 377 children with total anomalous pulmonary venous connection. Circulation<\/em>. 2007; 115:1591-1598 \r\n3.\tSchulz, A., Wu, DM., Ishigami, S., et al. Outcomes of total anomalous pulmonary venous drainage repair in neonates and the impact of pulmonary hypertension on survival. JTCVS Open<\/em>. 2022; 12: 335-343\r\n”,”hint”:””,”answers”:{“sroch”:{“id”:”sroch”,”image”:””,”imageId”:””,”title”:”A.\tPulmonary veins draining into the coronary sinus”},”7n5kz”:{“id”:”7n5kz”,”image”:””,”imageId”:””,”title”:”B.\tVertical vein with unobstructed flow”},”un2q4″:{“id”:”un2q4″,”image”:””,”imageId”:””,”title”:”C.\tPersistent pulmonary hypertension”,”isCorrect”:”1″}}}}}}

{“questions”:{“xxwqj”:{“id”:”xxwqj”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Anila B. Elliott, MD – University of Michigan, C.S. Mott Children\u2019s Hospital \r\nA 5-month-old male with a history of Tetralogy of Fallot (TOF) underwent complete repair with transannular patch and VSD closure. On arrival to the intensive care unit, the ECG shows narrow complex tachycardia with AV dissociation and heart rates between 170-210 beats per minute (bpm), with a systolic blood pressure in the 60s. Axillary temperature is 35.4 degrees celsius and most recent labs are within normal limits, with a potassium of 4.2 and magnesium 2.7. An amiodarone infusion is started after a loading dose. Which of the following is the BEST NEXT course of action?”,”desc”:”EXPLANATION \r\nJunctional ectopic tachycardia (JET) is a rare arrhythmia often seen in patients with congenital cardiac disease, originating from the atrioventricular (AV) junction or bundle of His^{1<\/sup>. JET is characterized by abnormal automaticity rather than reentrant mechanisms. It presents as a narrow complex tachycardia with AV dissociation, often at rates of 200-250bpm1<\/sup>. ECG findings include gradual acceleration and deceleration, distinguishing it from other tachyarrhythmias. Hemodynamic compromise is common due to rapid ventricular rates and loss of synchronized atrial contraction, resulting in decreased cardiac output. \r\n\r\nThere are two types of JET: congenital and post-operative. Congenital JET presents without a history of cardiac surgery with etiologies ranging from genetic predisposition, intrinsic abnormalities of the conduction system, ion channel dysfunction or histopathologic changes such as AV nodal fibrosis. Congenital JET tends to be refractory to treatment, increasing the risk of heart failure and sudden cardiac death. Mortality has been reported as high as 35% in untreated or refractory cases of congenital JET. Post-operative JET typically occurs within the first 72 hours following congenital cardiac surgery3<\/sup>. Mechanisms for post-op JET include ischemia, mechanical stretching or trauma to the AV conduction system. Certain anatomical features and surgical procedures increase the risk, with those that involve structures near the AV node having the highest risk. Although post-operative JET is self-limited and will resolve spontaneously within 5-7 days, it can lead to significant morbidity and mortality3<\/sup>.\r\n\r\nA summary of risk factors that increase the risk of post-operative JET1<\/sup>: \r\n1.\tType of procedure (Repair of TOF, double-outlet right ventricle (DORV), ventricular septal defect (VSD), atrioventricular septal defect (AVSD), transposition of the great vessels) \r\n2.\tAge < 6 months \r\n3.\tHigher post-operative core temperature \r\n4.\tUse of inotropes (epinephrine, milrinone, dopamine) \r\n5.\tElectrolyte abnormalities (hypokalemia, hypomagnesemia) \r\n6.\tProlonged cardiopulmonary bypass times (\u2265 75 minutes)\r\n\r\nThe three main goals of managing JET are: rate control, restoring AV synchrony, and treatment of any underlying causes. Treatment focuses on correcting electrolyte abnormalities (specifically potassium, magnesium and calcium) administering antiarrhythmics, sedation, and cooling3<\/sup>. In refractory cases, catheter-directed ablation can be utilized. Although adenosine will not terminate JET, it may slow down the rhythm enough to confirm the absence of p waves, helping to distinguish it from other tachyarrhythmias. \r\n\r\nTreatment of JET includes the following1-4<\/sup>: \r\n1.\tReplace potassium, magnesium, and calcium as needed \r\n2.\tCorrect acid-base status (especially metabolic acidosis) \r\n3.\tDecrease inotropic agents if appropriate \r\n4.\tAvoid\/treat fever and consider instituting mild therapeutic hypothermia (34-35 degrees)\r\n5.\tAmiodarone (loading dose: 5mg\/kg over 30 minutes or slower, infusion 10-20mg\/kg\/day)\r\n6.\tConsider sedation (i.e. dexmedetomidine) to reduce sympathetic tone \r\n7.\tPacing to restore AV synchrony \r\n\r\nStudies have found other common agents used in anesthetic practice may be helpful in management, such as dexmedetomidine. In a recent study, prophylactic dexmedetomidine significantly lowered the rate of postoperative JET compared to placebo (3.3% versus 16.7%)4<\/sup>. Pacing can restore AV synchrony, suppressing the junctional automaticity, allowing for improvement in hemodynamics1<\/sup>. \r\n\r\nAcross major pediatric cardiac critical care centers, both medication and pacing are the most commonly utilized treatments. It is important to note that there may be significant variation in institutional practices for JET management. For example, although amiodarone is widely considered the first-line drug5<\/sup>, other medications, such as procainamide, are also used successfully. Cooling was used less frequently and typically in conjunction with other therapies, rarely as the sole management strategy4<\/sup>. \r\n\r\nThe correct answer is choice A, AV sequential pacing. The serum magnesium is within normal limits, and other treatment modalities are warranted prior to considering catheter-directed ablation for post-operative JET. \r\n\r\n \r\nREFERENCES \r\n\r\n1.\tHoffman, TM., Bush, DM., Wernovsky, G., et al. Postoperative junctional ectopic tachycardia in children: incidence, risk factors, and treatment. Ann Thorac Surg<\/em> 2002; 74(5): 1607-1611 \r\n2.\tSasikumar, N., Kumar, RK., Balaji, S. Diagnosis and management of junctional ectopic tachycardia in children. Ann of Pediatr Cardiol<\/em>. 2021; 14: 372-381\r\n3.\tKim, ME., Baskar, S., Janson, CM., et al. Epidemiology of postoperative junctional ectopic tachycardia in infants undergoing cardiac surgery. Ann Thorac Surg<\/em>. 2024; 117: 1178-1186 \r\n4.\tEl Amrousy, DM., Elshmaa, NS., El-Kashlan, M., et al. Efficacy of prophylactic dexmedetomidine in preventing postoperative junctional ectopic tachycardia after pediatric cardiac surgery. J Am Heart Assoc<\/em>. 2017; 6(3): e004780 \r\n5.\tEntenmann A, Michel M, Herberg U, et al. Management of postoperative junctional ectopic tachycardia in pediatric patients: a survey of 30 centers in Germany, Austria, and Switzerland. Eur J Pediatr<\/em>. 2017;176(9):1217-1226. doi:10.1007\/s00431-017-2969-x\r\n”,”hint”:””,”answers”:{“srx8p”:{“id”:”srx8p”,”image”:””,”imageId”:””,”title”:”A.\tAtrioventricular sequential pacing”,”isCorrect”:”1″},”q0x42″:{“id”:”q0x42″,”image”:””,”imageId”:””,”title”:”B.\t30mg\/kg IV magnesium sulfate”},”vtbhr”:{“id”:”vtbhr”,”image”:””,”imageId”:””,”title”:”C.\tConsult electrophysiology (EP) team for catheter ablation”}}}}}}

{“questions”:{“0bt44”:{“id”:”0bt44″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Amy Babb, MD AND Amanpreet Kalsi, MBBS, FRCA – Vanderbilt University Medical Center – Monroe Carell Jr. Children’s Hospital at Vanderbilt \r\nA 1-year-old patient is diagnosed with congenitally corrected transposition of the great arteries (cc-TGA) with intact ventricular septum and no pulmonary stenosis. Which of the following is the MOST appropriate initial surgical strategy with the end-goal of complete anatomic correction?”,”desc”:”EXPLANATION \r\nCongenitally corrected transposition of the great arteries (cc-TGA) or L-TGA is defined by the presence of both atrioventricular and ventriculoarterial discordance secondary to abnormal looping of the ventricles during embryologic development. The abnormal looping results in normally positioned atria, with the morphologic left ventricle (LV) in the subpulmonary position and the morphologic right ventricle (RV) in the subaortic position. The great vessels are L-looped with the aorta anterior and to the left of the pulmonary artery. Although this results in a physiologically \u201cnormal\u201d or \u201ccorrected\u201d circulation, it is associated with long-term morbidity and mortality due to failure of the morphologic right ventricle as the systemic ventricle and the development of tricuspid regurgitation.\r\n\r\n\r\nL-TGA is commonly associated with other cardiac lesions including a ventricular septal defect (VSD), subpulmonary stenosis, an \u201cEbstein-like\u201d tricuspid valve and conduction system anomalies. Roughly 75% of patients with cc-TGA will have a VSD and require surgical repair. A common approach involves restoring the morphologic LV as the systemic ventricle with a Rastelli approach and an atrial switch.^{1<\/sup> When a VSD is present, anatomic correction and VSD closure is predictably tolerated because the LV has been exposed to systemic pressures via the VSD. \r\n\r\n\r\nConversely, approximately 25% of patients with cc-TGA have an intact ventricular septum with a variable clinical course, ranging from minimal heart failure symptoms to significant RV dysfunction, tricuspid regurgitation and early death without surgical intervention.2<\/sup> Unfortunately, it remains difficult to predict which patients will develop heart failure, leading some experts to advocate for early surgical intervention to restore \u201cnormal cardiac anatomy\u201d.3<\/sup> The double switch operation describes one such approach where both an atrial baffle (Senning\/Mustard procedures) and arterial switch result in the morphologic left ventricle as the systemic ventricle.1<\/sup> \r\n\r\n\r\nFor the double switch operation to be successful, the morphologic left ventricle must be able to support a full cardiac output with normal systemic vascular resistance. However, the LV of patients born with cc-TGA and intact ventricular septum involutes within a few weeks of life due to the rapidly falling pulmonary vascular resistance, and may become unable to pump against a higher afterload if acutely challenged.3<\/sup> As a result, the first surgical procedure for these patients should be pulmonary artery (PA) band placement to increase morphologic LV afterload and stimulate muscle growth prior to pursuing a double switch procedure.1-4<\/sup> Some patients will require multiple PA band titrations before the LV is considered adequate for a double switch procedure.3<\/sup> Older patients have a lower likelihood of successful LV re-training, but some experts still advocate for PA banding in an effort to preserve tricuspid valve competence,2,4<\/sup> as the increased afterload to the subpulmonic ventricle creates septal shift, improving the morphological RV geometry. \r\n\r\n\r\nThe double switch operation would not be a successful option in a 1 year-old with cc-TGA and intact ventricular septum due to potential LV \u201cdetraining\u201d and a central shunt is not appropriate in a child with biventricular circulation without outflow stenoses or septation defects. \r\n\r\n\r\n \r\nREFERENCES \r\n1.\tMainwaring R, Hanley F. Double Switch With Hemi-Mustard and Bidirectional Glenn Procedure for \u201cAnatomical\u201d Repair of Corrected Transposition. Operative Techniques in Thoracic and Cardiovascular Surgery<\/em>. 2013; 18(3): 171 \u2013 189. \r\n\r\n2.\tCui H, Hage A, Piekarski B, Marx G, et al. Management of Congenitally Corrected Transposition of the Great Arteries with Intact Ventricular Septum: Anatomic Repair or Palliative Treatment?Circulation: Cardiovascular Interventions<\/em>. 2021; 14(7): Page e010154. \r\n\r\n3.\tMac Felmly L, Mainwaring RD, Ho DY, Arunamata A, Algaze C, Hanley FL. Results of the Double Switch Operation in Patients Who Previously Underwent Left Ventricular Retraining.World J Pediatr Congenit Heart Surg<\/em>. 2024;15(3):279-286. doi:10.1177\/21501351231224329 \r\n\r\n4.\tMainwaring R, Patrick W, Arunamata A. et al. Left Ventricular Retraining in Corrected Transposition: Relationship between Pressure and Mass. The Journal of Thoracic and Cardiovascular Surgery<\/em>. 2020; 159(6): 2356-66. \r\n\r\n”,”hint”:””,”answers”:{“gf24w”:{“id”:”gf24w”,”image”:””,”imageId”:””,”title”:”A.\tDouble switch operation”},”x9cr9″:{“id”:”x9cr9″,”image”:””,”imageId”:””,”title”:”B.\tCentral shunt placement “},”glhph”:{“id”:”glhph”,”image”:””,”imageId”:””,”title”:”C.\tPulmonary artery banding”,”isCorrect”:”1″}}}}}}

{“questions”:{“ek71w”:{“id”:”ek71w”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Amy Babb, MD – Vanderbilt University Medical Center AND\r\nKaitlin Flannery, MD – Stanford University \r\n\r\nAn infant with Tetralogy of Fallot, pulmonary atresia and major aortopulmonary collateral arteries (TOF\/PA\/MAPCAs) presents for unifocalization. An intraoperative pulmonary artery flow study is requested by the surgeon. Which hemodynamic value obtained during the flow study is MOST likely to predict a successful repair with VSD closure and RV-PA conduit after unifocalization?\r\n”,”desc”:”EXPLANATION \r\nTOF\/PA\/MAPCAs describes a heterogeneous type of congenital heart disease with an outlet ventricular septal defect (VSD), pulmonary atresia (PA) and variable sources of pulmonary blood flow via collateral vessels. Standard surgical repair involves unifocalization of MAPCAs to form a reconstructed pulmonary artery tree using both native and homograft tissue. After the pulmonary arteries have been unifocalized, the next step consists of closure of the VSD and addition of an RV-PA conduit. Some patients will undergo unifocalization with complete intracardiac repair in one procedure, while others will require a staged approach.\r\n\r\nIt remains difficult to predict if a newly reconstructed pulmonary artery bed will be adequate to accommodate a full cardiac output after VSD closure. An insufficient pulmonary bed will result in elevated right ventricular systolic pressure (RVSP) and RV failure. Methods of predicting successful intracardiac repair based on anatomic metrics, such as neopulmonary artery index and pulmonary segment artery ratio, have been tried. In 2009, a study by Honjo et al concluded that a mean pulmonary artery pressure (mPAP) less than 30 mmHg at a cardiac index of 2.5 L\/min\/m^{2<\/sup> could predict a reasonable RV pressure after unifocalization with VSD closure better than anatomic characteristics.1<\/sup> In 2016, Zhu et al demonstrated that VSD closure with mPAP greater than 25 mmHg on flow study is a predictor of mortality following unifocalization.2<\/sup>\r\n\r\nIntraoperative pulmonary artery flow study is performed after PA unifocalization. The surgeon will place an aortic-sized cannula into the newly reconstructed PAs for flow from the cardiopulmonary bypass circuit.3<\/sup> A small needle is placed into the PAs and attached to pressure tubing with a transducer to monitor PA pressures. The anesthesiologist will ventilate the lungs while the perfusionist ramps up flows into the pulmonary arteries with the goal of achieving a cardiac index of 2.5 \u2013 3.0 L\/min\/m2<\/sup>. Ventilation with tidal volumes of 2-5 mL\/kg with respiratory rate of 30-35 breaths\/min will simulate normal cardiopulmonary interactions.4<\/sup> If mPAPs are higher than 25-30 mmHg at the target cardiac index, the right ventricle will likely struggle with VSD closure. Significant bleeding from the reconstructed PAs should be ruled out for an accurate interpretation. Flow studies have been shown to have reasonable correlation with post-operative RVSP, and be a better predictor than simple anatomic assessments.1<\/sup> Alternative strategies to VSD closure after failed flow study include central shunt placement or VSD closure with fenestration. \r\n\r\n\r\n \r\nREFERENCES \r\n\r\n1.\tHonjo O, Al-Radi O, MacDonald C, Tran K. et al. The Functional Intraoperative Pulmonary Blood Flow Study is a More Sensitive Predictor than Preoperative Anatomy for Right Ventricular Pressure and Physiologic Tolerance of Ventricular Septal Defect Closure after Complete Unifocalization in Patients with Pulmonary Atresia, Ventricular Septal Defect, and Major Aortopulmonary Collaterals. Circulation<\/em>. 2009; 120(11) supp 1: s46-s52. \r\n2.\tZhu J, Meza J, Kato A, et al. Pulmonary flow study predicts survival in pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries. J Thorac Cardiovasc Surg<\/em>. 2016; 152(6):1494-1503.e1. doi:10.1016\/j.jtcvs.2016.07.082 \r\n3.\tMargetson TD, Sleasman J, Kollmann S, McCarthy PJ, et al. Perfusion Methods and Modifications to the Cardiopulmonary Bypass Circuit for Midline Unifocalization Procedures. J Extra Corpor Technol<\/em>. 2019; 51(3):147-152. \r\n4.\tQuinonez ZA, Laura D, Abbasi RK, et al. Anesthetic management during surgery for tetralogy of Fallot with pulmonary atresia and major aortopulmonary collateral arteries. World J Pediatr Congenit Heart Surg<\/em>. 2018; 9(2): 236-41.\r\n”,”hint”:””,”answers”:{“ojlgz”:{“id”:”ojlgz”,”image”:””,”imageId”:””,”title”:”A.\tmPAP less than 15 mmHg at 1.5 L\/min\/m2″},”iiqbf”:{“id”:”iiqbf”,”image”:””,”imageId”:””,”title”:”B.\tmPAP greater than 30 mmHg at 2.5 L\/min\/m2″},”8vfaa”:{“id”:”8vfaa”,”image”:””,”imageId”:””,”title”:”C.\tmPAP less than 25 mmHg at 3.0 L\/min\/m2\r\n\r\n”,”isCorrect”:”1″}}}}}}

{“questions”:{“yl7ni”:{“id”:”yl7ni”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Amy Babb, MD AND Amanpreet Kalsi, MBBS, FRCA – Vanderbilt University Medical Center – Monroe Carell Jr. Children’s Hospital at Vanderbilt \r\n\r\nA teenage boy with history of dilated cardiomyopathy supported with a continuous flow left ventricular assist device (LVAD) presents for heart transplant. After separation from cardiopulmonary bypass (CPB), he is hypotensive despite adequate biventricular function, normal central venous pressure, and epinephrine, vasopressin, and norepinephrine infusions. Which of the following factors is MOST likely associated with vasoplegia in this patient?\r\n\r\n”,”desc”:”EXPLANATION \r\nVasoplegia presents as severe hypotension secondary to vasodilation with low systemic vascular resistance (SVR) despite normal or elevated cardiac index. Vasoplegia after cardiac surgery is a known entity associated with significant morbidity and mortality in adults^{1<\/sup>. In addition, vasoplegia immediately post cardiac surgery may be difficult to diagnose when balancing the other potential causes of shock such as myocardial failure or hemorrhage. \r\n\r\nPatients undergoing procedures with CPB are at risk of vasoplegia secondary to multiple proinflammatory insults, including surgical trauma, transfusion, and exposure to foreign materials from the circuit. Patients preoperatively supported with continuous-flow ventricular assist devices (CF-VADs) are at even higher risk for vasoplegia post-transplant2<\/sup>. Proposed mechanisms for this include a unique proinflammatory profile and dysregulation of vasomotor tone thought secondary to continuous flow physiology.\r\n\r\nA study by Sacks et al. in 2019 describes a small cohort of pediatric patients supported preoperatively with either pulsatile or continuous flow ventricular assist devices who met criteria for vasoplegia after orthotopic heart transplant3<\/sup>. One third of all patients were diagnosed with vasoplegia, 79% of which had been supported with a CF-VAD prior to transplant. This article also proposed a definition of pediatric vasoplegia using the typical monitors and parameters seen in pediatric patients. The definition of pediatric vasoplegia published in their study consisted of:3<\/sup>\r\n\r\n1.\tUse of any of the following medications: \r\na.\tNorepinephrine, vasopressin, high dose epinephrine (>0.08 mcg\/kg\/min), or high dose dopamine (>8 mcg\/kg\/min) \r\n2.\tDiastolic blood pressure below the 10th percentile \r\n3.\tSystolic ejection fraction greater than 60% on echocardiogram \r\n4.\tRight atrial or central venous pressure greater than 5 mmHg \r\n5.\tAbsence of positive blood or urine cultures\r\n\r\nThis small study concluded that preoperative continuous-flow ventricular assist devices are a likely risk factor for post-operative vasoplegia after heart transplant in the pediatric population. Because there is no strong consensus on the definition of vasoplegia in either adults or pediatrics4<\/sup>, understanding the risk factors may help with early identification of vasoplegia and prevent delay in treatment. Both dilated cardiomyopathy and pulmonary hypertension may occur concomitantly with vasoplegia, especially in the setting of prolonged CPB, but are not recognized independent risk factors. \r\nREFERENCES \r\n \r\n\r\n1.\tAsleh R, Alnsasra H, Daly RC, et al. Predictors and Clinical Outcomes of Vasoplegia in Patients Bridged to Heart Transplantation With Continuous-Flow Left Ventricular Assist Devices. J Am Heart Assoc<\/em>. 2019;8(22):e013108. doi:10.1161\/JAHA.119.013108 \r\n2.\tPatarroyo M, Simbaqueba C, Shrestha K, et al. Pre-operative risk factors and clinical outcomes associated with vasoplegia in recipients of orthotopic heart transplantation in the contemporary era. J Heart Lung Transplant<\/em>. 2012; 31(3): 282-287. \r\n3.\tSacks L, Hollander S, Zhang Y, et al. Vasoplegia After Pediatric Cardiac Transplantation in Patients Supported with Continuous Flow Ventricular Assist Devices. The Journal of Thoracic and Cardiovascular Surgery<\/em>. 2019; 157(6): 2433 \u2013 2440. \r\n4.\tOrtoleva J, Cobey F. A Systematic Approach to the Treatment of Vasoplegia Based on Recent Advances in Pharmacotherapy. Journal of Cardiothoracic and Vascular Anesthesia<\/em>. 2019; 33(5): 1310 \u2013 1314.\r\n\r\n”,”hint”:””,”answers”:{“6alp6”:{“id”:”6alp6″,”image”:””,”imageId”:””,”title”:”A.\tPreoperative continuous flow LVAD support”,”isCorrect”:”1″},”k7ybv”:{“id”:”k7ybv”,”image”:””,”imageId”:””,”title”:”B.\tHistory of dilated cardiomyopathy”},”0ufj3″:{“id”:”0ufj3″,”image”:””,”imageId”:””,”title”:”C.\tPost-operative pulmonary hypertension”}}}}}}